9 C 9605231 F 6972 Adbd

EFFECTS OF THE MENSTRUAL CYCLE AND ORAL CONTRACEPTIVES
ON ATHLETIC PERFORMANCE
by
CONSTANCE MARIE THERESE LEBRUN
B.Sc., University of Manitoba, 1976
M.D.C.M., McGill University, 1981
A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF

THE REQUIREMENTS FOR THE DEGREE OF
MASTER OF PHYSICAL EDUCATION
in
THE FACULTY OF GRADUATE STUDIES
Department of Sport Science
School of Physical Education
We accept this thesis as conforming to the required standard:
THE UNIVERSITY OF BRITISH COLUMBIA

December, 1991
Constance Marie Lebrun, 1991
In presenting this thesis in partial fulfilment of the requirements for an advanced

degree at the University of British Columbia, I agree that the Library shall make it
freely available for reference and study. I further agree that permission for extensive
copying of this thesis for scholarly purposes may be granted by the head of my
department or by his or her representatives. It is understood that copying or
publication of this thesis for financial gain shall not be allowed without my written
permission.
(Signature
Department of
The University of British Columbia

Vancouver, Canada
Date
DE-6 (2/88)
99(
11
ABSTRACT:
There have been few well-controlled studies to date on the influence of different phases
of the menstrual cycle on athletic performance, and information is even more sparse on potential
effects of oral contraceptive agents (OCAs) on performance. Many of the earlier studies failed
to accurately document the phase of the cycle, or used a variety of different oral contraceptives
with higher dosages of estrogens and progestins than those in current usage. Thus, the purpose
of this study was to examine the effects of the endogenous hormonal variations of a normal
menstrual cycle and the administration of a low-dose triphasic oral contraceptive agent (OCA)
on selected measures of athletic performance in a group of elite female athletes. Nineteen
eumenorrheic women were studied during the midfollicular (day 5.7 0.5; mean + SE) and
midluteal (day 23.3 0.9) phases of a normal menstrual cycle. Cycle phases were confirmed by
plasma estradiol and progesterone assays. Following the two menstrual cycle tests, subjects were
randomly assigned in a double blind fashion to either a placebo group (n=7, age=28.3 + 1.6 yr,
height=168.6 2.0 cm, weight=60.0 3.5 kg) or an OCA group (n=7, age=27.1 1.6 yr,
height=168.5 1.9 cm, weight=60.2 1.7 kg). A third test was carried out during the midcycle
(day 14.4 0.54) of the second cycle of the placebo/OCA administration.
In the 16 women with hormonal evidence of ovulation, no significant differences were
observed between the follicular phase and luteal phase tests in weight, percent body fat, sum of
skinfolds, maximum heart rate, maximum minute ventilation, maximum respiratory exchange
ratio, anaerobic performance, endurance time to fatigue (at 90% of V0 2..), or isokinetic strength
of knee flexion and extension. There was, however, a small decrease seen from the follicular to
the luteal phases in absolute V0 2..; from 3.19 0.09 lmin -1 to 3.13 0.08 1.min -1 (p=0.04),
iii
as well as in relative V0 2,,,,; from 53.7 0.9 mlkg -i min-1 to 52.8 0.8 mlkg -i min-1 (p=0.06).
There was a very slight increase in both hemoglobin and hematocrit during the luteal phase.
With regards to the effect of the OCA on performance, there was a significant difference
in the responses of the two groups while on medication or placebo, in both absolute V0 2..
(p=0.05) and in relative V0 2,. (p=0.02). The 7 subjects on OCA had a slight decrease in
maximal oxygen consumption from follicular phase values to the third test (absolute VOA :
3.29 0.12 lmizi l to 3.18 + 0.09 limin 4 ; relative VO2, ax : 54.7 + 1.2 mlkg -l min- i to 52.0 + 1.0
mlketnin -1 ); while the 7 women on placebo showed a slight increase over the same time period
(absolute V02.: 3.16 0.15 Lmin -1 to 3.18 0.13 lmin 1 ; relative V02.: 53.0 1.1 mlkg
nnin4 to 53.8 1.7 mlkg -l min-1 ). Weight and percent body fat did not vary significantly in -i
either group, but the sum of skinfolds changed differentially with a significant increase (p<0.01)
in the OCA group as compared to placebo. There were no associated alterations in maximum
heart rate, maximum respiratory exchange ratio, maximum minute ventilation, hemoglobin
concentration or hematocrit as a consequence of OCA administration. There were no significant
differences over all three tests between the two groups in anaerobic performance, endurance time
to fatigue, or isokinetic strength of knee flexion and extension.
There were, therefore, no statistically significant changes in selected physiological
variables or in the majority of the tests of performance occurring as a function of either the phase
of the menstrual cycle or administration of a low-dose triphasic OCA. However, the small
decreases in V0 2. during the luteal phase and while on OCA suggest that the female steroid
hormones, estrogen and progesterone, both endogenous and exogenous, may exert a slight
deleterious effect on aerobic capacity with potential implications for elite level performance.
iv
TABLE OF CONTENTS:
ABSTRACT ^
ii
TABLE OF CONTENTS ^
iv
LIST OF SYMBOLS ^
vi
LIST OF TABLES ^
LIST OF FIGURES ^
viii
ix
ACKNOWLEDGEMENTS ^
DEDICATION ^
xi
INTRODUCTION ^
METHODS AND MATERIALS ^

SUBJECTS ^
EXPERIMENTAL PROTOCOL ^
BODY COMPOSITION ^
BLOOD SAMPLES ^
AEROBIC CAPACITY ^
ANAEROBIC PERFORMANCE ^
ENDURANCE PERFORMANCE ^
ISOKINETIC STRENGTH ^
8
8
11
12
12
13
14
14
15
STATISTICAL ANALYSIS ^
15
RESULTS ^
SUBJECTS ^
GROUPS ^
EFFECT OF MENSTRUAL CYCLE PHASE ^
BODY COMPOSITION ^
BLOOD TESTS ^
EXERCISE PERFORMANCE ^
EFFECT OF THE ORAL CONTRACEPTIVE: ^
BODY COMPOSITION ^
BLOOD TESTS ^
17
17
17
20
20
23
23
25
25
26
26
DISCUSSION ^
EFFECTS OF MENSTRUAL CYCLE PHASE ^
BODY COMPOSITION ^
BLOOD TESTS ^
EFFECTS OF THE ORAL CONTRACEPTIVE ^
BODY COMPOSITION ^
BLOOD TESTS ^
33
33
34
35
36
42
42
43
43
SUMMARY ^
48
REFERENCES ^
50
APPENDIX A. REVIEW OF LITERATURE ^

NATURE OF THE PROBLEM/IMPORTANCE OF TOPIC ^
EFFECT OF THE MENSTRUAL CYCLE ON PERFORMANCE ^
BACKGROUND AND EARLY STUDIES ^
STUDIES WITHOUT HORMONAL DOCUMENTATION. ^
STUDIES UTILIZING SERUM PROGESTERONE MEASUREMENTS ^
CARDIOVASCULAR AND HEMODYNAMIC RESPONSES ^
TEMPERATURE REGULATION AND HEAT EXCHANGE ^
RESPIRATORY DRIVES AND VENTILATION ^
METABOLIC RESPONSES ^
EFFECTS OF ORAL CONTRACEPTIVES ON PERFORMANCE ^
BACKGROUND ^
CARDIOVASCULAR AND HEMODYNAMIC RESPONSES ^
RESPIRATORY DRIVES AND VENTILATION ^
METABOLIC RESPONSES ^
EFFECTS OF ORAL CONTRACEPTIVES ON EXERCISE
PERFORMANCE ^
59
59
63
63
66
69
71
74
75
77
80
80
81
81
82
83
APPENDIX B. RAW DATA ^
86
LIST OF SYMBOLS:
ADH^.ântidiuretic hormone
AST^.ânaerobic speed test
ATP^.âdenosine triphosphate
BBT^.^basal body temperature
bpm^.^beats per minute
C^
Centigrade
Cl'^.^chloride ion
CO2^.^carbon dioxide
CP^.^creatine phosphate
ECG^ electrocardiogram
ET^ endurance time to fatigue
F^
follicular phase
FFA^ free fatty acids

FO^ force output
GH^ growth hormone
Ir^
hydrogen ion
Hct^ hematocrit
HCVR^hypercapnic ventilatory response
Hg^^mercury
Hgb^ hemoglobin
vii
HR(max)^
maximum heart rate
HVR^
hypoxic ventilatory response
IOC^
International Olympic Commission
luteal phase
LH^
luteinizing hormone
MPA^medroxy-progesterone acetate
MVC^maximal voluntary contraction
Na+^sodium ion
/in^ newton meter
02ôxygen
OCA^ oral contraceptive agent
pH^ negative logarithm of 11+ concentration
RER(max)^maximum respiratory exchange ratio
RX^ treatment
SE^
standard error
''CO2^carbon dioxide production
VEêxpired minute ventilation

VE(max)^maximum minute ventilation
VO2ôxygen uptake
V02.^maximal oxygen consumption
viii
LIST OF TABLES:
TABLE I. SUBJECT PROFILES AND HORMONAL VALUES ^ 18
TABLE Ha. EFFECT OF MENSTRUAL CYCLE PHASE ON ANTHROPOMETRIC,
HORMONAL AND HEMATOLOGICAL VARIABLES ^ 21
TABLE Hb. EFFECT OF MENSTRUAL CYCLE PHASE ON PERFORMANCE
VARIABLES ^
22
TABLE Ella. EFFECT OF CYCLE PHASE AND OCA ON ANTHROPOMETRIC,

HORMONAL AND HEMATOLOGICAL VARIABLES ^ 30
TABLE Mb. EFFECT OF CYCLE PHASE AND OCA ON PERFORMANCE
VARIABLES ^
31
ix
LIST OF FIGURES:
FIGURE 1. EFFECT OF MENSTRUAL CYCLE PHASE ON V0 2,. ^ 24
FIGURE 2. EFFECT OF TREATMENT ON SUM OF SKIN FOLDS ^ 28
FIGURE 3. EFFECT OF TREATMENT ON V0 2.,, ^
29
ACKNOWLEDGEMENTS:
The realization of a project of this magnitude seems viable when it is first conceived,
totally insurmountable in the middle of it, and nothing short of miraculous when it is finally
achieved. I would like to gratefully recognize the contributions of the many people who have
encouraged me along the way, through numerous setbacks including personal injury and illness.
Special acknowledgment must go to all of my advisors, but especially to my committee
chairman, Dr. Don McKenzie, for his endless patience and guidance over the past five years. I
am deeply indebted as well to Dr. Jerilynn Prior, and to her research nurse, Yvette Vigna, for
their advice and suggestions. Their enthusiasm for research on the female athlete, and their
experience and knowledge on this subject were invaluable to me. Particular thanks also go to Dr.
Jack Taunton for his cheerful optimism and his role as a mentor in sports medicine. Both he and
Dr. Stan Herring from Seattle deserve much credit for my continuing and improving good health.
My close friends have played a singular role in this process, and I would like to thank
Alison Forbes for her dependable good humor and continued belief in me, and my secretary Pat
Morgan for her wonderful ability to keep both me and my office functioning and my patients
placated during my many absences. Dr. Bill Milsom also deserves very special appreciation for
his selfless and unquestioning moral support over the past year, and for his attempts to make me
share his ardour for the entire research process. Finally, I am totally indebted to all of my
subjects, who faithfully kept their basal body temperature charts and their training logs, and ran
their hearts out on the treadmill for me, not just once, but three times. This project was assisted
by financial support from Sport Canada, and from Syntex, Inc. In addition, I am grateful to
Dusan Benicky and Dr. Ted Rhodes for their technical assistance and laboratory support.
xi
DEDICATION:
This work is dedicated to my parents: to my mother, who is always interested in and

