Sie sind auf Seite 1von 4

Trends in Biosciences 8(5), Print : ISSN 0974-8, 1203-1206, 2015

Anovulation, Delayed Ovulation and Luteal Insufficiency


College of Veterinary Science & Animal Husbandry, Anand Agricultural University, Anand – 388 001, Gujarat, India email:


Ovulation in the cow occurs 10 to 12 hours after the end of behavioral estrus and 18 to 26 hours after the ovulatory LH peak. During estrus and after the end of estrus, several follicles undergo development but usually only one, it ovulates & the other follicles regress and become atretic. The consequences for fertility of an ovulatory defect are two-fold; either the oocyte is not liberated and hence cannot be fertilized, or it is liberated too late so that the spermatozoa are now incapable of fertilization, or the oocyte has aged and is not capable of normal development. Ovulatory defects occur due to endocrine deficiency or imbalance, failure of the development of hormone receptors at the target tissue or mechanical factors. If the quantity of pituitary hormone released is insufficient, or its timing is incorrect, then ovulation is delayed or fails to occur. In a minority of cases, because of extensive lesions involving adhesion of the ovarian bursa to the surface of the ovary, the physical process of ovulation is prevented.

Key words

Anovulation, Corpus luteum, Estrus, Follicle, Ovulation


Anovulation is failure of cows to ovulate. These animals have abnormal follicular development and abnormal estrous cycles. A syndrome that is associated with those conditions that lead to both true anoestrus or to cystic ovarian disease is that of ovulation failure. Sometimes anovulation is observed before the onset of a period of anovulatory anoestrus, with the follicle regressing and becoming atretic. Similarly, during the puerperium, before the onset of normal cyclical ovarian activity, a similar situation may arise, which is comparable with that observed in seasonal polyestrous species at the start of the breeding season (Jolly, et al., 1995; Beam and Butler, 1999).

If cows are examined per rectum during the first few weeks after calving, a number of enlarged anovulatory follicles can often be detected; they are incorrectly described as being cysts but they

are transient and do not persist even if no treatment is given (Webb, et al., 1999, 2004). Sometimes, a follicle does not regress but, having reached its maximum size of 2 to 2.5 cm in diameter, the wall becomes luteinized. This structure functions in the same way as a corpus luteum, either regressing after 17 to 18 days or frequently much earlier so that the cow returns to estrus at a shorter than normal interval. After the demise of the luteinized follicle, the subsequent estrus will probably be followed by a normal ovulation (Butler, 2000, 2001). Such a structure will be <2.5 cm in diameter and fluid-filled, with a rim of luteal tissue lining the follicle and with no evidence of a point of ovulation. (Lucy, 2003; Wathes, et al., 2003).

Successful ovulation of a dominant follicle during early lactation depends upon an appropriate pattern of LH secretion with the re-establishment of pulsatile LH secretion conducive to preovulatory follicular growth and estradiol secretion being recognized as a key element (Lamming, et al., 1982; Canfield and Butler, 1991; Hampton, et al., 2003). Both LH pulse frequency (Canfield and Butler, 1990) and the ovarian responsiveness to LH pulse signaling (Lamming, et al., 1982) increase during the first 2 weeks post partum. The strong suckling stimulus from a large litter suppresses gonadotropin secretion in the lactating sow and effectively blocks ovarian function and estrus until after weaning (Britt, et al., 1985; Varley and Foxcroft, 1990).

Ovulation failure may be classified into three categories








2. Anovulation with Follicle Growth to Deviation

3. Anovulation with Follicle Growth to Ovulatory or Larger Size







This condition is very rare. It may result as a genetic problem with chromosomal abnormalities


Trends in Biosciences 8 (5), 2015

or in severely malnourished animals. Complete ovarian hypoplasia (underdevelopment or incomplete development) may result from a single recessive autosomal gene with incomplete penetration. These animals have few primordial follicles (Roberts, 1986). Ovarian hypoplasia is also associated with freemartinism. The failure of follicular growth beyond emergence may be due to a deficiency of follicle stimulating hormone (FSH).







