395 Impact of thermal load on muscle and fat metabolism in meat animals.

Abstract Heat stress (HS) is an escalating challenge in livestock production, impairing growth performance, altering carcass traits, and reprogramming energy metabolism in skeletal muscle and adipose tissues. In a 28-day trial, crossbred beef steers (n = 32) were exposed to a temperature–humidity index (THI) of 75–80 for 8 hours daily. Heat stress significantly reduced average daily gain, final body weight, and hot carcass weight. Although rectal temperatures remained stable, elevated respiratory rates and increased muscle temperatures indicated localized thermal load. Dry matter intake also trended lower. Muscle tissue exhibited a shift toward oxidative fiber types, with increased expression of myosin heavy chain I (MHC I) and markers of mitochondrial biogenesis. Upregulation of heat shock proteins (HSP27, HSP70) at both transcript and protein levels was associated with preserved satellite cell function and reduced proteolysis. Complementary in vitro studies revealed that bovine myofiber exposed to 40 °C in the presence of oleic acid accumulated more intramyocellular lipid without signs of oxidative damage. This was accompanied by suppressed lipogenic gene expression and increased expression of fatty acid oxidation regulators, including PPARγ and. Despite overall increases in adipose tissue mass, HS did not enhance marbling. Instead, lipid deposition was biased toward subcutaneous and visceral compartments. Moreover, current findings indicate that short-term thermal fluctuations, absent sustained heat, can similarly induce cellular stress. These fluctuations elevated HSP expression, modulated myogenic regulators, and activated adipogenic pathways, indicating that temperature variability itself may influence muscle and fat development. These findings emphasize HS and temperature fluctuation as both stressors and metabolic signals, capable of directing energy partitioning and tissue remodeling in beef cattle.