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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]

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 CO2 partial pressure (an index of arterial CO2 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. [ABSTRACT FROM AUTHOR]

Hyperthermia stimulates ventilation in humans. This hyperthermia-induced hyperventilation may be mediated by the activation of peripheral chemoreceptors implicated in the regulation of respiration in reaction to various chemical stimuli, including reductions in arterial pH. Here, we investigated the hypothesis that during passive heating at rest, the increases in arterial pH achieved with sodium bicarbonate ingestion, which could attenuate peripheral chemoreceptor activity, mitigate hyperthermia-induced hyperventilation. We also assessed the effect of sodium bicarbonate ingestion on cerebral blood flow responses, which are associated with hyperthermia-induced hyperventilation. Twelve healthy men ingested sodium bicarbonate (0.3 g/kg body weight) or sodium chloride (0.208 g/kg). One hundred minutes after the ingestion, the participants were passively heated using hot-water immersion (42°C) combined with a water-perfused suit. Increases in esophageal temperature (an index of core temperature) and minute ventilation (V̇E) during the heating were similar in the two trials. Moreover, when V̇E is expressed as a function of esophageal temperature, there were no between-trial differences in the core temperature threshold for hyperventilation (38.0 ± 0.3 vs. 38.0 ± 0.4°C, P = 0.469) and sensitivity of hyperthermia-induced hyperventilation as assessed by the slope of the core temperature-V̇E relation (13.5 ± 14.2 vs. 15.8 ± 15.5 L/min/°C, P = 0.831). Furthermore, middle cerebral artery mean blood velocity (an index of cerebral blood flow) decreased similarly with heating duration in both trials. These results suggest that sodium bicarbonate ingestion does not mitigate hyperthermia-induced hyperventilation and the reductions in cerebral blood flow index in resting heated humans. NEW & NOTEWORTHY: Hyperthermia leads to hyperventilation and associated cerebral hypoperfusion, both of which may impair heat tolerance. This hyperthermia-induced hyperventilation may be mediated by peripheral chemoreceptors, which can be activated by reductions in arterial pH. However, our results suggest that sodium bicarbonate ingestion, which can increase arterial pH, is not an effective intervention in alleviating hyperthermia-induced hyperventilation and cerebral hypoperfusion in resting heated humans. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the effect of voluntary hypocapnic hyperventilation or moderate hypoxia on metabolic and heart rate responses during high-intensity intermittent exercise.Methods: Ten males performed three 30-s bouts of high-intensity cycling [Ex1 and Ex2: constant-workload at 80% of the power output in the Wingate anaerobic test (WAnT), Ex3: WAnT] interspaced with 4-min recovery periods under normoxic (Control), hypocapnic or hypoxic (2500 m) conditions. Hypocapnia was developed through voluntary hyperventilation for 20 min prior to Ex1 and during each recovery period.Results: End-tidal CO2 pressure was lower before each exercise in the hypocapnia than control trials. Oxygen uptake ([Formula: see text]) was lower in the hypocapnia than control trials (822 ± 235 vs. 1645 ± 245 mL min-1; mean ± SD) during Ex1, but not Ex2 or Ex3, without a between-trial difference in the power output during the exercises. Heart rates (HRs) during Ex1 (127 ± 8 vs. 142 ± 10 beats min-1) and subsequent post-exercise recovery periods were lower in the hypocapnia than control trials, without differences during or after Ex2, except at 4 min into the second recovery period. [Formula: see text] did not differ between the control and hypoxia trials throughout.Conclusions: These results suggest that during three 30-s bouts of high-intensity intermittent cycling, (1) hypocapnia reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate during the first but not subsequent exercises; (2) HRs during the exercise and post-exercise recovery periods are lowered by hypocapnia, but this effect is diminished with repeated exercise bouts, and (3) moderate hypoxia (2500 m) does not affect the metabolic response during exercise. [ABSTRACT FROM AUTHOR]

