Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training

Abstract

RESISTANCE TRAINING PROGRAMS have been developed with the aim of improving variables of muscle function such as strength, power, speed, local muscular endurance, coordination, and flexibility (21). Resistance training is now considered an important part of training and rehabilitation programs for healthy subjects and for various types of patients, such as cardiac patients (45), patients with pulmonary diseases (10), patients undergoing prolonged bed-rest periods (2), or elderly subjects (28). In these populations, the combination of resistance training with the more conventional endurance exercise improves the patients’ outcomes and quality of life (45). An increase in the cross-sectional area of skeletal muscle fibers and a shift of fiber-type distribution toward type 2 fibers are typical adaptations induced by resistance training; these adaptations enhance the muscle force-generating potential (12) but could represent an impairment to skeletal muscle oxidative metabolism. On the other hand, muscles with higher maximal force would need to recruit a lower number of motor units, and therefore more oxidative (and more efficient) muscle fibers (20, 26). According to other authors, strength training may increase skeletal muscle efficiency (4) and enhance skeletal muscle “metabolic stability” (50). Other studies reported, after resistance training, unchanged values of maximal O2 uptake (V˙ O2) (6), as well as unchanged (19) or lower (42, 43) mitochondrial volume density, oxidative enzyme activity, and capillary density in the hypertrophic muscles. Thus the specific effects of resistance training, with the related changes in muscle phenotype, on oxidative metabolism appear difficult to reconcile in a unifying scenario. The aim of the present study was to determine whether increases in muscle mass induced by chronic resistance training are associated, in humans, with alterations in skeletal muscle oxidative function and aerobic performance. Experiments were carried out on a group of resistance-trained athletes (RTA), in whom muscle adaptations to resistance exercise are expected to be particularly marked. An integrative approach was applied by analyzing oxidative metabolism at different levels, spanning from pulmonary gas exchange to skeletal muscle function and mitochondrial respiration. Oxidative function was assessed in vivo during incremental cycle ergometer (CE) exercise and dynamic knee extension (KE) exercise with one leg (3). During KE, the recruitment of a relatively small muscle mass, i.e., the quadriceps femoris of one leg, significantly reduces constraints to oxidative function deriving from cardiovascular O2 delivery, thereby allowing a more direct assessment of quadriceps muscle oxidative capacity in vivo. The intrinsic properties of mitochondria were assessed ex vivo in permeabilized muscle fibers obtained by biopsy by high-resolution respirometry (36). We hypothesized, in RTA vs. control subjects (CTRL), an impaired skeletal muscle oxidative function in vivo and an impaired mitochondrial respiratory function ex vivo.