Search

Dairy farming is vulnerable to global warming and climate change. Improving and maintaining conception rates (CRs) have a paramount importance for the profitability of any dairy enterprise. There is an antagonistic relationship between fertility and milk yield, and intensive selection for milk yield has severely deteriorated reproductive efficiency. Irrespective of geography and husbandry, modern dairy cows experience heat stress (HS) effects leading to fertility declines, but it worsens in tropical climates. The threshold of HS experience among modern dairy cow has lowered, leading to decreased thermal comfort zone. Studies show that this threshold is lower for fertility than for lactation. HS abatement and robustness response to lactation yield lead to negative energy balance, and cow's reproductive requirements remain unfulfilled. The adverse effects of HS commence from developing oocyte throughout later stages and its fertilization competence; the oestrus cycle and oestrus behaviour; the embryo development and implantation; on uterine environment; and even extend towards foetal calf. Even cows can become acyclic under the influence of HS. These harmful effects of HS arise due to hyperthermia, oxidative stress and physiological modifications in the body of dairy cows. Proper assessment of HS and efficient cooling of dairy animals irrespective of their stage of life at farm is the immediate strategy to reduce fertility declines. Other long‐ and short‐term mitigation strategies to reduce fertility declines during HS include feeding care, reducing disease and mastitis rates, using semen from cooled bulls, timed artificial inseminations (AI), allied hormonal interventions and use of embryo transfer technology. Ultimate long‐term solution should be well‐planned breeding for fertility improvement and HS tolerance. [ABSTRACT FROM AUTHOR]

Simple Summary: Modern dairy cows have elevated internal heat loads caused by high milk production, and the effects of accumulating incremental heat are exacerbated when temperature and humidity increases in the surroundings. To shed this additional heat, cows initiate a variety of adaptive mechanisms including increased respiration rate, panting, sweating, reduced milk yield, vasodilatation, and decreased reproductive performance. Hormonal changes based on reciprocal alterations to the energetic metabolism are particularly accountable for reduced efficiency of the dairy production under the heat stress. As animals experience negative energy balance; glucose, which is also a precursor of milk lactose, becomes the preferential energy fuel. In the absence of proper mitigations, heat stress possesses potential risk of economic losses to dairy sector. Besides physical measures for the timely prediction of the actual heat stress coupled with its proper amelioration, nutritional mitigation strategies should target modulating energetic metabolism and rumen environment. Higher milk yield and prolificacy of the modern dairy cattle requires high metabolism activities to support them. It causes high heat production by the body, which coupled with increasing environmental temperatures results in heat stress (HS). Production, health, and welfare of modern cattle are severely jeopardized due to their low adaptability to hot conditions. Animal activates a variety of physiological, endocrine, and behavioral mechanisms to cope with HS. Traditionally, decreased feed intake is considered as the major factor towards negative energy balance (NEBAL) leading to a decline in milk production. However, reciprocal changes related to insulin; glucose metabolism; failure of adipose mobilization; and skeletal muscle metabolism have appeared to be the major culprits behind HS specific NEBAL. There exists high insulin activity and glucose become preferential energy fuel. Physiological biochemistry of the heat stressed cows is characterized by low-fat reserves derived NEFA (non-esterified fatty acids) response, despite high energy demands. Besides these, physiological and gut-associated changes and poor feeding practices can further compromise the welfare and production of the heat-stressed cows. Better understanding of HS specific nutritional physiology and metabolic biochemistry of the dairy cattle will primarily help to devise practical interventions in this context. Proper assessment of the HS in cattle and thereby applying relevant cooling measures at dairy seems to be the basic mitigation approach. Score of the nutritional strategies be applied in the eve of HS should target supporting physiological responses of abatement and fulfilling the deficiencies possessed, such as water and minerals. Second line of abatement constitutes proper feeding, which could augment metabolic activities and synergizes energy support. The third line of supplemental supports should be directed towards modulating the metabolic (propionates, thiazolidinediones, dietary buffers, probiotics, and fermentates) and antioxidant responses (vitamins). Comprehensive understanding of the energetic metabolism dynamics under the impact of incremental heat load and complete outlook of pros and cons of the dietary ameliorating substances together with the discovery of the newer relevant supplementations constitutes the future avenues in this context. [ABSTRACT FROM AUTHOR]

Simple Summary: Heat stress can have large effects on most aspects of reproductive function in dairy cows. A hot environment can increase blood, rectal, and uterine temperatures, alter ovarian folliculogenesis, suppress fertility, oogenesis, and embryogenesis and ultimately reduce conception and pregnancy rates. Among the components of the female reproductive tract, the ovarian pool of follicles and their enclosed granulosa cells and oocytes are highly sensitive to hyperthermia. Many effects of elevated temperature on granulosa cells and developing oocytes involve increased production of reactive oxygen species, subsequently induce cellular apoptosis, and decrease the developmental ability of oocytes to be fertilized. Furthermore, heat stress-associated reproductive disorders are associated with altered progesterone and reduced estradiol production by ovarian follicles. The review mainly focuses on the follicle-enclosed granulosa cells and oocytes, provides new insights into the cellular and molecular adaptations of granulosa cells and oocyte under heat stress, depicts the role of the follicle microenvironment, and discusses some mechanisms that might underlie oocyte impairment. This study provides a possible way for the genetic adaptation to heat stress both for the regulation of body temperature and cellular resistance to elevated temperature. Heat stress has long been recognized as a challenging issue that severely influences the reproductive functions of dairy cattle, disrupting oocyte development during fetal growth. These detrimental effects of heat stress are the result of either the hyperthermia associated with heat stress or the physiological adjustments made by the heat-stressed animal to regulate body temperature. In addition, elevated temperatures have been implicated in increasing the production of reactive oxygen species. Thus, understanding the impact of heat stress on reproductive functions, from a cellular to molecular level, might help in selecting heat-resilient dairy cattle and developing heat stress mitigation strategies. In the present paper, we have attempted to describe the changes in the reproductive system and function of dairy cattle in response to heat stress by reviewing the latest literature in this area. The review provides useful knowledge on the cellular and genetic basis of oocyte and granulosa cells in heat-stressed dairy cattle, which could be helpful for future research in this area. [ABSTRACT FROM AUTHOR]