Biomedical subjects

Megan S Thorburn

Publications and source records attributed to Megan S Thorburn.

2 recordsLinked to original sources

PubMed2006

Exercise can be pyrogenic in humans.

Exercise increases mean body temperature (T(body)) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE(2) can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised T(body) in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), Vo(2 max): 53 ml x kg(-1) x min(-1) (SD 5)] consumed rofecoxib (50 mg/day; NSAID) or placebo (PLAC) for 6 days, 2 wk apart. Exercising thermoregulation was measured on day 6 during 45-min running ( approximately 75% Vo(2 max)) followed by 45-min cycling and 60-min seated recovery (28 degrees C, 50% relative humidity). Plasma cytokine (TNF-alpha, IL-10) concentrations were measured at rest and 30-min recovery. T(body) was similar at rest in PLAC (35.59 degrees C) and NSAID (35.53 degrees C) and increased similarly during running, but became 0.33 degrees C (SD 0.26) lower in NSAID during cycling (37.39 degrees C vs. 37.07 degrees C; P = 0.03), and remained lower throughout recovery. Sweating was initiated at T(body) of approximately 35.6 degrees C in both conditions but ceased at higher T(body) in PLAC than NSAID during recovery [36.66 degrees C (SD 0.36) vs. 36.39 degrees C (SD 0.27); P = 0.03]. Cardiac frequency averaged 6 x min(-1) higher in PLAC (P < 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W x m(-2); P = 0.56). A modest increase in both cytokines across exercise was similar between conditions. COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans.

Adult↗

PubMed2006

Attenuated gastric distress but no benefit to performance with adaptation to octanoate-rich esterified oils in well-trained male cyclists.

We investigated the effects of modifying a normal dietary fatty acid composition and ingestion of high-fat exercise supplements on gastrointestinal distress, substrate oxidation, and endurance cycling performance. Nine well-trained male cyclists completed a randomized triple-crossover comprising a 2-wk diet high in octanoate-rich esterified oil (MCFA) or twice long-chain fatty acids (LCFA). Following the diets, participants performed 3-h of cycling at 50% of peak power followed by 10 maximal sprints while ingesting either 1) a carbohydrate (CHO)+MCFA-rich oil emulsion after the 2-wk MCFA-rich dietary condition (MC-MC, Intervention) and 2) after one of the LCFA-rich dietary conditions (LC-MC, Placebo) or 3) CHO only following a LCFA-rich diet (LC-CHO, Control). During the 3-h ride MCFA-adaptation decreased octanoic-acid oxidation by 24% (90% confidence interval: 14-34%). The CHO+MCFA-rich oil emulsion reduced endogenous fat oxidation by 61% (33-89%) and 110% (89-131%) in the MC-MC and LC-MC conditions, respectively, and MCFA-adaptation reduced endogenous-carbohydrate oxidation by 10% (-3-23%). MCFA-adaptation attenuated gastrointestinal distress and nausea during the sprints, but the effect of the oil emulsion was to lower sprint power by 10.9% (7.7-14.1%) in the LC-MC condition and by 7.1% (5.7-8.5%) in the MC-MC condition, relative to the LC-CHO control; every one unit increase in nausea decreased mean power by 6.0 W (3.2-8.8 W). We conclude that despite some attenuation of endogenous-carbohydrate oxidation and gastric distress following adaptation to a MCFA-rich diet, repeat sprint performance was substantially impaired in response to the ingestion of a CHO+MCFA-rich oil emulsion.

Adaptation, Physiological↗