Abstract Endurance training commenced with reduced endogenous and exogenous carbohydrate eCHO) availability enhances training-induced oxidative adaptations of skeletal muscle. However training with reduced endogenous CHO has been shown to compromise absolute training intensity. Additionally, contractile-induced protein degradation and synthesis is increased and decreased, respectively, to a greater extent when exercise is commenced with reduced glycogen availability, compared to when the same exercise is commenced with normal muscle glycogen content. Taken together, chronic exposure to endurance training with low muscle glycogen availability could not only result in a de- training effect due to an inability to maintain high absolute workloads, this approach to training could also lead to a progressive loss of lean muscle mass. There is accumulating data to suggest that protein provision before during and after endurance exercise (EE) enhances post-exercise skeletal muscle protein synthesis as well as activation of signalling molecules regulating translation initiation and elongation. Furthermore, there is evidence that the consumption of branched-chain amino acids during exercise improves exercise performance and reduces perceptions of effort during exercise undertaken in a glycogen depleted state. This thesis investigated the effects of protein ingestion before, during and after exercise commenced with reduced eRO availability on exercise capacity and cell signalling responses associated with the regulation of mitochondrial biogenesis and muscle protein synthesis. It was anticipated that the findings obtained from this research would provide practical nutritional implications to combat the proposed negative effects associated with commencing EE with reduced eHO availability. In a fully randomised cross-over design separated by 7-10 days, ten participants reported to the laboratory on the evening before each trial to perform a glycogen depleting bout of intermittent exhaustive cycling. The following morning, participants arrived at the laboratory in a fasted state and performed 45 rnin of steady-state cycling at 50% peak power output (PPO) and a subsequent bout of intermittent exhaustive cycling at 40 and 80 % PPO as a measure of exercise capacity. Subjects ingested protein (PRO) or placebo (PLA) before (1 L), during (500 ml) and after exercise (1 L). Muscle biopsies were sampled from'the vastus lateralis immediately before and after exercise, and also 3 hours after exercise. Followinz the completion of the 45 min steady-state cvclinz protocol. -- '" ." '-" .1 ' ·f i "' r • i ! 1 there was no difference in time to exhaustion (P = 0.61) between trials during the subsequent exercise capacity test (24.7 ± 10.2 and 25.6 ± 8.7 mm for placebo and protein, respectively). Phosphorylation of AMPKThr172 increased by approximately 3-4 fold post- exercise (P = 0.03) with no difference (P = 0.545) between trials and returned to basal levels at 3 h post-exercise. In contrast, exercise did not alter phosphorylation of p38MAPKThrlSO/TYrlS2 (P = 0.54) or total protein content of POC-la at any time-point post-exercise (P = 0.77). Although not statistically significant (P = 0.09), our results illustrate a physiological trend for greater dephosphorylation of eEF2 Th66 (i.e. activation) in the protein trial post-exercise and at 3 h post-exercise, implying greater signalling for protein synthesis to occur in this trial. Whilst the present thesis provides further evidence that protein supplementation enriched with BCAAs does not improve exercise capacity in a glycogen depleted state, we do provide novel data implicating that protein ingestion may prove beneficial during low CHO endurance training. We demonstrate that protein ingestion before, during and after exercise still allows for activation of cell signalling pathways associated with regulating mitochondrial biogenesis in response to exercise commenced with reduced muscle glycogen availability. Additionally, we have shown that under identical conditions, protein ingestion before, during and after EE enhances the activation of eEF2, a proxy marker of muscle protein synthesis, therefore providing efficacy for use of protein supplementation as a nutritional strategy to combat the evident increased and decreased protein degradation and synthesis, respectively, during low CHO EE.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:576639 |
| Date | January 2012 |
| Creators | Taylor, Conor William |
| Publisher | Liverpool John Moores University |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
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