Records of late-gestation heat stress studies conducted over 10 consecutive years in Florida were pooled and analyzed to test the hypothesis that maternal hyperthermia during late gestation impairs performance of the offspring across multiple generations and lactations, ultimately impeding the profitability of the US dairy sector. Dry-pregnant multiparous dams were actively cooled (CL; shade of a freestall barn, fans and water soakers, n = 196) or not (HT; shade only, n = 198) during the last 46 d of gestation, concurrent with the entire dry period. After data mining, records of 156 daughters (F 1 ) that were born either to CL (CL F1 , n = 77) or HT dams (HT F1 , n = 79) and 45 granddaughters (F 2 ) that were born either to CL F1 (CL F2 , n = 24) or HT F1 (HT F2 , n = 21) were used in the analysis. Life events and daily milk yield for 3 lactations of daughters and granddaughters were obtained. Milk yield, reproductive performance, and productive life data were analyzed using MIXED and GLIMMIX procedures, and lifespan was analyzed using PHREG and LIFETEST procedures of SAS (SAS Institute Inc., Cary, NC). Milk production of HT F1 was reduced in their first (2.2 kg/d), second (2.3 kg/d), and third lactations (6.5 kg/d) compared with CL F1 . More HT F1 were culled before first calving, and the productive life and lifespan of HT F1 were reduced relative to CL F1 (4.9 and 11.7 mo, respectively). The granddaughters (HT F2 ) born to HT F1 produced less milk in their first lactation (1.3 kg/d) relative to granddaughters (CL F2 ) born to CL F1 . More HT F2 were culled before first breeding relative to CL F2 ; however, productive life and lifespan were not different between HT F2 and CL F2 animals. An economic analysis was then performed based on the number of heat stress days, dry cows per state, and the aforementioned impairments on daughters' lifespans and milk production. Collectively in the United States, the economic losses for additional heifer rearing cost, reduced productive life, and reduced milk yield of the F 1 offspring were estimated at $134, $90, and $371 million per year, respectively. In summary, late-gestation heat stress exerts carryover effects on at least 2 generations. Providing heat abatement to dry-pregnant dams is important to rescue milk loss of the dam and to prevent losses in their progeny.

Prenatal heat stress during late gestation exerts longterm effects on growth and productivity of the dairy calf. Further, direct exposure to heat stress during the preweaning period impairs calf thermoregulation and performance. We examined the effects of heat stress abatement during the prenatal period, postnatal period, or both on calf performance. We hypothesized that calves exposed to pre-and postnatal heat stress abatement would perform most optimally in terms of thermoregulation, growth, and health responses when compared with calves that are heat-stressed at any time in the pre-or postnatal periods. Holstein calves born to heat-stressed (HT) or cooled (CL) dams during late gestation (44 ± 5 d; prenatal HT or CL) were exposed to heat stress or cooling postnatally for 56 d (postnatal HT or CL), resulting in 4 treatments: HT-HT, HT-CL, CL-HT, and CL-CL; n = 12/treatment. Calves were administered 4 L of pooled colostrum and after 2 d of age allotted 10 L/d milk replacer and up to 3 kg/d concentrate in automatic feeder group pens (n = 6/pen). Postnatal cooling was achieved by 2 fans (average wind speed 2 m/s). Thermoregulatory responses (respiration rate and heart rate; rectal, body, and skin temperature), feed intake, growth parameters including average daily gain and medication events were recorded, and blood samples were collected weekly. Thermoregulatory responses were lower in postnatal CL calves compared with postnatal HT. In the afternoon, HT-HT calves had the highest respiration rate and rectal temperature, HT-CL calves had the lowest respiration rate, and CL-HT calves had the lowest heart rate compared with the other treatment groups. Prenatal CL calves weighed more at birth and weaning with a tendency for greater average daily gain compared with prenatal HT calves, whereas postnatal CL calves had increased milk replacer and concentrate intake and a tendency for reduced fever, infection, and total medication events relative to postnatal HT. Prenatal HT calves were esophageal tube fed more often than prenatal CL. Blood hematocrit and 24-h serum IgG concentration were greater in prenatal CL calves relative to prenatal HT. Prenatal heat stress abatement improves weight gain, hematocrit, and immunoglobulin transfer, whereas postnatal heat stress abatement modulates thermoregulatory responses, feed intake, and calf health. This study is the first to characterize the combined effects of pre-and postnatal heat stress or active cooling on the dairy calf.

