Thermoregulatory responses of lactating dairy cows to an acute heat stress after a pharmacologically-induced LH surge

The objective of this study was to develop an in vivo model to assess thermoregulatory response of lactating dairy cows to heat stress. Hyperthermia occurring for 10 to 12 hours after LH surge reduces quality of maturing oocyte, thereby reducing fertility. Between the months of February through May, cows were transported to a climate-controlled facility and maintained at a temperature-humidity index (THI) of 65.9 ± [plus or minus] 0.2 (thermoneutral) or exposed to increases in THI of 0.8 ± 0.1 units per hour (heat stress) for 12 hours before rapidly cooling to thermoneutral conditions. Mixed model regressions with repeated measures were used to test respiration rates (RR) and rectal temperature (RT). Within 40 and 110 min of increasing THI, RR increased in a quadratic fashion (P < [less than] 0.001); RT increased by 0.04 ± 0.1° [degree] C (P < 0.001) per unit THI. Changes in RR lagged THI and preceded rises in RT by 30 min. Average THI 3-days prior to treatment influenced changes in RR (P = [equal] 0.050) and RT (P < 0.001). Increased RR was more noticeable in heat-stressed cows when prior THI was in the 40s than low 60s. Rectal temperature of heat-stressed cows was 0.8 ± 0.02°C lower when prior THI was in the 40s versus low 60s. Progesterone and LH levels before treatment were predictive of thermoregulatory response in heat-stressed cows. Rapid cooling decreased RR by 0.6 ± 0.1 bpm (P < 0.001) and RT by 0.02 ± 0.002°C per min (P < 0.002). Speed and magnitude of thermoregulatory changes to an acute heat stress and after sudden cooling emphasizes the importance of strategic cooling before ovulation. Efforts to do so when prior THI approaches levels expected to induce mild stress are especially important. Respiration rate is a useful indicator of the degree of hyperthermia a lactating cow is experiencing during an acute heat stress event.