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Matthew Krause



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Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.


Skeletal muscle exists on a continuum of pure and hybrid fibres (I ↔ I/IIa ↔ IIa ↔ IIa/IIx ↔ IIx ↔ IIx/IIb ↔IIb) which can change phenotypes via external stimuli such as chronic exercise training. The various fibre types differ across characteristics such as shortening velocity, fatigue resistance, and mitochondrial content that provide skeletal muscle the ability to meet different metabolic, physiological, and structural demands. Another feature of skeletal muscle is its innate ability to regenerate after injury, which is a period of fibre type malleability and when fibres may be more responsive to treatments that switch phenotypes. Mitochondrial content and oxidative capacity are secondary indicators of fibre phenotype and may be similarly affected by external stimuli during exercise and regeneration due their overlapping regulatory pathways. Previous research observed an increase in fast twitch IIa/IIx hybrid fibres in the mouse soleus muscle following injury in response to endurance exercise training. Thus, this study aimed to elucidate the effect of exercise and regeneration on mitochondrial content and oxidative capacity on these hybrid fibres in the soleus. Twelve-week-old C57BL/6J mice participated in two weeks of endurance treadmill running. Fibre type-specific SDH (succinate dehydrogenase) content of type I, IIa, IIx and IIa/IIx fibres was compared between activity groups (sedentary vs exercise trained) at 14 and 50 days post-cardiotoxin-induced injury. Interestingly, 14 days of endurance exercise after an acute injury was detrimental to mitochondrial content and oxidative capacity, especially in the type IIa and IIa/IIx fibres. After 36 days of sedentary behaviour, the injured exercised group’s SDH content increased to a level comparable to the control group. Thus, it appears that injury and exercise may delay the mitochondrial regenerative process and impair the early restoration of skeletal muscle oxidative capacity and fibre phenotype.

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