The influence of high-intensity bicycle exercise on the redox level and lactate accumulation in skeletal muscle (m. quadriceps femoris) of man has been investigated. Six subjects exercised to exhaustion at a load corresponding to 100%VO2max.
Muscle content of NADH, determined by the bioluminescense technique, increased from (x±SEM) 0.089±0.007 mmol/kg dry wt. at rest to 0.190±0.031 after 2 min of exercise (P<0.05) and to 0.213±0.021 at exhaustion (P<0.05). Values after 2 min exercise and at exhaustion were not statistically different (P>0.05). Muscle lactate was increased 13-fold after 2 min of exercise and 22-fold at exhaustion as compared to the resting value.
After 10 min recovery NADH was restored back to the pre-exercise level whereas muscle lactate was still elevated.
The increase of muscle NADH during exercise is in contrast to earlier studies on isolated animal muscles, where an oxidation of NADH was observed during contractions. The difference might be due to the experimental model (isolated muscle vs. in vivo) or to the analytical method (qualitative data by reflectance fluorimetri from the surface of intact muscle vs. quantitative data from muscle extracts).
Calculations of the cytosolic NADH concentration from the lactate dehydrogenase equilibrium show that 95% or more of the NADH is confined to the mitochondrial compartment. The observed increase of muscle NADH therefore imply that the redox potential of the mitochondria is decreased during intense exercise.
The results are in conformity with that local hypoxia in the muscle cell is the mechanism for lactate production during exercise but an alternative explanation could be that the capacity of the respiratory chain to oxidize the formed NADH has been exceeded.
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Sahlin, K. NADH in human skeletal muscle during short-term intense exercise. Pflugers Arch. 403, 193–196 (1985). https://doi.org/10.1007/BF00584099
- Muscle contraction
- Muscle metabolism