Abstract
Simple SummaryHeat stress encountered during late gestation will not only reduce subsequent lactation performance, it will also affect the health and growth performance of calves. This study investigated the effects of seasonal heat stress during late gestation on the growth, metabolism, and immunity of calves. We found that heat stress during this period can impair hormones, oxidative stress, and immunity of calves before weaning and increase the risk of diarrhea in the first week after birth.Heat stress during late gestation could affect subsequent lactation performance, resulting in damage to the immune function, health, and growth performance of calves. This study aimed to compare the effects of 33 days of summer stress (Summer group, 70.15 < THI < 74.28) with 33 days of winter during late gestation (Winter group, 57.55 < THI < 67.25) on the growth, hormones, oxidative stress, and immune function of calves. Calves (Summer, n = 28; Winter, n = 23) were separated from cows immediately after birth and fed with 2 L colostrum within 2 h and 8–10 h after birth, respectively, and weaned at 60 days of age. Bodyweight (BW) was measured at birth and weaning. Withers height (WH), body length, and chest girth were measured at birth, 30 days, and 60 days of age. The health of calves ranging in age from 1 to 7 days was recorded. Plasma interferon-γ (IFN-γ), superoxide dismutase (SOD), adrenocorticotropin (ACTH), gonadotropin-releasing hormone (GnRH), IgG, cortisol, heat shock protein 70 (Hsp70), growth hormone (GH), insulin, lipid peroxide (LPO), and tumor necrosis factor-α (TNF-α) levels were measured in calves at 0 (before colostrum feeding), 3, 7, 14, 28, and 56 days of age. The pregnancy period of the Summer group was shortened by 1.44 days. The Winter and Summer groups had the same birth weight. One week after birth, the incidence of diarrhea was 57.14% and 21.74% in Summer and Winter groups, respectively. Compared with the Winter group, TNF-α in the Summer group increased significantly before colostrum feeding. ACTH and LPO decreased significantly at 3 days of age, ACTH and TNF-α decreased significantly at 7 days of age, Hsp70 increased significantly, ACTH was significantly reduced at 14 days of age, and Hsp70 increased dramatically at 7 days of age. SOD and TNF-α increased statistically at 28 days of age, LPO decreased significantly, and IFN-γ decreased significantly at 56 days of age, while IgG and GH increased significantly. We conclude that maternal heat stress during late gestation can damage the oxidative stress and immune plasma indexes of offspring before weaning.
Highlights
Heat stress disrupts the dairy cow’s production cycle, causing decreased feed intake, metabolic shift, and decreased production efficiency [1]
Heat stress during the dry period harms the function of immune cells in dairy cows preparing for calving, and this effect has been extended to the following lactation [2]
The problem of heat stress in summer is of great concern as it has a severe impact on the entire production cycle of dairy cattle and has become one of the most serious challenges faced by dairy cattle breeders due to the continuous rise in global temperature [5] and intensification of animal farming around the globe [6]
Summary
Heat stress disrupts the dairy cow’s production cycle, causing decreased feed intake, metabolic shift, and decreased production efficiency [1]. Heat stress during the dry period harms the function of immune cells in dairy cows preparing for calving, and this effect has been extended to the following lactation [2]. Heat stress during late gestation significantly impacts dairy calves’ health, growth, and ultimate performance [4]. When dairy cows are exposed to heat stress, they experience increased rectal temperatures and respiratory rates and reduced lying time [7]. Heat stress during lactation changes metabolic rate and reduces feed intake, both resulting in decreased milk yield [8]. The cooling of heat-stressed dairy cows after delivery is beneficial to control and maintain the metabolic compliance changes needed for the beginning of lactation, while ensuring the proper control of inflammation and oxidative metabolites [9]
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