Acute and chronic heat stress alters the metabolic profile of skeletal muscle in growing swine

Heat stress (HS) causes significant losses to the U.S. swine industry in several production and health areas including efficient lean tissue accretion. Perturbations in skeletal muscle metabolism may participate in this defect. The study objectives were to examine the cellular bioenergetic profile in skeletal muscle of piglets subjected to thermal stress in utero and/or during postnatal life. To accomplish this, 96 offspring from 14 sows were prenatally exposed to 1 of 4 environmental treatments involving thermal neutral (TN, 25°C) or HS conditions (cyclical 28-34°C). Sows exposed to TN or HS throughout gestation are denoted TNTN and HSHS, respectively whereas sows heat-stressed for the first or second half of gestation are denoted HSTN and TNHS, respectively. At 14 weeks of age, offspring were exposed to one of two postnatal thermal environments, constant TN (21°C) or HS (35°C) for 24 hrs (acute study) or 5 weeks (chronic study). Pigs were sacrificed after treatment and longissimus dorsi skeletal muscle samples collected for molecular analyses. Differences (p<0.05) were observed in protein abundance of p-4eBP1 and total Rs6 and gene expression of Cox5B, CytB, EEF2, HK2, MURF, ND1, PGC-1α, SDHA, and TFAM during the acute heat stress study. Differences (p<0.05) were observed in protein abundance of 4eBP1, total Akt, and p-Rs6 and gene expression of CytB, MURF, and PGC-1α during the chronic heat stress study. These data indicate that acute postnatal HS alters skeletal muscle metabolism, which may favor a reduction in mitochondrial respiration and protein synthesis potentially via the mTOR pathway.