Heat stress (HS) markedly affects postabsorptive energetics and protein metabolism. Circulating urea nitrogen increases in multiple species during HS and it has been traditionally presumed to stem from increased skeletal muscle proteolysis; however, this has not been empirically established. We hypothesized HS would increase activation of the calpain and proteasome systems as well as increase degradation of autophagosomes in skeletal muscle. To test this hypothesis, lactating dairy cows (~139 d in milk; parity ~2.4) were exposed to thermal neutral (TN) or HS conditions for 7 d (8 cows/environment). To induce HS, cattle were fitted with electric blankets for the duration of the heating period and the semitendinosus was biopsied on d 7. Heat stress increased rectal temperature (1.3°C) and respiratory rate (38 breaths per minute) while it decreased dry matter intake (34%) and milk yield (32%). Plasma urea nitrogen (PUN) peaked following 3 d (46%) and milk urea nitrogen (MUN) peaked following 4 d of environmental treatment and while both decreased thereafter, PUN and MUN remained elevated compared with TN (PUN: 20%; MUN: 27%) on d 7 of HS. Contrary to expectations, calpain I and II abundance and activation and calpain activity were similar between groups. Likewise, relative protein abundance of E3 ligases, muscle atrophy F-box protein/atrogin-1 and muscle ring-finger protein-1, total ubiquitinated proteins, and proteasome activity were similar between environmental treatments. Finally, autophagosome degradation was also unaltered by HS. Counter to our hypothesis, these results suggest skeletal muscle proteolysis is not increased following 7 d of HS and call into question the presumed dogma that elevated skeletal muscle proteolysis, per se, drives increased AA mobilization.

The consequences of prolonged environment-induced heat stress (EIHS) on heart health are largely unknown. We discovered that a 24-h exposure to environmental conditions sufficient to cause EIHS resulted in cardiac edema and histopathologic changes in the right and left ventricles. Furthermore, among other biochemical changes, EIHS increased autophagic flux and caused endoplasmic reticulum stress. These data raise the possibility that thermic injury, even when insufficient to cause heat stroke, can damage the myocardium.

Heat stress is a global threat to human health and agricultural production. We demonstrated that following 7 days of heat stress, skeletal muscle from females was more susceptible to oxidative stress than muscle from males in a porcine model, despite cooler muscle temperatures. The vulnerability to heat stress-induced oxidative stress in females may be driven, at least in part, by decreased antioxidant capacity and calcium dysregulation.

Environment‐induced heat stress (EIHS) results from sustained body temperature elevation owing to prolonged exposure to heat and humidity. We hypothesized that EIHS would cause kidney injury and cellular dysfunction. To test this hypothesis, female C57 mice were exposed to EIHS (n = 14; 37.6°C, 42.0% relative humidity) or thermoneutral (TN) conditions (n = 12; 31.2°C, 35.0% relative humidity) for 24 h. EIHS increased rectal temperature by 2.1°C (p < 0.001), decreased body mass by 10% (p = 0.036), decreased absolute kidney mass by 10% (p = 0.026), increased renal water content by 19% (p < 0.007) and increased blood urea nitrogen by 102% (p < 0.001) compared with TN. Histological analysis revealed that EIHS caused proximal tubule vacuolation (p = 0.001) and alterations in glomerular structure, supported by markers of lipid accumulation, tubular injury and inflammatory signalling. EIHS increased relative protein abundance of heat shock proteins 70 (48%, p = 0.002), 90 (37%, p = 0.001) and 60 (36%, p = 0.026), in addition to heat shock factor 1 (2‐fold, p = 0.020) compared with TN. In addition, there was biochemical evidence of mitochondrial remodelling, increased autophagic flux and robust activation of endoplasmic reticulum stress in kidneys from EIHS mice compared with TN mice. Collectively, these data suggest that 24 h of EIHS is sufficient to cause histological injury and cellular dysfunction, which might undermine renal health and function.