Abstract
Aim: The current study aimed to examine the effects of resistance exercise with concomitant consumption of high vs. low daily doses of non-steroidal anti-inflammatory drugs (NSAIDs) on mitochondrial oxidative phosphorylation in skeletal muscle. As a secondary aim, we compared the effects of eccentric overload with conventional training.Methods: Twenty participants were randomized to either a group taking high doses (3 × 400 mg/day) of ibuprofen (IBU; 27 ± 5 year; n = 11) or a group ingesting a low dose (1 × 75 mg/day) of acetylsalicylic acid (ASA; 26 ± 4 year; n = 9) during 8 weeks of supervised knee extensor resistance training. 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 (CI+IIP) from permeabilized skeletal muscle bundles was assessed using high-resolution respirometry. Citrate synthase (CS) activity was assessed using spectrophotometric techniques and mitochondrial protein content using western blotting.Results: After training, CI+IIP decreased (P < 0.05) in both IBU (23%) and ASA (29%) with no difference across medical treatments. Although CI+IIP decreased in both legs, the decrease was greater (interaction p = 0.015) in WS (33%, p = 0.001) compared with FW (19%, p = 0.078). CS activity increased (p = 0.027) with resistance training, with no interactions with medical treatment or training modality. Protein expression of ULK1 increased with training in both groups (p < 0.001). The increase in quadriceps muscle volume was not correlated with changes in CI+IIP (R = 0.16).Conclusion: These results suggest that 8 weeks of resistance training with co-ingestion of anti-inflammatory drugs reduces mitochondrial function but increases mitochondrial content. The observed changes were not affected by higher doses of NSAIDs consumption, suggesting that the resistance training intervention was the prime mediator of the decreased mitochondrial phosphorylation. Finally, we noted that flywheel resistance training, emphasizing eccentric overload, rescued some of the reduction in mitochondrial function seen with conventional resistance training.
Highlights
It is widely recognized that both high-volume and high-intensity (Granata et al, 2015; Vincent et al, 2015) aerobic exercise training is a potent stimulus for improving mitochondrial content and function (Holloszy, 1975), less is known about the effects of resistance training
complex I and II linked respiration (CI+IIP) decreased in both legs, the decrease was greater in weight stack device (WS) (33%, p = 0.001) than in flywheel training device (FW) (19%, p = 0.078) with no difference across medical treatments (Figure 1)
Main effects of time were found for ETFP and CIP (p < 0.05)
Summary
It is widely recognized that both high-volume and high-intensity (Granata et al, 2015; Vincent et al, 2015) aerobic exercise training is a potent stimulus for improving mitochondrial content and function (Holloszy, 1975), less is known about the effects of resistance training. When comparing eccentric vs concentric contractions, animal models have shown that mitochondrial respiration is mainly improved after concentric work (Isner-Horobeti et al, 2014). This could be due to the known fact that concentric work is much more energy consuming than eccentric work (Hoppeler, 2016), thereby triggering adaptations in the ATP-producing mitochondria. It remains to be explored how coupled concentriceccentric muscle actions, favoring eccentric overload, affects mitochondrial adaptations
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