Low Intensity Exercise Attenuates Acute Lipid Loading‐Induced Alterations in Mitochondrial Function in Rat Skeletal Muscle

Abstract

A single high‐fat meal acutely increases skeletal muscle mitochondrial H2O2 emitting potential (mEH2O2), shifts the intracellular redox environment to a more oxidized state, and increases circulating markers of oxidative stress. Bioenergetically, this implies an acute lipid load may elevate the reducing pressure/membrane potential (Δ Ψm) within mitochondria and, conversely, that even a mild increase in energy expenditure may be sufficient to prevent these effects. To test this hypothesis, male Sprague‐Dawley rats received an oral lipid gavage (20% intralipid, 45 Kcal/kg lean body mass) or water followed either by 2h of rest or 1h of rest plus 1h of low intensity treadmill exercise (15 m/min, 0% grade). Permeabilized fiber bundles were prepared from red gastrocnemius muscle for testing mitochondrial function. In rats receiving lipid, Δ Ψm and mEH2O2 were higher (P<0.05) and calcium retention capacity (mCa2+ RC, an index of resistance to mitochondrial permeability transition) was lower under state IV and/or “clamped” ADP‐stimulated state III conditions. All three effects were prevented when lipid gavage was followed by low‐intensity exercise. Respiratory capacity was unaffected by any of the interventions. These findings provide evidence that mitochondrial Δ Ψm, mEH2O2, and mCa2+ RC are acutely affected by nutritional overload in skeletal muscle, but can be prevented by low intensity exercise. NIH DK073488