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1 Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, ON, Canada
2 Department of Medicine, McMaster University, Hamilton, ON, Canada
* To whom correspondence should be addressed. E-mail: gibalam{at}mcmaster.ca.
We tested the theory that links the size of the muscle TCA cycle intermediate (TCAI) pool with the capacity to perform prolonged exercise. We hypothesized that aerobic training (TR) would attenuate the exercise-induced expansion of the TCA cycle pool, however the lower [TCAI] would not compromise cycle endurance capacity. Eight men (22±1 y) cycled at ~80% of pre-TR VO2peak before and after 7 wks of TR (1 hr.d-1, 5 d.wk-1). Biopsies (m. vastus lateralis) were obtained during both trials at rest, after 5 min and at the point of exhaustion during the pre-TR trial (EndEx1, 42±6 min). A biopsy was also obtained at the end of exercise during the post-TR trial (EndEx2; 91±6 min). In addition to improved performance, TR increased (P<0.05) VO2peak and citrate synthase maximal activity. The sum of 4 measured TCAI was similar between trials at rest, but lower after 5 min of exercise post-TR (2.7±0.2 vs 4.3±0.2 mmol.kg-1 dry weight (dw) (P<0.05). There was a clear dissociation between TCAI pool size and aerobic energy provision, since the [TCAI] at EndEx1 was not different between trials (Post: 2.9±0.5 vs Pre: 3.5±0.2 mmol.kg-1 dw), and yet cycle endurance time more than doubled in the post-TR trial. TR did not alter the resting concentrations of two measured amino acids, but attenuated the exercise-induced decrease in [glutamate] (Post: 4.5±0.7 vs Pre: 7.7±0.6 mmol.kg-1 dw) and increase in [alanine] (Post: 3.3±0.2 vs Pre: 5.6±0.3 mmol.kg-1 dw) (P<0.05), which is consistent with reduced carbon flux through AAT. We conclude that, following aerobic training, cycle endurance capacity is not limited by a decrease in the muscle TCAI pool.
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