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Abstract Twenty minutes of voluntary hypocapnic hyperventilation prior to exercise reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate without affecting exercise performance during the Wingate anaerobic test (WAnT). Thus, pre-exercise hypocapnic hyperventilation may be a useful means of stressing the anaerobic energy system during training, ultimately improving anaerobic exercise performance. However, it remains unclear whether a shorter (e.g., 5 min) pre-exercise hypocapnic hyperventilation is sufficient to reduce the aerobic metabolic rate during high-intensity exercise. We therefore compared the effects of 5-min and 20-min pre-exercise hypocapnic hyperventilation on aerobic metabolism during the 30-s WAnT. Ten healthy young males and one female performed the WAnT following 20 min of spontaneous breathing (control trial) or 5 or 20 min of voluntary hypocapnic hyperventilation. Both the 5-min and 20-min hyperventilation reduced end-tidal CO 2 partial pressure (an index of arterial CO 2 partial pressure) to ∼23 mmHg, whereas it remained unchanged during the spontaneous breathing. The peak, mean and minimum power outputs during the WAnT did not differ among the three trials. Oxygen uptake during the WAnT was lower in both the 5-min (1493 ± 257 mL min -1 ) and 20-min (1397 ± 447 mL min -1 ) hyperventilation trials than during the control trial (1847 ± 286 mL min -1 ), and was similar in the two hyperventilation trials. These results suggest that 5 min of pre-exercise hypocapnic hyperventilation reduces aerobic metabolism during the 30-s WAnT to a level similar to that seen with the 20-min hyperventilation. Moreover, exercise performance was unaffected, which implies anaerobic metabolism was enhanced.

Hypothermia can occur during aquatic exercise despite production of significant amounts of heat by the active muscles. Because the characteristics of human thermoregulatory responses to cold during exercise have not been fully elucidated, we investigated the effect of low-intensity exercise on the shivering response to core cooling in cool water. Eight healthy young men (24 ± 3 yr) were cooled through cool water immersion while resting (rest trial) and during loadless pedaling on a water cycle ergometer (exercise trial). Before the cooling, body temperature was elevated by hot water immersion to clearly detect a core temperature at which shivering initiates. Throughout the cooling period, mean skin temperature remained around the water temperature (25°C) in both trials, whereas esophageal temperature (T es ) did not differ between the trials ( P > 0.05). The T es at which oxygen uptake (V̇o 2 ) rapidly increased, an index of the core temperature threshold for shivering, was lower during exercise than rest (36.2 ± 0.4°C vs. 36.5 ± 0.4°C, P < 0.05). The sensitivity of the shivering response, as indicated by the slope of the T es -V̇o 2 relation, did not differ between the trials (-441.3 ±177.4 ml·min -1 ·°C -1 vs. -411.8 ± 268.1 ml·min -1 ·°C -1 , P > 0.05). The thermal sensation response to core cooling, assessed from the slope and intercept of the regression line relating T es and thermal sensation, did not differ between the trials ( P > 0.05). These results suggest that the core temperature threshold for shivering is delayed during low-intensity exercise in cool water compared with rest although shivering sensitivity is unaffected.

Hypoxia during supramaximal exercise reduces aerobic metabolism with a compensatory increase in anaerobic metabolism without affecting exercise performance. A similar response is elicited by preexercise voluntary hypocapnic hyperventilation, but it remains unclear whether hypocapnic hyperventilation and hypoxia additively reduce aerobic metabolism and increase anaerobic metabolism during supramaximal exercise. To address that issue, 12 healthy subjects (8 males and 4 females) performed the 30-second Wingate anaerobic test (WAnT) after (1) spontaneous breathing in normoxia (control, ∼21% fraction of inspired O2 [FiO2]), (2) voluntary hypocapnic hyperventilation in normoxia (hypocapnia, ∼21% FiO2), (3) spontaneous breathing in hypoxia (hypoxia, ∼11% FiO2), or (4) voluntary hypocapnic hyperventilation in hypoxia (combined, ∼11% FiO2). Mean power output during the 30-second WAnT was similar among the control (561 [133] W), hypocapnia (563 [140] W), hypoxia (558 [131] W), and combined (560 [133] W) trials (P =.778). Oxygen uptake during the 30-second WAnT was lower in the hypocapnia (1523 [318] mL/min), hypoxia (1567 [300] mL/min), and combined (1203 [318] mL/min) trials than in the control (1935 [250] mL/min) trial, and the uptake in the combined trial was lower than in the hypocapnia or hypoxia trial (all P <.001). Oxygen deficit, an index of anaerobic metabolism, was higher in the hypocapnia (38.4 [7.3] mL/kg), hypoxia (37.8 [6.8] mL/kg), and combined (40.7 [6.9] mL/kg) trials than in the control (35.0 [6.8] mL/kg) trial, and the debt was greater in the combined trial than in the hypocapnia or hypoxia trial (all P <.003). Our results suggest that voluntary hypocapnic hyperventilation and hypoxia additively reduce aerobic metabolism and increase anaerobic metabolism without affecting exercise performance during the 30-second WAnT. [ABSTRACT FROM AUTHOR]