supportive of my many endeavors, even when they lie outside her realm of experience; and to
my father, from whom I must have inherited this penchant for higher education and academia.
1
EFFECTS OF THE MENSTRUAL CYCLE AND ORAL CONTRACEPTIVES
ON ATHLETIC PERFORMANCE
INTRODUCTION:
From the time of the ancient Greeks and Romans, the athletic arena has historically been
regarded as a male domain. Indeed, it has only been since the beginning of the 20th century that
women have been participating in both recreational and competitive sport in significant numbers.
Today's female athlete is just as likely as her male counterpart to be testing the limits of her
physical capabilities, and engaging in strenuous and prolonged training programs in order to
achieve her best performance in elite sport. While the mechanisms of pulmonary, cardiovascular
and cellular adaptations to an exercise stimulus are continually being explored by the sport
scientist, much less is known about how the special physiological and hormonal variations of the
female athlete interact with these functions. The majority of research on the female athlete has
focused on the links between rigorous physical training and delayed menarche, alteration of
normal pubertal progression, shortened luteal phase, anovulation, athletic amenorrhea and
reversible infertility (see Highet, 1989; Loucks and Horvath, 1985; Loucks, 1991; Prior and
Vigna, 1985; Prior and Vigna, 1991). By comparison, the influence of these hormonal cycles on
physiological and exercise variables has not been studied extensively (Albohm, 1976). The female
athlete, from puberty through pregnancy and childbirth, to menopause and beyond, has to contend
with a shifting spectrum of hormonal alterations that have potential to affect performance,
especially at the elite level.
Considerable interest has also been generated lately in the usage of certain medications,
2
particularly anabolic steroids, for performance enhancement. Oral contraceptives contain potent
synthetic steroid hormones, albeit in minute quantities, yet relatively little is known about the
metabolic consequences of their administration. A significant number of elite female athletes are
prescribed the birth control pill at various times during their competitive careers, whether it be
for purposes of contraception, cycle regulation, control of dysmenorrhoea, or more recently, for
hormonal replacement in women with chronic amenorrhea (Shangold, 1988, 1990). Some
concerns have been expressed by others (Prior and Vigna, 1985) about this latter usage of OCAs
in women who already have a suppressed hypothalamic-pituitary axis. Side effects such as weight
gain and fluid retention, and long term risks related to cardiovascular disease, thromboembolism,
and alterations in lipid profiles have been substantially reduced by the newer low-dose triphasic
preparations. The question of potential effects of oral contraceptive agents (OCAs) on athletic
performance has not been answered conclusively; given the common usage of OCAs by athletes,
there may be profound implications for training and competition.
Early studies of the influence of the menstrual cycle on sport performance are largely
retrospective and anecdotal. Furthermore, their classifications of menstrual cycle phase were done
without any knowledge of actual levels of the ovarian hormones, and are consequently inaccurate,
and potentially misleading. The assumption that ovulation, and therefore a luteal phase occur if
the cycle is "regular" (i.e. 28 days long), is unfounded, but unfortunately widely held, even by
some modern-day researchers. With this in mind, in analyzing the impact of the "phase" of the
menstrual cycle on physical performance, investigators have documented no perceived influence
of cycle phase in 37% to 63% of athletes surveyed (Erdelyi, 1962; Ingman, 1953; Kral and
Markalous, 1937; Zaharieva, 1965). Estimates of cycle phase detriment range from 8% during
3
the menstrual phase (Kral and Markalous, 1937) to a high of 59% during the premenstrual phase
(Rougier and Linquette, 1962). In one study (Ingman, 1953), 24% of athletes did not ordinarily
compete during menses because of pain and/or fatigue. Performance was purportedly enhanced
during the menstrual phase in 13% (Erdelyi, 1962) to 29% (Kral and Markalous, 1937) of the
women surveyed. These results are both interesting and contradictory, but it is important to keep
in mind the notorious unreliability of such retrospective studies.
Early attempts to quantify this perceived difference in performance are marked with
discrepancies in the timing of the testing, as well as inadequate documentation (either by basal
body temperature monitoring or by serum progesterone measurements) of the cycle phase. The
testing procedures have usually involved either treadmill or cycle ergometry, and have measured
V02
or submaximal cardiorespiratory responses employing a variety of protocols. Many of the
studies have used relatively untrained subjects, or extremely small numbers. Some investigators
have found little or no difference in performance at various times during the menstrual cycle
(Allsen et al., 1977; De Bruyn-Prevost et al., 1984; Doolittle and Engebretsen, 1972; Gamberale
et al., 1975; Garlick and Bernauer, 1968; Stevenson et al., 1982a, 1982b). Others have
documented a decrement in performance in the premenstrual (Erdelyi, 1962) or menstrual phase
(Wearing et al., 1972), and the best performances in the intermenstrual (Erdelyi, 1962; Wearing
et al., 1972) or postmenstrual phases (Erdelyi, 1962, Fox et al., 1977). There have also been
several "field studies" (Bale and Nelson, 1985; Brooks-Gunn et al., 1986; Fomin et al., 1989;
Quadagno et al., 1991) with inconclusive results.
Of the studies that have utilized serum progesterone to confirm the luteal phase, only one
group of investigators (Jurkowski et al., 1978, 1981) has shown a dramatically significant change
4
in any measurable test of performance. In 9 moderately trained females (mean V0 2
of 42.8
1.7 mlIcemin -1 ), the time to exhaustion on a bicycle ergometer at 90% of 110 2. was
increased from 1.57 0.32 to 2.97 0.63 minutes in the luteal phase. Subsequent attempts to
explain this enhancement of endurance performance have focused on various aspects of substrate
metabolism as reflected by measurements of blood lactate and glucose, free fatty acids, insulin
and growth hormone (GH) responses, and glycerol and cortisol (Bonen et al., 1983; Lamont,
1986; Lavoie et al., 1987; Reinke et al., 1972; Sutton et al., 1980). Glycogen uptake and storage
in both liver and muscle have been shown to be facilitated by high concentrations of estradiol,
both in animal studies (Ahmed-Sorour and Bailey, 1981; Kendrick et al., 1987; Matute and
Kalkhoff, 1973) and in humans (Nicklas et al., 1989). Other metabolic actions of estradiol with
a potential impact on performance include effects on lipid availability and utilization, as well as
gluconeogenesis (Bunt, 1990). Progesterone has been shown in both men and women to cause
a shift in substrate metabolism towards a greater dependence on fat, as manifest by lower
respiratory exchange ratio (RER) values, and lower blood lactate levels during submaximal
exercise (Dombovy et al., 1987). However, with the exception of one study (Nicklas et al., 1989)
that found a strong tendency (p=0.07) towards an increase in endurance during the luteal phase,
no other group has successfully replicated the findings of Jurkowski et al., (1977, 1981) of
enhanced luteal phase performance in athletes.
Other researchers have examined the resting respiratory drives as a function of cycle
phase (Schoene et al., 1981). It has been shown that an increase in both hypoxic and hypercapnic
respiratory drives, as well as in minute ventilation, occurs under the influence of the increased
progesterone levels seen during the luteal phase (Schoene et al., 1981; Dombovy et al., 1987).
5
These changes can also be seen in men who are given a synthetic progesterone, medroxyprogesterone acetate (MPA) (Bonekat et al., 1987). Others (Regensteiner et al., 1989, 1990) have
suggested that the presence of estrogen potentiates these effects by its action on progesterone
receptors. Nevertheless, there have been no associated alterations in either V0 2,,,x or endurance
performance in the athletes, both male and female, involved in these studies. A recent study (De
Souza et al., 1990) reinforced the impression of no menstrual cycle influence on maximal and
submaximal exercise performance in a group of elite female athletes, but contrary to these earlier
studies, did not find any variation in minute ventilation.
Similarly, hormonally-mediated fluctuations have been documented throughout the
menstrual cycle in plasma volume and hemoglobin concentration (Gaebelein and Senay, 1982;
Jurkowski et al., 1981), as well as in body temperature (Hessemer and Bruck, 1985a, 1985b;
Wells and Horvath, 1973, 1974), but without any significant corresponding impact on
performance. From these and other studies (Stephenson et al., 1982a, 1982b), there appears to
be a dissociation of the hemodynamic and thermoregulatory responses to exercise during the
menstrual cycle from specific metabolic aspects of athletic performance.
Most of the research to date has concentrated on cardiopulmonary changes, and very little
information exists on any differential strength gains as a function of cycle phase. The studies that
have been carried out, as a rule, have not used either basal body temperature (BBT) monitoring
or measurement of serum progesterone to accurately document the cycle phase. The evidence to
date, albeit somewhat limited, suggests that isometric strength, as measured by maximum
voluntary contraction (MVC) of grip strength, is actually decreased during the luteal phase (Wirth
and Loman, 1982), and that there also appears to be a decrease in isometric endurance potentially
6
related to an increase in deep muscle temperature during this phase of the cycle (Petrofsky et al.,
1975, 1976). Other more recent studies (Dibrezzo et al., 1991, Quadagno et al., 1991) have failed
to demonstrate any meaningful changes across the menstrual cycle in either isokinetic strength
or maximal weight for bench press or leg lifts.
Surprisingly, even less is known about the effects of OCAs on any of the common indices
of athletic performance. The few anecdotal or retrospective studies that have been carried out are
inconclusive, and one even reported a performance enhancement in 8% of respondents (Bale and
Davies, 1983). Early controlled trials are difficult to interpret because of the diversity in both the
estrogen and progestin components of the OCA used, as well as in the range of fitness of the
subjects involved. It has been suggested by some that there is a decrease in VO2mu in subjects
taking an OCA (Daggett et al., 1983), in conjunction with a significant reduction in mitochondrial
citrate, but no associated alterations of post-exercise muscle glycogen or lactate. Other groups
of investigators maintain that there is no significant effect of OCAs (Huisveld et a., 1983;
McNeil and Mozingo, 1981), but they have only studied cross-sectional populations of exercising
females. Furthermore, none of these early studies have been carried out with the OCA most
frequently utilized today, a low-dose triphasic formulation. The only prospective investigation
to date involving such an OCA has also shown a slight, but statistically significant reduction in
functional aerobic capacity after a 6 month period on a low-dose monophasic OCA, that was
reversible upon discontinuation of the medication (Notelovitz et al., 1987). In terms of muscle
strength, extrapolation from the known effects of anabolic steroids might suggest that the
androgenic component of OCAs could have some positive effects, but the studies to date
(Petrofsky et al., 1976; Wirth and Loman, 1982) do not substantiate this premise, and in fact,
7
refute it to some degree.
Thus it can been seen that investigators are not in agreement on the effects of either the
phase of the menstrual cycle, or the administration of OCAs, on athletic performance. This study
was therefore undertaken to examine the performance of a group of elite female athletes using
four commonly utilized physiological measures: aerobic capacity (maximum oxygen consumption
or V02.), anaerobic capacity, aerobic endurance at 90% of V0 2., and isokinetic strength. The
purpose was to document whether or not the results of these tests are influenced by either the
endogenous hormonal variations during the phases of a normal menstrual cycle, and/or the
exogenous administration of a low-dose triphasic oral contraceptive containing both norethindrone
and ethinyl estradiol.
8
METHODS AND MATERIALS:
SUBJECTS:
Female subjects between the ages of 18 and 40 were recruited by means of advertisement
and word of mouth. Ethical approval was obtained from the Committee on Human
Experimentation of the University of British Columbia, and all subjects signed a written informed
consent. All of the women were having regular menstrual cycles from 24-35 days apart, and had
not taken oral contraceptives for at least three months prior to entering the study. Evidence for
ovulatory cycles was initially obtained by a menstrual history questionnaire determining the
existence of symptoms such as breast tenderness, fluid retention, appetite change, and mood
swings in the one to two weeks preceding a normal menstrual flow. The presence of such
symptoms has been shown to be due to, and thus be an indicator of the luteal phase elevation
in estrogen and progesterone (Prior and Vigna, 1987a). All subjects were "trained", and
participating in some type of regular intensive aerobic activity on a regular basis. In order to
more accurately document small differences in performance attributable to the experimental
conditions, the population of subjects studied was limited to elite female athletes, as defined by
an entrance V0 2
equal to or greater than 50 mlkg i nin-1 . Volunteers were recruited from a
variety of sports including running, cycling, triathlon, squash, cross-country skiing, ultimate
Frisbee, and rowing. An initial screening assessment of the level of their training activities was
carried out at the time of entrance into the study, and fitness level was confirmed at the time of
the first testing. Subjects who, on the first testing, did not meet the required aerobic capacity
were eliminated from the study.
9
A questionnaire was also administered to determine the general health of the subjects, and
to eliminate any potential risk factors for the administration of oral contraceptives. Subjects were
excluded if they were smokers, or if they had any significant past medical history, or were taking
any medication that might interfere with the exercise testing. Those who were on vitamin
supplements, or iron therapy, were asked to maintain the exact dosage throughout the entire
length of the study. Subjects were also required to have a physical examination, including a
pelvic examination and Pap smear, carried out by their own physician. If they experienced any
significant or untoward side effects from the oral contraceptive, they were free to discontinue it,
and withdraw from the study at any time.
Subjects were required to maintain a steady-state level of aerobic training throughout the
experimental period. They were asked to record a daily training log, as well as their basal body
temperature, menstrual and ovulatory symptoms, resting heart rate, weight, and subjective
sensations of performance. Basal body temperature was taken orally, before rising at the same
time of day, and recorded on a standard form, with comments in a separate column to explain
different times or concurrent illness or fever. The intensity and amount of training were reviewed
to ensure that there was no substantial training stimulus over the duration of the study.
Physiological testing was carried out in the midfollicular phase (between days 3 and 8 of
a normal cycle), and in the midluteal phase (between days 4 and 9 after ovulation, as determined
by a sustained rise in basal body temperature of 0.2 to 0.3 degrees Centigrade). These results
were later analyzed by a computerized (Maximina R) least mean squares technique (Prior et al.,
1990b) to determine day of ovulation and length of luteal phase. The estimated phase of the cycle
was verified by comparing the obtained measurements of ovarian hormones to normal values, as
10
follows:
Estradiol (pmo11 -1 ):^follicular range: 37-734 pmo11 -1
midcycle range: 440-1375 pmo1.1 -1 '
luteal range:^55-955 pmo11 4
Progesterone (nmo11 -1 ):^follicular range:0.3-4.8 nmo11 -1
luteal range:^8.0-89 nmolr i
mid-luteal range: 12.1-89 nmol1-1
However, the level of serum progesterone at rest that was required for absolute confirmation of
the luteal phase was greater than 16 nmo11 -1 (Abraham, 1974). Subjects who did not ovulate
during one cycle were followed through the next cycle and tested then after ovulation. If they
did not ovulate during the second cycle, then the first testing (midfollicular phase) was repeated
again prior to testing during the luteal phase. The order of testing during a normal cycle was
random, depending upon when subjects were enrolled in the study.
Following these two tests performed during the menstrual cycle, subjects were randomly
assigned in a double blind fashion to either an OCA (n=8) or a PLACEBO (n=9) group for a
total of two months. The oral contraceptive used in this study was a triphasic formulation
(Synphasic, Syntex, Inc.) and contained two different combinations of ethinyl estradiol and
norethindrone as follows: days 1-7: norethindrone 0.50 mg; days 8-16: norethindrone 1.0 mg.;
and day 17-21: norethindrone 0.50 mg; in combination with a constant concentration of 0.035
mg of ethinyl estradiol from days 1-21. This OCA was chosen because it conformed to prevailing
recommendations of Health and Welfare Canada (1985) in terms of starting patients on a lowdose triphasic preparation. Of the OCAs available at the time that the study was initiated,
11
Synphasic contained the lowest total norethindrone dose (15.0 mg over the 21 day cycle).
Moreover, for purposes of this study, it was deemed more appropriate to utilize an OCA with
a constant estrogen component, and only two different dosages of the progestin, in order to more
closely approximate the two phases of the menstrual cycle that were being studied.
All subjects took an unmarked lactose capsule containing either OCA or placebo, daily
for three consecutive weeks, and then stopped for a week, to simulate regular administration of
the oral contraceptive. This was carried out for a total of two months. They continued to record
both a training log, and their basal body temperature during this time. A third testing (treatment
or RX test) was carried out between days 14 and 17 of the second cycle of the OCA/placebo.
For subjects who were taking the OCA, this corresponded to the higher dose of norethindrone.
For subjects who were taking the placebo, however, this third test could have potentially taken
place during the follicular or luteal phase, or even during the mid-cycle estrogen peak. The
investigators were not aware to which group the subjects had been assigned.
EXPERIMENTAL PROTOCOL:
The experimental protocol was carried out on two successive days, and was virtually
identical for each testing. For the first day of testing, subjects were asked to refrain from any
vigorous exercise during the previous 24 hours, and to report to the laboratory in a rested state,
having fasted and abstained from any caffeine-containing compounds for at least three hours prior
to testing. The height and weight of each subject was measured. Room temperature and
barometric pressure were also recorded. Prior to warm-up, venous blood samples were taken
(Becton-Dickinson EDTA K3 tubes), and subsequently analyzed for estradiol and progesterone,
12
and a complete blood count, as described later. Aerobic capacity (V0 2,..) and anaerobic
performance (AST) were assessed. The second day of testing involved the measurement of
isokinetic strength, aerobic endurance, sum of skinfolds and percent body fat by underwater
densitometry.
BODY COMPOSITION:
Anthropometric measurements included height and weight (Detecto industrial scale),

measurement of skinfold thickness at six different sites (biceps, triceps, subscapular, suprailiac,
anterior thigh and medial calf) with a Harpenden skinfold caliper (John Bull, British Indicators
Ltd); and underwater densitometry using a hydrostatic weighing tank. Skinfold measurements
were simply summed Percentage of body fat was calculated by the method of underwater
densitometry (Brozeck et al., 1963) using the Sin formula (Siri, 1961).
BLOOD SAMPLES:
Venous blood samples were taken prior to any warm-up exercise. They were kept cool
(not refrigerated) for the duration of testing, and then processed as follows at the completion of
the testing: one tube was taken to the Laboratory at the University Hospital, U.B.C. Site, for
determination of an automated blood count (CoulterS + STKR). The remaining blood was spun
down in a refrigerated centrifuge (Damon/IEC Clini-Cool) for 10 minutes at 3000 rpm. The
plasma was then removed and stored in Venoject plain silicone-coated glass tubes at -20 degrees
C until it was subsequently analyzed in the laboratory at the Vancouver ni-nPral Hospital, using
commercially available no-extraction solid-phase ' 251 radioimmunoassays ,.t-A-Count Estradiol
13
and Coat-A-Count Progesterone, Diagnostic Products Corporation). To minimize interassay
variability, samples were coded and analyzed in three separate batches by an independent
observer. All samples from one subject were analyzed together, and at least one subject from
each of the two experimental groups was included in each assay. The intra-as say coefficient of
variations (CV) were 10.6% for estradiol and 10.3% for progesterone. Interassay CV's range
from 4.2% to 8.1% for estradiol and from 7.2% to 10.0% for progesterone (Diagnostic Products
Corporation). The sensitivities of these assays are 2.9 pmo11 -1 for estradiol and 0.16 nmo11 -1 for
progesterone.
AEROBIC CAPACITY:
Following a 5 to 10 minute warm-up at a speed of between 2.2 ms'' and 2.7 ms -1 , the
measurement of V0 2,nu was carried out on a Quinton 24-72 treadmill. The protocol utilized a
continuous progressive workload on a level grade, beginning at a speed of 2.2 ms', and
increasing by 0.22 ms -1 each minute until fatigue (as previously described by Parkhouse et al.,
1985). Heart rate was monitored with either an ECG tracing on a Burdick EKI5A
electrocardiograph, or a Polar Vantage heart rate monitor; and was recorded at 45 seconds into
each stage. Expired gases were continuously sampled and analyzed utilizing a Beckman
Metabolic Measurement Cart (0M-11 oxygen analyzer and LB-2 carbon dioxide analyzer), and
tabulated by a data acquisition system (Hewlett-Packard 3052A) that determined respiratory gas
exchange variables every 15 seconds. Calibration of the volume transducer was performed
utilizing a 1.0 liter syringe, and both gas analyzers were calibrated with standardized calibration
gases and room air prior to each test. A maximal test was defined by achievement of at least two
14
of the following three criteria: a plateau or decrease in V02
despite an increase in work load,
a respiratory exchange ratio (RER) greater than or equal to 1.1, or attainment of at least 90% of
predicted maximum heart rate. If a subject did not complete a satisfactory maximal test, the
testing procedure was repeated, following a short rest, but starting at a velocity of 3.08 tis'.
ANAEROBIC PERFORMANCE:
Subjects were allowed to rest for at least 1 and 1/2 hours following the V0 2 . test before
measurement of their anaerobic performance took place. High intensity running performance was
assessed by the anaerobic speed test (AST) of Cunningham and Faulkner (1969) employing time
in seconds to fatigue as the performance index. Fatigue was defined as an inability of the subject
to continue at the set treadmill speed. Following an adequate warmup, subjects performed the run
at 8 mph (3.52 ms -1 ) at a 20% incline until fatigue. Subjects were aware of the elapsed time. The
test-retest reliability of this test has been documented as r = 0.76 to 0.91 (MacDougall et al.,
1991).
ENDURANCE PERFORMANCE:
The results of the V02.. were used to calculate a treadmill velocity representing
approximately 90% of the maximal oxygen uptake. In fact, this workload was determined by
taking 90% of the treadmill speed at which the subject completed their last complete minute of
running before stopping the test. Therefore, because of the different lengths of time that the
various subjects were able to continue running in an anaerobic state, this value actually ranged
from 90 to 95% of their V0 2... Once set, this workload speed remained constant for the next
15
two testing sessions, regardless of any subsequent variations in the actual V0 2
measurement.
Endurance performance was assessed as the treadmill running time in seconds to fatigue.
ISOKINETIC STRENGTH:
Isokinetic strength was measured as peak torque in newton meters (Nm) generated by
knee flexion and extension on a Cybex H isokinetic dynamometer at a velocity of 30 degreess -1 .
The subjects were positioned on the Cybex table so that the lateral femoral condyle was aligned
with the axis of rotation of the isokinetic dynamometer. Subjects were secured to the backrest
by a seat belt at the waist, and the leg to be tested was stabilized with a strap above the knee at
mid-thigh. After a short warmup at a velocity of 240 degreess -1 , the best values of three different
attempts with each leg were taken. The coefficient of variation of this single joint test performed
at this velocity has been reported as 5.9% (MacDougall et al., 1991).
STATISTICAL ANALYSIS:
The data from different phases of the menstrual cycle were analyzed using paired
Student's t tests for dependent means. The data from the experimental protocol were analyzed
using a 2x3 analysis of variance (ANOVA) with repeated measures on the second factor. The
independent variables were treatment protocol (RX = OCA or PLACEBO) and test (follicular
phase, luteal phase, and test on OCA or placebo). The dependent variables analyzed in each
ANOVA were maximum aerobic consumption (V0 2 ), anaerobic capacity (AST), isokinetic
strength (Cybex II measurement of peak torque of knee flexion and extension), and aerobic
endurance (time to exhaustion at 90% of VO2m.). The baseline variables of age, height, weight,
16
percentage body fat and VO2
were reviewed to ensure that the subjects in each group were
homogeneous. At subsequent testing sessions, weight, sum of skin folds and percentage body fat
were remeasured and also analyzed for changes over time as a result of treatment protocol. The
results from the blood tests for estradiol, progesterone, hemoglobin concentration and hematocrit
were also analyzed in this manner.
Ideally, because of the multiple analyses that were performed, both Hotellings T 2 , and
multivariate analysis of variance (MANOVA) should be carried out, prior to exploring significant
differences between the two groups on any one variable. This was not possible, however, because
of the nature of the study and the small number of subjects involved in comparison to the
number of dependent variables. Therefore, to protect against an inflated Type I error rate, an
absolute level of significance that was acceptable was set at p<0.01. For purposes of analysis of
trends however, all p values up to 0.15 are reported and discussed. This was done to gain an
understanding of any potential effects of either the phase of the menstrual cycle or administration
of OCA that might be statistically significant in future studies, given a larger sample size and
decreased variability in the population studied. Furthermore, since the treatment was not initiated
until after both groups had completed both follicular and luteal phase tests, the F ratios and p
values that are reported refer for the most part to the interaction between the two independent
variables (treatment protocol and test). The only exception to this are the ANOVA results for
estrogen and progesterone values between all tests. Significant interactions were further explored
by graphing the means of each group over time. The statistical package utilized was Systat
version 5.01. All values are expressed as means + SE.
17
RESULTS:
SUBJECTS:
A total of 51 women were initially enrolled in the study based on predicted level of
fitness and a menstrual history suggestive of regular ovulation. Of these, 33 were actually tested
in order to obtain 27 subjects who satisfied the entry requirement of a V0 2,, greater than or
equal to 50 mlIcemin -1 . A final sample of only 19 women were determined to have ovulated
according to nonquantitative assessment of their BBT measurements. All of these subjects
successfully completed at least two parts of the study. The entry level data for these women (at
the time of the follicular phase test) and their plasma estradiol and progesterone levels (for all
three tests) are presented in Table I.
GROUPS:
EFFECT OF MENSTRUAL CYCLE PHASE:
Menstrual cycle phase was verified by comparison of the obtained measurements of
ovarian hormones to those previously reported in the literature. The absolute level of
progesterone accepted for confirmation of the luteal phase was 16 nmo1.1 -1 (Abraham, 1974). Two
of the women who did ovulate (VA and MO) were tested during both the follicular and the luteal
phases, but dropped out of the study prior to being assigned to a treatment protocol. Their data,
therefore, was included in the analysis of the effects of the menstrual cycle phase on
performance. Using the above criteria, it can be seen from Table I, that three of the subjects (SB,
DH, and EB) were not actually in the luteal phase of their cycle at the time of testing for this
^
^
18
TABLE I. SUBJECT PROFILES AND HORMONAL VALUES:
Subj Age^Height^Weight^V02maiÊstradiol^Progesterone
(yrs)^(cm)^(kg)^(mlkg-lmin-1)^(pmo1.14)^(nmo11-1)
F L RX F L^RX
NO TREATMENT:
VA'
27
169.4
MO' 27
159.0
53.0
59.0
54.7
50.5
255
101
497
697
-----
0.9
1.6
55.0
37.0
-----
PLACEBO GROUP:
S13 2 25
169.4
166.3
JF
34
JH
29
159.2
PW 32
167.1
26
JR
177.8
TE
25
171.4
30
169.2
SJ
ES
22
167.4
DIP 30
178.6
53.0
58.6
44.3
56.3
74.0
63.5
57.3
65.3
60.0
53.2
50.6
58.6
52.1
52.1
52.3
55.2
50.2
56.8
61
77
131
188
126
115
109
190
75
348
256
665
536
238
308
254
631
184
1043
298
397
517
370
174
340
455
122
1.2
1.0
1.2
1.6
1.1
1.1
0.6
1.4
1.4
1.8
17.5
65.0
73.0
45.0
34.0
24.0
41.0
0.9
1.8
1.0
43.0
63.0
8.6
1.3
11.5
8.2
1.0
OCA GROUP:
32
CL
AM 23
CS
26
KD
22
MM 25
MC 30
IL
32
EB3 23
64.7
61.1
60.1
51.8
64.5
58.5
61.1
55.8
51.3
55.2
51.4
52.4
53.1
64.2
55.3
52.2
47
178
154
280
102
88
122
83
437
558
433
414
376
581
501
632
31
548
926
241
70
75
36
87
1.3
1.5
2.0
1.2
1.2
1.2
0.6
1.5
25.0
40.0
34.0
46.0
51.0
28.0
34.0
3.1
0.8
27.0
63.0
52.0
0.8
0.6
1.2
1.4
172.5
172.9
169.2
159.9
172.5
168.5
164.1
155.6
SUBJ, subject; F, follicular phase; L, luteal phase; RX, treatment; OCA, oral contraceptive agent
'Subjects only completed menstrual cycle part of study.
2 Subject did not ovulate, so excluded from menstrual cycle part of study; third test was during
midcycle estrogen surge, so excluded from oral contraceptive part of study.
3 Subjects did not ovulate, so data excluded from menstrual cycle part of study.
19
phase. This occurred despite biphasic BBT charts suggestive of ovulation, at least by
nonquantitative analysis. The patterns of their cycles, as later analyzed by the computerized
Maximina R program (Prior et al., 1990b) showed that they had varying degrees'of luteal phase
dysfunction. One of these athletes (EB) was tested on days 23 and 24 of her cycle, following
visual estimation of the day of ovulation from her BBT charts as occurring on day 19. However,
the statistical computer analysis of her BBT data (which is of necessity done retrospectively)
showed that she did not actually ovulate until about day 25. Another athlete was tested during
the luteal phase, according to the quantitative analysis of her temperature data, but had a luteal
phase length of only 12 days. The third athlete probably did not ovulate, as even assessment of
her BBT pattern by the Maximina R program failed to give a result for the most likely day of
luteal phase onset. As a consequence, the data from these women was also excluded from the
analysis of the menstrual cycle phase effects on performance.
EFFECTS OF THE ORAL CONTRACEPTIVE:

