International journal of sport nutrition and exercise metabolism最新文献

Enhanced buffering capacity following sodium citrate (SC) ingestion may be optimized when subsequent exercise commences at individual time-to-peak (TTP) alkalosis (blood pH or bicarbonate concentration [HCO3-]). While accounting for considerable interindividual variation in TTP (188-300 min), a reliable blood alkalotic response is required for practical use. This study evaluated the reliability of blood pH, HCO3-, and sodium (Na+) following acute SC ingestion. Fourteen recreationally active males ingested 0.4 or 0.5 g/kg body mass (BM) of SC on two occasions each and 0.07 g/kg BM of sodium chloride (control) once. Blood pH and HCO3- were measured for 4 hr postingestion. Blood pH and HCO3- displayed good reliability following 0.5 g/kg BM SC (r = .819, p = .002, standardized technical error [sTE] = 0.67 and r = .840, p < .001, sTE = 0.63, respectively). Following 0.4 g/kg BM SC, blood HCO3- retained good reliability (r = .771, p = .006, sTE = 0.78) versus moderate for blood pH (r = .520, p = .099, sTE = 1.36). TTP pH was moderately reliable following 0.5 (r = .676, p = .026, sTE = 1.05) and 0.4 g/kg BM SC (r = .679, p = .025, sTE = 0.91) versus poor for HCO3- following 0.5 (r = .183, p = .361, sTE = 5.38) and 0.4 g/kg BM SC (r = .290, p = .273, sTE = 2.50). Although the magnitude of (and displacement in) blood alkalosis, particularly HCO3-, appears reliable following potentially ergogenic doses of SC, strategies based on individual TTP cannot be recommended.

Taurine (TAU) has been shown to improve time to exhaustion (TTE) and fat oxidation during exercise; however, no studies have examined the effect of acute TAU supplementation on maximal fat oxidation (MFO) and related intensity to MFO (FATmax). Our study aimed to investigate the effect of acute TAU supplementation on MFO, FATmax, VO2peak, and TTE. Eleven recreationally trained male endurance runners performed three incremental running tests. The first visit included a familiarization to the test, followed by two subsequent visits in which exercise was performed 90 min after ingestion of either 6-g TAU or placebo (PLA) using a triple-blind randomized crossover design. There was no effect of TAU on MFO (p = .89, d = -0.07, TAU: 0.48 ± 0.22 g/min; PLA: 0.49 ± 0.15 g/min or FATmax (p = .26, d = -0.66; TAU: 49.17 ± 15.86 %V˙O2peak; PLA: 56.00 ± 13.27 %V˙O2peak). TTE was not significantly altered (TAU: 1,444.8 ± 88.6 s; PLA: 1,447.6 ± 87.34 s; p = .65, d = -0.04). TAU did not show any effect on V˙O2peak in comparison with PLA (TAU: 58.9 ± 8.4 ml·kg-1·min-1; PLA: 56.5 ± 5.7 ml·kg-1·min-1, p = .47, d = 0.48). However, V˙O2 was increased with TAU at most stages of exercise with large effect sizes. The acute ingestion of 6 g of TAU before exercise did not enhance MFO, FATmax, or TTE. However, it did increase the oxygen cost of running fixed intensities in recreationally trained endurance runners.

