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)
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/22560 |
| Date | 06 1900 |
| Creators | Howarth, Krista R. |
| Contributors | Gibala, Martin J., Human Biodynamics |
| Source Sets | McMaster University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis |
Page generated in 0.002 seconds