CHAPTER 56 Effects of Environment on Bovine Reproduction
Whoever would study medicine aright must first learn of the following subjects. First, he must consider the effect of each of the seasons of the year and the differences between them.
Originally domesticated in the Near East around 8000 years ago, domestic cattle have become distributed throughout most of the world. The rate of geographic dispersion of cattle has been slow until recently, and distinct genetic populations of cattle have arisen that are adapted to specific environments. Beginning in the latter half of the 19th century, and progressing rapidly in the 20th century to the present, however, technologic advances in transportation and management practices have led to rapid changes in the environment in which cattle are reared and in the genetic composition of cattle. These advances involved geographic change in location of specific breeds, management practices that confer environmental stress, and alterations in the genetics and physiology of cattle that have reduced adaptation to the local environment. As a result, cattle often are placed in environments in which physiologic and productive functions are not optimal. Cattle, like most mammals, are very adaptable animals and possess many homeokinetic mechanisms to maintain critical body functions at the expense of changes in other physiologic functions. Unfortunately, reproduction is one of the physiologic functions that often is most expendable in homeokinetic control systems. In fact, reproductive function is dictated in large part by the environment, and heritability estimates for reproductive traits are low.
At least four general approaches can be taken to manipulate environmental effects on reproduction. First, the environment can be altered to provide cows with conditions more conducive to reproduction. Second, it also is possible to change the cow genetically so that it is more adapted to local environmental conditions. Third, it often is possible to schedule reproductive activity so it occurs when climatic conditions are optimal. Finally, it sometimes is possible to alter the physiology of the cow to modify the effects of environment on reproduction. Successful development of any of these schemes will depend on knowledge of the magnitude of environmental effects and of the physiologic alterations mediating environmental effects. This chapter discusses in detail what is known about these subjects for two environmental inputs—heat stress and photoperiod—and suggests management approaches to enhance reproductive function of cattle through manipulation of these environmental influences. Also provided is some information about other environmental regulators of reproduction.
EFFECTS OF HEAT STRESS ON REPRODUCTIVE FUNCTION
Among the highest physiologic priorities of all homeotherms is maintenance of body temperature. The cow maintains a constant core body temperature of approximately 38.5° C by matching internal heat production with net loss of heat to the environment. In situations leading to hyperthermia (internal heat production greater than net loss of heat), thermoregulatory regions of the central nervous system engage physiologic systems to reduce internal heat production and increase net heat flow from the body. Several physiologic changes that stabilize body temperature are deleterious to reproduction. In addition, the hyperthermia experienced by heat-stressed cows can itself compromise reproductive function. Taken together, these effects lead to a severe reduction in reproductive performance of cattle.
All cattle are at risk of becoming hyperthermic, but the problem of heat stress is greatest in lactating dairy cattle populations. Genetic selection for milk yield has produced an animal with high internal heat production, thus increasing susceptibility to hyperthermia. In lactating cows, the upper critical temperature (the ambient temperature at which hyperthermia occurs) is as low as 24° to 27° C. Effects of heat stress are therefore not limited to the tropics but sometimes occur during the summer in temperate zones. By contrast, many beef breeds are adapted for tropical or semitropical conditions. Indeed, some reports indicate that reproductive function of Zebu cattle is highest in summer and lowest in winter.
Detection of Estrus
As shown in Figure 56-1, ability to detect estrus in Bos taurus declines during periods of heat stress. This decline occurs in large part because of a reduction in duration of estrous behavior. In contrast with B. taurus, evidence for decreased duration of estrus in Bos indicus by heat stress is scarce. Under Florida conditions, estrus in Brahman heifers averaged 8.6 ± 2.3 hours in spring, 5.5 ± 1.2 hours in summer and 5.4 ± 0.5 hours in fall and 6.8 ± 1.6 hours in winter.1 In this same study, under conditions in which variation in feed availability was minimal, the proportion of ovulations without detected estrus was greater in winter (59.7%) than in summer (40.3%).
Fig. 56-1 Seasonal variation in estrus detection in hot climates in dairy cattle. A, Seasonal variation in the duration of estrus in Arizona. B, Data from dairy cows in Virginia on the total number of mounts per estrus detected using a radiotelemetric surveillance system. C, Seasonal variation in the estimated frequency of undetected estrus in a lactating Jersey herd in Florida.
