**1. Introduction**

Global warming has multifaceted consequences for livestock today, which exhibits as heat stress, lack of feed and fodder, and alters in epidemiological patterns of vector borne diseases among other things resulting in decline in reproduction performance in production. In Dairy and Beef industries heat stress is the major cause for production loss. Bovines are homoeothermic organisms sustain a balanced body temperature by balancing the quantity of metabolic activities generated heat and also the heat depletion to the surroundings [1]. The heat development and loss keep body temperatures in a narrow range, but illness, inadequate nutrition, and extreme environmental temperatures can disturb the metabolism.

At the time of heat stress, animal productivity and reproduction output reduced dramatically. It also declines the rate of food consumption, milk production, dairy cow health, and reproduction. The upper crucial limit of thermo-neutral zone cattle is approximately 25°C. When the temperature exceeded above the 25°c denotes that dairy cattle can get affected by heat stress [2]. In Lactating cattle's are further vulnerable to heat stress for that reason lactation causes high metabolic energy production, which can lead to hyperthermia. Heat stress appears to have an impact on fertility in the autumn [3]. The lack of fertility, usually related with the June, September, October and November. Thus, cattle are no longer being affected to heat stress [3]. The antral follicle may get affected by the heat stress for long term which further developed 40th to 50th days later into an enlarged dominant follicle [3]. The oocyte get effected by heat stress at the time of pre-ovulatory cycle with involvement of oxidative stress detected in vivo and vitro studies [4, 5]. The administration of antioxidants reduced heat shock in vitro [5]. The embryo pre-implantation is vulnerable towards heat stress, but this vulnerability show reduction in developing embryo. The state of energy balance in lactating cattle's influenced the pattern of follicular growth as well [6]. The negative energy balance and their factors affect the lactation phase, milk productivity level, intake of calcium salts of long-chain fatty acids in energy-rich nutrients and vaccination of bovine somatrophin under the pressure of follicular dynamics. The post-partum lactating and non-lactating cattle's have different numbers of large follicles and E2 ratios during the preovulatory phase. The Temperature-Humidity Index (THI) is a commonly used environmental assessment index for assessing heat stress in dairy production [7]. The values of THI can be categorised into four groups based on the degree of heat stress faced by dairy cattle's. According to Armstrong [2] normal heat stress (71), middle heat stress up to (72 to 79) moderate heat stress (80 to 90), and harsh heat stress (> 90). In tropical and subtropical climates, the THI 72 level is the threshold for high output in terms of lactating and reproduction. The recent studies on THI in temperate climates, on have found that a THI of less than 68 is appropriate for cattle efficiency and welfare.

Heat stress can described with the help of temperature-humidity index (THI) reading with the purpose of is consistently above the thermo-neutral region and has a negative impact on a cattle's efficiency. Thus, the THI > 72 has been linked to heat stress in beef cattle [8] while THI 75 has been linked to heat stress in bulls [8]. Since THI does not account for exposure to radiation or wind velocity, it may underestimate climatic stress in beef cattle.

The objective of this chapter is to describe what could be known about the mitigated strategies for following to overcome heat stress which impairs embryo development and to address physiological, genetic and environmental problems and to enhance bovine production in hot weather.

## **2. Heat stress imbalances reproductive hormones**

The ovarian functions are controlled by gonadotropin hormone (GnRH) which are secreted from the hypothalamus which help in the activation of pituitary gland which further secrete the luteinizing hormones (LH), follicle stimulating hormone (FSH) and gonadotropin hormones [2]. The impact of heat stress on peripheral blood Luteinizing hormone yet to be determined, as some studies have found an increase, decrease or even no effect [2] of heat stress on LH. The lack of LH levels can also disturbs the secretion of estradiol from dominant follicle which causes greater impact on oestrus cycle, maturation of follicles and also decreases the ovarian functions [2]. However, estradiol is essential for ovarian follicle growth, oocyte maturation, and endometrial proliferation. Furthermore, FSH and LH [9], insulin-like growth factor (IGF), LH [9] and anti-Mullerian hormone (AMH) LH [9] have distinct receptors in granulosa cells (GCs) any disruption in GC quality or proliferation capacity can

*Adverse Impact of Heat Stress on Bovine Development: Causes and Strategies for Mitigation DOI: http://dx.doi.org/10.5772/intechopen.99307*

have an indirect impact on follicle growth, disrupting oocyte maturation resulting in impaired embryo development and an unsatisfactory pregnancy outcome LH [9]. Heat stress reduces plasma estradiol concentrations in dairy cattle's [10] which is consistent with lower luteinizing hormone (LH) concentrations and reduced follicle dominance, though this outcomes has not always been seen [10]. There is also widespread consensus that FSH secretion increases in the summer, owing to reduced inhibit secretion from small follicles. When a stressor affect the hypothalamic–pituitary–adrenal axis (HPA) which are responsible to stimulate the hormone such as gonadotropin releasing hormone (GnRH), vasopressin, releasing hormone (CRH) and glucocorticoids [11]. while progesterone, gonadotropins, prolactin, and glucagon rises [11]. Furthermore, glucocorticoids minimise the vulnerability of target tissues to sex steroids by inhibiting pituitary development of gonadal steroids. The rapid initial release of LH is induced by arachidonic acid and its metabolites, whereas the prolonged release of LH is mediated by protein kinase C-dependent mechanisms. By inhibiting the hydrolysis of phospholipids and thus, preventing the synthesis of arachidonic acid, glucocorticoids reduces the release of LH. Gonadal steroids also have ability to control pituitary gonadotropin activity is also influenced by glucocorticoids [11]. The amount of gonadal steroid hormones will decline in the presence of glucocorticoids over hours or even days [11] disrupting reproductive physiology, behaviour and lowering feeding and appetite [11].