Anovulation with follicular growth to deviation but not ovulatory size is a common occurrence, especially in prepubertal animals and in the postpartum period. The characteristic signs of this condition are small ovaries caused by the absence of a corpus luteum (CL) or ovulatory size follicles. However, daily ultrasound evaluation of the small ovaries of these anovulatory cows has demonstrated the presence of follicular waves. Heifers as young as two weeks have follicular waves. Follicular waves occur throughout pregnancy, and the first postpartum wave begins approximately four days postpartum. Although in dairy cows the first postpartum dominant follicle may ovulate, more commonly the first ovulation occurs approximately 33 days postpartum. Malnutrition, suckling or peripartum disease can prolong the time to first ovulation (Wathes, et al.,


In prepubertal animals the hypothalamus is extremely sensitive to the negative feedback effect of estradiol, resulting in inhibition of luteinizing hormone (LH) pulses. As puberty approaches, the number of hypothalamic estradiol receptors decreases, reducing the negative feedback effect of estradiol. The subsequent LH increase supports the growth of the follicle to ovulatory size resulting in sufficient estradiol to induce an LH surge and ovulation (Lucy, 2003).

The postpartum dairy cow is in negative energy balance until approximately eight weeks. The time to first ovulation is variable but is related to the timing of the nadir in negative energy balance for the individual cow. A return to positive energy balance allows an increased maximal size of the dominant follicle, increased follicular estradiol and an increase in pulsatile LH secretion resulting in ovulation. The state of negative energy balance may be similar to that of the prepubertal animal in which

low estradiol level is inhibitory to hypothalamic GnRH secretion (Hampton, et al., 2003).

Anovulation with Follicle Growth to Ovulatory or Larger Size

Cystic Ovarian Disease (COD) is a common and economically significant condition of dairy cattle (Johnson and Coates, 2004). The condition is expressed as two syndromes. Follicular cysts are anovulatory follicles that persist for a minimum of 10 days, have a diameter greater than 2.5 cm and are characterized by either continuous estrus or anestrus. Luteal cysts are anovulatory follicles over 2.5 cm in diameter that are partially luteinized and persist for a prolonged period, and are usually characterized by anestrous. Both follicular and luteal cysts occur in the absence of a CL. However, approximately 40% of cows diagnosed with cysts may also have a CL. This definition has limitations as a cyst is seldom monitored for 10 days prior to diagnosis and the presence of a CL is difficult to determine without the use of ultrasonography. Recent ultrasound data indicates that follicles normally ovulate at approximately 17 mm diameter, suggesting that follicles that persist and have a diameter greater than 17 mm be considered cysts. Follicles destined to become cysts grow at the same rate as those destined to regress or ovulate until approximately 16 mm, following which the cysts continue to increase in size.

Diagnosis of anovulation can only be made retrospectively, by noting on trans rectal palpation or ultra sonography that a follicle persists longer than one would have suspected. In the case of the luteinized follicle it will remain for 17–18 days before regressing; the ovary containing it will be rounded, smooth and fluctuating, rather than irregular and solid as it is with a corpus luteum. Treatment is directed towards ensuring that ovulation occurs at the next oestrus, hence hCG or GnRH administered.

Delayed ovulation

Delayed ovulation is generally assumed to be one of the causes of failure of conception. Certain cows have prolonged estrus. However, this is opined to be related to a delay in corpus luteum (CL) assuming normal steroidogenesis rather than to the delayed ovulation. Conception rate is reduced in cows that ovulated by the second day after estrus (Singh, et al., 2005). Ovulatory defects may be due to endocrine deficiency or imbalance and mechanical factors.

PARMAR, et al., Anovulation, Delayed Ovulation and Luteal Insufficiency


Delayed ovulation is one of the major causes of repeat breeding in cattle. Delayed ovulators have longer interval from onset of estrus to ovulation (Bage, et al., 2002 and Singh, et al., 2005). Therefore the importance of insemination timing with respect to ovulation has repeatedly been emphasized for ensuing fertilization (Rodriguez- Martinez, 2001). Asynchrony in timing of insemination with ovulation results in low pregnancy rate due to fertilization failure (Hunter, 1994). Therefore single insemination following AM- PM rule may lead to poor conception due to shortage of motile/ fertile spermatozoa. This problem might be alleviated if high numbers of fertilizable spermatozoa are available at ovulation. Under this condition, either re-inseminations during estrus (Stevenson, et al., 1990) or single insemination with hormonal therapy to induce ovulation may marginally improve fertility in repeat breeder cow. Diagnosis is difficult and requires sequential rectal palpation of the ovaries. Graafian follicle over one the ovary and same ovary 24 hrs later if same follicle persist then diagnosed as delayed ovulation. In the treatment, give repeated AI at 24 hr interval for two or three times.

