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    Adaptation to an MCFA-rich diet : effect on gastric tolerance, the capacity for MCFA oxidation, and performance while ingesting exogenous carbohydrate and structured oils during endurance exercise : a thesis presented in partial fulfilment of the requirements for the degree of Master of Sport Science at Massey University

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    Abstract
    Introduction: Elevating the availability of fatty-acids to the muscle can potentially benefit endurance exercise performance by reducing intramuscular-glycogen utilisation. Digestion of triglycerides containing long-chain fatty acids (LCFAs) is slow, and fatty acids must pass through the carnitine palmityl transferase (CPT) transport system to enter the mitochondria, which potentially limits fat oxidation during prolonged-heavy exercise. Conversely, medium-chain triglycerides (MCTs) are rapidly digested and their constituent fatty acids (MCFAs) by-pass the CPT transport system. Ingestion of MCFAs may therefore supply mitochondrial acetyl-CoA, potentially reducing the requirement for glycolytic flux during exercise. However, studies comparing carbohydrate (CHO) with CHO-containing MCFA-rich exercise supplements have revealed inconsistent results, probably because of the variation in gastrointestinal (GI) distress suffered by participants associated with MCT ingestion. Purpose: To investigate whether 2-weeks of dietary adaptation to MCFA-rich supplements reduces the severity of gastrointestinal (Gl) distress, or increases the rate of MCFA oxidation during endurance exercise. A decrease in ratings of GI distress, or an increase in MCFA oxidation was anticipated to lead to performance benefits. Method: Nine well-trained male endurance cyclists participated in a double-blind, pseudo-randomised. triple-crossover protocol. Participants were 37 ± 7.26 years, 81.36 ± 7.67 kg. training at least 8-10 h per week and riding competitively. Mean VO2 max and peak power output (PPO) were 4.84 ± 0.46 L-min-1 and 357.33 ± 20.55 W respectively. The effects of a 2-week MCFA-rich diet +13 C-enriched MCFA+CHO exercise supplement (MC-MC) on GI distress, MCFA-oxidation rate and sprint performance variables were compared against a 2-week LCFA-rich diet with either: (a) a13 C-enriched MCFA+CHO exercise supplement (LC-MC), or (b) a CMO-only supplement (LC-CHO). Dietary and exercise MCFA-rich supplements were consumed in the form of randomised-structured triacylglycerols made with a 3:1 molar ratio of MC- and LCFAs randomly esterified to glycerol backbones. Participants followed a controlled training regime whilst on the diets. The performance test consisted of a 3-h ride at 50% PPO followed by 10 maximal sprints. At rest and every 20-min throughout the ride, participant ratings of GI and exertion sensations were recorded, followed by external respiratory-gas analysis, collection of a breath sample for breathl3 C-enrichment analysis, a venous blood sample and ingestion of a supplement. Similarly, after sprints 1, 4, 7 and 10 participants recorded their GI ratings followed by a blood sample. Results: Peak MCFA-oxidation rates were 0.38 g-min-1(95% Cl 0.31-0.47) and 0.43 g-min-1(0.30-0.61, p-value = 0.21) in the MC-MC and LC-MC conditions respectively, but there was no evidence for CHO sparing following MCFA adaptation. Participant ratings of GI distress decreased slightly during exercise with 2-weeks of a diet high in MCFAs relative to LCFAs. Ratings of reflux, bloatedness, nausea, and urge to vomit were, respectively, 1.34 (0.88-3.14), 1.03 (0.74-2.27), 0.81 (0.62-1.69) and 0.93 (0.64-245) scale units lower in the MC-MC condition relative to LC-MC. The attenuation in GI distress corresponded with a tendency toward increased sprint mean power, which was 3.4% (± 5.9%, 0.25) higher in the MC-MC condition relative to LC-MC. However, sprint mean power was still lower in both the MC-MC (6.8% ± 2.8%, <0.0001) and LC-MC (10.4% ± 5.5%, 0.0004) conditions relative to LC-CHO. Mechanism covariate analysis illustrated a negative effect of the GI distress marker nausea on sprint performance. For every 1 unit increase in nausea for the MC-MC and LC- MC conditions, sprint power decreased by 6 W (± 3.8,0.004) relative to LC-CHO. Conclusion: No clear metabolic adaptation was evident with high dietary MCFA relative to LCFA. In addition, MCFA-rich exercise supplements caused a decrement in performance relative to CHO ingestion in both MC-MC and LC-MC conditions, suggesting that light- moderate GI distress still causes substantial performance detriments. There was little evidence to support the ingestion of randomised structured triglycerides high in MCFA with the intention of enhancing endurance performance.
    Date
    2005
    Author
    Thorburn, Megan
    Rights
    The Author
    Publisher
    Massey University
    URI
    http://hdl.handle.net/10179/11694
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    DSpace software copyright © Duraspace
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