(A, Data from Monty DE, Wolff LK: Am J Vet Res 1974;35:1496–1500; B, data from Nebel RL, Jobst SM, Dransfield MBG, et al: J Dairy Sci 1997;80:179 Suppl 1; C, data from Thatcher WW, Collier RJ: In Morrow DA [ed]: Current therapy in theriogenology, 2nd ed. Philadelphia: WB Saunders, 1986.)
Reduced estrous behavior probably is related, at least in part, to reduced locomotor activity experienced by heat-stressed animals. An endocrine cause also is possible, because heat stress has been reported to reduce peripheral concentrations of estradiol-17β around the time of estrus in some studies. Heat stress also has been observed to decrease gonadotropin responses to injection of gonadotropin-releasing hormone (GnRH) in cows with low circulating concentrations of estradiol-17β.
Effects of Heat Stress on Establishment of Pregnancy
Data in Figure 56-2 illustrate the marked seasonal depression in pregnancy rates per insemination of artificially inseminated dairy cattle in warm months of the year. This depression is most apparent in regions of the world with hot climates but can occur in more temperate areas also. Heat stress is the major environmental factor responsible for lowered pregnancy rates in the summer. Experimental exposure of cattle to heat stress reduced pregnancy rate and embryonic survival, whereas provision of cooling during the summer improved the frequency of cows’ becoming pregnant after insemination (Table 56-1). Moreover, the magnitude of the depression in pregnancy rate is proportional to the degree of hyperthermia; this has been demonstrated for both dairy and beef cows.
Fig. 56-2 Seasonal variation in pregnancy rates per insemination (i.e., conception rates) for lactating dairy cows in Arizona, Florida, South Africa, and Minnesota.
(Data for Arizona: from Monty DE, Wolff LK: Am J Vet Res 1974;35:1496–1500; for Florida: from Cavestany D, El-Wishy AB, Foote RH: J Dairy Sci 1985;68:1471–1478; for South Africa: from Du Preez JH, Terblanche SJ, Giesecke WH, et al: Theriogenology 1991;35: 1039–1049; and for Minnesota: from Udompraset P, Williamson NB: Theriogenology 1987;28: 323–336.)
It is important to define the phases of the reproductive process leading to fertilization and embryonic development that are sensitive to maternal hyperthermia, because together these phases dictate the critical windows in which cows must be kept homeothermic to maintain high pregnancy rates. Disruption of the reproductive process can occur quite early—during oocyte growth or maturation. Although little seasonal effect on fertilization rate for oocytes subjected to in vitro fertilization (IVF) has been observed, fertilized oocytes collected from cows during the summer are less likely to give rise to an embryo capable of development to the blastocyst stage than are embryos collected during the winter. Seasonal variation in performance of embryo production systems based on IVF has been observed even in a relatively cool region like Wisconsin. Additional evidence from Israel suggests that oocyte quality gradually improves as season progresses from early to late autumn, as supported by data from studies in which cows were subjected to multiple oocyte recoveries.
The periovulatory period represents another period during which the establishment of pregnancy can be disrupted by heat stress. For example, heat stress of superovulated cows for 10 hours beginning at the onset of estrus had no effect on fertilization rate but reduced the proportion of normal embryos recovered on day 7 after estrus. This effect of heat stress was not caused by effects on spermatozoa within the reproductive tract, because insemination was not performed until body temperatures of heat-stressed cows had returned to normal. Rather, heat stress altered the oocyte or the reproductive tract so that normal embryonic development was compromised.
In another study, it was demonstrated that heat stress of superovulated cows reduced development and viability of embryos if cows were exposed to heat stress at day 1 after estrus but not if heat stress was given on day 3, 5, or 7 after estrus (Fig. 56-3). Moreover, the reduction in development to the blastocyst stage caused by exposure of cultured embryos to elevated temperature declined as embryos proceeded through development (see Fig. 56-3). Thus, embryos become more resistant to effects of heat stress as pregnancy proceeds. Nonetheless, the embryo can still be damaged by severe heat stress even late in development. For example, heat stress of beef cows from days 8 to 16 of pregnancy reduced conceptus size at day 17.
