- Heat stress can occur nearly everywhere, but its duration varies among locations.
- Heat stress can negatively affect all aspects of reproduction. These effects can occur within days.
- Heat stress increases embryo loss and reduces estrous expression, embryo quality and size, endocrine hormones, and immune function. These effects can occur within days.
- Heat stress reduces sperm quantity and quality. Using AI versus bulls may improve the number of pregnant cows.
- Implementing a robust synchronization and timed AI program can reduce days open and improve the number of pregnant cows compared to AI on detected estrus during summer.
- Administration of hCG or GnRH on or after AI may improve pregnancy rates during summer; however, results are variable.
- Utilizing in vitro embryo production with sexed semen and timed embryo transfer during heat stress can drastically improve pregnancy rates and the number of heifers born.
Heat stress (HS) negatively impacts all aspects of dairy cattle production. Decreased milk production and reproduction losses during the summer substantially impact the economic potential of dairy farms. Factors such as global warming, population growth in more temperate climates, and an increase in the number of food-producing animals in hotter climates further increase the susceptibility of the dairy industry to HS-related issues (Hulme, 1997; Roush, 1994). The annual economic impact of HS on U.S. animal agriculture has been estimated at $2 billion, with the dairy industry alone accounting for $900 million of this loss. Consequently, strategies should be initiated to lessen the severity of HS on both reproduction and milk production to improve cow performance and farm profitability.
Heat stress occurs over a wide combination of solar radiation levels, ambient temperatures, and relative humidity. This is further aggravated by increased metabolic heat production due to greater dry matter intake, which is assumed to elevate the sensitivity of the lactating dairy cow to HS. The dairy industry continues to focus on selecting for production traits which, in turn, may increase the dairy cow’s susceptibility to HS, further intensifying the summer decline in milk production and reproduction. In addition, selecting for milk yield reduces the thermoregulatory range of the dairy cow (Berman et al., 1985). Breeds predominantly used in the U.S. dairy industry were developed in temperate climates and are most productive between the temperatures of 41° and 59°F. Cows experience a loss in production when temperatures increase from 59° to 77°F (Hahn, 1985). However, dramatic reductions are observed when the temperature exceeds 77°F.
The objective of this paper is to disseminate past and recent information on HS effects in lactating dairy cattle. Although proper cow cooling is still the number one way to improve milk production and reproduction during HS, the intent of this article is to discuss additional approaches to improve summer fertility. Traditional strategies and novel approaches to reduce the negative impact of HS will be discussed with an emphasis on reproductive approaches.
Interrelationships of Heat Stress and Reproduction
As mentioned earlier, genetic selection for milk production has increased metabolic heat output per cow. This has considerably increased the lactating dairy cows’ susceptibility to HS. In addition, during the first several days to weeks following calving, the cow is vulnerable to infectious diseases and metabolic disorders. These stress factors, coupled with physiological, nutritional, and environmental changes occurring at calving, can reduce reproductive performance.
Estrous Activity, Hormone Function, and Follicular Development
Heat stress reduces the length and intensity of estrus. For example, in summer, motor activity and other manifestations of estrus are reduced (Hansen and Arechiga, 1999), and incidences of anestrous and silent ovulations are increased (Gwazdauskas et al., 1981). Nebel et al. (1997) reported that Holsteins in estrus during the summer had 4.5 standing events versus 8.6 standing events/estrus for those in winter. One possible reason for the reduction in expression of estrus observed during HS is that physical activity is reduced as a response to limit heat production.
On a commercial dairy in Florida, undetected estrous events were estimated at 76 to 82% during June through September compared to 44 to 65% during October through May (Thatcher and Collier, 1986). Another possible reason for reduced estrous expression is from suppressed endocrine hormones such as luteinizing hormone and estradiol, important for follicle growth and initiation of estrous behavior (Rensis and Scaramuzzi, 2003). Seasonal studies report lower steroid concentrations in the follicular fluid obtained from large follicles during the hot season associated with reduced viability of granulosa cells and impaired aromatase activity (Badinga et al., 1993; Wolfenson et al., 1995). In a study by Wolfenson et al. (1997), androstenedione production by thecal cells was reduced, and low estradiol concentrations were observed in follicular fluid collected from dominant follicles during autumn. The authors concluded that alteration of steriodogenic capacity induced by HS carry over to the final stages of follicle development. In addition, Roth et al. (2000) observed decreased estradiol and androstenedione production from granulosa and thecal cells obtained from follicles three to four weeks after acute HS. In a similar study, low concentrations of estradiol were observed in the follicular fluid of cows during summer, which increased throughout autumn (Roth et al., 2004).
