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Training for improvement of oxidative capacity of muscle fibers may be attenuated when concurrently training for peak power. However, because of fiber type-specific recruitment, such attenuation may only account for high-oxidative muscle fibers. Here, we investigate the effects of concurrent training on oxidative capacity (as measured by succinate dehydrogenase (SDH) activity) by using task-specific recruitment of the high- and low-oxidative compartment of rat medial gastrocnemius muscle (GM). Forty rats were subjected to 6 wk of peak power training (PT, n = 10), endurance training (ET, n = 10), concurrent peak power and endurance training (PET, n = 10), or no training (control, n = 10). SDH activity, mRNA expression of SDH, peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), receptor-interacting protein 140, and BCL2/adenovirus E1B 19 kDa-interacting protein 3 as well as PGC-1α protein levels were analyzed in the low- and high-oxidative region of the GM. In the low-oxidative compartment, PT and PET induced a 30% decrease in SDH activity of Type IIB fibers compared with controls and ET (P < 0.001) without changes in mRNA or protein levels. In the high-oxidative compartment, after ET, SDH mRNA levels were 42% higher and RIP140 mRNA levels 33% lower compared with controls, which did not result in changes in SDH activity. These results indicate that in compartmentalized rat GM, peak power on top of endurance training attenuated transcription of mRNA for mitochondrial proteins in high-oxidative muscle fibers. In low-oxidative Type IIB fibers, peak power training substantially decreased SDH activity, which was not related to lower SDH mRNA levels. It is concluded that PT and PET enhanced mitochondrial degradation in the low-oxidative compartment of rat GM.


Regula Furrer, Arnold DE Haan, Nathalie Bravenboer, Dorien Kos, Paul Lips, Richard T Jaspers. Effects of concurrent training on oxidative capacity in rat gastrocnemius muscle. Medicine and science in sports and exercise. 2013 Sep;45(9):1674-83

PMID: 23475169

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