Abstract
Simple SummaryEnvironmentally induced hyperthermia, also called heat stress (HS), compromises reproductive physiology in mammals. The number of oocytes is fixed after birth and they are stored in the ovary in a quiescent state (at the stage of the first meiotic prophase) in primordial follicles. There is evidence that HS alters the oocyte quality, the dynamics of follicular growth and ovulation. The dairy cow, submitted to the metabolic stress of high milk production, is a good model for studying the effects of HS on ovarian function. The aim of this review is to describe the influence of HS during the stages of follicular development in dairy cattle, from the activation of primordial follicles to ovulation. Some clinical aspects are also considered.Follicular organization starts during mid-to-late fetal life with the formation of primordial follicles. The bilateral interplay between the oocyte and adjoining somatic cells during follicular growth and ovulation may be sensitive to heat stress (HS). Mechanisms giving rise to pre-ovulatory temperature gradients across reproductive tissues are mostly regulated by the pre-ovulatory follicle, and because the cooling of the gonads and genital tract depends on a counter-current transfer system of heat, HS may be considered a major factor impairing ovulation, fertilization and early embryo development. There is evidence of a long-lasting influence of HS on oogenesis and final follicular maturation. Follicular stages that are susceptible to HS have not been precisely determined. Therefore, the aim of this review was to describe the influence of HS during the staged follicular development in dairy cattle, from the activation of primordial follicles to ovulation. Some clinical prospects are also considered.
Highlights
Induced hyperthermia (heat stress (HS)) compromises reproductive physiology in mammals
Zona pellucida material is deposited around the oocyte, cortical granules are produced within the oocyte cytoplasm and follicles appear to become responsive to gonadotropins [22,23]
As cooling of the gonads and genital tract depends on a counter-current transfer system of heat, HS may be considered a major factor impairing ovulation, fertilization and early embryo development
Summary
Induced hyperthermia (heat stress (HS)) compromises reproductive physiology in mammals (reviewed in [1]). The assumed upper critical temperature under shade is about 25–28 ◦ C, with a maximum temperature-humidity index (THI) of 78.2 [2,3]. These given values, the rectal temperature rises, and the conception rate can decline by an average of 20 to 30% [4,5]. HS compromises hypothalamic GnRH secretion, and the circulating concentrations of LH and FSH are reduced [12,13] It follows that this reduced cascade of neuroendocrine and endocrine events leads to impaired selection and development of ovulatory follicles, ovulation and the development of a functional corpus luteum.
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