Heat stress impairs follicle selection and increases the length of follicular waves, thus reducing the quality of oocytes and modulating follicular steroidogenesis (Roth et al., 2001). Summer HS has been shown to increase the number of subordinate follicles while reducing the degree of dominance of the dominant follicle and decreasing inhibin and estrogen levels (Wolfenson et al., 1995; Wilson et al., 1998). In another experiment, Wolfenson et al. (1995) detected a tendency for reduction in plasma inhibin concentrations in HS lactating dairy cows, and Paltra et al. (1997) observed similar results for cyclic water buffaloes. Subsequently, exposure of lactating dairy cows to HS during an entire estrous cycle induced a 50% increase in the number of large (>10 mm) follicles during the first follicular wave (Wolfenson et al., 1995). Also, a similar result was observed in heat-stressed heifers during days 17 to 21 of the estrous cycle (Wilson et al., 1998). This may account for the increase in twinning rate following insemination of cows during the summer, in that increases in the number of large follicles occur in summer compared with winter months (Ryan and Boland, 1991). Summer HS reduces follicular dominance, allowing more than one dominant follicle to develop, thereby explaining the increased twinning seen in summer months. In addition, either due to direct actions of elevated temperature or alterations of follicular function, the oocyte has potential to be compromised. Further investigation is warranted to ascertain HS effects on the endocrine system and subsequent follicle and oocyte growth.
Oocytes, Fertilization, and Early Developing Embryos
During summer, HS reduces pregnancy and conception rates which can carry over into the fall months (Wolfenson et al., 2000). Presently, it is not known at what stage in follicular development that HS damages the ovarian follicle and/or oocyte. This may be an important area for future investigation since the negative effects of HS on the ovary are comparable to negative effects on the testis in which a time lag of 60 days is required before completion of the spermatogenic cycle leading to the production and ejaculation of new sperm that were not damaged by HS. A comparable time lag for recovery in the female ovary/oocyte most likely accounts for a considerable portion of the delay in restoration of fertility seen well into the fall (Roth et al., 2001). Oocytes obtained from dairy cows during the summer HS period had reduced developmental competence in vitro (Rocha et al., 1998). Rutledge et al. (1999) also reported a decrease in the number of Holstein oocytes that developed to the blastocyst stage during July and August compared to cooler months. In both of these studies, fertilization rate was not affected by season, but the lower development following fertilization during summer was indicative of oocyte damage. In contrast, Sartori et al. (2002) showed a significant reduction in the summer for fertilization rate, embryo quality, and nuclei/embryo in lactating cows versus virgin heifers. When superovulated donor heifers were exposed to HS for 16 hours beginning at the onset of estrus, there was no effect on fertilization rate. However, a reduced number of normal embryos were recovered on day 7 after estrus (Putney et al., 1988a). This illustrates that brief HS can still affect oocyte competence within the preovulatory follicle. In addition, exposure of cultured oocytes to elevated temperatures during maturation decreased cleavage rate and the proportion of oocytes that became blastocysts (Edwards and Hansen, 1997). Effects of HS on the developing and ovulated oocyte could significantly impact growth and quality of the subsequent embryo, contributing to the increased amount of embryo loss observed in lactating dairy cattle.
Heat stress can also affect the early developing embryo. When HS was applied from days 1 to 7 after estrus, there was a reduction in quality and development of embryos flushed from the reproductive tract on day 7 after estrus (Putney et al., 1989). In addition, embryos collected from superovulated donor cows in summer months were less able to develop in culture than embryos collected from superovulated cows during fall, winter, and spring months (Monty and Racowsky, 1987). Drost et al. (1999) demonstrated that transfer of in vivo-produced embryos from cows in thermoneutral conditions increased pregnancy rate in HS recipient cows compared to that of HS cows subjected to AI. Embryos appear to have developmental stages in which they are more susceptible to the deleterious effects of HS as shown in vitro. In vitro HS at the 2- to 4-cell stage caused a larger reduction in embryo cell number than HS at the morula stage (Paula-Lopes and Hansen, 2002). An earlier study also observed that HS caused a greater reduction in embryo development when applied at the 2-cell stage than the morula stage (Edwards and Hansen, 1997) or at day 3 following fertilization than at day 4 (Ju et al., 1999). Utilizing techniques (i.e., embryo transfer) to bypass the critical stage at which embryos are most sensitive to HS can dramatically improve fertility as discussed in later sections.
