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Heat stress increases respiratory exchange ratio while reducing daily energy expenditure in growing pigs.

Heat stress (HS) alters animal metabolism causing reduced performance (muscle growth) while increasing the incidence of disease and mortality. HS is particularly detrimental in the swine industry where the global economic burden of heat stress is in the billions of dollars annually. Excess environmental heat promotes a HS response increasing the expression of heat shock factors and heat shock proteins which coordinate a shift in metabolic substrate preference. The net result of these changes is a metabolic phenotype with limited lipid oxidation that relies on aerobic and anaerobic glycolysis as a predominant source of energy production. This study was designed to evaluate the effect of HS on substrate utilization and overall animal metabolic rate in growing pigs. Crossbred barrows (15.2±2.4 kg) were exposed to 5 days of TN (thermal neutral, 24 C°) or HS ( 35 C°) (n=8 per treatment), after a 5‐day acclimation period (24 C°). Pigs were fed ad libitum and monitored regularly for respiratory rate (RR) and rectal temperature (3x daily). A metabolic cart was used to assess daily energy expenditure (DEE), and respiratory exchange ratio (RER, CO2:O2), pigs were placed in an enclosed chamber and gas exchange was measured for 1 hour after a 30 min washout. Muscle biopsies were taken from the longissimus dorsi to evaluated palmitate, pyruvate, and leucine oxidation capacity and metabolic flexibility (metflex). Metabolic measures and muscle biopsies were taken after five days of acclimation (pre) and immediately following (post) the 5‐day environmental treatments. Initial DEE was positively correlated to weight (r2=0.55, p<0.01) and feed intake (r2=0.40, p<0.01), initial DEE relative to bodyweight (DEE/BW) correlated to metflex (r2=0.29, p=0.03). HS increased RR (94.3±4.5 vs 55.9±2 BPM, p<0.01) and rectal temperature (39.6±0.1 vs 39.2±0.1 C°, p<0.01) compared to TN controls. Weight gain and feed intake did not differ between HS and TN groups. Seven days of HS increased RER (0.91±0.02 vs 1.02±0.02 VCO2:VO2, p<0.01) and decreased DEE/BW (68.8±1.7 vs 49.7±4.8 kcal/kg, p<0.01) compared to baseline values. Heat stress also decreased muscle palmitate oxidation (−20.1%, p=0.04) and metflex (28.8±3.5 vs 19.2±3.7, P=0.01), while causing an increase in leucine oxidation (14.1±0.9 vs 19.0±2.2 nmol/mg‐pro/hr, p=0.02) compared to baseline values. Growth rates of HS animals were positively correlated to post DEE/BW (r2=0.75, p<0.01), while negatively correlated to changes in rectal temperature (r2=0.54, p=0.04). Previous research has shown a J‐shaped relationship between environmental temperature and energy expenditure, with both cold and hot environments increasing energy expenditure. However, these data demonstrate that chronic HS may decrease energy expenditure at least relative to body weight in growing pigs. This reduction in energy expenditure appears to be mechanistically controlled through substrate regulation as HS increased RER and decreased lipid oxidation and metflex. To overcome limits in lipid oxidation, amino acid use for energy may be upregulated which can further limit potential for muscle growth.