Seventeen women participated in this part of the study. They were randomly assigned to
either PLACEBO (n=9) or OCA (n=8). The three women who did not show objective hormonal
evidence of ovulation were excluded from the final analysis. It is interesting to note that one of
these subjects, (SB) in the PLACEBO group appeared to be in the midcycle estrogen surge at the
time of her third test (i.e. high estradiol and low progesterone). The remainder of the subjects
in the PLACEBO group, could be classified as either being in the follicular (low estradiol, low
progesterone) or the luteal (high estradiol, high progesterone) phase during their third test, based
on their hormonal data. Further examination of the hormonal values for the third and final test
20
indicated that 5 of 8 subjects taking the OCA had suppression of their endogenous ovarian
hormones to varying degrees. This was not true however, for 3 of them (AM, CS, and KD), who
had values of both estradiol and progesterone equivalent to luteal phase levels. This was an
unexpected finding, and may indicate incomplete or inadequate suppression of ovulation by the
OCA in these subjects. Plasma levels of the synthetic steroid hormones in the OCA (ethinyl
estradiol and norethindrone) were not measured, but were assumed to be high during this test.
EFFECT OF MENSTRUAL CYCLE PHASE:

The data from both the OCA and placebo group were pooled to obtain a total of 16
subjects (mean SE; age = 27.6 3.8 yr; height = 167.9 + 5.3 cm; follicular phase weight =
59.6 + 6.7 kg; VOA . = 53.7 0.9 mlkg -1 min -1 ) who demonstrated both subjective
(nonquantitative assessment of BBT charts) and objective (plasma estrdiol and progesterone
values in the mid-luteal range) evidence of ovulation. Their body composition measurements and
the results of their blood tests and exercise performance tests are presented in Tables Ha and Ilb.
Testing took place during the midfollicular phase (day = 5.7 + 0.5) and the midluteal phase (day
= 23.3 + 0.9). Room temperature was 22.9 + 0.4 degrees Centigrade and barometric pressure was
760.9 0.7 mm Hg.
BODY COMPOSITION:
There were no significant differences found between the two tests (i.e. between the
follicular and luteal phases of the cycle in the same subject) with regards to weight, percent body
fat or sum of skinfolds.
21
TABLE Ha. EFFECT OF MENSTRUAL CYCLE PHASE ON ANTHROPOMETRIC,
HORMONAL AND HEMATOLOGICAL VARIABLES:
VARIABLE
PHASE OF CYCLE
FOLLICULAR^LUTEAL
Weight
kg
59.6 1.7
59.5 1.8
NS
Body Fat
17.4 0.3
17.1 1.0
NS
Sum of
skinfolds
75.2 3.9
76.1 + 3.7
NS
Estradiol
pmo11 -1
141.4 15.8
461.4 + 36.9
T=8.58, p<0.01
Progesterone
nmo11 -1
122 .09
40.6 + 3.7
T=10.57, p<0.01
Hemoglobin
gin.1-1
131.4 + 1.5
133.2 + 1.2
T=1.72, p=0.11
Hematocrit
%
38.5 0.4
39.2 0.3
T=1.98, p=0.07
MCV
fL
91.8 + 0.9
91.8 + 0.9
Values are means SE. (n=16)

Sum of skinfolds = total in mm; MCV, mean cell volume.
No other significant differences were observed.
PAIRED t-TEST
(df = 15)
NS
22
TABLE Hb. EFFECT OF MENSTRUAL CYCLE PHASE ON PERFORMANCE
VARIABLES:
VARIABLE
PHASE OF CYCLE
FOLLICULAR^LUTEAL
PAIRED t-TEST
(df = 15)
V02.
lmin-1
3.19 .09
3.13 + .08
T=2.28, p=0.04
V0 2,,.
mlkg i nie
53.7 0.9
52.8 0.8
T=2.04, p=0.06
HR(max)
189.4 + 2.3
189.5 2.6
NS
RER(max)
1.17 0.01
1.15 0.01
NS
VE(max)
1min-1 (BTPS)
105.4 + 2.3
106.3 2.4
NS
AST
seconds
28.5 2.2
28.3 + 2.3
NS
ET
seconds
753.8 + 58.8
769.3 + 64.1
NS
R Quadriceps
143.9 7.9
142.4 + 6.1
NS
R Hamstrings
80.5 4.5
83.3 + 4.8
NS
L Quadriceps
Nm
144.4 8.2
141.7 7.2
NS
L Hamstrings
Nm
82.5 5.6
83.6 + 4.4
NS
bpm
Nm
IsTm
Values are means SE. (n=16)

V0 2,. , maximum oxygen consumption; VE (max), maximum recorded minute ventilation;
HR(max), maximum heart rate; RER(max), maximum respiratory exchange ratio; AST,
anaerobic speed test; ET, endurance time; R, right, L, left; (measurements of muscle strength are
peak torque, measured at 30 degreess -1 , best of three trials).
No other significant differences were observed.
23
BLOOD TESTS:
The levels of both estradiol (mean follicular = 141.4 + 15.8 pmo11 -1 ; mean luteal = 461.4
+ 36.9 pmo11 -1 ) and progesterone (mean follicular = 1.22 + 0.09 nmo11-1 ; mean luteal = 46.6 +
3.7 nmo11 -1 ) were significantly different (p<0.01) between the two phases, as would be expected
in women with ovulatory cycles. Mean red cell volume did not change from the follicular to
luteal tests. There was a trend towards a slightly increased hemoglobin (mean follicular = 131.4
+ 1.5 gm1-1 , mean luteal = 133.2 + 1.2 gm1 -1 ) and hematocrit (mean follicular = 38.5 0.4
percent, mean luteal = 39.2 0.3 percent) during the luteal phase, although the increase did not
reach statistical significance.
EXERCISE PERFORMANCE:
In examining the effects of cycle phase on athletic performance, the data show that
absolute VO2 L, decreased slightly from 3.19 + 0.09 limin -1 to 3.13 + 0.08 lmie from the
follicular to luteal phase (p=0.04), while relative V0 2. also decreased in parallel, from 53.7 +
0.9 mlkg-l mie to 52.8 + 0.8 mlkeirnin -1 (p=0.06). These changes are represented graphically
in Figure 1 for all subjects. There were no significant alterations in maximum VE (highest
recorded minute ventilation), maximal heart rate, or maximum RER attributable to phase of the
cycle. The remainder of the tests of performance: the anaerobic speed test (AST), the endurance
run at 90% V02., and the Cybex II measurements of isokinetic strength of quadriceps and
hamstrings; were also not influenced by the menstrual cycle phase to any significant degree in
these 16 subjects.
24
Figure 1: Effect of Menstrual Cycle Phase

on VO 2max
65
so
55
EL 50
45
Follicular^Luteal
25
EFFECT OF THE ORAL CONTRACEPTIVE:
A subgroup of 14 of the original 19 subjects successfully completed all three parts of the
study, and it was thus possible to compare their results from the follicular, -luteal and the
TREATMENT tests. The effect of administration of the triphasic OCA (Synphasic) was
compared to a PLACEBO, (OCA n=7; PLACEBO n=7) for differences in the trends across both
groups. The descriptive statistics for both groups during the follicular phase were similar (mean
+ S.E.; PLACEBO: age = 28.3 1.58 yr, height = 168.6 + 2.0 cm, weight = 60.0 + 3.5 kg;
OCA: age = 27.1 1.6 yr, height = 168.5 + 1.9 cm, weight = 60.2 + 1.7 kg). The measurements
of body composition, and the results of the blood tests, and tests of exercise performance for both
groups are presented in Tables Ma and DD. Testing took place during the midfollicular and
midluteal phases, as previously described and then at approximately midcycle (day 14.4 0.5)
during the second month of administration of the treatment. Testing conditions were similar to
those for the first part of the study.
BODY COMPOSITION:
There were no significant overall mean differences between the two groups in weight or
percentage body fat for the follicular and luteal phase tests, and the treatment tests. There was
a tendency for a slight increase in weight (mean follicular = 60.2 + 1.7 kg to mean treatment =
61.2 1.6 kg) in the group on OCA, compared to the PLACEBO group. There was also a slight
increase in body fat in the OCA group from 16.5 1.6 percent in the follicular phase to 17.5 +
1.6 percent on treatment, and a concomitant decrease in the PLACEBO group from 17.4 + 1.9
percent in the follicular phase to 16.9 1.9 percent over the same time frame. These results,
26
however, did not quite attain statistical significance. There was an overall significant difference
between the two groups (p<0.01) in the change in the sum of the skinfolds. The OCA group
increased from 68.8 + 5.3 mm in the follicular phase to 73.1 + 4.1 mm in the luteal phase to
79.2 + 6.2 mm on treatment, while the PLACEBO group decreased slightly from 80.1 + 6 6 mm
in the follicular phase to 78.9 7.5 in the luteal phase to 76.3 8 0 mm on treatment. These
results are presented graphically in Figure 2.
BLOOD TESTS:
There was a significant difference in the estradiol values obtained in the follicular, luteal,
and treatment tests for all subjects (p<0.01), but this effect was to be expected, and did not vary
as a function of the treatment. Likewise, progesterone values varied between each test for both
groups (p<0.01), but there was no significant difference between the two groups as a result of
the treatment protocol. Hemoglobin and hematocrit values and mean red cell volume did not vary
significantly either between the two groups, or within each group across the three tests.
There was an overall difference in response between the OCA and PLACEBO group in
both the absolute V02
(p4.05), and the relative V0 2. (p=0.02). This occurred between the
luteal phase and the treatment test measurements (i.e. when the athletes were taking the
medication). Absolute V0 2. continued to decrease in the OCA group from the follicular to the
luteal phases (3.29 + 0.12 1.min -1 to 3.26 + 0.11 1min" 1 ), to the treatment tests (3.18 0.09
lmin-1 ); while in the PLACEBO group, there was a slight decrease between the follicular and
27
luteal phase tests (3.16 0.15 lmin -1 to 3.08 0.13 lmin -1 ), but an increase in the third test (to
3.18 + 0.13 1.min"). Relative V0 2. followed the same pattern in the OCA group with follicular
to luteal phase decreases (from 54.7 + 1.7 mlkg -l inain-1 to 53.7 + 1.2 mllcesmin -1 ) followed by
a further decrease on OCA (to 52.0 1.0 mlkg -1 min-1 ); while the PLACEBO group decreased
concomitantly from the follicular to luteal phases (53.0 1.1 mllcg 1 min-1 to 51.9 1.3 mlkg
min-1 ) and then increased again during the third test (to 53.8 + 1.7 m1.14 1 .min-1 ). These-1
changes are depicted graphically in Figure 3. There were no significant accompanying
fluctuations in maximum recorded minute ventilation (V E), maximum heart rate or maximum
respiratory exchange ratio (RER).
28
Figure 2: Effect of Rx on Sum of Skin Folds

90
V)
60
Follicular Luteol
Rx
29
Figure
3: Effect of Rx on VO 2max
58
56
xoo
54
c%) 52
50
Follicular Luteal
Ex
30
TABLE ma. EFFECT OF CYCLE PHASE AND OCA ON ANTHROPOMETRIC,
HORMONAL AND HEMATOLOGICAL VARIABLES:
VARIABLE
PLACEBO (n=7)
RX
ORAL CONTRACEPTIVE (n=7)

F^L
RX
Weight
kg
59.9
3.5
59.9
3.6
59.8
3.8
60.2
1.7
60.6
1.7
61.2
1.6
Body Fat
17.4
1.9
17.1
1.5
16.9
1.9
16.5
+1.6
16.5
1.4
17.5
1.6
Sum of
skinfolds
80.1
+6.6
78.9
+7.5
76.3
+8.0
68.8
+5.3
73.4
+4.1
79.21
+6.2
Est
pmo11-1
133.7
15.7
412.7
72.0
364.4
+41.9
138.7
28.6
471.4
29.1
275.3*
+128.9
Progest
nmolr l
1.14
+.12
42.8
+7.7
19.5
+9.0
1.29
+.16
36.9
+3.6
12.7*
+7.5
Hgb
gm1-1
133.1
1.9
134.4
1.9
135.7
1.7
131.3
2.3
132.6
1.8
130.7
+1.8
Hct
39.0
+0.6
39.3
+0.4
39.9
+0.5
38.5
+0.5
39.2
+0.4
38.7
+0.6
MCV
fl.
92.0
+0.6
91.7
+0.9
92.9
+1.0
91.9
+1.8
92.3
+1.8
91.8
+1.9
Values are means + SE.