Fig. 56-3 Developmental changes in resistance of bovine embryos to heat shock. A, Left panel: Effect of heat stress on day 1, 3, 5, and 7 of pregnancy (day 0 = estrus) in superovulated cows on the proportion of embryos recovered as blastocysts. B, Left panel: Data illustrating how stage of embryonic development affects response of embryos to an elevated temperature of 41° C for 12 hours, compared with control conditions of 39° C.
(A, Left panel: Data from Ealy AD, Drost M, Hansen PJ: J Dairy Sci 1993;76:2899–2905; B, left panel: data from Edwards JL, Hansen PJ: Mol Reprod Dev 1997;46:138–145, 1997.)
Causes of Heat Stress–Associated Pregnancy Failure
Potentially, heat stress could cause pregnancy loss by exerting actions on either the oocyte, embryo, or reproductive tract. Furthermore, disruption of pregnancy could occur because of direct effects of elevated temperature on cellular function or as an indirect consequence of physiologic changes for regulation of body temperature.
Heat stress could compromise oocyte competence by at least three possible mechanisms: (1) Disruption in patterns of folliculogenesis could lead to ovulation of an aged oocyte with lowered potential for fertilization. Consistent with this idea is the finding that heat stress beginning at day 1 of the estrous cycle caused earlier emergence of the dominant follicle of the second follicular wave. Such an effect could conceivably alter the quality of the oocyte ovulated at the subsequent estrus, because oocytes from persistent dominant follicles have reduced competence. This mechanism must not be the only one operational, however, because it does not explain why season (and presumably heat stress) adversely affects multiple oocytes in the cohort of follicles ovulated after superovulation, collected by transvaginal ultrasound–guided recovery, or aspirated from excised ovaries. (2) Heat stress also has been reported to affect follicular steroidogenesis. Perhaps alterations in the steroidal environment disrupt oocyte development. (3) Finally, oocytes may be similar to male germ cells in that they have heightened sensitivity to elevated temperature. Unlike most cells, the oocyte in developing follicles is transcriptionally inactive after it reaches a diameter of approximately 110 μm (i.e., at about the 3-mm follicle stage). This means that the range of cellular adjustments to elevated temperature that are possible in the oocyte are limited to those not involving transcription. For example, bovine oocytes cannot undergo increased synthesis of heat shock protein 70 (HSP70) in response to elevated temperature.
Sensitivity to elevated temperature persists for several cleavage divisions after fertilization, with the embryo acquiring increased resistance to heat shock as it proceeds through development. Thus, the increased resistance of cows to heat stress as pregnancy proceeds may reflect developmental changes in the embryo that lead to greater cellular resistance to elevated temperatures (see Fig. 56-3). The molecular basis for increased embryonic thermotolerance is not known. Heat shock protein synthesis in embryos exposed to elevated temperature occurs as early as the four-cell stage, and other biochemical changes may therefore also be important.
The process by which the embryo causes maintenance of the corpus luteum also is potentially sensitive to disruption by heat stress. Culture at 43° C reduced secretion of the antiluteolytic hormone interferon-τ by day 17 conceptuses. Heat shock also increased release of prostaglandin F2α (PGF2α) and prostaglandin E2 from endometrial explants and uterine production of PGF2α in response to oxytocin.
Effects of Heat Stress in Late Pregnancy and the Postpartum Period
Abortion caused by heat stress is rare, but placental function is compromised by heat stress in the last third of pregnancy. Thus, in one study, secretion of the placental hormone estrone sulfate, placental size, and calf birth weight were reduced in the summer or by experimental heat stress (Table 56-2). These effects of heat stress probably are caused primarily by the reduction in blood flow to the placenta that occurs with heat stress. In one study in California, calf mortality in the summer increased as environmental temperature increased. This relationship could reflect the lower calf birth weights caused by heat stress, as well as reduced immunoglobulin transfer to the neonate.
Table 56-2 Heat Stress during Late Gestation and Calf Birth Weight and Subsequent Milk Yield in Dairy Cows
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