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Enzymatic down regulation with exercise in rat skeletal muscle
L L Ji1, F W Stratman, H A Lardy
1Institute for Enzyme Research, University of Wisconsin, Madison 53705.
Archives of Biochemistry and Biophysics
|May 15, 1988
Summary
Intense exercise suppressed key mitochondrial enzymes in rat skeletal muscle, especially in untrained individuals. This effect, linked to oxidative stress, may be mitigated by training-induced increases in antioxidant enzymes like glutathione peroxidase.
Area of Science:
- Exercise Physiology
- Mitochondrial Biochemistry
- Enzymology
Background:
- Acute and exhaustive exercise can impact skeletal muscle metabolism.
- Mitochondrial function is crucial for energy production during exercise.
- The effects of exercise on specific mitochondrial enzymes and their regulation are not fully understood.
Purpose of the Study:
- To investigate the impact of a single bout of exhaustive exercise on key mitochondrial enzyme activities in rat skeletal muscle.
- To determine the time course of enzymatic changes post-exercise and compare effects in trained versus untrained rats.
- To explore the relationship between exercise-induced enzymatic suppression, proteolysis, and oxidative stress markers.
Main Methods:
- Maximal enzyme activities of citrate synthase (CS), malate dehydrogenase (MDH), and alanine aminotransferase (ALT) were measured in rat skeletal muscle mitochondria post-exercise.
- Proteolysis was assessed using [3H]leucine clearance.
- Mitochondrial protein sulfhydryl content and glutathione peroxidase (GPX) activity were quantified.
Main Results:
- Exhaustive treadmill running significantly suppressed CS, MDH, and ALT activities in skeletal muscle mitochondria, an effect sustained for 48 hours, particularly in untrained rats.
- Decreased enzyme activities correlated with reduced mitochondrial protein sulfhydryl content, suggesting thiol oxidation.
- Increased GPX activity in trained rats correlated with endurance time, indicating enhanced antioxidant capacity.
Conclusions:
- Exercise-induced enzymatic down-regulation is not solely due to proteolysis but involves oxidative modification of enzyme active sites.
- Prolonged exercise generates reactive oxygen species that oxidize mitochondrial thiols, impairing enzyme function.
- Exercise training enhances antioxidant defenses, potentially protecting against exercise-induced mitochondrial dysfunction.