F, follicular phase; L, luteal phase; RX, treatment.
Est, estradiol; Progest, progesterone; Hgb, hemoglobin; Hct, hematocrit; MCV, mean cell
volume.
significant F(2,24)=6.94, p<0.01.
* significant between phases, but not between groups: estradiol F(2,24)=13.58, p<0.01;
progesterone F(2,24)=34.18, p<0.01.
No other significant differences were observed for the interaction.
31
TABLE Mb. EFFECT OF CYCLE PHASE AND OCA ON PERFORMANCE
VARIABLES:
VARIABLE
PLACEBO (n=7)
ORAL CONTRACEPTIVE (n=7)

F^L^RX
RX
V0 2,,^3.16
lmind^+.15
3.08
+.13
3.18
+.13
3.29
+.12
3.26
+.11
3.18'
+.09
17 0 2,.^53.0
mlkemiri l 1.1
51.9
1.3
53.8
1.7
54.7
+1.7
53.7
1.2
52.02
1.0
VE (max)^108.4
lminABTPS) +4.2
109.3
3.8
107.6
5.2
104.5
3.0
105.2
3.5
102.6
2.4
HR(max)^188.9
BPM^+4.3
188.3
+5.1
191.0
+5.4
189.9
+3.3
190.0
+3.2
190.5
+4.6
RER(max)
1.17
.02
1.15
.02
1.12
.02
1.17
.02
1.16
.03
1.16
.02
AST
seconds
26.1
+3.2
24.9
+2.8
26.6
+3.4
33.0
+3.0
33.0
+3.2
33.0
+2.8
ET
seconds
790.4
+83.8
761.7
+95.0
842.4
+120.7
753.6
+88.9
781.6
+111.0
703.1
+148.9
RQuad
Nm
138.7
+9.8
135.2
+9.4
140.2
+12.7
161.5
+10.2
157.8
+5.5
149.1
+4.7
RHs
Nm
77.1
+6.5
76.9
+5.6
78.8
+6.0
89.9
+5.8
94.5
+7.7
93.0
+7.5
LQuad
Nm
146.4
+10.9
148.1
+9.7
138.3
+12.8
154.5
+12.7
148.0
+9.2
141.0
+8.0
LHs
Nm
75.9
+5.7
80.9
+6.6
75.9
+6.8
98.0
+7.2
92.0
+5.7
86.0
+5.5
Values are means SE.

F, follicular phase; L, luteal phase; RX, treatment.
V0 2,.., maximum oxygen capacity; V E (max) maximum minute ventilation; HR(max), maximum
heart rate; RER(max), maximum respiratory exchange ratio; AST, anaerobic speed test; ET,
endurance time; RQuad, right quadriceps; RHs, right hamstrings; LQuad, left quadriceps; LHs,
left hamstrings; measurements are peak torque at 30 degreess 1 .
significant F(2,24)=3.39, p=0.05^2 significant F(2, 24)=4.91, p=0.02
No other significant differences were observed for the interaction.
32
There was an initial slight dissimilarity between the two groups in the anaerobic speed
test (26.1 3.2 seconds for the PLACEBO group, compared to 33.0 + 3.0 seconds in the OCA
group), but neither group varied in their performance to any significant degree across all three
tests, or as a function of treatment. There was no significant alteration in endurance performance
due to the treatment protocol, although there was a trend towards a decrease in the OCA group
from 753.6 + 88.9 seconds in the follicular phase to 703.1 + 148.9 seconds while on treatment,
while the performance in the PLACEBO group increased from 790.4 83.8 seconds in the
follicular phase to 842.4 + 120.7 seconds on treatment. Similarly, there was an initial discrepancy
in the left hamstrings peak torque measurements (75.9 5.7 Nin in the PLACEBO group vs.
92.0 5.7 Nm in the OCA group) but no overall significant difference in the performance over
time. There was a trend for all measurements of strength to decrease slightly in the OCA group
from follicular to treatment tests, and to stay relatively the same in the PLACEBO group, but this
did not reach statistical significance.
33
DISCUSSION:
EFFECTS OF MENSTRUAL CYCLE PHASE:

