The Effect of Heat on the Pig Industry

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During HS, the utilization of carbohydrates (i.e. glucose) as an energy source is altered (Streffer, 1988), and this has been demonstrated by our lab in pigs (Pearce et al., 2013) and cattle (Wheelock et al., 2010). Acute HS was originally thought to be responsible for reduced worker productivity in summer months (Baumgard and Rhoads, 2013), and was first reported to cause hypoglycemia in cats (Lee and Scott, 1916). In addition, athletes exercising during times of HS have increased hepatic glucose output and glucose oxidation at the expense of lipids (Fink et al., 1975; Febbraio, 2001). Moreover, exogenous glucose is unable to blunt the formation of hepatic glucose (Angus et al., 2001) likely due to increased glycogenolysis (Febbraio, 2001), and gluconeogenesis (Collins et al., 1980). A proposed mechanism for the enhanced hepatic glucose output is increased pyruvate carboxylase expression (a rate limiting enzyme that controls lactate and alanine entry into the gluconeogenic pathway) during times of HS (O’Brien et al., 2008; White et al., 2009) likely resulting from increased plasma lactate (presumably due to an increase in muscle lactate production). This indicates that peripheral tissues increase aerobic glycolysis, and thus resembles the Warburg effect (used in cancer cells) where aerobic glycolysis in skeletal muscle is accelerated and lipolysis is reduced (Baumgard and Rhoads, 2013). Despite the well-documented reduction in nutrient intake and increase in body

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