Heat Stress Reduces Metabolic Rate While Increasing Respiratory Exchange Ratio in Growing Pigs.

Abstract

Simple SummaryCellular growth, particularly muscle hypertrophy, requires substantial energetics. In animals, proper substrate utilization is essential. Maximal growth is dependent on both carbohydrates and lipids being oxidized to provide as much energy as possible for protein syntheses, while amino acids must be spared from oxidation to provide an ample supply of proteogenic building blocks. However, maximal cellular growth is not a default metabolic state and is easily overridden by environmental factors such as heat stress (HS). HS has previously been hypothesized to increase metabolic rate, as is typical of a general stress response. Newer evidence, however, suggest that HS may limit energy production by inhibiting the use of lipids as a fuel source. HS metabolism instead depends on carbohydrates and even amino acids as energetic substrate, potentially limiting energy production. This study demonstrates that, contrary to current recommendations, HS reduces metabolic rate. Findings demonstrated a 38% reduction in relative energy expenditure (kcal/day/kg) due to HS. HS also caused a 33% increase in amino acid oxidation. A combination of decreased energy production and increased amino acid oxidation creates a metabolic state with severely limited growth potential which cannot be solved by simply increasing feed.Heat stress (HS) diminishes animal production, reducing muscle growth and increasing adiposity, especially in swine. Excess heat creates a metabolic phenotype with limited lipid oxidation that relies on aerobic and anaerobic glycolysis as a predominant means of energy production, potentially reducing metabolic rate. To evaluate the effects of HS on substrate utilization and energy expenditure, crossbred barrows (15.2 ± 2.4 kg) were acclimatized for 5 days (22 °C), then treated with 5 days of TN (thermal neutral, 22 °C, n = 8) or HS (35 °C, n = 8). Pigs were fed ad libitum and monitored for respiratory rate (RR) and rectal temperature. Daily energy expenditure (DEE) and respiratory exchange ratio (RER, CO2:O2) were evaluated fasted in an enclosed chamber through indirect calorimetry. Muscle biopsies were obtained from the longissimus dorsi pre/post. HS increased temperature (39.2 ± 0.1 vs. 39.6 ± 0.1 °C, p < 0.01) and RER (0.91 ± 0.02 vs. 1.02 ± 0.02 VCO2:VO2, p < 0.01), but decreased DEE/BW (68.8 ± 1.7 vs. 49.7 ± 4.8 kcal/day/kg, p < 0.01) relative to TN. Weight gain (p = 0.80) and feed intake (p = 0.84) did not differ between HS and TN groups. HS decreased muscle metabolic flexibility (~33%, p = 0.01), but increased leucine oxidation (~35%, p = 0.02) compared to baseline values. These data demonstrate that HS disrupts substrate regulation and energy expenditure in growing pigs.