Menstrual cycle phases were confirmed by measurement of plasma estradiol and
progesterone levels taken before exercise for each test. The wide range of values found within
each phase attests to both the interindividual and intercycle variability. Some studies (Prior and
Vigna, 1991, Shangold et al., 1979) have suggested that trained subjects who are menstruating
may have a shortened luteal phase with lowered progesterone levels. Many of the subjects in this
study, however, despite V02.. values in excess of 50 mgkg 'inin ' that would define them as
-
elite athletes, had normal progesterone levels, indicating that low concentrations of progesterone
are not a consistent finding in accomplished athletes. Nor is there necessarily an association of
altered menstrual status with low body weight, as initially suggested by others (Frisch 1974,
1987). Nevertheless, this level of aerobic training is still associated with a fairly high degree of
luteal phase dysfunction, as evidenced by quantitatively determined luteal phase lengths between
9 to 14 days in this group of elite female athletes. Furthermore, most athletes with "regular"
menstrual cycles would not likely be aware of this process without monitoring of their BBT
and/or premenstrual symptoms.
The fact that three of the subjects were not actually in the luteal phase at the time of this
test, despite nonquantitative BBT evidence to the contrary, underscores the importance of
accurate measurements of plasma levels of ovarian hormones in any research involving phases
of the menstrual cycle. Quantitative computer analysis of BBT patterns by programs such as
Maximina R (Prior et al.,1990) can further add to the accuracy of timing of luteal phase tests,
34
as can newer assays to detect the midcycle urinary peak of luteinizing hormone (LH). Neither
technique is completely infallible, and the accuracy of each method increases with the user's
familiarity with the procedures. The former program is helpful also to document the length of
the follicular and luteal phases, as determined by the least mean squares method. However, prior
to comparative analysis of data from different phases of the menstrual cycle, it is still essential
to know the resting plasma levels of estradiol and progesterone values at the time of testing, in
order to accurately ascertain the menstrual cycle phase.
BODY COMPOSITION:
There were no significant alterations in body weight, percentage body fat, or sum of
skinfolds between the two phases of the cycle in this group of 16 subjects. Many women
complain of a subjective feeling of weight gain in the premenstrual phase but there is evidence
(Prior and Vigna, 1987b) that regular physical exercise can ameliorate some of the symptoms of
premenstrual syndrome, including fluid retention. This group of athletes was engaged in regular
aerobic training, and this factor may have accounted for the lack of variation in their weight.
Recent work by Bunt et al., (1989) has questioned the validity of underwater body
densitometry measurements in women at various phases of the menstrual cycle, because the
menstrual cycle changes in plasma volume and total body water may lead to errors in the
determination of the percentage of body fat using conventional formulas. There also exists a
current controversy about the reliability and reproducibility of the usage of skinfold
measurements in determining body fatness (for review, see Lohman, 1981). Many of the
regression formulas use varying combinations of the skinfold measurements in their calculations,
35
and this may limit comparison of values between different studies. Furthermore, there is marked
disparity between men and women, as well as between young and old individuals in the
distribution of their subcutaneous fat. Therefore, formulas that are derived for a population of
men or middle-aged women, are totally inaccurate and unacceptable for usage in a selected group
of young athletic women, such as were involved in this study. It is thus more appropriate to use
the sum of the obtained skinfold measurements for comparative purposes, rather than alter these
values by any complex mathematical transformations that have the inherent potential for
erroneous assumptions.
BLOOD TESTS:
There was a slight, but nonsignificant increase in both hemoglobin concentration and
hematocrit in the luteal phase as compared to the follicular phase of the menstrual cycle. This
is in disagreement with the results of a very early study (Vellar, 1974), which reported
significantly lower hematocrits and hemoglobin concentrations during the premenstrual phase,
as a consequence of the plasma volume shifts that occur from the physiological actions of
estradiol. Both hemoglobin concentrations and hematocrit values reached a peak at about the 18th
day of the cycle, a time which Vellar termed the postovulatory phase. However, in that study,
the blood samples were drawn from women at unsubstantiated phases of the cycle, and blood
estrogen concentrations were not measured. A recent study (Fortney et al., 1988) suggests that
blood progesterone levels must be low in order to see this estrogenic effect. In the present study,
both estradiol and progesterone levels were high during the luteal phase. Other investigators have
also noted a slight increase in resting hemoglobin concentration (Jurkowski et al., 1978) and
36
hematocrit (Fox et al., 1977) during the luteal phase, but have not offered any biological
explanation for this phenomenon, nor have they linked it to any alteration in performance.
AEROBIC CAPACITY:
Both absolute and relative V0 2,. declined slightly during the luteal phase, (p=0.04 and
0.06 respectively). This is of borderline significance, bearing in mind the small number of
subjects and the number of tests that were carried out, and should therefore be interpreted with
some caution. Because of the multiple comparisons involved in this study, the fiduciary level of
confidence was set to p<0.01. However, it is still important to consider this as a potentially
meaningful trend, that may be significant in a larger study with more subjects. To date, this
represents the largest series of this nature that has been carried out in elite level athletes, with
proper documentation of menstrual cycle phases. In comparison, the most recent study by De
Souza et al., (1991) did not find any significant differences in VO2max between the follicular and
luteal phases in their group of 8 eumenorrheic subjects. It does emphasize the fact, however, that
investigators doing studies on female athletes should be careful to standardize the phase of the
cycle in which testing is being carried out, i.e. 3-8 days post menses, in order to eliminate the
confounding factor of these possibly significant changes in V0 2.,. between the two phases of the
menstrual cycle. It is also quite conceivable, that given the different hormonal milieu at midcycle
(high estradiol, low progesterone), that aerobic capacity might be altered as well, potentially in
a different fashion. There has been no well-documented research to date on performance during
this part of the menstrual cycle.
37
None of the other measurements taken during exercise in this group of athletes showed
any variation between the follicular and luteal phases. Again, these findings corroborate the
conclusions reached by previous investigators. Both early studies without hormonal measurements
(Fox et al., 1977, Garlick and Bernauer, 1968; Wells and Horvath, 1974) and more recent work
utilising progesterone and estradiol levels for confirmation of cycle phase (Jurkowski et al., 1978,
Shoene et al., 1981, De Souza et al., 1990) have failed to document any significant alterations
in maximum heart rate or respiratory exchange ratio related to phase of the cycle.
The lack of change in maximum minute ventilation in this study is also in agreement with
the results of Schoene et al. (1981), who found changes in normally menstruating nonathletes,
but not in normally menstruating athletes or amenorrheic controls. Progesterone is thought to
stimulate respiration through a central mechanism during both the luteal phase of the menstrual
cycle (England and Fahri, 1976), and during pregnancy (Moore et al., 1987; Pernoll et al., 1975).
This hyperventilation has also been seen in men given medroxy-progesterone acetate (MPA), a
synthetic progesterone (Dombovy et al., 1987; Skatrud et al., 1978) and is thought in part to be
due to increased metabolism, as reflected by increased body temperature after ovulation. The lack
of a significant progesterone effect on ventilation in athletes, however, is consistent with the
observation that outstanding endurance athletes have a decreased ventilatory drive in response
to chemotactic stimuli (Byrne-Quinn et a., 1971; Martin et al., 1979). This characteristic is
inherited to a certain degree (Martin et al., 1979), and may be a contributing factor in their ability
to successfully compete at an elite level.
38
Little information exists in the literature on the effects of cycle phase on anaerobic
performance. In this study, there was no significant variation in the anaerobic speed test as a
-
function of phase of the cycle. The metabolic effects of estradiol on substrate utilization mostly
come into play in prolonged exercise, and therefore would not be expected to have any effect on
short term (around 30 seconds) anaerobic metabolism which relies more on ATP and creatine
phosphate. Likewise, elevation of progesterone levels in the luteal phase do not seem to have any
consequences on this type of energy turnover. The variation and the range of values seen in the
subjects in this study can most likely be attributed to sport-specific training, and the energy
demands of the various sports that these subjects were participating in (i.e. the squash players
had the highest time for the anaerobic speed test (35-40 seconds). These AST values are only
indicative of their anaerobic capacity, and do not reflect the state of their aerobic fitness. In
actual fact, low anaerobic performance is a common finding in aerobically or endurance trained
athletes, such as those involved in this study.
With regards to the effects of phase of the cycle on aerobic endurance performance, in
contrast to the work of Jurkowski et al., (1978, 1981), the present study did not demonstrate any
significant differences relative to the two phases of the cycle. Their group documented a doubling
in endurance time at 90% V0 2, between the follicular and luteal phases; from 1.57 minutes to
2.97 minutes. They postulated a shift in metabolism towards free fatty acids (PM), and a
glycogen sparing effect secondary to the increased estradiol and progesterone in this phase of the
39
cycle. They also measured a higher blood lactate in the follicular phase during heavy and
exhaustive exercise. To substantiate their hypothesis of a decrease in lactate production during
the luteal phase, they further confirmed no effect of the cycle phase on the disappearance of a
bolus of infused lactate (Jurkowski et al., 1981). Similarly, other investigators (Dombovy et al.,
1987) found a decrease in blood lactate and respiratory exchange ratio under the influence of
endogenous progesterone during the luteal phase in women, and also in men given medroxyprogesterone acetate. Earlier studies (Reinke et al., 1971; Lamont, 1986) and work by Bonen et
al. (1983, 1991) and Nicklas et al., (1988) have not substantiated these findings. In addition, there
is some disagreement about whether or not there actually is an increment in circulating FFA
during the luteal phase (Reinke et al., 1971; Bonen et al., 1991).
One of these groups of researchers (Nicklas et al., 1989) has actually performed muscle
biopsies in both the follicular and luteal phases following a bout of depletion exercise on a
bicycle ergometer (90 minutes at 60%V0 2. and 4 x 1 minute at 100% VO2
), and then before
and after exercise to exhaustion three days later. During the three days between these exercise
tests, the subjects consumed a controlled diet of 60% carbohydrate in order to maximize repletion
of glycogen stores. Although there was no difference in glycogen utilization per se, during
exercise in either phase of the cycle, muscle glycogen repletion was greater in the luteal phase
following depletion exercise. Furthermore, even though the change did not attain statistical
significance, there was a strong tendency (p<0.07) towards a longer duration of endurance
exercise during the luteal phase. Other authors have found either no phase difference in
endurance performance (Stephenson et al., 1982a; Dombovy et al., 1987), or even a longer work
time during the follicular phase, albeit in nonathletes only (Schoene et al., 1981).
40
One possible explanation for the inconsistency in results is the difference in the various
protocols used to assess endurance performance. The subjects in this study performed the
endurance run on the second day of testing, and had only completed the strength tests, and a
short warmup prior to beginning this test. In the study of Jurkowski et al., (1978) endurance
performance was tested on a bicycle ergometer as part of a continuous progressive protocol,
where the subjects had already completed 20 minutes at 33% of VO2mx , and 20 minutes at 66%
of V02,.. prior to being tested at 90% V0 2,. Furthermore, one of their subjects was unable to
complete any work at the highest intensity of the protocol during the follicular phase, and with
only 9 women in the study, this may have biased the results. It may be that the progressive
protocol is a more sensitive test of changes in aerobic endurance; nevertheless, the fact remains
that the subjects in the present investigation were able to maintain an output of at least 90% of
V02. 0 for anywhere from 4.5 to 22 minutes independent of menstrual cycle phase. The subjects
in the study of Nicklas et al., (1989), on the other hand, were tested at 70% of VO zn., and were
able to sustain this somewhat lower exercise intensity for up to 150 minutes.
Studies on strength performance throughout the menstrual cycle are sparse and employ
a variety of strength tests. In the current protocol, there were no differential effects on isokinetic
strength of knee flexion or extension attributable to the phase of the cycle. The majority of
previous investigators did not confirm menstrual cycle phases with estradiol and progesterone
measurements, so interpretation of their findings must be made with caution. None-the-less,
Quadagno et al., (1991), studied twelve recreational weight-lifters, and found no differences in
41
their performance in lifting 70% of their maximum weight for bench and leg press at any time
during the menstrual cycle, as monitored by menstrual cycle charts only. Dibrezzo et al., (1991)
found little or no effect of the menstrual cycle phase upon the relationships among body weight,
percent body fat, knee extension and flexion strength or endurance (tested on the Cybex II
dynamometer at 60, 180 and 240 degreess -1 ). The definitions of menstrual cycle phases (mensus,
ovulation and luteal) in that study were, however, based only on assigned days of an ideal cycle.
Wirth and Loman (1982), on the other hand, measured handgrip endurance time and force
output at 50% of a maximal voluntary contraction. They found that the maximal voluntary
contraction (MVC) was significantly greater during the follicular phase, but there was no
documentation of the luteal phase in their subjects by either BBT measurements or serum
progesterone. In another study, Petrofsky et al., (1976) noted a decrease in maximal endurance
of isometric forearm contraction during the luteal phase compared to midway during the
ovulatory phase (as determined by a rise in BBT temperature), suggesting an inverse relationship
between muscle temperature and isometric endurance. This tendency was reversed when the
temperature of the muscle was held constant at 37 degrees Centigrade. The increased body
temperature in the luteal phase that occurs as a result of the elevation in progesterone has been
shown by others (Quadagno et al., 1991; Wearing et al., 1972) not to have any substantial
adverse effects on either the speed or force of muscle contraction. Thus the findings in the
current study are in agreement with most of the previous studies, despite the fact that these have
not been carried out with accurate documentation of the cycle phase.
42
EFFECTS OF THE ORAL CONTRACEPTIVE:
BODY COMPOSITION:
Early studies using the original high-dose oral contraceptive formulations have
documented many potentially detrimental side effects, including fluid retention and weight gain,
whereas today's new biphasic and triphasic pills contain between 30% to 40% less hormone and
can thus be expected to have a corresponding decrease in adverse effects (Greenblatt, 1985).
There was a slight weight gain of about 1 kg in the subjects on the OCA as compared to the
placebo group, but these athletes were only followed for two months. It is possible that this effect
would stabilize over time with continued administration of the OCA, but it is equally conceivable
that this metabolic influence of the synthetic steroid hormones would be cumulative. Whether
the increased weight is fat, muscle or water is somewhat difficult to ascertain. If the weight gain
was muscle, then one might expect a slight increase in absolute, but not in relative V0 2,.., as
a function of increased metabolically active tissue. The increase in the sum of skinfolds would
suggest that it was primarily fat or water, but the lack of associated change in percentage body
fat does not substantiate this entirely.
Furthermore, it has been suggested that variations in bone mineral content in young adult
women may also have an impact on the estimation of percent body fat (Bunt et al., 1990) by
underwater densitometry methods. It has been shown that women with episodic amenorrhea may
be at risk of lowering their bone density in proportion to the number of missed cycles
(Drinkwater et al., 1990) It is also quite probable that a group of elite female athletes such as
were involved in this study, experience frequent anovulatory cycles and luteal phase disturbances,
despite having seemingly "regular" menstrual bleeding (Bonen and Keizer, 1984). It has recently
43
been documented (Prior et al., 1990a) that this may, over time, also have an insidious influence
on their bone density that they may not be aware of. Therefore, in terms of the impact of these
variations in bone density on the determination of body density using underwater densitometry,
it would require an extremely large change in percentage of body fat to exceed the limits of both
experimental and calculation error. These factors need to be kept in mind when doing
comparative research on similar groups of exercising females (see Martin and Drinkwater, 1991).
BLOOD TESTS:
Some of the potential benefits of oral contraceptives for athletic performance include an
amelioration of dysmenorrhea, and a reduced risk of both iron deficiency and anemia. None of
the subjects in this study were clinically anemic (ie. hemoglobin concecntration < 120 gm1 -1 ),
but iron status was not determined. Nevertheless, there were no significant changes in either
hemoglobin concentration or hematocrit as a result of OCA treatment compared to placebo. This
is in agreement with other studies (Notelovitz et al., 1987).
AEROBIC CAPACITY:
A slight decrease in V0 2. was measured in the subjects on OCA as compared to the
subjects on placebo, with no alteration in any of the other cardiorespiratory measures. This is in
concordance with several of the previous investigations. One study (Daggett et al., 1983) has
shown a slight but statistically significant (p<0.05) reduction in V0 2.. (from 44.6 to 39.8 nalkg '.miri l ) in a group of seven relatively untrained subjects after 1 to 2 months use of an
44
unspecified oral contraceptive. Another study (Notolovitz et al., 1987) used a design similar to
the present investigation, with both a control group (n=6) and an OCA group (n=6). They had
similar findings, but to a lesser degree following a 6 month usage of a lower dose monophasic
preparation. The control group increased their V0 2. values from a mean SD of 42.6 2.8
to 45.9+ 5.8 mlkg -1 min-1 over the duration of the study, but in contrast, the oral contraceptive
users decreased from 41.2 11.8 to 38.4 9.8 mlkg -I min-1 (a 7% difference in aerobic capacity
relative to body weight). This was associated with an 8% decrease in the absolute oxygen uptake
(from 2.34 2.17 limin -1 ), and in the oxygen pulse (12.1 3.2 to 11.2 + 2.2 ml per beat). These
changes were reversible on discontinuation of therapy. It may well be that there is a continuum
of effects of OCA on aerobic capacity, and as the concentrations of hormones decrease (with a
corresponding decrease in most of the other side effects), the effects on V02. become less
significant. As these decreases in V0 2. have not been linked with any significant alterations in
02 carrying capacity of the blood (hemoglobin concentration or hematocrit), or the majority of
the other physiological measurements influencing 0 2 uptake or delivery to the tissue (such as
minute ventilation, heart rate or cardiac output), there may be significant changes at the cellular
level. The study by Daggett et al., (1983), for example, found a decrease in muscle mitochondrial
citrate in their subjects on OCA. It is worth emphasizing, however, that even a small variation
in performance, even though it does not quite reach statistical significance, may be of tremendous
importance to the high performance athlete, where success or failure is frequently measured in
tenths of a second.
Another caveat in research of this nature is the relative impossibility of carrying out
double blind studies in this type of situation. Approximately half of the subjects in this study
45
were aware that they were taking the OCA by the alteration in the pattern of their normal
menstrual cycles, and frequently by nuisance side effects such as breakthrough bleeding
throughout the cycle. It is also important to point out that at the time of the third test, 2 of the
subjects on the placebo were actually definitely in the follicular phase, and 2 of them were in
the luteal phase, while the remaining 3 subjects were possibly just entering or finishing the luteal
phase of their cycles. Therefore no substantial generalizations or comparisons can be made with
regards to the means of these results with their performance on the earlier tests. Nevertheless,
the fact remains that overall, the placebo group increased their V0 2. from the baseline follicular
phase measurements, as compared to the subjects on the OCA who had a mean slight decrease
over the same time frame. Furthermore, although the mean values for the OCA group only
declined from 54.7 1.7 to 52.0 1.0 mlkg-l min -1 from the follicular phase test to the
treatment test, 6 out of the 7 subjects showed at least a minimal decrease in V0 2,,,, over this
period, and two subjects had dramatic decreases, in the range of 4 to 9 mlkg-l Miti l . There is
thus a degree of intersubject variability in this response to exogenously administered hormones.
There was no alteration in the capacity of the subjects to carry out the anaerobic speed
test, as a function of administration of the OCA or placebo. There does not appear to be any
impact of OCA on energy metabolism for short term anaerobic work. The scores for this test
were relatively low in the majority of the athletes, indicating a low anaerobic capacity. This is
consistent with the fact that these subjects were well trained for predominantly aerobic-type
activities.
46
There were no significant differences between the two groups with respect to their
performance on the endurance run, although there was a trend towards a slight decrease in the
group on OCA. This may be related to some influence of the OCA on substrate metabolism, such
as alteration in carbohydrate or lipid metabolism (Beck, 1973; Bonen et al., 1991). Oral
contraceptives are known to potentiate diabetes and have also been shown to cause a decrease
in blood glucose with heavy exercise as compared to a eumenorrheic control group (Bonen et
al., 1991). This action would be more likely to decrease endurance performance, than to enhance
it, by decreasing the available fuel for the exercising muscles. Blood glucose was not measured,
but this may have been one of the mechanisms accounting for the dramatic difference in
endurance performance in some of the subjects. All subjects had fasted for at least three hours
prior to the testing, and they were not allowed to take anything other than water until completion
of the endurance run.
Likewise, there was a trend for all strength measurements in the OCA group to decrease
over time, as compared with the subjects on placebo, but this did not reach statistical significance
either. With regards to the effects of OCA on strength, only one study (Petrofsky et al., 1976)
has looked at this in any detail. They found that the isometric endurance of subjects on oral
contraceptives did not vary during the course of a cycle, compared to normal controls who did
show an alteration in isometric endurance in response to different times during the menstrual
cycle, with a decrease during the luteal phase. They postulated that this latter trend was due to
47
the increase in deep muscle temperature occurring in the luteal phase of the cycle. The women
on the OCA did not show any variation in their core temperature over the course of a cycle.
Unfortunately, they did not test women before putting them on an oral contraceptive to determine
the effect of the medication itself in the same subject. The oral contraceptives certainly provide
a relatively stable hormonal milieu, as compared to the variations within a normal cycle, but the
important question of their overall effect on strength still remains unanswered.
48
SUMMARY:
The results of this study demonstrate that although there are small decreases in both
absolute and relative V02. during the luteal phase of the menstrual cycle in" trained female
athletes, these do not impact to any significant degree upon commonly utilized measurements of
anaerobic performance, aerobic endurance performance, or isoldnetic muscle strength .
Furthermore, there are no associated alterations in maximum minute ventilation, maximum heart
rate, maximum respiratory exchange ratio, body composition or any hematological variables to
explain these changes in aerobic capacity. The administration of a low-dose triphasic oral
contraceptive pill (Synphasic), over a one and one half month time span resulted in a small
increase in the sum of skin folds and a lesser (nonsignificant) increase in weight, as well as a
slight decrease in both absolute and relative V0 2.., as compared to a similar group of subjects
on placebo. There were no statistically significant changes in any of the other measures of
performance, or physiological variables.
Therefore the results of this study indicate that neither phase of the menstrual cycle or
nor administration of a low-dose triphasic oral contraceptive have any apparent or measurable
effects on certain aspects of athletic performance in this group of elite female athletes. However,
the small decreases in ' 02
,
that occurred during the luteal phase and while on OCA suggest
that the female steroid hormones, estrogen and progesterone, both endogenous and exogenous,
may exert a slight deleterious effect on aerobic capacity with potential implications for elite
performance. In addition, the magnitude of this effect appears to vary between subjects.
Therefore, this type of study needs to be repeated with a larger number of subjects, and perhaps
with varying doses of the OCA, and for a longer duration, in order to further investigate this
49
possibility. Further studies should also focus on the potential mechanisms of this possible change
in functional aerobic capacity, as well as on other more sport-specific measures of performance
in the elite athlete.
50
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59
APPENDIX A. REVIEW OF LITERATURE:
NATURE OF THE PROBLEM/IMPORTANCE OF TOPIC:
Women have been an integral part of the work force for hard manual labour for centuries
and they continue to labour in this capacity in underprivileged and third world countries.
Nevertheless, little research exists on the physical effects of such toil on their reproductive
systems, or on their physical work capacity as affected by their hormonal status (Gamberale et
al., 1975). In more affluent and developed countries, women have ever-increasing opportunities
to challenge themselves outside the workplace, in both competitive and recreational sport.
Considering that women have only been allowed to compete in the Olympic Games since 1912,
and that events such as the women's marathon were just added in 1984, it is easy to see what
giant strides women have taken, both physiologically and psychologically, over the past few
decades. The momentum is not likely to abate; more and more sports such as hockey, rugby, etc.
continue to expand to include women's teams, and the International Olympic Committee itself
designated 1990 as the year of "Women in Sport", as well as announcing that their goal was to
include more womens' sports in 1996 and beyond. In Canada, the Sport Canada branch of the
federal government has issued a policy paper focusing on strategies to ensure equity for women
in sport (Sport Canada Policy on Women in Sport, 1986).
Concomitant with this rise in popularity of physical recreation and sport for women has
been a concern about the effects of strenuous exercise on their reproductive and neuroendocrine
systems. Menstrual irregularities such as delayed menarche, primary and secondary amenorrhea,
shortened luteal phase, oligomenorrhea and infertility, once thought to be purely a result of a
critical set point of percentage body fat (Frisch, 1974, 1987) have been shown to have
60
multifactorial causes. Family history, previous menstrual history, nutrition and body composition
have all been implicated in these hormonal disruptions, and so have sport specificity (with a
heavy emphasis on aerobic type activities such as running, aerobics and gymna stics or ballet),
.
rigorous training programs, excessive mileage and psychological stress of training and
competition (for a review of athletic amenorrhea, see Bonen and Keizer, 1984; Highet, 1989).
Hans Selye (1939) demonstrated that it was possible to induce changes in the estrous cycle of
female rats with a program involving abrupt onset of intense exercise. Bullen et al., (1985) were
able to reproduce these findings in women, causing menstrual dysfunction such as altered luteal
phase and anovulation which were reversible on discontinuing the exercise stimulus. Numerous
other studies have also substantiated these fmdings (see Shangold et al., 1979; Shangold and
Levine, 1982, Keizer and Rogol, 1990, Prior and Vigna, 1991).
Conversely, relatively little work has been done on the influence of hormones such as
estrogen and progesterone on various components of athletic performance. There is much indirect
evidence to suggest that they should have some impact. In pregnancy, profound alterations in
body composition, cardiorespiratory function, hemodynamics and exercise performance are known
to occur in different trimesters (Arta! et al., 1981, 1986). There are also volume and
biomechanical changes as well as significant hormonal shifts. Estrogen and progesterone, when
administered therapeutically, either together or separately, can influence a variety of metabolic
processes. Estradiol, for example, has been shown to directly impact upon substrate utilization
by increasing lipid availability and utilization, and by decreasing gluconeogenesis and
glycogenolysis (for a review, see Bunt, 1990). It also has profound effects on plasma volume
(Fortney et al., 1988). Progesterone, either endogenous (Schone et al., 1981) or synthetic
61
(Dombovy et al., 1987) causes an increase in ventilation, and an alteration in respiratory drives.
Therefore, it is highly conceivable that the fluctuations in hormonal concentrations that occur
during both normal and abnormal menstrual cycles might have effects of some consequence to
the competitive athlete.
Oral contraceptive agents (OCAs) were initially developed to prevent pregnancy, but their
predictable control of the menstrual cycle and the decrease in cramps and menstrual flow have
prompted their use in many other clinical situations. Elite athletes troubled by dysmenorrhea may
utilize them for manipulating both the timing and the symptoms of their normal menstrual cycles
(Shangold, 1988). More recently, concerns have surfaced about the effects of altered menstrual
function on bone density and subsequent problems with premature osteoporosis (Drinkwater et
al., 1981, 1990; Prior et
at, 1990a). The majority of investigators believe that lack of estrogen
is the determining factor in rate of bone turnover (similar to the postmenopausal woman), and
therefore recommend the utilization of estrogen for therapy (Drinkwater et al., 1981, Shangold,
1982, Shangold et al., 1990). Another school of thought believes that progesterone is the principal
bone-trophic hormone (Prior et al., 1990). Clinically, both hormones are frequently used together
in estrogen replacement therapy in postmenopausal women, or in the combination oral
contraceptive pill in younger women. Side effects of OCAs have been reduced or eliminated by
a gradual decrease in the concentration and composition of both the estrogen and the
progestational agents in the pills currently on the market (Greenblatt, 1985; Percival-Smith et al.,
1990). However, there is little or no accurate information on the influence of OCAs on any of
the many components of athletic performance (Schelkun, 1991).
62
Performance is multi-faceted and sport-specific, and difficult to predict with any degree
of accuracy. Furthermore, there are many different criteria that may be measured. Events such
as long-distance running require a well-trained cardiovascular system, and a high aerobic
capacity. Other sports, such as squash, demand a high degree of anaerobic fitness for the short
bursts of intense activity during rallies. Still others, such as judo, rowing, and the field events
in athletics, are weight and strength-dependent. The majority of sports also require a refined level
of hand-eye coordination and quick reaction time, and more and more sports rely on sports
psychology and visualization techniques to enhance performance. To date, there is no single
accurate method of predicting performance; there are just too many factors to take into account.
Nevertheless, there are some physiological tests of performance that have been
consistently utilized in the laboratory setting. Aerobic capacity, anaerobic capacity and isokinetic
muscle strength can be measured reliably, accurately, and with a high degree of intersubject
reproducibility (MacDougall et al., 1991). Aerobic endurance can be determined by recording the
length of time that an athlete can sustain a continuous effort at a given percentage of VO2m,x ,
usually from 70 to 90%. Body composition and percentage of body fat are conventionally
assessed using skinfold calipers and the underwater densitometry method (Brozek et al., 1963;
Lohman, 1981; Ski, 1961). These, and other measures can be utilized to help predict sport
performance in the athlete, both male and female.
63
EFFECT OF THE MENSTRUAL CYCLE ON PERFORMANCE:
BACKGROUND AND EARLY STUDIES:
Early studies dealing with the influence of the menstrual cycle on performance were based
on retrospective surveys. Furthermore, definitions of cycle "phase" were not documented by
hormonal measurements, and are thus more accurately interpreted using the specific name of the
stage, such as "post menses", "premenstrual" or "menstrual flow". A report from Kral and
Markalous (1937) involving an unspecified number of athletes found that 63% did not notice any
differential effects during the menstrual cycle. Despite the fact that 8% reported a decrement in
performance during menses, another 29% found that their performance was enhanced during this
time. Ingman (1953) surveyed 104 Finnish athletes with regards to their performance. There was
no perceived effect in 43% of this group, while 19% actually reported enhanced performance
during the time of menstrual flow. Another 38% of the women described the opposite
phenomenon - performance decrement during their menses, and in fact, a significant number of
these women (24%) did not normally compete during their menses because of pain and/or
fatigue. Erdelyi (1962) studied 557 Hungarian female athletes from a variety of sports. On
average, 48.2% of these women did show any change in their performance during the menstrual
flow, 30.7% showed worse performance and 13% showed better performance that their usual
average. The results of his survey were consistent with the findings of other authors of that era
(see Erdelyi, 1962). The "best" performances were generally reported during the immediate
"postmenstrual" days, while the worst performances were in the "premenstrual" interval, and
during the first few days of menstrual flow. It is important to remember, however, that although
the timing of these "postmenstrual" and "premenstrual" stages may correspond to the timing of
64
"follicular phase" and "luteal phase", current definitions of these phases includes accurate
documentation by serum hormone measurements (Abraham, 1974).
Rougier and Linquette (1962) had the largest series of respondents, and compared 1435
athletes of varying calibre. Of the 553 engaged in regular intensive exercise, 59% noticed an
impairment in their performance during the premenstrual time concomitant with an increase in
their premenstrual symptoms. Another 309 women only exercised for 2-4 hours per week, and
11% of these related the same decrement, but without any increase in their symptoms. A further
1% who suffered no recognizable symptoms also showed a definite decrease in performance as
regards speed, accuracy, strength and fatigue in the pre-menstrual and menstrual phase. This
suggests that the elite female athlete may be more sensitive to and cognizant of any variation in
her athletic efficiency. Conversely, small differences in performance are significantly more
important to this group of women, especially considering the importance of their competitive
careers.
Zaharieva (1965) found that amongst 66 Olympians from a variety of sports surveyed at
the Tokyo Olympics, 34% of the women continued to train during the menses, but 12% of the
athletes overall, and an astonishing 33% of the swimmers always interrupted their training during
the menstrual flow. It is possible that this may have been associated with the prevailing customs
of the times when tampons were not yet popular or acceptable, and there were still a large
number of superstitious beliefs about menstrual flow. Of the sportswomen competing during
menstruation, 36.9% noticed no difference in their performance, 27.7% stated that the effect
varied, but 17% found that their performance was worse. With regards to the feeling of fitness,
46% of these Olympians did not notice any change, but 32% felt weaker during the menstrual
65
flow. Bale and Davies (1983) administered a questionnaire to 109 specialist physical education
students, and found that 45% of women not taking the contraceptive pill felt that menstruation
affected their performance, as compared to 31% of women taking the pill. The other studies are
similarly inconsistent, but it has been generally recognized and accepted that gold medals have
been won and world records set during any part of the menstrual cycle.
Menstrual symptoms such as dysmenorrhea, fatigue, fluid retention and weight gain are
postulated to have potential adverse effects on sports activity and performance. Indeed, these
symptoms were noted by many of the women surveyed in these retrospective studies. Another
factor that is more difficult to quantify is the possible negative impact on performance of earlier
misconceptions about menstrual flow. A more recent prospective study (Moller-Nielsen and
Hammar, 1989) has suggested that women soccer players were more susceptible to traumatic
injuries during the premenstrual and menstrual period than during the rest of the menstrual cycle,
especially amongst players with premenstrual symptoms such as irritability/irrascibility,
swelling/discomfort in the breasts, and swelling/discomfort in the abdomen. However, despite
current knowledge about the variability of menstrual cycles in athletes, this study approximated
the length of the menstrual cycles to be 28 days (14 day duration of premenstrual and menstrual
period, and 14 day duration for the rest of the cycle). Thus, the investigators did not adequately
document the existence of ovulatory cycles, and furthermore, may have under or overestimated
the length of the premenstrual phase of the cycle. These results therefore, should be interpreted
with caution. The authors also found that women using oral contraceptives had a lower rate of
traumatic injuries as compared to women who were not on OCAs. They postulated that oral
contraceptives might exert a protective effect by ameliorating some symptoms of the
66
premenstrual and menstrual period which might affect coordination and hence the risk of injury.
Other studies (Dalton, 1960, Posthuma et al., 1987, Wearing et al., 1972) have also investigated
general accident proneness, neuromuscular coordination, and reaction time and manual dexterity
at different times during the cycle. In general, women with premenstrual symptoms have showed
a decrement in these indices of performance during the premenstrual stage of their cycles and
have performed best in the "intermenstrual phase".
STUDIES WITHOUT HORMONAL DOCUMENTATION:

The majority of the early clinical studies which attempted to document aerobic
performance during different times in the menstrual cycle did not include ovarian hormone
measurements. Furthermore, the definitions of cycle "phase", and the range of days over which
testing was carried out, make accurate interpretation of the results both confusing and hazardous.
Doolittle and Engebretsen (1972) tested 16 university women during four different stages:
"follicular" (day 7-10 of the cycle), "ovulatory" (day 13-15),"luteal" (day 18-20) and "premenses"
(day 23-26); and found no performance variations due to the menstrual cycle in the maximum
02 consumption, the 12 minute run-walk, the 600 yard run-walk or the 1.5 mile run-walk tests.
They were the earliest group of investigators to even think of documenting the cycle phase by
serum progesterone levels. However, their blood test results for progesterone showed that one
subject may not have ovulated, and two others may have ovulated late or not at all. Furthermore,
the blood samples were drawn between five and seven minutes after exercise. It has since been
shown that both estrogen and progesterone levels increase with exercise over resting values.
These increases appear to be independent of pituitary control, and are dependent upon exercise
67
intensity, and phase of the cycle, being higher in the luteal than in the follicular phase of the
menstrual cycle (Jurkowski et al., 1978). Other authors have documented similar changes in one
or both female steroid hormones (Bonen et al., 1979; Shangold et al., 1980; Sutton et al., 1980).
These increases likely occur as a result of decreased metabolic clearance (Keizer et al., 1981),
although recent work suggests that there may actually be increased secretion of these ovarian
hormones with exercise (Bonen et al., 1991).
Gamberale and his group (1975) tested 12 subjects with severe menstrual distress at three
different intervals during the cycle, the 1st or 2nd day of menstruation ("menstrual"), 10-18 days
after the start of menstruation ("postmenstrual") and 6-2 days prior to the estimated start of
menstruation ("premenstrual"). Testing was carried out on a bicycle ergometer for 6 minutes at
40% and 70% VO2inaz. They did not find any significant change in either heart rate or 0 2 uptake
at any phase of the cycle. Interestingly, however, at the same heart rate, exercise was perceived
as more exerting in the menstrual stage than in either the premenstrual or postmenstrual stages.
Another study that was reported in abstract form only (Fox et al., 1977) involved trained
and untrained women tested on a treadmill at three specific points in the cycle: 13 days after the
onset of menstruation ("postmenstrual"), 7 days after ovulation ("premenstrual"), and 3 days after
the onset of menstruation ("menstrual"). Of note is the fact that, according to this classification
system, the women in the "postmenstrual phase" could potentially have been ovulating. They
found that in the trained group, the submaximal VO 2 was highest 13 days after the onset of menstruation, but that there were no differences in the untrained group. In contrast, Allsen et al.,
(1977) tested 10 trained women on a treadmill at four different times in the cycle across four
cycles and were not able to demonstrate any differences in maximal aerobic capacity. Their tests
68
included Phase I: 24 hours after the onset of the menstrual period, Phase II: within 24 hours of
Phase I, Phase III: 10 days from the Phase II test; and Phase IV: 10 days from the Phase III test;
and again, did not include verification of the cycle phase by serum progesterone.
Some investigators (Stevenson et al., 1982a, 1982b) have even monitored their subjects
at 5 different points during the cycle (days 2, 8, 14, 20 and 26), and failed to demonstrate any
significant variations in peak 0 2 uptake or submaximal cardiorespiratory responses to exercise
on a bicycle ergometer. However, mean core temperature was elevated on day 14 and 20, as
compared to days 2 and 8. They thus postulated a dissociation of the metabolic responses from
the thermoregulatory responses to exercise during the menstrual cycle (1982b). In a separate
paper, (1982a), they also noted that there was no difference in either the anaerobic threshold or
in the level of perceived exertion at any exercise level that they could attribute to the timing of
the test within the menstrual cycle.
In contrast, a recent "field" study (Brooks-Gunn et al., 1986) looked at the performance
times of 6 adolescent swimmers over a 12 week period and found that they were slowest during
the premenstruum, and fastest during the menstrual phase. Menstrual phase was determined by
a biweekly questionnaire (the Moos Menstrual Distress Questionnaire), and oral basal body
temperature. However subsequent analysis of the basal body temperature data of the cycles, by
the method of Vollman (1977), showed that 5 of 10 cycles were biphasic, 2 of the 10 were
monophasic, and 3 were biphasic with a short luteal phase.
A group of investigators in the USSR (Fomin et al., 1989) assessed the working capacity
of 164 female cross-country skiers by testing their performance during a 5-km test race on the
standard track and during a 12.5-km test race on ski rollers. They also analyzed personality and
69
reactive anxiety at different times during the menstrual cycle. They divided the biologic cycle
into 5 stages including menstrual, postmenstrual, ovulatory, postovulatory, and premenstrual, (but
again without documentation by either BBT or serum progesterone). The best test results were
achieved by women who were in the postovulatory and postmenstrual stages. Their conclusions
were that in order to achieve maximum benefit, training loads should be selected with special
attention to volume and intensity, based on the phase of the cycle.
STUDIES UTILIZING SERUM PROGESTERONE MEASUREMENTS:

A few investigators have adequately documented cycle phase by serum progesterone
and/or estradiol concentrations, and therefore, their findings can be considered as more
scientifically acceptable. Jurkowski et al., (1978, 1981) looked at the performance of 9
moderately trained women (mean 1 .102,. 42.8 + 1.7 mlkemin -1 ) on a bicycle ergometer.
Testing was carried out in the midfollicular phase (6-9 days after beginning of menstruation), and
in the midluteal phase (6-9 days after ovulation as determined by a sustained rise in BBT of 0.3
degrees Centigrade. The procedure involved a predetermination of VO
V0 2
, and then a progressive
incremental exercise protocol of sustained testing for 20 minutes at 33% and then at 66% of this
level of exertion, followed by time to exhaustion at 90% of this value. The first two exercise
loads were termed light and heavy exercise respectively. There were no significant differences
in maximum work load, heart rate, cardiac output or ventilation between the two phases at light
and heavy exercise, or in heart rate at exhaustion; but time to exhaustion doubled in the luteal
phase from 1.57 0.32 minutes to 2.97 + 0.63 minutes (p<.02). There were no significant
differences in 02 uptake, CO2 output, cardiac output or stroke volume to account for this marked
70
improvement in endurance performance. There was, however, an increase in maximum
inspiratory ventilation (VI) during the luteal phase, from 80 +5.4 limin -1 to 88 + 5.6 and,
as will be discussed later, differences in venous blood lactate between the two phases.
Schoene et al., (1981) also tested women in the midfollicular phase (6-10 days after the
onset of menstruation) and the midluteal phase (4-9 days after ovulation), and measured serum
progesterone, both before and after the exercise protocol. They compared three groups of women:
6 nonathletic women with normal cycles, 6 athletic women with normal cycles, and 6 athletic
women who were also amenorrheic. Interestingly, there were no significant differences in
performance or in the time to onset of the anaerobic threshold in the athletic women, irrespective
of their menstrual status. In the nonathletic group, however, maximal exercise response,
expressed either as total exercise time or maximum VO2
or CO2 production, was better in the
follicular phase than during the luteal phase. They postulated that in the nonathletes there might
be some effect of subjective dyspnea, possibly associated with the increase in VE, or change in
respiratory drives during this part of the cycle, which limited maximal exercise performance. The
athletes, on the other hand, did not have any associated alterations in their ventilatory responses
due to the menstrual cycle phase.
Hessemer and Bruck (1985a, 1985b) investigated the influence of the menstrual cycle on
thermoregulatory, metabolic and heart rate responses to exercise at night. They studied 10 women
with normal cycles during the follicular phase (4-7 days after the onset of menses) and the luteal
phase (4-8 days after a sustained rise in BBT) Both phases were properly substantiated by serum
progesterone measurements. Along with their other findings they did note a 5.2% increase in
mean V02 during the luteal phase as compared to the follicular phase. Metabolic rate actually
71
increased by 5.6% in the luteal phase, but surprisingly, net efficiency was 5.3% lower. They did
not document significant differences in any other exercise variables to explain these results; and
thus postulated that it was the elevated body core temperature during the postovulatory phase that
had a negative influence on exercise efficiency.
CARDIOVASCULAR AND HEMODYNAMIC RESPONSES:
Investigators have attempted to implicate hormonally mediated shifts in plasma volume,

hemoglobin concentration and hematocrit, and cardiac output at different phases of the menstrual
cycle in these variations in performance. It has been well documented that one of the long-term
adaptations to endurance exercise is a significant increase in plasma volume. There is a
concomitant but proportionately smaller increase in the red blood cell volume leading to a
subsequent fall in hematocrit termed the "runner's anemia". This phenomenon is postulated to
be effective in lowering blood viscosity, thus facilitating movement of the blood through the
system of vessels and capillaries. It is possible, that this is a "preadaptation" to exercise, as the
commencement of exercise from rest causes a fairly immediate decrease in plasma volume that
continues as exercise is prolonged. This loss of fluid occurs primarily through sweating, but
transcapillary fluid flux in exercising muscle also plays a role in this process.
Significant alterations in the distribution of body fluids occur throughout the normal
menstrual cycle. During the luteal phase, the increase in progesterone acts at the level of the
kidney to block the action of aldosterone resulting in loss of Na + and H20. This stimulates the
renin/angiotensin system to increase aldosterone secretion, and also promotes an increase in
antidiuretic hormone (Gaebelein and Senay, 1982). This is one of the mechanisms felt to be
72
responsible for the fluid retention reported in the postovulatory phase. Estrogen has also been
shown to have a water-retaining effect, potentially due to either an effect on the kidneys, or an
alteration in the synthesis or release of antidiuretic hormone (ADH). The effect on plasma
volume is more pronounced with exogenously administered estrogens (Fortney et al., 1988),
especially in the presence of low blood progesterone concentrations. It appears that estrogen and
progesterone may have opposing influences on the control of body fluids, and this may then
potentially be of significance to the exercising woman both during the course of a normal
menstrual cycle, or during the administration of a combination oral contraceptive agent.
In resting subjects, the luteal "phase" has been associated with decreases in both
hemoglobin and hematocrit (Vellar, 1974). In this study, however, the phase of the cycle was not
accurately determined, and serum estrogen was not measured. Measurements during exercise of
plasma volume, cardiac output, hemoglobin concentration and hematocrit have intermittently
documented significant differences between phases of the menstrual cycle, but there has been no
associated alteration of any of the measurements of performance. Wells and Horvath (1973),
studied the effects of heat stress responses in 7 untrained and unacclimatised subjects at three
times during the cycle: within 36 hours of commencement of menstrual flow, at the estimated
time of ovulation, and midway between ovulation and the day of the next expected menstrual
flow. The time of estimated ovulation was determined on the basis of early morning rectal
temperature recordings taken over a period of 4-5 months. Unfortunately, there was no
documentation by steroid hormone measurements. They found a higher hemoglobin concentration
and hematocrit in the ovulatory tests, and the lowest values during the menstrual flow. There was
essentially no difference in serum electrolytes (except for a higher serum Cr) or plasma proteins.
73
However, total body sweat losses of Na* and C1 were lower during heat exposure in the tests
conducted between the time of supposed ovulation and menstrual flow, suggesting that high
levels of both female sex hormones decreased electrolyte loss in sweat. However, as previously
mentioned, there is no assurance that either estrogen or progesterone were high during this time
period. Interestingly, though, with the addition of moderate exercise to the heat stress, these
effects were no longer observed to any significant extent. Fox et al., (1977) noted an increased
hematocrit in conjunction with an increase in submaximal mean Vol at 13 days after the onset
of menstruation, as compared to measurements obtained 7 days after ovulation, and 3 days after
the onset of menstruation. They did not document any differences in other cardiorespiratory
variables relative to time during the cycle, either at rest or during exercise.
The hydration status of the subjects has also been shown to have a significant effect on
these hemodynamic alterations. Gaebelein and Senay (1982) studied 5 women on a bicycle
ergometer, early in the follicular phase, and in the mid-luteal phase, as documented by an
increase in serum progesterone. They observed a more rapid increase in hemoglobin
concentration and osmoconcentration as well as decreases in plasma volume during exercise in
the follicular phase, especially following hypohydration. Their data are more convincing, and
suggest that both the phase of the menstrual cycle, and the pre-exercise fluid status may be
important determinants of vascular volume dynamics during exercise.
74
TEMPERATURE REGULATION AND HEAT EXCHANGE:
It has been shown that women are less tolerant of heat stress than men, but controversy
still exists regarding the effects of the different phases of the menstrual cycle on
thermoregulation, and there is even more debate as to whether or not there are any significant
implications for performance. Wells & Horvath (1973) investigated the effects of heat stress
responses at 48 degrees Centigrade and 11 mm. Hg water vapor pressure, during three separate
times of the cycle in 7 subjects with "normal" menstrual cycles. They were tested within 36
hours of commencement of menstrual flow, at the estimated time of ovulation (as determined by
basal body temperature recordings), and midway between ovulation and the day of the next
expected menstrual flow. Although there was a tendency towards a higher heart rate and lower
ventilation volumes in the ovulatory tests, there were no differences in core or skin temperature,
02 consumption, or total body sweating rate; and they concluded that cycle phase had no
significant effects on generalized thermoregulatory or metabolic responses to acute short-term
heat exposure. Even the addition of an exercise stress (a 40 minute treadmill walk at 50% of
roC)2z..x) exercise to that of the hot environment did not potentiate any differences in these
variables across the different times of the cycle (Wells & Horvath, 1974). These findings are in
keeping with a previous study by Sargent and Weinman (1966) where the activity of the eccrine
sweat glands was not significantly affected by the stage of the menstrual cycle. Other
investigators (Frye and Kamon, 1981) have also not been able to document any significant
variation in heat stress responses in women in relation to any "phase" during the menstrual cycle.
In contrast, Hessemer and Bruck (1985a, 1985b) documented the cycle phase by
measurement of serum progesterone, and tested their subjects between 3:00 and 4:00 am. when
75
the difference between the temperature in the luteal and follicular phases is at its maximum. They
did demonstrate a higher pre-exercise and postexercise core temperature during the luteal phase,
as well as an elevation in the thresholds for shivering, chest sweating, and cutaneous vasodilation.
There was also a luteal phase increase in the above threshold of chest sweat rate and cutaneous
heat clearance. Others (Stephenson et al., 1982a, 1982b) have 4hown the variation in core
temperature, but have not found any significant variation in performance. They have thus
postulated a dissociation of the metabolic responses from the thermoregulatory responses to exercise during the menstrual cycle.
RESPIRATORY DRIVES AND VENTILATION:

