3 research outputs found

    Blinded and unblinded hypohydration similarly impair cycling time trial performance in the heat in trained cyclists

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    Knowledge of hydration status may contribute to hypohydration-induced exercise performance decrements, therefore, this study compared blinded and unblinded hypohydration on cycling performance. Fourteen trained, non-heat acclimated cyclists (age 25 ± 5 y; V̇O2peak 63.3 ± 4.7 mL∙kg-1∙min-1; cycling experience 6 ± 3 y) were pair-matched to blinded (B) or unblinded (UB) groups. After familiarisation, subjects completed euhydrated (B-EUH; UB-EUH) and hypohydrated (B-HYP; UB-HYP) trials in the heat (31˚C); 120 min cycling preload (50% Wpeak) and a time trial (~15 min). During the preload of all trials, 0.2 mL water∙kg body mass-1 was ingested every 10 min, with additional water provided during EUH trials to match sweat losses. To blind the B group, a nasogastric tube was inserted in both trials and used to provide water in B-EUH. The preload induced similar ( P=0.895) changes in body mass between groups (B-EUH -0.6 ± 0.5%; B-HYP -3.0 ± 0.5%; UB-EUH -0.5 ± 0.3%; UB-HYP -3.0 ± 0.3%). All variables responded similarly between B and UB groups ( P≥0.558), except thirst ( P=0.004). Changes typical of hypohydration (increased heart rate, RPE, gastrointestinal temperature, serum osmolality and thirst, decreased plasma volume; P≤0.017) were apparent in HYP by 120 min. Time trial performance was similar between groups ( P=0.710) and slower ( P≤0.013) with HYP for B (B-EUH 903 ± 89 s; B-HYP 1008 ± 121 s; -11.4%) and UB (UB-EUH 874 ± 108 s; UB-HYP 967 ± 170 s; -10.1%). Hypohydration of ~3% body mass impairs time trial performance in the heat, regardless of knowledge of hydration status

    Chronic ingestion of a low dose of caffeine induces tolerance to the performance benefits of caffeine

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    This study examined effects of 4 weeks of caffeine supplementation on endurance performance. Eighteen low-habitual caffeine consumers ( 0.05). Before supplementation, all participants completed one V̇O2peak test, one practice trial and 2 experimental trials (acute 3 mg · kg−1 caffeine [precaf] and placebo [testpla]). During the supplementation period a second V̇O2peak test was completed on day 21 before a final, acute 3 mg · kg−1 caffeine trial (postcaf) on day 29. Trials consisted of 60 min cycle exercise at 60% V̇O2peak followed by a 30 min performance task. All participants produced more external work during the precaf trial than testpla, with increases in the caffeine (383.3 ± 75 kJ vs. 344.9 ± 80.3 kJ; Cohen’s d effect size [ES] = 0.49; P = 0.001) and placebo (354.5 ± 55.2 kJ vs. 333.1 ± 56.4 kJ; ES = 0.38; P = 0.004) supplementation group, respectively. This performance benefit was no longer apparent after 4 weeks of caffeine supplementation (precaf: 383.3 ± 75.0 kJ vs. postcaf: 358.0 ± 89.8 kJ; ES = 0.31; P = 0.025), but was retained in the placebo group (precaf: 354.5 ± 55.2 kJ vs. postcaf: 351.8 ± 49.4 kJ; ES = 0.05; P > 0.05). Circulating caffeine, hormonal concentrations and substrate oxidation did not differ between groups (all P > 0.05). Chronic ingestion of a low dose of caffeine develops tolerance in low-caffeine consumers. Therefore, individuals with low-habitual intakes should refrain from chronic caffeine supplementation to maximise performance benefits from acute caffeine ingestion

    24 h severe energy restriction impairs post-prandial glycaemic control in young, lean males

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    Intermittent energy restriction (IER) involves short periods of severe energy restriction interspersed with periods of adequate energy intake, and can induce weight loss. Insulin sensitivity is impaired by short-term, complete energy restriction, but the effects of IER are not well known. In randomised order, 14 lean men (age: 25 (SD 4) y; BMI: 24 (SD 2) kg·m-2; body fat: 17 (4) %) consumed 24 h diets providing 100% (10441 (SD 812) kJ; EB) or 25% (2622 (SD 204) kJ; ER) of estimated energy requirements, followed by an oral glucose tolerance test (OGTT; 75g glucose drink) overnight fasted. Plasma/ serum glucose, insulin, non-esterified fatty acids (NEFA), glucagon-like peptide-1 (GLP-1), glucose-dependant insulinotropic peptide (GIP) and fibroblast growth factor-21 (FGF21) were assessed before and after (0 h) each 24 h dietary intervention, and throughout the 2 h OGTT. Homeostatic model assessment of insulin resistance (HOMA2-IR) assessed the fasted response and incremental (iAUC) or total (tAUC) area under the curve were calculated during the OGTT. At 0 h, HOMA2-IR was 23% lower after ER compared to EB (P<0.05). During the OGTT, serum glucose iAUC (P<0.001) serum insulin iAUC (P<0.05) and plasma NEFA tAUC (P<0.01) were greater during ER, but GLP-1 (P=0.161), GIP (P=0.473) and FGF21 (P=0.497) tAUC were similar between trials. These results demonstrate that severe energy restriction acutely impairs postprandial glycaemic control in lean men, despite reducing HOMA2-IR. Chronic intervention studies are required to elucidate the long-term effects of IER on indices of insulin sensitivity, particularly in the absence of weight loss
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