Biol Trace Elem Res
DOI 10.1007/s12011-014-9983-x
Relationships Between Blood Mg2+ and Energy
Metabolites/Enzymes After Acute Exhaustive Swimming Exercise
in Rats
Md. Mahbubur Rahman & Sei-Jin Lee & A-Reum Mun & Gareeballah Osman Adam &
Ra-Mi Park & Gi-Beum Kim & Hyung-Sub Kang & Jin-Shang Kim & Shang-Jin Kim &
Sung-Zoo Kim
Received: 8 March 2014 / Accepted: 14 April 2014
# Springer Science+Business Media New York 2014
Abstract Magnesium (Mg) plays a central role in neuronal
activity, cardiac excitability, neuromuscular transmission,
muscular contraction, vasomotor tone, and blood pressure,
all of which are significantly related to physical performance.
To date, the available data about detection of blood total Mg
(tMg; free-ionized, protein-bound, and anion-complex forms)
are inconsistent, and there is limited information on blood
free-ionized Mg (Mg2+) in relation to physical exercise. The
aim of this study was to determine the biochemical changes
related to energy metabolism after acute exhaustive swimming
exercise (AESE) in rats in an attempt to correlate the role of
M. M. Rahman and S. J. Lee contributed equally to this study as co-first
authors.
M. M. Rahman : A.<R. Mun : G.<B. Kim : H.<S. Kang : J.<S. Kim :
S.<J. Kim
Department of Veterinary Pharmacology and Toxicology,
College of Veterinary Medicine, Chonbuk National University,
567 Baekje-daero, Deokjin-gu, Jeonju-si, Jeollabuk-do 561-756,
Republic of Korea
S.<J. Lee
Korea Basic Science Institute Jeonju Center, 567 Baekje-daero,
Deokjin-gu, Jeonju-si, Jeollabuk-do 561-756, Republic of Korea
G. O. Adam
Department of Clinical Studies, Sudan University
of Science and Technology, Khartoum 11111, Sudan
R.<M. Park
Department of Chemical Engineering, College of Engineering,
Chonbuk National University, 567 Baekje-daero, Deokjin-gu,
Jeonju-si, Jeollabuk-do 561-756, Republic of Korea
S.<Z. Kim (*)
Department of Physiology, Chonbuk National University Medical
School, Chonbuk National University, 567 Baekje-daero,
Deokjin-gu, Jeonju-si, Jeollabuk-do 561-756, Republic of Korea
e-mail: szkim@jbnu.ac.kr
blood Mg2+ with metabolites/enzymes related to energy pro-
duction. After AESE, blood Mg2+, tMg, K+, partial pressure of
carbon dioxide, lactate, total protein (T-PRO), high-density
lipoprotein (HDL), creatinine (CRE), blood urea nitrogen
(BUN), uric acid (UA), alanine aminotransferase (ALT), as-
partate aminotransferase (AST), alanine phosphatase (ALP),
lactate dehydrogenase (LDH), and creatinine kinase (CK)
were significantly increased, whereas pH, partial pressure of
oxygen, oxygen saturation, the Mg2+/tMg and Ca2+/Mg2+
ratios, HCO3−, glucose, triglyceride (TG), and low-density
lipoprotein (LDL) were significantly decreased. During
AESE, lactate, T-PRO, albumin, AST, ALP, LDH, CK,
CRE, BUN, and UA showed significant positive correlations
with changes in blood Mg2+, while glucose, TG, and LDL
correlated to Mg2+ in a negative manner. In conclusion, AESE
induced increases in both blood Mg2+ and tMg, accompanied
by changes in blood metabolites and enzymes related to
energy metabolism due to increased metabolic demands and
mechanical damages.
Keywords Mg2+ . Acute exhaustive swimming exercise .
Energy metabolism . Rat
Introduction
During exercise, magnesium (Mg) plays a central role of
neuronal activity, cardiac excitability, neuromuscular trans-
mission, muscular contraction, vasomotor tone, and blood
pressure significantly related to physical performance [1]. In
blood, total Mg (tMg) is divided into three forms as follows:
free-ionized, protein-bound, and anion-complex forms [2].
The free-ionized Mg (Mg2+), as the physiologically active
form, is an essential cofactor for over 325 physiological and

