Does Extreme Muscle Hypertrophy Determine an Impairment of Skeletal Muscle Oxidative Metabolism?

Abstract

PURPOSE: The purpose was to evaluate the effects of marked skeletal muscle hypertrophy induced by chronic resistance training on skeletal muscle oxidative function. METHODS: Eleven male resistance-trained athletes (RTA, age: 25.4±1.8 [mean±SE] years) and eleven active control subjects (CTRL) were evaluated. Quadriceps femoris muscle volume was determined by magnetic resonance imaging. During incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercise we determined: pulmonary O2 uptake (V'O2); skeletal muscle (vastus lateralis) fractional O2 extraction, as estimated from concentration changes in deoxygenated hemoglobin+myoglobin (delta[deoxy(Hb+Mb)]), determined by near-infrared spectroscopy and expressed as a percentage of the maximal values obtained by a transient limb ischemia. Mitochondrial respiration was evaluated by high-resolution respirometry in permeabilized ("skinned") vastus lateralis fibers obtained by biopsy. RESULTS: Body mass and quadriceps femoris muscle mass were higher in RTA (102.6±2.2 kg and 3.14±0.13 kg, respectively) vs. CTRL (77.7±1.8 and 2.36±0.08). Peak O2 uptake (V'O2peak) was lower in RTA vs. CTRL both during CE (39.6±1.6 mL/min/kg BM vs. 45.9±0.9, respectively) and KE (49.2±2.3 mL/min/100g of quadriceps muscle mass vs. 61.4±3.3). Delta[deoxy(Hb+Mb)]peak was lower in RTA vs. CTRL both in CE (52±3% vs. 72±3) and in KE (51±3% vs. 73±4). On the other hand, rather surprisingly, maximal ADP-stimulated mitochondrial respiration was higher in RTA (56.7±7.1 pmolO2/s/mg wet weight) vs. CTRL (35.7±3.1), also after the values were normalized per citrate synthase activity. CONCLUSIONS: Peak oxidative function in vivo was impaired in RTA, also after eliminating, by the adopted KE protocol, constraints related to cardiovascular O2 delivery. This finding may appear to be in contradiction with the higher maximal ADP-stimulated mitochondrial respiration observed in isolated fibers. The main limitation to oxidative function in RTA in vivo may reside in peripheral O2 diffusion. Financial support by ASI - OSMA Contract I/007/06/0, Workpackage 1B-31-1 is acknowledged.