Endurance training does not affect diaphragm mitochondria respiration

We sought to determine if chronic endurance training would increase mitochondrial respiration or protein content in rat diaphragm muscle. To this end, 20 male Wistar rats were randomly assigned to control (C) or an 8-week endurance training (T) group, n = 10 per group. At the end of T, V̇_O2 max was 13% greater in T (83.3 vs 73.8 ml·kg^-1·min^-1) and peak max power output was 32% greater (2.63 vs 1.98 kg·m·min^-1). Mitochondrial specific activities of pyruvate-malate and cytochrome oxidase (expressed per mg mitochondrial protein) in both plantaris and diaphragm were similar in C and T rats, as were ADP/O and respiratory control ratios. When expressed per gram wet weight, whole muscle homogenate oxygen uptake (pyruvate + malate) and cytochrome oxidase activity increased 36 and 23%, respectively (P < 0.05) in plantaris from T rats but did not change in diaphragm. Control oxidative capacity and mitochondrial protein content in the diaphragm were ca. 2-fold those in control plantaris. Plantaris mitochondrial protein content increased ca. 50% with T while the diaphragm was unaffected. We conclude that: (1) plantaris muscle oxidative capacity adapts to training by increasing mitochondrial protein content, since there was no evidence for functional improvement of existing mitochondria, and (2) in the face of a substantial training effect in whole animal and plantaris, the T stimulus was not sufficient to induce mitochondria protein changes in the diaphragm. This finding is the result of either a 'pre-adaptation' secondary to the diaphragm's high chronic activity, or a sub-threshold increase in diaphragn recruitment during the exercise conditions studied.