Adaptation of mitochondrial ATP production in human skeletal muscle to endurance training and detraining.
Level 3 - non-randomized controlled study
Uncontrolled prospective longitudinal before-and-after physiological study in humans.
PubMed 1474078 · doi:10.1152/jappl.1992.73.5.2004
What was done
Nine healthy men completed six weeks of endurance training followed by three weeks of detraining. Skeletal muscle biopsies (~60 mg) were collected before training, after training, and after detraining. Mitochondrial ATP production rate (MAPR) was measured in isolated mitochondria via bioluminometry across various substrate mixtures, alongside assessments of muscle mitochondrial and glycolytic enzyme activities and maximal oxygen uptake (VO2 max).
What was found
Training increased MAPR by 70% with pyruvate + palmitoyl-L-carnitine + alpha-ketoglutarate + malate, by 50% with pyruvate + malate, and by 92% with palmitoyl-L-carnitine + malate. When normalized to protein content in the mitochondrial fraction, no differences in MAPR were observed. Training increased enzyme activities for cytochrome-c oxidase (78%), glutamate dehydrogenase (45%), citrate synthase (40%), and succinate cytochrome c reductase (18%), while VO2 max increased by 9.6%. Three weeks of detraining decreased MAPR by 12% to 28% (not statistically significant for all substrate combinations) and reduced VO2 max by 6.0%.
Why it matters
This study directly quantifies changes in human mitochondrial ATP production capacity, showing that endurance-induced gains in ATP synthesis are driven primarily by expanded mitochondrial content rather than changes per unit of mitochondrial protein, and that these metabolic adaptations begin to reverse within weeks of inactivity.
Limits
The study had a very small sample size (n = 9) restricted to young healthy men and lacked a non-training control group. Detraining-induced reductions in MAPR did not achieve statistical significance for all tested substrate combinations.
Cited by
- supports Detraining leads to rapid loss of mitochondrial capacity in skeletal muscle.