Later Stages of Embryo Development
Not only can HS affect the oocyte and early embryo, it can also reduce embryo growth up to day 17, which is a critical time point for embryo production of interferon-tau. Adequate amounts of interferon-tau are critical for reducing pulsatile secretion of prostaglandin F2α, thus blocking CL regression and maintaining pregnancy. Biggers et al. (1987) indicated that HS reduced weights of embryos recovered on day 17 from beef cows. This reduction in embryo size was associated with reduced interferon-tau available to inhibit prostaglandin F2α pulsatile secretion, which causes CL regression. Putney et al. (1988b) incubated embryos and endometrial explants obtained on day 17 of pregnancy at thermoneutral (39°C, 24 hour) or HS (39°C, 6 hour; 43°C, 18 hour) temperatures. The HS conditions decreased protein synthesis and secretion of interferon-tau by 71% in embryos; however, endometrial secretion of prostaglandin F2α and embryo secretion of prostaglandin E2 increased in response to HS by 72%. Wolfenson et al. (1993) observed that secretion of prostaglandin F2α was increased in vivo when heifers were exposed to high ambient temperatures. Collectively, these studies demonstrate that both the embryo and uterine environment can be disrupted due to HS inhibiting the embryo’s ability to secrete interferon-tau (signal to block CL regression) and maintain pregnancy and (or) manipulating production of important proteins from the uterine lining.
A reduction in the amount of growth factors due to an increased level of milk production and (or) decline in nutritional status due to HS may reduce the amount of necessary embryotrophic growth factors. Secretion of embryotrophic growth factors into the uterine lumen may be controlled by nutritional status of the cow as embryo transfer pregnancy rates were reduced in recipients with low BCS (Mapletoft et al., 1986). Plasma concentrations of insulin, insulin-like growth factor-1, and glucose are decreased in summer compared to winter months, most likely due to low DMI and increased negative energy balance. This reduction in important growth factors and nutrients for reproduction hampers the embryo’s ability for normal growth and production of interferon-tau. Bilby et al. (2006a) reported that supplementing lactating dairy cows with recombinant bovine somatotropin (bST or growth hormone) at the time of AI and 11 days later increased growth factors, conceptus lengths, interferon-tau production, and pregnancy rates in lactating dairy cows compared to cows without bST supplementation. Increasing the availability of important growth factors during HS may improve embryo growth and survival. This strategy combined with feeding bypass fats enriched in eicosapentaenoicacid (EPA) and docosahexaenoic acid (DHA) may benefit reproductive performance during summer HS (Bilby et al., 2006 a,b,c). However, when using techniques such as improved nutrition or a pharmaceutical such as bST to improve embryo viability and growth in vivo, the inherent increase is shifted toward enhancing milk production at the expense of reproduction, in turn, possibly masking the true benefits on fertility. Further studies are warranted to develop tools to target hormonal or nutrient delivery to the reproductive organs in order to improve fertility without losing the benefits of additional nutrients and hormones focused on increased milk production.
Embryo loss, another important factor that affects fertility, is increased during HS. Dairy cows conceiving with singletons or twins are 3.7 and 5.4 times more likely to lose their embryo, respectively, during the hot versus cool season (Lopez-Gatius et al., 2004). In addition, the likelihood of pregnancy loss has been shown to increase by a factor of 1.05 for each unit increase in the mean maximum temperature-humidity index (THI) from days 21 to 30 of gestation. Pregnancy losses with a maximum THI of 55, 55-59, 60-64, 65-69, and > 69 were 0, 1, 2, 8, and 12%, respectively (Garcia-Ispierto et al., 2006). Interestingly, the maximum THI at which embryo loss dramatically increases is 60-64 to 65-69. This is much lower than the generally accepted THI of 72 which has historically been thought to be the threshold at which cows become heat-stressed. This provides additional evidence that reproductive failure occurs at lower temperatures than once expected.
