Abstract #T161
Section: Physiology and Endocrinology (posters)
Session: Physiology and Endocrinology II
Format: Poster
Day/Time: Tuesday 7:30 AM–9:30 AM
Location: Exhibit Hall A
Session: Physiology and Endocrinology II
Format: Poster
Day/Time: Tuesday 7:30 AM–9:30 AM
Location: Exhibit Hall A
# T161
Thermoregulatory response of lactating Holsteins to an acute heat stress after a pharmacologically induced LH surge.
Chelsea R. Abbott*1, Arnold M. Saxton1, Tate Walker1, Roger Long1, Louisa A. Rispoli1, Rebecca R. Payton1, Ramiro Oliviera Filho1, Felipe G. Dantas1, Kelly A. Campen1, Rafael Carvalho1, Ky G. Pohler1, Neal Schrick1, Lannett Edwards1, 1University of Tennessee, Knoxville, TN.
Key Words: heat stress, estrus, thermoregulation
Thermoregulatory response of lactating Holsteins to an acute heat stress after a pharmacologically induced LH surge.
Chelsea R. Abbott*1, Arnold M. Saxton1, Tate Walker1, Roger Long1, Louisa A. Rispoli1, Rebecca R. Payton1, Ramiro Oliviera Filho1, Felipe G. Dantas1, Kelly A. Campen1, Rafael Carvalho1, Ky G. Pohler1, Neal Schrick1, Lannett Edwards1, 1University of Tennessee, Knoxville, TN.
Objective was to examine thermoregulatory response of lactating cows to an acute heat stress occurring after an LH surge. Cows with a corpus luteum were given PGF2α, and 11 d later, CIDR and GnRH were administered. Seven day thereafter, CIDR was removed and PGF2α was given. Cows with a dominant follicle (15.2 ± 2.6 mm) were transported to a climate-controlled room 35 h after final PGF2α. Forty hours after final PGF2α, GnRH was given to induce LH surge. Thermoneutral cows (TN; n = 17) were kept at a THI of 65.8 ± 1.5; heat-stressed cows (HS; n = 12) experienced THI increases of 2.1 units per h for 12 h (up to a final THI of 85.2 ± 0.2). Frequent rectal temperature (RT) and respiration rate (RR, breaths/min, bpm) were recorded. Blood samples were taken at last GnRH, 2, 3, and 4 h thereafter, and after HS ceased. Mixed model regression with repeated measures with various combinations of treatment, THI, previous THI, DIM, milk yield, parity, RT, and RR was used to address a priori hypotheses. Elevating THI increased (P = 0.001) RT and RR in HS (39.5 ± 0.6°C and 105.4 ± 22.2 bpm) versus TN (38.3 ± 0.4°C and 47.0 ± 10.5 bpm) cows. Changes in RT and RR by increasing THI were noted within 40 and 110 min, respectively (0.05 ± 0.3°C and 3.4 ± 0.1 bpm per unit rise in THI). Changes in RR lagged THI and preceded rises in RT by 30 min. Average THI 3 d before imposing HS conditions influenced RT and RR (P < 0.0001). Serum progesterone 2 h after final GnRH was negatively related to RT changes (P = 0.0001); serum estradiol was positively related (P = 0.009). After HS ceased, cows were returned to TN conditions; RT and RR decreased by 1.08 ± 0.4°C and 45.9 ± 9.4 bpm per 15 min. At 45 min, HS and TN cows were similar (38.9°C and 66.9 bpm vs 38.7°C and 59.6 bpm). Rapid changes in RT after an acute heat stress event emphasizes the importance of strategically cooling periovulatory cows, especially since estradiol levels may heighten heat-induced elevations in RT. Project was supported by Agriculture and Food Research Initiative Competitive Grant no. 2016-67015-24899 from USDA National Institute of Food and Agriculture.
Key Words: heat stress, estrus, thermoregulation
