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Heat Stress & Animal Reproduction

Dr. Bhaskar Ganguly Doctoral Fellow Veterinary Physiology & Biochemistry College of Veterinary & Animal Sciences Pantnagar - 263145 (INDIA).


Endotherms maintain high core body temperatures The set-point varies diurnally and/ or seasonally Low body temperatures are better tolerated HIBERNATING MAMMALS MAY MAINTAIN CORE BODY TEMPERATURES AS LOW AS 6 - 10 C! High temperatures disrupt membranes & proteins, & cause loss of fluids & electrolytes Homoeothermy is a priority over several other physiological functions Mechanisms by which Heat Stress affects Reproduction Re-distribution of blood flow from core to periphery Reduced feed intake Effects on cellular functions viz. oxidative stress, membrane integrity, etc.

Heat Stress & Male Reproduction

Most mammalian testes & epididymis are suspended outside the abdomen in scrotal sacs Tunica dartos regulates surface area, Cremaster regulates distance from abdomen, Pampiniform plexus allows counter-current heat exchange Heat stress: Environmental heat, Fever, Cryptorchidism Susceptibility: spermatocyte > spermatid > Bspermatogonia Initially concentrated semen is produced which becomes dilute with increasing heat stress Thermal damage is associated with oxidative stress, resulting in apoptosis & DNA breakage Effects of cryptorchidism are enhanced in Superoxide dismutase knockout mice

a. Spermatogenesis

Fertilization by spermatozoon exposed to heat stress results in poor developmental competence of embryos; the conceptuses are small & have lower placental weights Semen characteristics are not immediately affected because damaged spermatogenic cells do not enter ejaculates for some time after heat stress In the bull, where spermatogenesis takes 61 days, alterations in semen occur about two weeks after heat stress & persist up to eight weeks Ejaculated spermatozoa do not show apoptosis or loss of fertilizing capacity when cultured at temperatures characteristic of heat stress However, pre- & post-implantation survival of resulting embryos is compromised X & Y spermatozoa are affected differentially by elevated temperature; ratio is skewed towards female embryos when males experiencing scrotal heat treatment are used for mating

b. Hormone secretion
Pulsed heat stress causes decline in circulating concentrations of testosterone lasting for about two weeks Concentrations are restored in the face of continued heat stress Severe heat stress may compromise LH secretion in males as well

Heat Stress & Female Reproduction

Heat Stress & Female Reproduction

The lactating dairy cow & laying hen are particularly sensitive to heat stress because of the metabolic demands of lactation & oviposition, respectively The magnitude of the summer decline in fertility is much less for non-lactating heifers or cows producing low amounts of milk than for high milk yielders

a. The oocyte
Heat stress compromises the oocyte & the follicle in which it is encased High air temperatures 10 days before estrus were associated with low fertility Steroid production by cultured granulosa & theca cells was low when cells were obtained from cows exposed to heat stress 2026 days previously Follicular changes due to heat stress are nearpermanent; the resumption of fertility seen in lactating dairy cows in the autumn could be hastened by removing follicles formed in the summer

The oocyte
Alterations in follicular function involve those of follicular growth, steroid secretion & gene expression In goats, heat stress reduces plasma concentrations of estradiol & lowers follicular estradiol concentration, aromatase activity & LH receptor level, & delays ovulation In rats, heat stress reduces the levels of gonadotropin receptors & aromatase activity of granulosa cells & the follicular fluid concentrations of estradiol Heat stress can reduce LH secretion Number of small & medium follicles increases due to a decrease in circulating concentrations of inhibin & increased FSH secretion

The oocyte
Heat stress coincident with ovulation & oocyte maturation may not have an effect on their capacity to be fertilized but the resultant embryos develop slowly or abnormally Damage to the oocyte during the pre-ovulatory period by heat shock seems to involve the generation of reactive oxygen species, as the effects are reduced by administration of antioxidants Approx. 1530% of oocytes exposed to elevated temperature undergo apoptosis & inhibitors of apoptosis can reduce the effect of elevated culture temperature on oocyte competence for fertilization & subsequent development

b. Embryonic Development
The pre-implantation embryo is susceptible; susceptibility declines as development proceeds Exposure of lactating cows to Heat stress at day 1 after estrus, when embryos are one to two cells, reduces the proportion of embryos that develop to the blastocyst stage at day 8 after estrus Heat stress at days 3 (816 cells), 5 (morula) and 7 (blastocysts) has no effect on the proportion of embryos that are blastocysts at day 8

Embryonic Development

The adverse effect of heat shock on development of pre-implantation bovine embryos is less for breeds of cattle that evolved in hot climates (Brahman, Romosinuano, Nelore) than for breeds that evolved in cooler climates (Angus, Holstein) The fertility of Holstein cows inseminated during heat stress is greater if semen is from bulls of the Gir breed, than if semen is from Holstein bulls

Embryonic Development
Actions of elevated temperature on the preimplantation embryo probably involve increased production of reactive oxygen species In the mouse, maternal heat stress results in increased reactive oxygen species activity in oviducts and embryos, and reduced glutathione content in recovered embryos Treatment of female mice with either melatonin or vitamin E reduces the effects of heat stress on embryonic development Female embryos are better able to survive than male embryos due to reduced reactive oxygen species production in females

Embryonic Development
Generation of reactive oxygen species in response to heat shock declines as bovine embryos advance in development while intracellular concentrations of the cytoplasmic antioxidant glutathione increase Induced thermo-tolerance response develops (day 4 in cattle; 8 cell stage in mice): exposure to a mild elevation in temperature makes cells more resistant to a subsequent severe elevation in temperature Induced thermo-tolerance involves synthesis of heat shock protein 70 (HSP70); glutathione is required in mice Apoptosis inhibitors increase the magnitude of the reduction in development caused by elevated temperatures; apoptosis of the damaged cells of the embryo allow the embryo to develop normally Heat stress may reduce circulating concentrations of progesterone

c. Fetal Development
Heat stress during gestation causes reduced fetal growth Exposure of pregnant ewes to heat stress causes reduced fetal and placental weights and concentrations of placental hormones in the blood Effects on growth are greater when occurring during mid gestation than when occurring during later gestation

Fetal Development
Reduced fetal weights are not caused due to reduced perfusion to the placenta; placental blood flow per gram of fetus is similar between heat-stressed and control ewes Rather, the cause is an increase in placental vascular resistance due to altered angiogenesis as reflected by aberrant expression of genes such as vascular endothelial growth factor and its receptors and placental growth factor Heat stress probably has more effects during mid-gestation than late gestation because angiogenesis is more extensive in the former period Glucose transport across the placenta is also reduced by maternal heat stress due to reduced expression of GLUT8 in cotyledonary placenta

Reduced secretion of placental hormones as a result of heat stress can cause reduced milk yield: inadequate nutrition for the neonate Maternal hyperthermia can also increase the incidence of teratologies Fetal stress caused by hyperthermia results in changes in physiological functions in adulthood In guinea pigs, heat stress in utero reduces learning activity in adulthood

Fetal Development