Uterine Environment and Immune Function
Reproduction can be compromised during HS via a suboptimal environment for fertilization, embryo growth, and implantation. Further, HS causes redistribution of blood flow from the visceral organs to the periphery, resulting in decreased availability of nutrients and hormones and ultimately compromising uterine function. Increases in uterine blood flow caused by injection of estradiol-17β were reduced in cows not exposed to shade in summer compared with those receiving shade (Thatcher and Collier, 1986). Also, as mentioned earlier, prostaglandin production is increased and embryo growth and interferon-tau produced by the embryo are reduced due to HS. A culmination of reduced blood flow (which provides the essential nutrients for embryo development) and increased prostaglandin production will severely inhibit embryo survival during summer months.
The effect HS has on immune function has not been evaluated in detail, especially in agriculturally important species. However, the incidence of some health problems certainly appears to increase during the summer months as increased rates of mastitis, retained placenta, metritis, and ketosis have been reported (Collier et al., 1982a). Several epidemiological studies reveal a reduction in fertility for cows affected by disorders of the reproductive tract, mammary gland, and feet and by metabolic diseases such as ketosis, milk fever, and left-displaced abomasum. Retained placenta, metritis, and ovarian cysts are risk factors for conception. Cows had lower conception rates of 14% with retained placenta, 15% with metritis, and 21% for those with ovarian cysts (Grohn and Rajala-Schultz, 2000). Mastitis also significantly reduces fertility in lactating dairy cattle (Hansen et al., 2004). In addition, general stress enhances glucocorticoid levels, which reduces neutrophil function. Therefore, HS-induced increases in cortisol levels may partially explain the negative effects HS has on health.
An additional cause of compromised immune function may be negative energy balance. Negative energy balance in early lactation is associated with a variety of health and reproductive issues (Drackley, 1999). The HS cow also enters negative energy balance and thus (probably not surprisingly) experiences many of the same health problems and reduced reproductive parameters as transitioning cows. The calculated negative energy balance during HS (approx. -5 Mcal/d) is not as severe as in early lactation (i.e., approx. d 7:approx. -15 Mcal/d), but it almost certainly is not a coincidence that both situations have increased rates of similar disorders.
Placental and Fetal Development
When HS is imposed the last two to three months of pregnancy, there are clear effects on placental function and endocrine parameters. Prepartum HS may decrease thyroid hormones and placental estrogen levels while increasing non-esterified fatty acid concentrations in blood, all of which can alter growth of the udder and placenta, nutrients delivered to the unborn calf, and subsequent milk production (Collier et al., 1982a). Collier et al. (1982b) also reported that dairy cows experiencing HS during late gestation had calves with lower birth weights and produced less milk than cows not exposed to HS. This was associated with a reduction in circulating thyroxine, prolactin, growth hormone, and glucocorticoid concentrations. Other researchers have suggested that cooling prepartum cows may increase birth weights, improve colostrum quality, decrease calving-related health disorders, and increase subsequent milk production (Avendano-Reyes et al., 2006; Wolfenson et al., 1988). Feed intake and metabolic rate are adversely affected by HS during the immediate prepartum period, and this may adversely affect the ability of the dairy cow to increase production postpartum.
Modifications to Reproduction Programs
Natural Service Fertility
A majority of dairy producers still use natural service as a component of their reproductive program, further accentuating the effects of HS on reproductive performance in dairy cattle. HS significantly impairs natural service sires by effects on spermatogenesis and reduced libido. Semen quality decreases when bulls are continually exposed to ambient temperatures of 86°F for five weeks or 99.5°F for two weeks despite no apparent effect on libido. Heat stress decreases sperm concentration, lowers sperm motility, and increases the percentage of morphologically abnormal sperm in an ejaculate. After a period of HS, semen quality does not return to normal for approximately two months because of the length of the spermatogenic cycle, adding to the carryover effect of HS on reproduction. However, the use of frozen-thawed conventional semen and AI bypasses effects of heat stress on male fertility. For example, many dairy producers in the United States use AI for a set number of breedings (i.e., three AI breedings) and then move the cow to a corral with natural breeding; however, it may be advantageous to continue to use AI for several more breedings to bypass the deleterious effects described above, especially during, and for a two-month period after, HS. Also, the use of AI will improve genetic progress and eliminate the chance of cows contracting a disease introduced by natural mating.