Hypoxia (HY) and sleep deprivation have opposite effects on appetite. As HY may alter sleep, it may be informative to assess the accumulative effects of these two stressors on hunger, energy intake (EI), and food reward. Seventeen young, active, healthy males completed four 5-hr sessions in normoxia (NO) or normobaric HY (FIO2 = 13.6%, ∼3,500 m) after a night of habitual sleep (HS; total sleep time >6 hr) or sleep restriction (SR; total sleep time <3 hr). Subjective appetite was assessed regularly using visual analogic scales and EI during an ad libitum lunch after 3.5 hr of exposure. Food reward was assessed using the Leeds Food Preference Questionnaire just before the lunch. As expected, EI was lower for the HY-HS (4.32 ± 0.71 MJ; p = .048) and HY-SR (4.16 ± 0.68 MJ, p = .013) sessions than the NO-HS (4.90 ± 0.84 MJ) session without acute mountain sickness-related gastrointestinal symptoms. No significant effect of SR alone was observed (NO-SR: 4.40 ± 0.68 MJ). Subjective appetite was not affected. Explicit liking for high-fat foods was higher with SR than HS (main effect: p = .002) and implicit wanting for high-fat foods was higher for the NO-SR, HY-HS, and HY-SR sessions than the NO-HS session (p < .006). Thus, acute SR did not modify subjective appetite or EI despite the increasing food reward for high-fat foods and did not alter the HY-induced changes of appetite or food reward.

Marine-derived proteins, such as blue whiting-derived protein hydrolysates (BWPH), represent high-quality sources of dietary protein, but their ability to support postexercise anabolism is not established. The impact of BWPH on whole-body anabolism was compared with an isonitrogenous whey protein isolate (WPI) and nonessential amino acid (NEAA) control in 10 trained young males (31 ± 4 years) who, on three separate visits, performed a session of whole-body resistance exercise and then consumed, in randomized crossover fashion, BWPH, WPI, or NEAA (0.33 g/kg; 19, 33, and 0 mg/kg leucine, respectively) with L-[1-13C]leucine. Breath, blood, and urine samples were collected for 6-hr postprandial to assess dietary leucine oxidation, amino acid (AA) concentrations, and 3-methylhistidine: creatinine ratio. Peak and area under the curve concentrations for leucine, branched-chain amino acids, and essential amino acids were greater in WPI compared with BWPH (all p < .05) but with no differences in time to peak concentration. Total oxidation reflected leucine intake (WPI > BWPH > NEAA; p < .01), whereas relative oxidation was greater (p < .01) in WPI (28.6 ± 3.6%) compared with NEAA (21.3 ± 4.2%), but not BWPH (28.6 ± 8.8%). Leucine retention, a proxy for whole-body protein synthesis, was greater in WPI (185.6 ± 9.5 μmol/kg) compared with BWPH (109.3 ± 14.1 μmol/kg) and NEAA (5.74 ± 0.30 μmol/kg; both p < .01), with BWPH being greater than NEAA (p < .01). Urinary 3-methylhistidine: creatinine ratio did not differ between conditions. Both WPI and BWPH produced essential aminoacidemia and supported whole-body anabolism after resistance exercise, but a higher intake of BWPH to better approximate the leucine and EAA content of WPI may be needed to produce an equivalent anabolic response.

Introduction: This study aimed to analyze the effect of caffeine (CAF) intake on pulmonary oxygen uptake (V˙O2) kinetics, muscle fatigue, and physiological and perceptual parameters during severe-intensity cycling exercise.

Methods: Twelve physically active men (age: 26 ± 5 years; V˙O2peak: 46.7 ± 7.8 ml·kg-1·min-1) participated of this placebo (PLA)-controlled, randomized, double-blinded, and crossover design study. Participants performed on separate days (a) a ramp incremental test to determine V˙O2peak and gas exchange threshold and (b) four 8-min constant work rate tests at 60% of the difference between gas exchange threshold and maximal V˙O2peak (i.e., Δ60%) 1 hr after taking either 6 mg/kg of body mass of CAF or PLA. Before and immediately after constant work rate tests, a 5-s all-out isokinetic sprint was performed to assess the muscle torque. V˙O2 kinetics, blood lactate concentration ([La]), and rating of perceived exertion were analyzed during constant work rate tests.

