VO2max during whole-body exercise is presumably constrained by oxygen delivery to mitochondria rather than by mitochondria's ability to consume oxygen. Humans and animals have been reported to exploit only 60-80% of their mitochondrial oxidative capacity at VO2max. However, ex vivo quantification of mitochondrial overcapacity is complicated by isolation or permeabilization procedures. An alternative method for estimating mitochondrial oxidative capacity is via enzyme histochemical quantification of succinate dehydrogenase (SDH) activity. We determined to what extent V̇O2max attained during cycling exercise differs from mitochondrial oxidative capacity predicted from SDH activity of m. vastus lateralis in chronic heart failure patients, healthy controls and cyclists. VO2max was assessed in 20 healthy subjects and 28 cyclists and SDH activity was determined from biopsy cryosections of m. vastus lateralis using quantitative histochemistry. Similar data from our laboratory of 14 chronic heart failure patients and 6 controls were included. Mitochondrial oxidative capacity was predicted from SDH activity using estimated skeletal muscle mass and the relationship between ex vivo fiber VO2max and SDH activity of isolated single muscle fibers and myocardial trabecula under hyperoxic conditions. Mitochondrial oxidative capacity predicted from SDH activity was related (r2=0.89, p<0.001) to VO2max measured during cycling in subjects with VO2max ranging from 9.8 to 79.0 ml kg-1 min-1. VO2max measured during cycling was on average 90±14% of mitochondrial oxidative capacity. We conclude that human VO2max is related to mitochondrial oxidative capacity predicted from skeletal muscle SDH activity. Mitochondrial oxidative capacity is likely marginally limited by oxygen supply to mitochondria.
- succinate dehydrogenase
- oxygen supply
- Copyright © 2016, Journal of Applied Physiology