We hypothesized that the exercise-induced increase in muscle tricarboxylic acid (TCA) cycle intermediates (TCAI) would be lower after aerobic training (TR), due to a better match between pyruvate production and subsequent oxidation and lower flux through the alanine aminotransferase (AAT) reaction. Eight men [22 ± 1 y; maximal aerobic capacity (V02max) = 3.9 ± 0.2 L/min] cycled at 75% of their pre-TR V02max to exhaustion (Exh), before and after 7 wk ofTR (1 hr/d, 5 d/wk). Muscle biopsies (v. lateralis) were obtained at rest, 5 min of exercise and Exh. The effect ofTR was evidenced by an increased time to fatigue (91 ± 6 vs 42 ± 6 min), increases in resting [glycogen] and citrate synthase maximal activity, and decreases in glycogen degradation, lactate accumulation and phosphocreatine utilization during exercise. 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 dw, P<0.05). Importantly, the [TCAI] at Exh post- TR (2.9 ± 0.2 mmol.kg-1 dw) was not different compared to 5 min of exercise and thus fatigue was not attributable to a decline in TCAI. The net change in glutamate (Post: 4.5 ± 0.7 vs Pre: 7.7 ± 0.6 mmol.kg-1 dw) and alanine (Post: 3.3 ± 0.2 vs Pre: 5.6 ± 0.3 mmol.kg-1 dw) from Rest-5 min of exercise was attenuated post-TR (P<0.05), which is consistent with lower flux through the AA T reaction. We conclude that changes in muscle TCAI during exercise are not causally related to aerobic energy provision. / Thesis / Master of Science (MSc)