Results: CAF did not alter the primary time constant of V˙O2 kinetics (PLA: 38.3 ± 14; CAF: 36.7 ± 7.5 s), V˙O2 slow component (PLA: 0.5 ± 0.2; CAF: 0.5 ± 0.2 L/min), or peak torque (PLA: 144.6 ± 18.6; CAF: 143.9 ± 18.7 N·m). CAF decreased rating of perceived exertion (15.9 ± 1.8 vs. 17.0 ± 1.5 a.u.) and increased blood lactate concentration (9.0 ± 2.5 vs. 8.3 ± 2.2 mmol/L; p < .05) after constant work rate tests compared with PLA.

Conclusion: CAF ingestion does not alter V˙O2 kinetics or muscle torque production during 8 min of severe-intensity cycling exercise.

Background: Preexercise caffeine intake has proven to exert ergogenic effects on cycling performance. However, whether these benefits are also observed under fatigue conditions remains largely unexplored. We aimed to assess the effect of caffeine ingested during prolonged cycling on subsequent time-trial performance in trained cyclists.

Methods: The study followed a triple-blinded, randomized, placebo-controlled cross-over design. Eleven well-trained junior cyclists (17 ± 1 years) performed a field-based 8-min time trial under "fresh" conditions (i.e., after their usual warm-up) or after two work-matched steady-state cycling sessions (total energy expenditure∼20 kJ/kg and ∼100 min duration). During the latter sessions, participants consumed caffeine (3 mg/kg) or a placebo ∼60 min before the time trial. We assessed power output, heart rate, and rating of perceived exertion during the time trial and mood state (Brunel Mood Scale) before and after each session.

Results: No significant condition effect was found for the mean power output attained during the time trial (365 ± 25, 369 ± 31, and 364 32 W for "fresh," caffeine, and placebo condition, respectively; p = .669). Similar results were found for the mean heart rate (p = .100) and rating of perceived exertion (p = 1.000) during the time trial and for the different mood domains (all p > .1).

Conclusions: Caffeine intake during prolonged exercise seems to exert no ergogenic effects on subsequent time-trial performance in junior cyclists. Future studies should determine whether significant effects can be found with larger caffeine doses or after greater fatigue levels.

Purpose: This study investigated the effect of menthol (MEN) mouth rinsing (MR) on cycling performance during a modified variable cycle test (M-VCT) in adolescent athletes under hot conditions (31.4 ± 0.9 °C, 23.4 ± 3.7% relative humidity).

Methods: Trained adolescent male cyclists (n = 11, 16.7 ± 1.3 years, height 176.6 ± 8.8 cm, body mass 65.8 ± 11.6 kg, maximal oxygen uptake 62.97 ± 7.47 ml·kg-1·min-1) voluntarily completed three trials (familiarization and two experimental) of a 30-min M-VCT, which included five 6-min laps consisting of three 6-s accelerations and three 10-s sprints throughout each lap. In a randomized crossover design, MEN (0.01%) or placebo (PLA) (crystal-light), was swilled for 5 s before the start of each lap (total of 6 MR). Power output, distance (in kilometers), core temperature, heart rate, perceptual exertion, thermal stimulation (thermal comfort and thermal sensation), and blood lactate concentration were recorded.

Results: MEN MR significantly improved M-VCT mean power output by 1.81 ± 1.57% compared to PLA (MEN, 177.8 ± 31.4 W; PLA, 174.7 ± 30.5 W, p < .001, 95% confidence interval [1.73, 4.46], d = 1.53). For maximal intermittent sprints, 6- and 10-s mean power output was significantly higher with MEN than PLA (6 s, p = .041, 95% confidence interval [0.73, 27.19], d = 0.71; 10 s, p = .002, 95% confidence interval [11.08, 35.22], d = 1.29). There was no significant difference in core temperature, heart rate, blood lactate concentration, or any perceptual measure between trials (p > .05) despite significantly higher work with MEN.

Conclusion: 64% of athletes (7/11) improved M-VCT performance with MEN. The results of this investigation suggest that a MEN MR may improve power output during a sport-specific stochastic cycling task in elite adolescent male cyclists.