Luteal insufficiency

Luteal defects could result from an abnormality inherent to the follicle that ovulate (DiZerega and Hodgen, 1981). For example, Follicular maturity is not synchronized with the ovulatory hormonal signal. To the same extent, the nature of the gonadotropic stimulus provided for ovulation could be of relevance to luteal function. Corpora lutea formed by LH-stimulated ovulation secreted progesterone normally, whereas corpora lutea induced by FSH did not secrete progesterone. Premature stimulation of ovulation with either gonadotropin was followed by suppressed luteal function. Corpora lutea of gonadotropin treated animals appeared older (further developed) which secrete low progesterone. Premature induction of follicular rupture in the ewe is followed by an insufficient luteal phase.

Two distinct irregularities of corpus luteum function are known to occur, The short luteal phase and The inadequate or insufficient luteal phase (Inskeep and Murdoch, 1980; DiZerega and Hodgen, 1981). Secretion of progesterone from the corpus luteum is aberrantly reduced, while the interval to the next ovulation (unlike the shortened luteal phase) is normal. Ovulation attendant with an insufficient luteal condition which leads to the

improper development of corpora lutea and due to either under developed or over developed corpora lutea secrete low amount of progesterone than the normal.

The luteal insufficiency mostly occurs due to follicle destined to ovulate undergoes dramatic maturational changes during the period of time immediately preceding the pre ovulatory surge of gonadotropins (Richards, 1980; Webb and England, 1982). Follicle lacked its potential maturity (i.e. Did not have a complete complement of gonadotropin receptors and follicular cells). Follicular maturity is most critical to the subsequent level of function of the corpus luteum. Hence, the necessity of enhanced follicular maturity, that taking place during the immediate pre ovulatory period, in terms of a requirement for ovulation. This condition is very difficult to diagnose by clinical examination because all such cases they show irregular cycle. Diagnostic method is estimation of milk (12-18 ng/ml) or blood plasma (4-6 ng/ml) progesterone level (usually low level). Treatment is directed towards use of luteotropic drugs.

It could be concluded that the anovulatory estrus rate in dairy cattle is closely connected to parity, breed, and quartile of the year. It may also be concluded that inappropriate release of GnRH at the time of estrus. Once diagnosed, anovulatory estrus can be successfully treated using GnRH analogues. Delayed ovulation is a significant component of the repeat-breeder syndrome in animals. Thus, treatments or management practices oriented toward preventing delayed ovulation in animals. Luteal insufficiency has been associated with decreased fertility in domestic farm animals. Luteal insufficiency is most commonly found at puberty and during resumption of ovarian activity following seasonal or postpartum anestrous.


Bage, R., Gustafsson, H., Larsson, B., Forsberg, M. and Rodrýiguez-Martýinez, M. 2002. Repeat breeding in dairy heifers: follicular dynamics and estrous cycle characteristics in relation to sexual hormone patterns. Theriogenology., 57(9): 2257-2269.

Beam, S. W. and Butler, W. R., 1999. Effects of energy balance on follicular development and first ovulation in postpartum dairy cows. J. Reprod. Fertil. Suppl., 54:


Britt, J. H., Armstrong, J. D., Cox, N. M. and Esbenshade, K. L. 1985. Control of follicular development during and after lactation in sows. J. Reprod. Fertil. Suppl., 33:



Trends in Biosciences 8 (5), 2015

Butler, W. R., 2000. Nutritional interactions with reproductive performance in dairy cattle. Anim. Reprod. Sci., 60: 449-457.

Butler, W. R., 2001. Nutritional effects on resumption of ovarian cyclicity and conception rate in postpartum dairy cows. Anim. Sci. Occas. Publ., 26: 133-145.

Canfield, R. W. and Butler, W. R. 1990 Energy balance and pulsatile LH secretion in early postpartum dairy cattle. Domest. Anim. Endocrinol., 7: 323–330.