biochemical processes, especially cellular energy production,
glycogen breakdown, and modulation of the activity of aden-
osine triphosphatase (ATPase) as source of energy for cells
[2]. Thus, physical performance during exercise is highly
dependent on body magnesium levels. Adequate levels of
magnesium could delay time to exhaustion [3] and improve
exercise performance by increasing the levels of erythrocyte,
hemoglobin [4], and blood Mg2+ [5] but its deficiency could
affect metabolic response during exercise [6]. In turn, exercise
is a potent stressor with high-energy demand that might lead
to alterations on body Mg2+ levels as most ATP in cells is
bound to Mg2+ [7] and MgATP2− as the active species in
enzyme binding and the energy producing form in active
transport and muscular contraction [8]. Indeed, exercise-
induced alterations of Mg2+ could have significant conse-
quences in metabolism and enzyme activities [1].
Conflicting findings regarding on the change in blood tMg
and Mg2+ levels after acute high-intensive swimming exercise
have been reported. Some studies showed that tMg in blood
did not change after acute swimming exercise in rat [9, 10] or
that tMg in blood decreased after acute swimming exercise in
human [11, 12] and rat [13]. It has also been reported that tMg
in blood increased after acute swimming exercise in rat
[14–16] and gerbil [17]. We have previously demonstrated
that acute high-intensive swimming exercise increased in
blood Mg2+ and lactate but decreased in Ca2+ and glucose
accompanied with metabolic and respiratory acidosis in rat
[18]. However, there has been considerable interest in the
relationships between blood ions and metabolites/enzymes
related to energy metabolism during exhaustive exercise.
The present study was undertaken to determine changes in
blood tMg, Mg2+, Ca2+, Na+, K+, Cl−, and HCO3− after
exhaustive swimming exercise in rats seeking for a correlation
between blood Mg2+ and the metabolites/enzymes involved in
energy metabolism.
Methods
All experimental protocols employed herein were approved
by the committee on the care of laboratory animal resources,
Chonbuk National University, and were conducted in accor-
dance with the Guide for the Care and Use of Laboratory
Animals published by the US National Institute of Health
(NIH Publication no. 85-23, revised 1996).
Animals
Twenty-five male Sprague-Dawley rats (220–250 g, Samtako
Biokorea, Daejeon, Korea) were used. They were housed in
cages maintained at 23±2 °C and 50±5 % humidity in a 12 h
light/dark cycle. Food and water were available ad libitum
before exercise.
Rahman et al.
Acute Exhaustive Swimming Exercise
We designed a forced swimming pool especially
planned for rats. The system consists of a glass chamber
(70 cm in height, 60 cm in length, and 90 cm in width)
filled with water 55 cm high, with a heating system and
an air pumping system. To prevent floating during
swimming, water bubbles were produced by tubes con-
nected to the air pump system. The temperature of the
water within the glass chamber was kept at 36±1 °C via a
thermostatically controlled heater located at the base of the
chamber. The rats were individually forced to swim until
exhaustion (about 3–4 h).
Measurement of Blood Ions, Metabolites, and Enzymes
Blood was collected from tail vein just before swim-
ming and caudal vena cava after immediately follow-
ing swimming. A published procedure was used for
blood collection, storage, and measurement for ion-
ized magnesium in blood [19]. We used Nova Stat
Profile 8 CRT (NOVA Biomedical Corp, Waltham,
MA, USA) for measuring pH, partial pressures of
carbon dioxide (pCO 2 ) and oxygen (pO 2 ), oxygen
saturation (O 2sat), glucose, lactate, hematocrit (Hct),
hemoglobin (Hb), and the concentrations of Na + , K+ ,
Ca 2+ , Mg 2+ , and Cl − . The concentration of HCO 3 −
was calculated using the Henderson-Hasselbalch equation.
The values of anion gap were calculated by the formula
[Na+ −(Cl− +HCO3−)].
Immediately after swimming, serum was separated by cen-
trifugation at 3,000 rpm for 10 min and stored at −20 °C until
needed for biochemical analysis using Hitachi 2070
(Hitachi, Tokyo, Japan) measuring total protein (T-
PRO), albumin (ALB), triglyceride (TG), total choles-
terol (T-CHO), high-density lipoprotein (HDL), low-
density lipoprotein (LDL), creatinine (CRE), blood urea
nitrogen (BUN), uric acid (UA), alanine aminotransfer-
ase (ALT), aspartate aminotransferase (AST), alkaline
phosphatase (ALP), lactate dehydrogenase (LDH), creat-
inine kinase (CK), and tMg. The values of osmolality
(Osm) were calculated by the formula [1.86×Na++(Glu-
cose/18)+(BUN/2.8)+9].
Statistical Analysis
The Prism 5.03 software (GraphPad Software Inc., San Diego,
CA, USA) was used for the statistical analysis of the data.
Results are expressed as mean±standard error of the mean
(SEM). The paired Student’s t test or Wilcoxon matched pairs
test were used as appropriate for discrimination and correlated
with the Spearman’s rank correlation coefficient. The level of
significance was set at p<0.05.
Blood Mg2+ and Energy Metabolites/Enzymes After Exercise