Although dairy calves are more thermotolerant relative to mature cows, they are still susceptible to heat stress, as demonstrated by elevated physiological responses and reduced feed intake under high ambient temperature and relative humidity. However, indicators of heat stress have not been well-characterized in calves. Herein, we evaluated associations between environmental and thermoregulatory and productive animal-based indicators of heat stress in dairy calves exposed to chronic heat stress or continuous cooling in a subtropical climate. Holstein calves were exposed to heat stress (HT; shade of barn, n = 24) or continuous cooling (CL; shade of barn plus 2 fans, n = 24) from 2 to 42 d of age. Environmental indices, including ambient temperature, relative humidity, temperature-humidity index (THI), and wind speed, and animal-based indices, including respiration (RR), heart rate (HR), rectal (RT), and skin temperature (ST) were recorded thrice daily (0900, 1300, and 1900 h). Milk replacer (MI) and grain intakes were recorded daily from 15 to 42 d of age. Using segmented regression models, we then estimated THI thresholds for significant changes in physiological responses. We found a strong, positive correlation between animal-based indicators (except for HR, MI, and grain intakes) and ambient temperature and THI, with the highest correlation obtained with ST and THI (r ≥ 0.72). Ambient temperature and ST and ambient temperature or THI and MI were the only correlations that differed between treatments. The coefficient of determination (R 2 ) obtained from regression analyses to model animal-based indicators was substantially improved by the inclusion of environmental indicators, with the greatest improvement achieved with THI. Overall, continuous cooling by fans promoted calf heat loss as CL calves had lower RR, RT, ST, and higher feed intake compared with HT calves. Temperature-humidity index breakpoints could be determined for RT (THI = 67), RR (THI = 65), and MI (THI = 82) in HT calves, and only for RR (THI = 69) in CL calves. Skin temperature variables had no detectable breakpoints in either treatment due to the strong linear relationship to THI. Collectively, our results suggest that ST is appropriate to estimate chronic heat stress and that THI is the best environmental indicator of heat stress in dairy calves raised in a shaded, subtropical environment. At a practical level, calves should be closely monitored when THI reaches 65 to 69 to minimize the risk of heat stress-related impairments.

The bovine dry period is a dynamic non-lactating phase where the mammary gland undergoes extensive cellular turnover. Utilizing RNA sequencing, we characterized novel genes and pathways involved in this process and determined the impact of dry period heat stress. Mammary tissue was collected before and during the dry period (−3, 3, 7, 14, and 25 days relative to dry-off [day 0]) from heat-stressed (HT, n = 6) or cooled (CL, n = 6) late-gestation Holstein cows. We identified 3,315 differentially expressed genes (DEGs) between late lactation and early involution, and 880 DEGs later in the involution process. DEGs, pathways, and upstream regulators during early involution support the downregulation of functions such as anabolism and milk component synthesis, and upregulation of cell death, cytoskeleton degradation, and immune response. The impact of environmental heat stress was less significant, yet genes, pathways, and upstream regulators involved in processes such as ductal branching morphogenesis, cell death, immune function, and protection against tissue stress were identified. Our research advances understanding of the mammary gland transcriptome during the dry period, and under heat stress insult. Individual genes, pathways, and upstream regulators highlighted in this study point towards potential targets for dry period manipulation and mitigation of the negative consequences of heat stress on mammary function.

Earth’s rising temperature has substantial repercussions for food-producing animals by increasing morbidity and mortality, diminishing reproductive potential, and reducing productivity. In the dairy industry this equates to massive losses in milk yield, which occur when cows are exposed to heat stress during lactation or during the non-lactating period between lactations (i.e. dry period). Furthermore, milk yield is significantly lower in first-lactation heifers that experienced fetal heat stress. The mechanisms underlying intrauterine effects of heat stress on the offspring’s future lactation have yet to be fully elucidated. We hypothesize that heat stress experienced through the intrauterine environment will alter the mammary gland microstructure and cellular processes involved in cell turnover during the cow’s first lactation. Mammary biopsies were collected from first-lactation heifers that were exposed to heat stress or cooling conditions while developing in utero (IUHT and IUCL; respectively, n = 9–10). IUHT heifers produced less milk compared to IUCL. The mammary glands of IUHT heifers differed morphologically from IUCL, with the IUHT heifers having smaller alveoli and a greater proportion of connective tissue relative to their IUCL herdmates. However, intrauterine heat stress had little impact on the proliferation and apoptosis of mammary cells during lactation. Our results indicate that fetal exposure to heat stress impairs milk production in the first lactation, in part, by inducing aberrant mammary morphology. This may result from alterations in the developmental trajectory of the fetal mammary gland that persist through the first lactation rather than to alterations in the cellular processes controlling mammary cell turnover during lactation.