Canfield, R. W. and Butler, W. R. 1991. Energy balance, first ovulation and the effects of naloxone on LH secretion in early postpartum dairy cows. J. Anim. Sci., 69: 740-


DiZerega, G. J. and Hodgen, G. D. 1981. Luteal phase dysfunction infertility: A sequel to aberrant folliculogenesis. Fertil. Steril., 35: 489.

Hampton, J. H., Salfen, B. E., Bader, J. F., Keisler, D. H. and Garverick, H. A. 2003. Ovarian follicular responses to high doses of pulsatile luteinizing hormone in lactating dairy cattle. J. Dairy Sci., 86: 1963-1969.

Hunter, R. H. F. 1994. In: Embryonic Mortality in Domestic Species. (Zavy MT and Geisert R.D. Eds): CRC Press, Boca Raton, p. 1-22.

Inskeep, E. K. and Murdoch, W. J. 1980. Relation of ovarian functions to uterine and ovarian secretion of prostaglandins during the estrous cycle and early pregnancy in the ewe and cow. In: R. O. Greep (Ed.) Reproductive Physiology III. International Review of Physiology, Vol. 22. pp 325— 356. University Park Press, Baltimore, MD.

Johnson, W. H. and Coates, A. E. 2004. An update on cystic ovarian disease. In Proceedings International Cong. Anim. Repro., Porto Seguro, Brazil 60-65.

Jolly, P. D., McDougall, S., Fitzpatrick, L. A., Macmillan, K. L. and Entwistle, K. 1995. Physiological effects of undernutrition on postpartum anestrous in cows. J. Reprod. Fertil. Suppl. 49: 477-492.

Lamming, G. E., Peters, A. R., Riley, G. M. and Fisher, M. W. 1982. Endocrine regulation of postpartum function. Current Topics of Vet. Med. Anim. Sci., 20: 148-172.

Lucy, M. C. 2003. Mechanisms linking nutrition and reproduction in postpartum cows. Reprod. Suppl., 61:


Richards, J. S. 1980. Maturation of ovarian follicles: Actions and interactions of pituitary and ovarian hormones on follicular cell differentiation. Physiol. Rev., 60: 51.

Roberts, S. J. 1986. In Veterinary Obstetrics and Genital Disease. Published by the author, Woodstock, Vermont,


Rodriguez-Martinez, H. 2001. Oviduct function in cows and pigs: with special reference to sperm capacitation. Asian-Aust. J. Anim. Sci., 14: 28–37.

Singh, B., Saravia, F., Bage, R. and Rodriguez-Martinez, H. 2005. Pregnancy Rates in Repeat-breeder Heifers Following Multiple Artificial Inseminations during Spontaneous Oestrus. Acta vet. Scand., 46: 1-12.

Stevenson, J. S., Call, E. P., Scoby, R. K. and Phatak, A. P.

1990. Double Insemination and Gonadotropin-Releasing

Hormone Treatment of Repeat-Breeding Dairy Cattle.

J. Dairy Sci., 73: 1766-1772.

Varley, M. A. and Foxcroft, G. R. 1990. Endocrinology of lactation. J. Reprod. Fertil. Suppl., 40: 47-61.

Wathes, D. C., Taylor, V. J., Cheng, Z. and Mann, G. E.

2003. Follicle growth, corpus luteum function and their

effects on embryo development in postpartum dairy cows. Reprod., Suppl., 61: 219-237.

Webb, R. and England, B. G. 1982. Identification of the ovulatory follicle in the ewe: Associated changes in follicular size, thecal and granulosa cell luteinizing hormone receptors, antra/ fluid steroids, and circulating hormones during the preovulatory period. Endocrinology., 110: 873.

Webb, R., Garnsworthy, P. C., Gong, J. G. and Robinson, R.

S. 1999. Consequences for reproductive function of

metabolic adaptation to load. Anim. Sci. Occas. Publ., 24: 99-112.

Webb, R., Garnsworthy, P. C., Gong, J. G., and Armstrong,

D. G. 2004. Control of follicular growth: local interactions

and nutritional influences. J. Anim. Sci., 82: 63-74.

Received on 03-02-2015

Accepted on 07-02-2015