Progesterone has been implicated as a causative factor in the hyperventilation seen during
pregnancy (Moore et al., 1987; Pernoll et al., 1975) and the luteal phase of the cycle (Dombovy
et al., 1987); and a synthetic progestin, medroxyprogesterone-acetate (MPA), is often
administered to patients with central hypoventilation syndromes in order to stimulate ventilation.
It has been shown that giving this same hormone to men will induce all of the ventilatory
changes seen during the luteal phase of the menstrual cycle, but does not cause any significant
alteration in overall exercise performance as measured on a bicycle ergometer (Bonekat et al.,
1987).
It is currently widely held that highly accomplished endurance athletes commonly have
altered respiratory drives, in terms of a decreased ventilator)/ response to hypoxia and
hypercapnia (Byrne-Quinn et al., 1971, Martin et al., 1979). Decreased hypoxic and hypercapneic
ventilatory responses are postulated to have a positive effect in endurance athletes, by decreasing
76
the subjective sensation of dyspnea that may be a factor in limiting maximal exercise
performance, as well as allowing them to continue exercising despite the onset of hypoxia. It has
been suggested that the endogenous surge of progesterone during the menstrual cycle may exert
a deleterious effect on performance due to alterations in these respiratory drives. It is also
possible, that in the luteal phase, the effects of an increased sensitivity of the respiratory center
and a lower W ion concentration may combine to account for a lack of difference in ventilation
during exercise. England and Fahri (1976) noted a decrease in end tidal P an (from a mean value
of 39.8 torr to 36.7 torr) and in base excess during the luteal stage, but failed to measure serum
progesterone, and in fact, calculated the probable time of ovulation by subtracting 14 days from
the date of the first menstrual bleeding.
There are relatively few studies of this nature with accurate hormonal documentation of
the phase of the menstrual cycle. Schoene et al., (1981) examined the relationship between
respiratory drives and exercise performance during different phases of the menstrual cycle (as
determined by serum progesterone measurements) in 6 eumenorrheic athletes, 6 amenorrheic
athletes and in 6 nonathletic controls. They documented an increase in both the hypoxic and
hypercapnic ventilatory responses in the luteal phase in all groups, with the hypoxic ventilatory
response being lower in the athletes in both test periods. Maximal exercise response, expressed
either as total exercise time or maximum 0 2 consumption was significantly decreased during the
luteal phase in the nonathietes only. Ventilatory equivalent was also increased during the luteal
phase. The amenorrheic athletes, on the other hand, showed no changes between the two test
periods on any of the parameters including serum progesterone. Although this study did not
demonstrate an overall difference between the two phases of the cycle in the athletic group, it
77
is interesting that the three athletes who did show luteal increases in hypoxic ventilatory
responses, and hypercapnic ventilatory responses, as well as substantial luteal phase decreases
in V02. related poor performance in training and national competition with the-luteal phase of
their cycle. There was thus a suggestion of a correlation between augmentation of drives and
a decrease in performance as measured by V0 2. and maximal exercise time, at least in the
nonathletic group. In contrast, other investigators (Chen and Tang, 1989) have documented an
interesting finding, that of increased inspiratory muscle endurance (by 26%) in the luteal phase,
and postulated that this was due to a higher level of circulating progesterone, as measured in their
study. Obviously the responses of the ventilatory system to endogenous variation in the female
steroid hormones during the menstrual cycle are myriad and extremely complex.
METABOLIC RESPONSES:
The luteal phase elevations in progesterone and estrogen may in some way impact upon
either substrate utilization or hormonal response patterns during exercise. Glucose uptake and
storage in the liver and muscle is known to be facilitated by estrogens (Bunt, 1990) and
progesterone (Matute and Kalkhoff, 1987); both in animals (Ahmed-Sorour and Bailey, 1981;
Kendrick et al, 1987; Matute and Kalkhoff, 1987), and also in humans (Nicklas et al., 1989).
During prolonged exercise, glycogen is spared when estrogen levels are high. Furthermore, these
responses may be altered or affected by the pre-exercise nutritional status of the subjects, in
addition to the phase of the menstrual cycle. Bonen et al., (1983) tested 19 subjects on a
treadmill under fasting (n=6), glucose-loaded (n=5) and control (n=8) conditions, and found that
for all the groups, the metabolic and endocrine responses to exercise were similar in both the
78
follicular and the luteal phase for glucose, lactate, glycerol, LH, FSH, and cortisol. However, in
the glucose group, the FFA response was lower in the luteal phase, while in the fasted group, the
insulin and GH responses were elevated in the luteal phase. The progesterone response to
exercise in both the control group and the glucose group was found to be greater in the luteal
phase. In the fasted group, there was no alteration in progesterone response in either phase.
Furthermore, this group had a lower LH response and a greater GH response than the other
groups. Earlier studies (Bonen et al., 1979) have also shown that the progesterone and estradiol
increment induced by exercise is relatively greater in the luteal than in the follicular phase. They
postulated that a greater reliance on fat metabolism through oxidation of fatty acids may result
in retardation of the rate of utilization of glycogen and therefore production of lactate.
Several experiments by Jurkowski et al., (1978, 1981) tested trained female athletes during
both the midfollicular phase (6-9 days after the beginning of menstruation, and the midluteal
phase (6-9 days after ovulation). Ovulation was documented by a sustained rise in basal body
temperature of at least 0.3 degrees Centigrade, and cycle phase was subsequently confirmed by
an increase in serum progesterone from a mean of 0.58 ngmr 1 to 8.8 ngrn1 -1 . At work loads of
approximately 33%, 66% and 90% of V0 2., there were no significant differences in maximum
work load, heart rate or ventilation between the two phases, but the time to exhaustion at 90%
of V02.. was increased in the luteal phase from 1.57 + 0.32 to 2.97 + 0.63 minutes. It was
further noted that the exercise-induced increase in plasma lactate during heavy and exhaustive
exercise was greater during the follicular phase than in the luteal phase. A hormonally-mediated
shift towards a greater reliance on free fatty acid metabolism during exercise was postulated to
account for the lower respiratory exchange ratio and the delayed appearance of plasma lactate
79
during the luteal phase. In a separate part of the study, they showed that the phase of the cycle
had no effect on the disappearance of a bolus of infused lactate, thus implying that the difference
during exercise somehow reflected a true difference in production. As these studies were not able
to document any differences in central components of performance such as heart rate, ventilation
and cardiac output, perhaps the variation in performance can be attributed to contributions at the
metabolic and cellular levels.
The only other study to show a potentially significant increase in endurance time during
the luteal phase was also carried out utilizing plasma estradiol and progesterone concentrations
to confirm the phase of the cycle. In their study, Nicklas et al., (1989) performed muscle biopsies
on a group of six eumenorrheic athletes after a bout of depletion exercise on a bicycle ergometer.
Following three days of rest and diet control, these subjects carried out an endurance test to
fatigue (at a workload of 70% of V02.), with pre and post exercise muscle biopsies taken from
the vastus lateralis. These authors were able to document a strong tendency (p=.07) for an
increase in endurance time during the luteal phase (139.2 + 14.9 minutes as compared to 126
17.5 minutes during the follicular phase). This was accompanied by, and potentially due to, a
greater glycogen repletion in the three days following the depletion exercise test during the luteal
phase, but was not associated with any significant alterations in glycogen utilization. Thus, the
interactions of both estrogen and progesterone at the substrate level, are intricate, and as yet,
incompletely understood.
80
EFFECTS OF ORAL CONTRACEPTIVES ON PERFORMANCE:
BACKGROUND:
In terms of the effects of the oral contraceptive agents (OCA) on performance, the evidence
presented so far has been contradictory. Again, the early studies were mostly anecdotal or
retrospective surveys. Bale and Davies (1983) administered a questionnaire to 109 specialist
physical education students. Of these, 69.7% felt that menstruation adversely affected their
performance. They complained of feelings of lethargy and tiredness, and a lack of interest in
physical activity during this time. Of the 50 girls (46%) that were on the birth control pill, it is
interesting that no student thought that her performance had deteriorated as a result, and in fact
8% even felt that their performance had improved. As previously mentioned, Moller-Nielsen and
Hammar (1989) prospectively followed 86 female soccer players over a one year period. They
found a decreased incidence of traumatic injuries in the women who were taking oral
contraceptives as compared to the women who were not (P< 0.05). They attributed-these findings
to an amelioration of premenstrual symptoms such as fluid retention, mood swings, breast
tenderness, etc., that might influence neuromuscular coordination, and thus reduce the rate of
injury. However, an assumption in their statistical analysis was that the cycles were all exactly
28 days in length. This is unlikely to have occurred, and furthermore, without hormonal
documentation of the cycle phases, it cannot be assumed that all of the women in the control
group were even ovulatory.
81
CARDIOVASCULAR AND HEMODYNAMIC RESPONSES:
Various controlled studies have looked at the different components of the cardiovascular
and pulmonary systems. Littler et al., (1974) measured pulmonary blood flow and cardiac output
using N20 whole body plethysmography, and found no significant difference in cardiac index,
pulmonary arterial distensibility, heart rate or systemic blood pressure in any phase in women
on a combined estrogen-progestin pill, a progestin only pill or on no pill at all. When expressed
as cardiac output, however, the estrogen-progestin group had a significantly greater cardiac
output, followed by the progestin only group, as with the control group being the lowest. In
another study, Lehtovirta et al., (1977) also documented a higher blood volume, stroke volume
and cardiac output during exercise, as well as an increase in blood volume at rest, in a group of
13 women taking an OCA containing 0.075 mg of mestranol and 2.5 mg of lynestrenol for 1 to
2 months.
There have been relatively few studies specifically on alterations in either hemoglobin or
hematocrit in women taking OCAs, but since they decrease menstrual blood loss, they are known
to decrease the risk of iron deficiency and anemia, so there may be a differential effect of OCAs
on performance simply by enhancement of the oxygen-carrying capacity of the blood.
RESPIRATORY DRIVES AND VENTILATION:

Just as endogenous progesterone has significant effects on respiratory drives in women,
and medroxy-progesterone acetate (MPA) has been shown to induce similar changes in men; the
possibility exists that synthetic progestins in OCAs may also have deleterious effects. Montes et
al., (1983) examined the effects of oral contraceptives on respiration and found an increase in
82
VE, and VCO2 (but no change in V02 , either at rest, or during exercise) in subjects taking OCA.
This effect was shown to be greater at three months than after six months of use, suggesting that
some respiratory or metabolic adaptations may take place.
METABOLIC RESPONSES:
Others have also investigated the potential effects of oral contraceptive agents on substrate
metabolism. Bonen et al., (1991) have documented an increase in FFA concentrations during mild
exercise, and a lower glucose both at rest and during exercise in subjects taking OCAs. Many
other studies have yielded conflicting reports on the effect of OCAs on glucose and insulin
production or metabolism during exercise (see Bonen et al., 1991). Extrapolation of these results
to the level of muscle metabolism is limited. However, the majority of investigators infer that
a higher concentration of FFA in the blood means that more of this substrate is being
metabolised by the exercising muscle. Furthermore, greater availability of FFA can inhibit
carbohydrate metabolism in skeletal muscle. Conversely, during heavy exercise, muscle glycogen
is metabolised to a greater degree, resulting in higher circulating lactate concentrations, which
in turn, reduce the concentration of FFA. The study of Bonen et al., (1991) however, did not
document any alterations in lactate response in the subjects on OCA.
Another group, (McNeill and Mozingo, 1981) exercised a group of nonathietes on a
bicycle ergometer on the 4th, 10th, and 26th day of their menstrual cycle before taking OCA
(Norlestrin 21 1 mg), and then again during the second cycle of OCA. They demonstrated a
significant increase in the oxygen consumption for standardized work loads of 300 and 600 kpm
when the subjects were taking OCA. They hypothesized a shift in the mixture of substrates
83
utilized in submaximal work towards an increased dependence upon triglycerides and a decreased
dependence on glycogen as a result of taking OCA. Since more oxygen is required to release
each calorie of energy from the triglyceride molecule than from the glycogen -molecule, 'they
further postulated that such a shift in substrate utilization should be manifested by a concomitant
increase in the energy cost of standardized work, in keeping with their findings.
EFFECTS OF ORAL CONTRACEPTIVES ON EXERCISE PERFORMANCE:

Investigators are not in agreement on either the quantitative or directional effects of OCA
on various physiological tests. Interpretation of these studies is further complicated by the
diversity in both the estrogen and progestin components of the OCAs used, as well as in the
range of fitness of the subjects involved. Attempts have been made to examine the effects of
OCA on maximal aerobic capacity, but most studies have been carried out either with the higherdose OCAs, or with relatively untrained subjects. An abstract by Daggett, Davies and Boobis
(1983) has reported that there is a decrease in VO2max (from a mean of 44.6 mlkg-l min-1 to 39.8
mlkg-l min-1 ), as well as a decrease in muscle mitochondrial citrate during OCA use. They
studied 7 active females prior to, one and two months during, and six weeks following oral
contraceptive use, although there is no mention as to which OCA they were utilizing. There were
no fluctuations in post-exercise muscle glycogen and lactate as determined from muscle biopsies.
They did not find any change in respiratory quotient, blood lactate or blood glucose responses
to 60 minutes of exercise at 10% above the lactate inflection point between the two conditions,
but there was a significant increase in ventilatory equivalent during OCA use. They followed
their subjects through two months on OCA and found that the differences returned to normal by
84
6 weeks post-cessation of the medication.
In contrast, De Bruyn-Prevost et al., (1984) used a cross-sectional sample and tested two
different groups of subjects (a control group, and a group on OCA) on a bicycle ergometer for
both aerobic and anaerobic endurance at three times during the cycle: the 1st or 2nd day of
menstruation, at the ovulatory period (or the 14th day of the cycle for the OCA group) and at
the end of the cycle, one to two days before menstruation. There was no documentation as to the
content or composition of the OCAs that the subjects were taking. They concluded that there
were no significant differences either between the groups, or at different phases of the cycle, but
again, phase of the cycle was not identified by measurement of serum progesterone. Furthermore,
the subjects on OCA did not have any pre-OCA results to compare to, to assess any significant
effects in the same subject. Another study with a similar comparative design (Huisveld et al.,
1983) also did not find any significant differences in VO2m., maximal respiratory exchange ratio,
maximum heart rate or the duration of the exercise test on a bicycle ergometer between 10 users
of OCA and 10 nonusers. It is obviously dangerous and incorrect to make any generalizations
from this type of study to the general population of exercising women.
There has been only one prospective trial carried out to date with a low-dose oral
contraceptive. Notelovitz et al., (1987), examined the effects of 6 months of administration of
Ovcon 35 (35 micrograms of ethinyl estradiol and 0.4 mg of norethindrone) in 6 subjects as
compared to 6 controls. The controls were fitted with diaphragms and/or IUD's. The VO2,.0 in
the OCA users declined significantly from 41.2 + 11.8 mlkg -l miti l to 38.4 + 9.8 mlkg -l rnin-1
(a 7% difference) while the control group increased from 42.6 + 2.8 mlkg -l min-1 to 45.9 + 5.8
mlikemin1 over the same time frame (p<.03). There was an increase in weight on OCA from
85
a baseline of 57.5 6.5 kg to 59.3 6.3 kg. They also found an 8% decrease in both the
absolute oxygen uptake (2.4 0.67 1.min' to 2.2 0.5 1.min') and the oxygen pulse (the volume
of oxygen consumed per heart beat (12.2 3.2 mlbear l to 11.2 + 2.2 mlbear l ). The control
group, in contrast, increased their values by 9%, from 12.3 2.3 to 13.4 2.2 mlbear i (p<.02).
All values returned to baseline levels 1 month after stopping the oral contraceptives.
There have been few studies to date on the effects of OCAs on muscle strength, and these
suffer as well from problems of design, and small numbers of subjects. Petrofsky et al., (1976)
tested 7 women, 3 of whom were on two different OCAs; and found that although static muscle
strength on a hand-grip dynamometer was not different between the two groups, OCA use had
a significant deleterious action on isometric endurance. Wirth and Lohman (1982) measured
handgrip endurance time (ET) and force output (FO) at 50% of a maximum voluntary contraction
in three groups of subjects: nonusers, females on OCA, and females taking OCA and Vitamin
B6,
at two different phases in the cycles. The MVC was significantly greater during the follicular
phase in the control subjects, and both the ET and FO were lower in the subjects on OCA, with
no variation during the pill cycle. Unfortunately, neither author was able to offer a convincing
physiological explanation for any of these observed differences.
Thus, the studies to date suggest that there may be subtle variations in performance
throughout the normal menstrual cycle, and that the administration of oral contraceptive agents
to female athletes may potentially have undesirable effects in terms of aerobic capacity and
muscle strength and endurance. What has been lacking is a prospective controlled study involving
athletes at an elite level, using proper documentation of cycle phase by serum progesterone, and
utilizing a single OCA, preferably one of the new low-dose triphasic preparations.
86
APPENDIX B. RAW DATA:
SUBJECT: VA
GROUP: N/A
VARIABLE
FOLLICULAR^LUTEAL^TREATMENT
Weight
kg
Body fat
%
Sum of
skinfolds
mm
Estradiol
pmo111
Progesterone
nmo11 4
Hemoglobin
ginr i
Hematocrit
%
MCV
fL
53.0
53.1
15.1
14.5
76.4
67.6
255
497
0.9
55.0
131
134
38.7
40.0
86
87
2.90
2.94
54.71
55.29
99.1
104.7
187
188
1.14
1.14
AST
seconds
ET-90% V0 2.
seconds
27
35
343
542
R Quadriceps
Nm
R Hamstrings
lim
L Quadriceps
Nm
L Hamstrings
/im
89
100
57
62
92
84
49
60
V02.
lmin -1
V02.
mlkg-l inizi l
V5(max)
lmin -1 BTPS
HR(max)
bpm
RER(max)
MCV, mean cell volume; V0 2., maximum oxygen capacity; VE(max), maximum minute ventilation; HR(max),
maximum heart rate; RER(max), maximum respiratory exchange ratio; AST, anaerobic speed test; ET, endurance
time; R, right; L, left (peak torque measured at 30 degreess -1 , best of three trials)
87
SUBJECT: MO
GROUP: N/A
VARIABLE
FOLLICULAR^LUTEAL^TREATMENT
Weight
kg
Body fat
%
Sum of
skinfolds
58.0
55.7
25.4
23.6
85.1
85.6
101
497
1.6
55.0
120
128
34.9
36.7
96
94
2.93
2.76
50.45
49.62
97.0
94.1
192
196
1.16
1.12
15
14
909
963
111
127
62
70
111
111
54
68
Estradiol
pmo1.1-1
Progesterone
nmo11-1
Hemoglobin
gm1-1
Hematocrlt
%
MCV
fa,
V02.
1min-1
V02.
mlkg i miri l
Vs(max)
lmin -1 BTPS
HR(max)
bpm
RER(max)
AST
seconds
ET-90% V02.,
seconds
R Quadriceps
Nin
R Hamstrings
Nin
L Quadriceps
Nin
L Hamstrings
Nn
MCV, mean cell volume; V0 2., maximum oxygen capacity; V E(max), maximum minute ventilation; HR(max),
time; R, right; L, left (peak torque measured at 30 degreess 4 , best of three trials)
88
SUBJECT: IF
GROUP: Placebo
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
%
Sum of
skinfolds
58.6
57.5
56.5
19.4
17.0
17.1
90.0
89.0
90.0
Estradiol
pmolr l
Progesterone
nmolr i
Hemoglobin
gm1
Hematocrit
77
256
298
1.0
17.5
1.0
128
133
135
37.0
38.7
39.2
MCV
IL
92
95
96
V02.
1min -1
V02.
mlkg-i min-i
V$(max)
1min' BTPS
HR(max)
bpm
RER(max)
2.96
2.93
3.03
50.57
50.91
53.50
105.7
110.7
105.0
180
180
180
1.16
1.17
1.06
AST
seconds
ET-90%1/02.
seconds
23
18
18
798
677
893
R Quadriceps
Nm
R Hamstrings
Nm
L Quadriceps
Inn
L Hamstrings
138
125
155
60
65
84
133
138
149
62
65
70
MCV, mean cell volume; V0 2.,, maximum oxygen capacity; V E (max), maximum minute ventilation; HR(max),
89
SUBJECT: III
GROUP: Placebo
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
%
Sum of
skinfolds
443
44.2
44.0
10.0
112
10.1
44.4
35.8
36.0
Estradiol
pmo11: 1
Progesterone
nmolr i
Hemoglobin
grnl
Hematocrit
%
MCV
IL
131
665
397
1.2
65.0
43.0
129
128
138
37.8
37.6
39.1
92
89
91
V02.
lmin -1
V02.
mlkenie
VE(max)
1.min' BTPS
HR(max)
bpm
RER(max)
2.60
2.63
2.75
58.56
5958
62.16
88.6
90.5
89.3
187
185
190
1.16
121
1.09
AST
seconds
ET-90% V0,,
seconds
21
26
34
1005
1083
951
R Quadriceps
INIin
R Hamstrings
lim
L Quadriceps
Ntn
L Hamstrings
IsIn
106
92
75
65
57
49
117
103
87
68
62
46
90
SUBJECT: PW
GROUP: Placebo
VARIABLE
FOLLICULAR^LUTEAL
Weight
kg
Body fat
56.3
55.4
55.1
14.6
12.6
10.6
Sum of
skinfolds
85.4
81.6
65.4
Estradiol
pmolI' l
Progesterone
nmo11-1
Hemoglobin
gmr 1
Hematocrit
%
MCV
fL
188
536
517
1.6
73.0
63.0
134
143
140
38.8
41.4
413
93
93
93
2.94
2.84
2.94
52.14
51.33
53.44
104.0
104.9
105.5
176
176
176
1.17
1.10
1.21
AST
seconds
ET-90% V02.
seconds
39
33
37
1015
1082
1201
R Quadriceps
Nrn
R Hamstrings
Nin
L Quadriceps
Nm
152
152
149
92
92
89
184
184
157
103
103
98
VOzi.
lmin' l
V02.
mlkg-l min4
VE(max)
lrnin' l BTPS
HR(max)
bpm
RER(max)
L Hamstrings
TREATMENT
Nn
MCV, mean cell volume; V0 2., maximum oxygen capacity; V E (max), maximum minute ventilation; HR(max),
time; R, right; L, left (peak torque measured at 30 degreess'', best of three trials)
91
SUBJECT: JR
GROUP: Placebo
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
%
Sum of
skinfolds
74.0
74.5
74.4
18.8
18.5
17.2
99.8
97.8
101.2
Estradiol
pmo11 -1
Progesterone
nmo11-1
Hemoglobin
gm1" 1
Hematocrit
%
MCV
fi.,
126
238
370
1.1
45.0
8.6
136
137
136
39.0
39.5
39.5
93
93
95
3.85
3.62
3.72
52.10
48.76
50.03
121.6
116.5
116.3
185
175
180
1.19
1.15
1.14
30
26
26
999
771
1205
176
163
182
106
88
98
163
169
182
87
95
89
V02.
1min -1
V02.
mlkg-i mie
VE(max)
1min-1 BTPS
HR(max)
bpm
RER(max)
AST
seconds
ET-90% V0 2,
seconds
R Quadriceps
Isin
R Hamstrings
Nm
L Quadriceps
Nrn
L Hamstrings
Nin
92
SUBJECT: TE
GROUP: Placebo
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
63.5
64.6
66.5
13.1
17.3
18.9
Sum of
skinfolds
77.8
81.2
82.6
Estradiol
pmo11-1
Progesterone
nmo1.1-1
Hemoglobin
gmr i
Hematocrit
115
308
174
1.1
34.0
1.3
139
136
138
41.3
39.4
40.7
MCV
89
88
88
1/02,..
lmin -1
V02,,
mlkg i nnin' i
VE(max)
1min' BTPS
HR(max)
bpm
RER(max)
3.32
3.29
3.18
52.31
50.83
47.78
117.5
116.3
107.4
210
205
215
1.21
1.16
1.11
33
33
28
484
380
328
138
149
146
73
87
81
168
149
149
81
95
84
tL
AST
seconds
ET-90% V/0 2,
seconds
R Quadriceps
Nin
R Hamstrings
Isin
L Quadriceps
/in
L Hamstrings
Nm
MCV, mean cell volume; V0 2,, maximum oxygen capacity; V E(max), maximum minute ventilation; HR(max),
93
SUBJECT: S/
GROUP: Placebo
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
%
Sum of
skinfolds
57.3
57.4
56.1
21.6
21.1
23.7
77.0
83.4
73.6
109
254
340
0.6
24.0
11.5
139
134
137
41.1
39.5
41.8
94
93
94
*0 2.
1min -1
*02,...
mlkenie
V$(max)
1min -1 BTPS
HR(max)
bpm
RER(max)
3.16
2.95
3.11
55.17
51.37
55.46
105.8
105.6
97.4
197
208
204
1.07
1.09
AST
seconds
ET-90% V0 2,.
seconds
14
13
12
628
709
713
106
117
119
65
62
69
106
144
98
62
62
60
Estradiol
pmo114
Progesterone
nmolr i
Hemoglobin
gm1-1
Hematocrit
%
MCV
a,
R Quadriceps
Nrn
R Hamstrings
isin
L Quadriceps
Isin
L Hamstrings
lin
MCV, mean cell volume; VO 2., maximum oxygen capacity; iymax), maximum minute ventilation; HR(max),
94
SUBJECT: ES
GROUP: Placebo
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
%
Sum of
skinfolds
653
65.6
65.8
24.3
21.8
20.5
86.2
83.8
85.6
Estradiol
pmo11 -1
Progesterone
nmo11 -1
Hemoglobin
gmt i
Hematocrit
190
631
455
1.4
41.0
8.2
127
130
126
37.7
39.2
37.8
MCV
fL
91
91
93
V02.
lmin -1
V0 2,..,
mlkg i nie
Vz(max)
lmin -i BTPS
HR(max)
bpm
RER(max)
3.28
3.31
3.56
50.16
50.48
54.11
115.02
120.3
132.6
187
189
192
1.23
1.20
1.13
AST
seconds
ET-90% V0 2.,
seconds
23
25
31
604
630
606
R Quadriceps
Isin
R Hamstrings
Nrn
L Quadriceps
Nm
L Hamstrings
Nm
155
149
155
81
87
81
155
149
146
68
84
84
MCV, mean cell volume; V0 2,., maximum oxygen capacity; V z(max), maximum minute ventilation; HR(max),
95
SUBJECT: CL
GROUP: OCA
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
64.7
64.6
65.2
14.8
15.7
15.5
Sum of
skinfolds
63.4
65.8
69.8
Estradiol
pmo11-1
Progesterone
nmo11 -1
Hemoglobin
gmr 1
Hematocrit
%
MCV
fL
47
437
31
1.3
25.0
0.8
138
140
135
39.5
40.8
38.9
89
90
91
V02,..
lmin -1
V02,..,
mlkenie
V1 (max)
1min -1 BTPS
HR(max)
bpm
RER(max)
3.32
3.47
3.41
51.26
53.67
52.35
116.4
121.1
109.4
188
186
190
1.25
1.28
1.22
42
46
46
424
486
421
171
134
141
106
113
106
179
136
152
122
110
95
AST
seconds
ET-90% V0 2.,
seconds
R Quadriceps
Nm
R Hamstrings
N rn
L Quadriceps
Nnt
L Hamstrings
Nm
MCV, mean cell volume; 17 02,u , maximum oxygen capacity; V E(max), maximum minute ventilation; HR(max),
96
SUBJECT: AM
GROUP: OCA
TREATMENT
VARIABLE
FOLLICULAR^LUTEAL
Weight
kg
Body fat
%
Sum of
skinfolds
61.1
61.2
61.2
12.9
14.3
13.9
77.3
84.8
83.8
178
558
548
1.5
40.0
27.0
137
136
139
39.8
39.8
41.2
91
91
89
3.38
3.24
3.26
55.22
52.95
53.29
102.3
101.9
98.3
203
205
205
1.18
1.13
1.12
AST
seconds
ET-90% V0 2.,
seconds
45
39
35
716
740
651
R Quadriceps
/*In
R Hamstrings
/in
L Quadriceps
Ntn
L Hamstrings
Nm
152
165
138
68
79
65
160
171
141
79
87
65
Estradiol
pmo11-1
Progesterone
nmo114
Hemoglobin
gm1-1
Hematocrit
%
MCV
a.
V02.
lmin -1
V02.
mlkernie
Vs(max)
lmin' i BTPS
HR(max)
bpm
RER(max)
MCV, mean cell volume; V0 2,., maximum oxygen capacity, VE(max), maximum minute ventilation; HR(max),
97
SUBJECT: CS
GROUP: OCA
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
60.1
59.9
60.6^.
24.1
22.6
22.1
Sum of
skinfolds
63.4
73.0
79.6
Estradiol
pmo11-1
Progesterone
nmo1.1-1
Hemoglobin
gm1-1
Hematocrit
154
433
926
2.0
34.0
63.0
129
133
130
38.6
40.2
38.3
MCV
fL
88
89
90
V03.,
lmin -1
V02,,
mlkg i nnind
Vs(max)
1.min -1 BTPS
HR(max)
bpm
RER(max)
3.08
3.01
2.96
51.41
50.29
48.86
93.1
91.79
92.34
184
187
180
1.19
1.25
1.20
AST
seconds
ET-90% V0 2,,,,
seconds
23
19
21
834
695
721
R Quadriceps
106
152
152
R Hamstrings
bin
L Quadriceps
73
62
73
111
136
155
L Hamstrings
Zinn
73
65
76
MCV, mean cell volume; V0 2., maximum oxygen capacity; 'V E(max), maximum minute ventilation; HR(max),
time; R, right; L, left (peak torque measured at 30 degreess" 1 , best of three trials)
98
SUBJECT: KD
GROUP: OCA
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
51.8
51.6
53.4
20.5
20.4
23.2
Sum of
skinfolds
76.2
72.4
86.2
Estradiol
pmoll' i
Progesterone
nmo11 -1
Hemoglobin
gm1 1
Hematocrit
280
414
241
1.2
46.0
52.0
135
129
126
39.0
37.4
36.7
MCV
fi,
99
99
98
V02.
lmin -1
V02.
mlkg-i min-1
Vz(max)
1.min-1 BTPS
HR(max)
bpm
RER(max)
2.72
2.76
2.73
52.44
53.51
51.04
96.7
100.9
99.7
194
198
198
1.12
1.11
1.12
AST
seconds
ET-90% V0 2.
seconds
29
34
30
723
905
405
R Quadriceps
!im
R Hamstrings
Nin
L Quadriceps
Nin
L Hamstrings
163
155
146
108
122
78
155
155
127
103
106
76
MCV, mean cell volume; V0 2,., maximum oxygen capacity; V E(max), maximum minute ventilation; HR(max),
99
SUBJECT: MM
GROUP: OCA
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
64.5
65.3
66.3
16.4
16.9
20.1
Sum of
skinfolds
92.4
89.9
109.4
Estradiol
pmo11-1
Progesterone
nmo11-1
Hemoglobin
gmr 1
Hematocrit
102
376
70
1.2
51.0
0.8
131
134
130
38.5
39.6
39.8
MCV
88
87
85
Vo2.,
3.43
337
3.24
53.20
51.64
48.90
107.2
102.6
103.7
198
190
195
1.18
1.14
1.13
AST
seconds
ET-90% V01
seconds
35
29
33
537
451
261
R Quadriceps
Nin
R Hamstrings
IsIn
L Quadriceps
Nn
L Hamstrings
Nm
179
163
174
87
102
114
198
149
163
119
98
108
fi.,
lmin 4
V02.
mlkg-l min-1
Vz(max)
1min -1 BTPS
HR(max)
bpm
RER(max)
time; R, right; L, left (peak torque measured at 30 degrees -1 , best of three trials)
100
SUBJECT: MC
GROUP: OCA
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
58.4
60.5
59.7
14.8
15.8
15.3^-
Sum of
skinfolds
49.9
67.4
59.0
Estradiol
pmo11-1
Progesterone
nmo11 1
Hemoglobin
gmr i
Hematocrit
%
MCV
IL
88
376
581
1.2
51.0
28.0
128
130
128
38.1
38.9
38.2
90
91
91
3.75
3.65
3.31
64.22
60.36
55.52
110.9
110.6
104.6
181
182
205
1.08
1.18
1/02.
1min -1
V02.
mlkg i miri l
V1(max)
lmin -I BTPS
HR(max)
bpm
RER(max)
AST
seconds
ET-90% V0 2.,
seconds
29
29
34
1133
876
1285
R Quadriceps
Isln
R Hamstrings
Nm
L Quadriceps
/in
L Hamstrings
Nm
174
182
155
98
98
108
171
182
149
103
95
92
time; R, right; L, left (peak torque measured at 30 degreesg i , best of three trials)
101
SUBJECT: IL
GROUP: OCA
VARIABLE
FOLLICULAR^LUTEAL
TREATMENT
Weight
kg
Body fat
61.1
61.3
62.3
12.2
12.9
12.3^-
Sum of
skinfolds
59.0
58.7
66.6
Estradiol
pmolr 1
Progesterone
nmolr i
Hemoglobin
gm1-1
Hematocrit
122
501
36
0.6
34.0
1.2
121
126
127
35.9
38.0
37.6
MCV
98
99
99
V02,
inin-1
V02,
mllcemin' i
V1(max)
1min-1 BTPS
HR(max)
bpm
RER(max)
3.38
3.30
3.38
55.34
53.76
54.31
104.8
107.9
109.9
181
182
175
1.08
1.14
1.14
AST
seconds
ET-90% V02,,,
seconds
28
35
31
908
1318
1178
R Quadriceps
Nm
R Hamstrings
Nin
L Quadriceps
Nm
L Hamstrings
Nm
187
155
138
89
87
106
108
108
100
87
84
89
n.
MCV, mean cell volume; V0 2, maximum oxygen capacity; V E(max), maximum minute ventilation; HR(max),
time; R, right; L, left (peak torque measured at 30 degrees -1 , best of three trials)

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EFFECTS OF THE MENSTRUAL CYCLE AND ORAL CONTRACEPTIVES

A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF

THE UNIVERSITY OF BRITISH COLUMBIA

In presenting this thesis in partial fulfilment of the requirements for an advanced

The University of British Columbia

METHODS AND MATERIALS ^

APPENDIX A. REVIEW OF LITERATURE ^

APPENDIX B. RAW DATA ^

FFA^ free fatty acids

maximum heart rate

hypoxic ventilatory response

International Olympic Commission

''CO2^carbon dioxide production

VE^expired minute ventilation

TABLE Ella. EFFECT OF CYCLE PHASE AND OCA ON ANTHROPOMETRIC,

This work is dedicated to my parents: to my mother, who is always interested in and

or submaximal cardiorespiratory responses employing a variety of protocols. Many of the

equal to or greater than 50 mlkg i nin-1 . Volunteers were recruited from a

Anthropometric measurements included height and weight (Detecto industrial scale),

despite an increase in work load,

were reviewed to ensure that the subjects in each group were

EFFECTS OF THE ORAL CONTRACEPTIVE:

EFFECT OF MENSTRUAL CYCLE PHASE:

Values are means SE. (n=16)

Values are means SE. (n=16)

Figure 1: Effect of Menstrual Cycle Phase

(p4.05), and the relative V0 2. (p=0.02). This occurred between the

Figure 2: Effect of Rx on Sum of Skin Folds

ORAL CONTRACEPTIVE (n=7)

Values are means + SE.

ORAL CONTRACEPTIVE (n=7)

Values are means SE.

EFFECTS OF MENSTRUAL CYCLE PHASE:

), and then before

Graham. Effects of menstrual cycle on metabolic responses to exercise. J. Appl. Physiol.:

Jurkowski, J. E. H., N. L. Jones, C. J. Toews, and J. R. Sutton. Effects of menstrual cycle on

at, 1990a). The majority of investigators believe that lack of estrogen

STUDIES WITHOUT HORMONAL DOCUMENTATION:

STUDIES UTILIZING SERUM PROGESTERONE MEASUREMENTS:

, and then a progressive

or CO2 production, was better in the

CARDIOVASCULAR AND HEMODYNAMIC RESPONSES:

Investigators have attempted to implicate hormonally mediated shifts in plasma volume,

RESPIRATORY DRIVES AND VENTILATION:

RESPIRATORY DRIVES AND VENTILATION:

EFFECTS OF ORAL CONTRACEPTIVES ON EXERCISE PERFORMANCE:

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