Purpose: Although caffeine is known to possess ergogenic effects, previous studies demonstrated no effect of caffeine on 800-m run performance outdoors, which might be due to several uncontrolled factors including pacing strategies. We hypothesized that caffeine ingestion improves a pace-controlled simulated 800-m run performance. We also hypothesized that exercise-induced arterial hypoxemia occurs during the simulated 800-m run, and this response is mitigated by caffeine-induced increases in exercise ventilation. Methods: In a randomized, double-blind, placebo-controlled and crossover design, 16 (3 females) college middle-distance runners who have 800-m seasonal best of 119.97 ± 7.64 s ingested either 1) placebo (6 mg of glucose per kilogram of body weight) or caffeine (6 mg of caffeine per kilogram of body weight). Then they performed an 800-m run consisting of 30-s running at 103% of their 800-m seasonal best, followed by running at 98% of seasonal best until exhaustion, which mimics actual 800-m run pacing pattern. Results: Running time to exhaustion was extended by 7.3% ± 6.2% in the caffeine-ingested relative to placebo trial (123 ± 12 vs 114 ± 9 s, P = 0.04). Arterial oxygen saturation markedly decreased during the simulating running, but this response was similar (76.6% ± 5.7% vs 81.1% ± 5.2%, at 113 s of the simulating running) between the caffeine and placebo trials (P ≥ 0.23 for time–supplement interaction and main effect of supplement). Minute ventilation, oxygen uptake (all P ≥ 0.36 for time–supplement interaction and main effect of supplement), and rate of perceived exertion (all P ≥ 0.11) did not differ between the trials throughout the simulating running. Heart rate was higher in the caffeine-ingested trial throughout the simulated running (P < 0.01 for main effect of supplement). Postexercise blood lactate concentration was higher in the caffeine trial (P = 0.02). Conclusions: Caffeine ingestion improves simulated 800-m run performance without affecting exercise ventilation and severe exercise-induced arterial hypoxemia. [ABSTRACT FROM AUTHOR]

Introduction: Caffeine is an exercise performance enhancer widely used by individuals engaged in training or competition under heat-stressed conditions. Caffeine ingestion during exercise in the heat is believed to be safe because it does not greatly affect body temperature responses, heart rate, or body fluid status. However, it remains unknown whether caffeine affects hyperthermia-induced hyperventilation or reductions in the cerebral blood flow index. We tested the hypothesis that under conditions inducing severe hyperthermia, caffeine exacerbates hyperthermia-induced hyperventilation and reduces the cerebral blood flow index during exercise. Methods: Using a randomized, single-blind, crossover design, 12 physically active healthy young men (23 ± 2 yr) consumed a moderate dose of caffeine (5 mg·kg−1) or placebo in the heat (37°C). Approximately 60 min after the ingestion, they cycled for ~45 min at a workload equal to ~55% of their predetermined peak oxygen uptake (moderate intensity) until their core temperature increased to 2.0°C above its preexercise baseline level. Results: In both trials, ventilation increased and the cerebral blood flow index assessed by middle cerebral artery mean blood velocity decreased as core temperature rose during exercise (P < 0.05), indicating that hyperthermia-induced hyperventilation and lowering of the cerebral blood flow occurred. When core temperature was elevated by 1.5°C or more (P < 0.05), ventilation was higher and the cerebral blood flow was lower throughout the caffeine trial than the placebo trial (P < 0.05). Conclusions: A moderate dose of caffeine exacerbates hyperthermia-induced hyperventilation and reductions in the cerebral blood flow index during exercise in the heat with severe hyperthermia. [ABSTRACT FROM AUTHOR]