Table 1 Effects of acute exhausting swimming exercise on blood ions (mM/l)

Mg2+ tMg Mg2+/tMg Ca2+ Ca2+/Mg2+

Pre 0.49±0.01 0.74±0.02 0.67±0.02 1.23±0.01 2.51±0.03

Post 0.67±0.01*** 1.25±0.05*** 0.56±0.02*** 1.20±0.03 1.81±0.06***

Na+ K+ Cl− HCO3− Anion gap

Pre 149±1 5.0±0.1 107±1 29.3±0.7 12.6±0.7
Post 151±1 6.5±0.3*** 108±1 18.2±1.2*** 24.5±2.7***

Mg2+ free ionized magnesium, tMg total magnesium, Mg2+ /tMg the ratio of Mg2+ per tMg, Ca2+ /Mg2+ the ratio of Ca2+ per Mg2+ , Anion gap,
[Na+ -(Cl− +HCO3− )]. The data are reported as the mean±SEM (n=25). ***p<0.001; paired Student's t-test or Wilcoxon matched pairs test versus pre-
swimming

Results Correlation Between Blood Mg2+ and Metabolites/Enzymes

Effect of AESE on Blood Ions
As shown in Table 1, acute exhaustive swimming exercise
(AESE) produced significant increases in blood Mg 2+
(p<0.001), tMg (p<0.001), K+ (p<0.001), and anionic gap
(p<0.001), but significant decreases in HCO3− (p<0.001) and
the ratios of Mg2+ per tMg (Mg2+/tMg; p<0.001) and Ca2+ per
Mg2+ (Ca2+/Mg2+; p<0.001). The changes in Ca2+, Na+, and
Cl− were not significant.
Effect of AESE on Blood pH, Gas Composition, Hct, Hb,
and Osm
As shown in Table 2, AESE produced significant increase in
blood pCO2 (p<0.001), but significant decreases in pH
(p<0.001), pO2 (p<0.001), and O2sat (p<0.001). There were
no significant changes in Hct, Hb, and Osm.
Related to Energy Metabolism
As can be seen in Fig 1, the levels of lactate (r=+0.5281;
p < 0.001), T-PRO (r = +0.4780; p < 0.0001), ALB (r = +
0.4134; p<0.01), ALT (r=+0.5539; p<0.001), AST (r=+
0.7487; p<0.001), ALP (r=+0.4427; p<0.01), LDH (r=+
0.7337; p<0.001), CK (r=+0.7236; p<0.001), CRE (r=+
0.4626; p<0.001), BUN (r=+0.5064; p<0.001), and UA (r
=+0.7675; p<0.001) showed a significant positive correlation
with the blood Mg2+ levels. On the contrary, the correlation of
Mg2+ was significantly negative for glucose (r=−0.6173;
p < 0.001), TG (r = −0.7467; p < 0.001), and LDL (r =
−0.3646; p<0.01). No relevant correlations were found be-
tween Mg2+ and T-CHO (r=−0.1150; p=0.4265) and with
HDL (r=+0.2174; p=0.1294).
Discussion

Effect of AESE on Metabolites/Enzymes Related to Energy
Metabolism
As shown in Table 3, AESE produced significant increases in
blood lactate (p<0.001), T-PRO (p<0.001), HDL (p<0.05),
CRE (p < 0.001), BUN (p < 0.001), UA (p < 0.001), ALT
(p < 0.001), AST (p < 0.001), ALP (p < 0.001), LDH
(p<0.001), and CK (p<0.001), but significant decreases in
glucose (p<0.001), TG (p<0.001), and LDL (p<0.01). There
were no significant changes in ALB and T-CHO.
In blood, tMg divided into three fractions: 65 % free-ionized
(Mg2+), 27 % protein-bound (mainly to albumin), and 8 %
anion-complex (e.g., lactate, phosphate, and bicarbonate)
forms [2]. In body, only Mg2+ as the physiologically active
form can be transported in or out of the cell through its
membrane, regulating a number of rate-limiting enzymatic
steps including energy metabolism and the activity of ion
transporters [7]. While the percentage of Mg2+ in blood is
50–70 % of tMg2+, the percentage of Mg2+ in cell is 5–10 %
[2]. Normally, most of the intracellular Mg2+ is bound to ATP