Timed Artificial Insemination
The use of fixed timed AI (TAI) to avoid the deleterious effects of reduced estrous detection has been well documented. Utilizing some type of TAI protocol (i.e., Ovsynch, Cosynch72, or Ovsynch56), either coupled with or without estrous detection, can improve fertility during the summer. Past studies conducted in Florida during the summer months reported an increase in the number of cows pregnant at 90 days (Arechiga et al., 1998) or 120 days postpartum (De la Sota et al., 1998) compared to cows inseminated at observed estrus even though conception rate at first service was not different (Arechiga et al., 1998). In the study by De la Sota et al. (1998), positive effects of first service TAI during HS were consistent for the course of a year with fewer cows being culled (12.9 versus 22%) and additional cows conceiving (87% versus 78%) if TAI was utilized for first service versus AI at detected estrus. These results provide evidence that using TAI during HS decreased days open, interval from calving to first breeding, and services per conception versus insemination at detected estrus (De la Sota et al., 1998). Subsequently, Jordan et al. (2002) observed two different first-service TAI programs over the course of 11 months, and the effect of season on first insemination was not significant. Other studies have also reported more consistent pregnancy rates through the summer when a synchronization program was used compared with AI at detected estrus (Burke et al., 1996; Britt and Gaska, 1998). Although TAI ensures cows are inseminated by a certain day in milk and can reduce reliance on estrous detection rates during HS, these programs will not overcome the negative impacts of heat stress on oocyte maturation and embryo development.
Use of GnRH or hCG during or after Estrus
Ovulation failure and undetected ovulations increase during HS (Gwazdauskas et al., 1981; Thatcher and Collier, 1986). One possible way to circumvent the lack of ovulation and possibly improve fertility in the summer is through an injection of GnRH at estrus. Ullah et al. (1996) injected GnRH into lactating dairy cows at detected estrus during late summer in Mississippi and increased conception rate from 18% to 29%. In agreement with this study, lactating dairy cows were injected with GnRH at the first signs of standing estrus during the summer and autumn months in Israel, and conception rates increased compared to untreated controls (56% to 41%, respectively; Kaim et al., 2003). Interestingly, a study conducted during the summer in Spain increased conception rates only when GnRH was injected at the time of AI and 12 days later (35.4%) compared to injecting only at TAI (30.8%) or only 12 days after TAI (20.6%; Lopez-Gatius et al., 2006). The authors concluded that, although double treatment with GnRH was highest, strong benefits were also registered following a single GnRH treatment at insemination. In addition, treatment did not affect twin pregnancy rates, yet increased the incidence of an additional corpus luteum (CL).
Progesterone production by the CL is critical for the establishment and maintenance of pregnancy. In a review, Wolfenson et al. (2000) concluded that chronic heat stress reduces progesterone concentrations; however, progesterone concentrations may be increased after an acute heat stress. Several studies have shown that progesterone concentrations can be elevated by inducing an accessory CL with the use of GnRH or hCG from 5 to 14 days after AI. When injecting either hCG or a GnRH agonist on day 5 of the estrous cycle in lactating dairy cows during summer, formation of an accessory CL and elevated progesterone occurred (Schmitt et al., 1996). Nonetheless, conception rates were not improved during HS. Alternatively, Gandy et al. (2002) utilized a TAI program during summer and divided cows into three groups of either no treatment after TAI, GnRH on day 5, or GnRH on day 11 post-TAI. Pregnancy rates were improved for cows receiving GnRH on either day 5 (32.4%) or day 11 (38.2%) after TAI compared with no treatment (18.9%).
Further studies are warranted to ascertain when hormonal manipulation should be utilized post-TAI, which hormonal product to use, and at what degree of heat stress hormonal administration post-TAI is needed.
