We report a two-to three-fold increase in free radical (R') concentrations of muscle and liver following exercise to exhaustion.
Exhaustive exercise also resulted in decreased mitochondrial respiratory control, loss of sarcoplasmic reticulum (SR) and endoplasmic reticulum (ER) integrity, and increased levels of lipid peroxidation products.
Free radical concentrations, lipid peroxidation, and SR, ER, and mitochondrial damage were similar in exercise exhausted control animals and non-exercised vitamin E deficient animals, suggesting the possibility of a common R" dependent damage process.
In agreement with previous work showing that exercise endurance capacity is largely determined by the functional mitochondrial content of muscle (1-4), vitamin E deficient animals endurance was 40% lower than that of controls.
The results suggest that R" induced damage may provide a stimulus to the mitochondrial biogenesis which results from endurance training.
Daily exercise of low work intensity but prolonged duration (endurance training) results in an increased mitochondrial content of muscle, although the cellular stimulus for mitochondrial biogenesis is not known (1,2,5,6). The literature contains conflicting reports as to whether a single bout of exhaustive exercise can actually cause muscle subcellular damage (7,8), but Gale (9) has demonstrated an increased sensitivity to oxidizing agents and others have reported loss of lysosomal latency and release of proteolytic enzymes in both muscle and liver (i0,ii).
In addition, Dillard et al. ( 12) have measured increased levels of pentane (which may be formed as a lipid peroxidation product) in the expired air of exercising humans.
In this report we have investigated the possibility that exhaustive exercise may produce free radicals (R-), lipid peroxidation, and loss of mitochondrial, sarcoplasmic reticulum (SR), and