Table 2 Effects of acute exhausting swimming exercise on blood pH, gas compositions, hematocrit, hemoglobin, and osmolality

pH pCO2 (mmHg) pO2 (mmHg) O2sat (%) Hct (%) Hb (g/dl) Osm (mOsm/l)

Pre 7.31±0.02 48.2±1.9 63.0±2.6 81.3±2.7 42±1 13.6±0.2 300±2

Post 7.05±0.04*** 61.4±3.5** 32.8±2.7*** 46.5±3.3*** 44±1 14.0±0.2 304±3

pCO2 partial pressure of carbon dioxide, pO2 partial pressure of oxygen, O2sat oxygen saturation, Hct hematocrit, Hb hemoglobin, Osm osmolality. The
data are reported as the mean±SEM (n=25). *p<0.05, **p<0.01, and ***p<0.001; paired Student’s t-test or Wilcoxon matched pairs test versus pre-
swimming
 Rahman et al.

Table 3 Effects of acute exhausting swimming exercise on blood metabolites and enzymes

Glucose (mg/dl) Lactate (mM/l) T-PRO (g/dl) ALB (g/dl) TG (mg/dl) T-CHO (mg/dl) HDL (mg/dl) LDL (mg/dl)

Pre 125±3 3.04±0.14 4.9±0.1 2.5±0.1 108±6 67±1.3 33±1 11±1

Post 94±7*** 4.28±0.26*** 5.3±0.03*** 2.7±0.1 22±3*** 62±2.3 37±1* 9±0**

CRE (mg/dl) BUN (mg/dl) UA (mg/dl) ALT (IU/l) AST (IU/l) ALP (IU/l) LDH (IU/l) CK (IU/l)
Pre 0.5±0.0 21.0±0.4 0.8±0.1 68±3 133±6 602±19 214±8 1,209±38
Post 0.6±0.0*** 26.7±1.3*** 3.0±0.2*** 110±8*** 325±24*** 687±29** 698±58*** 3,187±303***

T-PRO total protein, ALB albumin, TG triglyceride, T-CHO total cholesterol, HDL high-density lipoprotein, LDL low-density lipoprotein, CRE
creatinine, BUN blood urea nitrogen, UA uric acid, ALT alanine aminotransferase, AST aspartate aminotransferase, ALP alkaline phosphatase, LDH
lactate dehydrogenase, CK creatinine kinase. The data are reported as the mean±SEM (n=25). *p<0.05, **p<0.01, and ***p<0.001; paired Student’s t
test or Wilcoxon matched pairs test versus pre-swimming

and changes in cytosolic ATP concentration results in the
changes in intracellular free Mg2+ [7]. Several studies have
shown that the ratio between the Mg2+ and tMg is not constant
[20, 21]. Although accumulating evidence has shown a direct
relationship between body Mg levels and exercise, data for blood
tMg and Mg2+ levels after exercise are inconsistent [1, 5, 9–18,
22] and only limited information is available on exercise effects on
Mg2+ as an important metabolic and regulatory species [18, 22].
Partially, such heterogeneity can be attributed to species, ex-
perimental designs, and intensity or duration of exercise. Also, the
time of blood sampling and the chosen analytical protocols must
be taken into account [1]. In general, short-term high intensive
exercise has been shown to be associated with increase in tMg,
hypermagnesemia, while long-term endurance exercise results in
decrease in tMg, hypomagnesemia [1]. In agreement with these
findings, our results show that AESE causes an increase in both
Mg2+ and tMg, together with increases in K+, HCO3−, and anion
gap. Other studies support these observations: increases in blood
Mg2+ [18] and tMg after swimming in rat [14–16] and gerbil [17].
Interestingly, we found that the Mg2+/tMg after AESE was