Embryo Manipulation and Transfer
Embryo transfer can significantly improve pregnancy rates during the summer months (Drost et al., 1999). Embryo transfers can bypass the period (i.e., before day 7) in which the embryo is more susceptible to HS. In a recent study, in vitro-produced embryos with sex-sorted semen were either frozen or remained fresh, then timed embryo transferred into lactating dairy cows during summer versus conventional AI (Stewart et al., 2011). Conception risk was nearly doubled with fresh embryos (39%), and no difference was found between vitrified embryos (27%) compared with conventional AI (21%). When calving rate and gender were evaluated, fresh embryos remained superior (27.5%) compared with vitrified (17.1%) or conventional AI (14.6%), and the number of heifers born was increased in both fresh and vitrified embryo groups versus conventional AI (88% and 84% versus 50%; Bilby et al., 2011). De Vries et al. (2011) evaluated the economic potential using a Markov chain dairy herd simulation model combined with linear programming. In this analysis, using in vitro-produced embryos with sex-sorted semen at a cost of $60 compared to $20 for conventional AI improved profit per cow $22 to $42 depending on different herd constraints used in the model. Costs included in the analysis were semen, AI, embryo transfer, and all associated hormones. Nevertheless, embryo transfer is not a widely adopted technique. Improvements need to be made in in vitro embryo production techniques, embryo freezing, timed embryo transfer, and lowering the cost of commercially available embryos before this becomes a feasible solution. Logistical implementation on a large scale with the need of a skilled technician will also slow commercial adoption. Hormonal treatments of embryos in vitro for improved post-transfer survival during summer have been investigated. Past studies have shown improved development of the embryo to the blastocyst stage when bovine embryos were stimulated with IGF-I (Moreira et al., 2002a,b; Block et al., 2003). The IGF-I has proven beneficial in not only stimulating embryo development but also in protecting embryos from deleterious effects of HS. Jousan and Hansen (2004) conducted a series of studies utilizing in vitro fertilized (IVF) bovine embryos cultured with or without IGF-I. For the first experiment, day 5 embryos (≥ 16 cells) were exposed to either a thermoneutral environment (101.3°F for 24 hours) or a heat stress environment (105.8°F for 9 hours followed by 101.3°F for 15 hours). Heat stress reduced the total cell number at 24 hours after the initiation of heat stress and elevated the number of apoptotic cells within the embryo. However, IGF-I blocked the reduction in cell number and reduced the percentage of cells within the embryo that were apoptotic. In addition, the second experiment utilized similar treatments but evaluated embryos at day 8, and similar results were obtained. This series of experiments, and others, illustrate that IGF-I can enhance embryo survival during HS in vitro.
Since IGF-I appears to have thermal protective properties in vitro, studies were designed to investigate whether transferring embryos cultured with IGF-I into recipient cows during HS would improve pregnancy rates (Block et al., 2003). Lactating Holstein, heat-stressed cows (n = 260) were synchronized with a TAI protocol and received an in vitro fertilization (IVF)-produced embryo cultured with or without IGF-I (100 ng/mL) on day 7. A single embryo was transferred to all recipients (n = 210) with a palpable CL. Transfer of IGF-I-treated embryos increased pregnancy rate at day 53, tended to increase pregnancy rate at day 81, and improved calving rates (Block et al., 2003). This proved that transferring IVF-produced embryos cultured with IGF-I can improve pregnancy rates in recipient heat-stressed, lactating dairy cows.
Although the results from these studies confirm that IGF-I affects the embryo in vitro to improve viability during thermal stress, the question remains if elevated peripheral IGF-I in vivo can increase pregnancy rates during summer. Additional studies were conducted in Florida utilizing recombinant bovine somatotropin (rbST) to stimulate IGF-I production and possibly improve fertility during summer (Jousan et al., 2007). Lactating dairy cows (n = 276) were synchronized and received sequential injections of rbST treatments beginning at approximately 60 DIM or no treatment with rbST. Pregnancy rates (day 45 to 80) did not differ between control and rbST-treated cows for first- (15.2% versus 16.7%) or second-service TAI (17.2% versus 14.8%). However, plasma concentrations of IGF-I, milk yield, and rectal and vaginal temperatures were greater for rbST-treated cows with a reduction in body condition score (Jousan et al., 2007).
Since elevated body temperature compromises fertility in lactating dairy cows (e.g., a 0.5°C increase in uterine temperature on the day of insemination resulted in a 12.8% decrease in fertility; Gwazdauskas et al., 1973), it is possible that increasing IGF-I via rbST treatment protected the developing embryo from the elevated body temperature associated with rbST, ultimately maintaining similar pregnancy rates.
Manipulation of embryos in vitro and (or) development of hormonal therapies for use in vivo may allow for improvements in summer fertility.
Reproductive programs can be modified through hormonal manipulations, embryo transfer, and continued AI to bypass critical time points of which HS appears to be most detrimental. Implementing aggressive reproductive programs during the summer can help improve reproductive performance but will not eliminate reproductive shortfalls. Research is still warranted in developing novel approaches to improve the already low fertility of lactating dairy cows during HS.
Todd R. Bilby, Ph.D.
Texas AgriLife Research and Extension, Texas A&M System
The Dairy Heat Stress Roadshow and proceedings were supported by Agriculture and Food Research Initiative Competitive Grant No. 2010-85122-20623 from the USDA National Institute of Food and Agriculture.
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