Quantitative and qualitative adaptation of skeletal muscle mitochondria to increased physical activity

Abstract

Endurance capacity rely on high muscle oxidative capacity but should also involve a tighter coupling between energy production and utilization within the myocyte. The present study examined the responses of muscle oxidative capacity and the regulation of oxidative phosphorylation by phosphate acceptors in locomotor muscles of voluntary running rats (n = 8), using saponin permeabilized fibers of the deep and superficial parts of plantaris muscle (dPLA and sPLA, respectively). Non-ADP stimulated respiration of skinned fibers increased by 33% (P < 0.05) and 100% (P < 0.001) in sPLA and dPLA, respectively. The maximal ADP-stimulated respiration was 57% (P < 0.001) and 32% (P < 0.01) higher in active rats than in sedentary rats (n = 8), in sPLA and dPLA, respectively. This finding was consistent with a 72% increase in the CS activity in plantaris muscle of exercising rats (P < 0.01). Voluntary running induced a 334% increase in the apparent Km for ADP in sPLA (P < 0.001), and a 61% increase in dPLA (P < 0.05), showing a lower affinity for cytosolic ADP of mitochondria present in both, predominantly glycolytic, and oxidative fibers. There was an increase in the creatine kinase efficacy in both sPLA and dPLA (131%, 75%, P < 0.001, respectively), consistent with an increase in the activity of the mitochondrial isoform of creatine kinase (106%, P < 0.01). It is concluded that, in addition to the well-known increased oxidative capacity, voluntary running is associated with changes in the regulation of oxidative phosphorylation by phosphate acceptors, in both glycolytic and oxidative fibers, in the direction of increased coupling between energy production and energy utilization.

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“…Such an increase would suggest a lower affinity and/or a lower permeability of the mitochondria for ADP (62). A high apparent K m for ADP as reported in oxidative fibers would correspond to a metabolic mechanism allowing better control of mitochondrial respiration by mitochondrial kinases (65). Thus, in our study, DHA would affect in a similar way the kinetic parameters of the respiration with a consequence on the mitochondrial function.…”

A Metabolomics-driven Elucidation of the Anti-obesity Mechanisms of Xanthohumol

“…8F). As an adaptation to exercise, the mitochondrial affinity for cytosolic ADP in muscle decreases as the myofibers become more oxidative (53). It is tempting to speculate that the long term increase we observed in ADP may be related to this switch.…”

Can we optimise the exercise training prescription to maximise improvements in mitochondria function and content?

“…Physical activity increases skeletal muscle energy demand many fold, and it is not surprising that cross-sectional studies suggest an association between physical activity levels and changes in both mitochondria content [33][34][35][36] and function [33,[37][38][39][40]. Interestingly, analysis of the cross-sectional data published to date indicates that higher physical activity levels are associated with relatively larger values for mitochondrial function (as measured by mitochondrial respiration) than content (as measured by Citrate Synthase activity) (Fig 1).…”