Mild heat stress effects on hepatic and mammary mitochondria of lactating dairy cattle

Abstract

Heat stress has a myriad of negative effects on dairy production through a disruption in animal homeostasis that often lingers past the exposure. Yet, the effects of heat stress on cellular processes are not fully elucidated. In the present study, we used an electric heat blanket (EHB), pair-feeding heat stress model to investigate the direct effects of heat stress on mitochondrial function and milk production. Multiparous Holstein cows (n = 24, 2.80 ± 0.84 lactations; mean ± SD) were assigned to 1 of 2 treatment groups: EHB-induced heat-stressed (HS) or pair-fed thermoneutral (PFTN) groups. During experimental period 1 (P1), all cows were under TN conditions for 10 d. During experimental period 2 (P2), cows in the HS group were subjected to EHB-induced heat stress for 10 d, while the PFTN group remained under thermoneutral conditions and was pair-fed according to the average reduction in feed intake of the HS group. The mild and chronic heat stimulus provided by the EHB was effective at inducing a physiological heat stress response as evidenced by increased rectal temperature and respiration rates, and reduced DMI, milk yield, and circulating nonesterified fatty acid concentrations of the HS group in P2 compared with P1. Mitochondrial respiration and biogenesis remained mostly unchanged in the liver. No differences were detected between HS and PFTN cows in tissue reactive oxygen species production, antioxidant activity, or oxidative damage. Heat stress decreased mitochondrial number while increasing mitochondrial size in mammary tissue of HS cows and altered the gene expression of stress and energy sensors. These data suggest that even mild heat stress can directly affect a tissue's energetic status and alter mitochondrial biogenesis.

Keywords: ATP; mitochondrial respiration; oxidative stress.