Resistance Exercise Attenuates Mitochondrial Function

Abstract

Although nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to modulate skeletal muscle adaptations and protein metabolism in response to resistance exercise, little is known about the effects of NSAIDs on mitochondrial function. Thus, the current study aimed to examine the effects of resistance exercise with concomitant NSAID consumption on mitochondrial oxidative phosphorylation in skeletal muscle. Twenty participants were randomized in a single-blinded fashion to either an experimental group receiving ibuprofen (IBU: 27±5 yr; n=11; 1200 mg/d) or a control group receiving a low-dose acetylsalicylic acid (CON: 26±4 yr; n=9; 75 mg/d) During this period, subjects performed 8 weeks of supervised resistance exercise involving the knee extensors muscles. Each of the subject’s legs were randomized to complete the training program using either a flywheel (FW) device emphasizing eccentric-overload, or a traditional weight stack machine (WS). Maximal mitochondrial oxidative phosphorylation (OXPHOS) from permeabilized skeletal muscle bundles was assessed using high resolution respirometry before and after the training intervention. Citrate synthase activity was assessed using spectrophotometric techniques. After training, OXPHOS decreased (P<0.05) in both IBU (23%) and CON (29%) with no difference across medical treatments. Although OXPHOS decreased in both legs, the decrease was greater (interaction P=0.015) in WS (33%, P=0.015) than in FW (19%, P=0.078). Citrate synthase (CS) did not change after the intervention. The increase in quadriceps muscle volume was not significantly correlated with the change in OXPHOS (R=0.15). These results suggest that 1) eight weeks of resistance training reduces mitochondrial function but not mitochondrial content, 2) The decreased mitochondrial function with resistance exercise was not affected by ibuprofen consumption, 3) flywheel resistance training, emphasizing eccentric overload, rescues some of the reduction in mitochondrial function seen with conventional resistance training.