Fig. 1 Spearman’s rank correlation between blood Mg2+ and metabo- creatinine, BUN blood urea nitrogen, UA uric acid, ALT alanine amino-
lites/enzymes via during acute exhausting swimming exercise. T-PRO transferase, AST aspartate aminotransferase, ALP alkaline phosphatase,
total protein, ALB albumin, TG triglyceride, T-CHO total cholesterol, LDH lactate dehydrogenase, CK creatinine kinase
HDL high-density lipoprotein, LDL low-density lipoprotein, CRE
Blood Mg2+ and Energy Metabolites/Enzymes After Exercise
significantly decreased, suggesting an increase in protein-bound
and anion-complex forms resulting from increases in proteins and
anions after exhaustion that would interact with Mg2+.
It would be expected that hypermagnesemia after AESE was
due to (1) a consequence of a decrease in plasma volume or (2)
an increase in Mg2+ efflux from cell to blood resulting from a
change in intracellular Mg2+ homeostasis following muscle
contraction, acidosis, and increased energy demand. Consider-
ing the exercise-induced plasma volume decrease (mean
change: −6.1±3.89), Hct and Hb values were used to estimate
relative changes in plasma volume [23]. This in turn resulted in
a slight decrease in Mg2+ from 0.67±0.02 to 0.64±0.02 and
tMg from 1.25±0.05 to 1.19±0.05 (corrected for volume
changes), with significant differences (p<0.001) when com-
pared to with preswimming values; 0.49±0.01 of Mg2+ and
0.74±0.02 of tMg. In spite of a decrease in plasma volume, the
Ca2+ and Ca2+/Mg2+ were decreased after swimming with no
significant change in Na+ and Cl−. Consequently, the change in
plasma volume did not alter Mg2+ homeostasis after AESE in
this study.
During exhaustive high-intensity exercise, muscle must get
sufficient ATP from oxidative and non-oxidative energy ca-
tabolism of glycogen, glucose, protein, amino acid, or fatty
acid, including mainly anaerobic glycolysis [24]. The in-
creased energy production produces an increase in CO2 and
lactic acid, which dissociates to lactate and free H+. In this
study, we demonstrated that AESE resulted in decreases in
blood pH, glucose, TG, HCO3−, pO2, and O2sat as well as
increases in lactate, T-PRO, CRE, BUN, UA, and pCO2,
suggesting increased energy production accompanied with
metabolic and respiratory acidosis. Exercise and muscle con-
tractions increased glucose uptake by skeletal muscles [25,
26]. The increased lactate level further lowers the pH, which
can result in various biochemical and physiological side ef-
fects on glycolysis, phosphofructokinase, and muscular con-
tractions caused by change in ionic homeostasis [27].
The increased energy production from proteins and amino
acids coincided with increases in BUN and UA and decreases in
phosphocreatine and pH values [28]. In energy metabolism
including glycolysis, the citric acid cycle, and oxidative
phospholylation, Mg2+ plays a predominant role as cofactors
including Mg2+-dependent seven enzymes for the formation of
pyruvate from glucose, thiokinase, pyruvate, succinate,
isocitrate, and glutamate dehydrogenases, etc [29]. Mg2+ is
essential for muscle contraction because actions of actin and
myosin filaments are ATP dependent [1]. Therefore, high-
energy demand during exercise could increase Mg2+ in skeletal
muscle as a result of an increase of H+ concentration [8] and
MgATP2− degradation due to the exercise associated ATP de-
pletion [30]. Furthermore, it was reported that extra- and intra-
cellular acidification in muscle produced a significant increase in
intracellular Mg2+ [31, 32], resulting in hypermagnesemia due
to an increase in consequent Mg2+ efflux [33].
The results of this study show that changes in blood Mg2+
during AESE have a significant negative correlation with
changes in glucose, TG, and LDL, but the opposite occurs
with respect to lactate, T-PRO, ALB, AST, ALP, LDH, CK,
CRE, BUN, and UA. As a consequence of both metabolic and
mechanical causes during AESE, the cell membrane integrity
of muscle fibers can be damaged and the cytosolic enzymes
including ALT, AST, ALP, LDH, and CK leak out into circu-
lating blood [34] with a concurrent increase in enzymatic
activities due to energy demands [35]. Indeed, metabolically
exhausted and mechanically damaged muscle fibers exhibit a
decrease in the membrane resistance following an increase in
the intracellular Ca2+, promoting activation of the K+ channel
[36] and hypermagnesemia due to increased Mg2+ leakage
[37].
In view of the above arguments and the new data presented
herein, we strongly propose that AESE induces an increase in
blood Mg2+ and tMg, accompanied by changes in blood
metabolites and enzymes due to increased metabolic demands
and mechanical damages.
Acknowledgments This paper was supported by research funds of
Chonbuk National University in 2012.
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