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1 Department of Kinesiology, McMaster University, Hamilton, Canada
2 Department of Kinesiology, University of Waterloo, Waterloo, Canada
3 Department of Human Biology, University of Guelph, Guelph, Canada
* To whom correspondence should be addressed. E-mail: gibalam{at}mcmaster.ca.
Skeletal muscle primarily relies on carbohydrate (CHO) for energy provision during high-intensity exercise. We hypothesized that sprint interval training (SIT), or repeated sessions of high-intensity exercise, would induce rapid changes in transport proteins associated with CHO metabolism, whereas changes in skeletal muscle fatty acid transporters would occur more slowly. Eight active men (22±1 y; peak oxygen uptake = 50±2 ml/kg/min) performed 4-6 x 30-s all out cycling efforts with 4 min recovery, 3 d/wk for 6 wk. Needle muscle biopsy samples (v. lateralis) were obtained before training (Pre), after 1 and 6 wk of SIT and after 1 and 6 wk of detraining. Muscle oxidative capacity, as reflected by the protein content of cytochrome c oxidase subunit 4 (COX4), increased by ~35% after 1 wk of SIT and remained higher compared to Pre even after 6 wk of detraining (P<0.05). Muscle GLUT4 content increased after 1 wk of SIT and remained ?20% higher compared to baseline during detraining (P<0.05). The monocarboxyate tranporter (MCT) 4 was higher after 1 and 6 wk of SIT compared to Pre, whereas MCT1 increased after 6 wk of training and remained higher after 1 wk of detraining (P<0.05). There was no effect of training or detraining on the muscle content of fatty acid translocase (FAT/CD36) or plasma membrane associated fatty acid binding protein (FABPpm) (P>0.05). We conclude that short-term SIT induces rapid increases in skeletal muscle oxidative capacity but has divergent effects on proteins associated with glucose, lactate and fatty acid transport.
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