Purpose: We investigated whether varying the number of repetitions of high-intensity exercise during work-matched warm-ups modulates physiological responses (heart rate, metabolic responses, and core temperature), perceptions (ratings of perceived exertion, effort of breathing), readiness for exercise, and short-term exercise performance. Methods: Ten physically active young males performed a 30-s Wingate anaerobic test (WAnT) following a warm-up consisting of submaximal constant-workload cycling at 60% maximal oxygen uptake with no high-intensity cycling (constant-workload warm-up) or with 1, 4, or 7 repetitions of 10 s of high-intensity cycling at 110% maximal oxygen uptake. All warm-ups were matched for duration (10 min) and total work. Results: Warm-ups with seven repetitions of high-intensity cycling resulted in higher ratings of perceived whole-body exertion and effort of breathing than the constant-workload warm-up. Warm-up with four repetitions of high-intensity cycling produced greater readiness for a 30-s WAnT (7.33 ± 0.73 AU) than the constant-workload warm-up (6.33 ± 0.98 AU) (P =.022). Physiological responses did not differ among the four warm-up conditions, though peak heart rate was slightly higher (~5 beats/min) during warm-up with four or seven repetitions of high-intensity cycling than during the constant-workload warm-up. Peak, mean, and minimum power output during the 30-s WAnT did not differ among the four warm-up conditions. Conclusions: These results suggest that the effects of warm-ups with intermittent high-intensity exercise on physiological responses and short-term high-intensity exercise performance do not greatly differ from a warm-up with a work-matched submaximal constant-workload. However, they appear to modulate perceptions and readiness as a function of the number of repetitions of the high-intensity exercise. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate the effects of a rise in arterial carbon dioxide pressure (PaCO2) on vascular and blood flow responses in the cerebral circulation and active skeletal muscles during dynamic exercise in humans. Thirteen healthy young adults (three women) participated in hypercapnia and normocapnia trials. In both trials, participants performed a two‐legged dynamic knee extension exercise at a constant workload that increased heart rate to roughly 100 beats min−1. In the hypercapnia trial, participants performed the exercise with spontaneous breathing while end‐tidal carbon dioxide pressure (PETCO2), an index of PaCO2, was held at 60 mmHg by inhaling hypercapnic gas (O2: 20.3 ± 0.1%; CO2: 6.0 ± 0.5%). In the normocapnia trial, minute ventilation during exercise was matched to the value in the hypercapnia trial by performing voluntary hyperventilation with PETCO2 clamped at baseline level (i.e., 40–45 mmHg) through inhalation of mildly hypercapnic gas (O2: 20.6 ± 0.1%; CO2: 2.7 ± 1.0%). Middle cerebral artery mean blood velocity and the cerebral vascular conductance index were higher in the hypercapnia trial than in the normocapnia trial. By contrast, vascular conductance in the exercising leg was lower in the hypercapnia trial than in the normocapnia trial. Blood flow to the exercising leg did not differ between the two trials. These results demonstrate that hypercapnia‐induced vasomotion in active skeletal muscles is opposite to that in the cerebral circulation. These differential vascular responses may cause a preferential rise in cerebral blood flow. [ABSTRACT FROM AUTHOR]

Whether high‐intensity exercise training and detraining combined with skeletal muscle pump (MP) could alter the magnitude of postexercise hypotension has not been investigated. We therefore sought to determine whether the combination of MP (unloaded back‐pedaling) with 4 weeks of high‐intensity exercise training and detraining could alter the magnitude of postexercise hypotension. Fourteen healthy men underwent 4 weeks of high‐intensity exercise training (5 consecutive days per week for 15 min per session at 40% of the difference between the gas exchange threshold and maximal oxygen uptake [i.e., Δ40%]) followed by detraining for 4 weeks. Assessments were conducted at Pre‐training (Pre), Post‐training (Post) and after Detraining with (MP) and without MP (Con). The exercise test in the Pre, Post and the Detraining consisted of 15 min exercise at Δ40% followed by 1 h of recovery. At all time‐points, the postexercise reduction in mean arterial pressure (MAP) was reduced in MP compared to Con (all p < 0.01). Four weeks of high‐intensity exercise training resulted in a reduction in the magnitude of postexercise hypotension (i.e., the change in MAP from baseline was mitigated) across both trials (All p < 0.01) when compared to Pre and Detraining. Following Detraining, the reduction of MAP from baseline was reduced compared to Pre, but was not different from Post. We conclude that high‐intensity exercise training combined with skeletal MP reduces the magnitude of postexercise hypotension, and this effect is partially retained for 4 weeks following the complete cessation of high‐intensity exercise training. [ABSTRACT FROM AUTHOR]

The effect of different exercise intensities on the magnitude of post‐exercise hypotension has not been rigorously clarified with respect to the metabolic thresholds that partition discrete exercise intensity domains (i.e., critical power and the gas exchange threshold (GET)). We hypothesized that the magnitude of post‐exercise hypotension would be greater following isocaloric exercise performed above versus below critical power. Twelve non‐hypertensive men completed a ramp incremental exercise test to determine maximal oxygen uptake and the GET, followed by five exhaustive constant load trials to determine critical power and W′ (work available above critical power). Subsequently, criterion trials were performed at four discrete intensities matched for total work performed (i.e., isocaloric) to determine the impact of exercise intensity on post‐exercise hypotension: 10% above critical power (10% > CP), 10% below critical power (10% < CP), 10% above GET (10% > GET) and 10% below GET (10% < GET). The post‐exercise decrease (i.e., the minimum post‐exercise values) in mean arterial (10% > CP: −12.7 ± 8.3 vs. 10% < CP: v3.5 ± 2.9 mmHg), diastolic (10% > CP: −9.6 ± 9.8 vs. 10% < CP: −1.4 ± 5.0 mmHg) and systolic (10% > CP: −23.8 ± 7.0 vs. 10% < CP: −9.9 ± 4.3 mmHg) blood pressures were greater following exercise performed 10% > CP compared to all other trials (all P < 0.01). No effects of exercise intensity on the magnitude of post‐exercise hypotension were observed during exercise performed below critical power (all P > 0.05). Critical power represents a threshold above which the magnitude of post‐exercise hypotension is greatly augmented. New Findings: What is the central questions of this study?What is the influence of exercise intensity on the magnitude of post‐exercise hypotension with respect to metabolic thresholds?What is the main finding and its importance?The magnitude of post‐exercise hypotension is greatly increased following exercise performed above critical power. However, below critical power, there was no clear effect of exercise intensity on the magnitude of post‐exercise hypotension. [ABSTRACT FROM AUTHOR]

A combined experimental and computational study on the key intermediates of NHC-catalyzed acylation reaction, Breslow intermediates (BIs), has been conducted in order to achieve a direct nucleophilic alkanoylation of N -heterocycles. Various BI precursors are alternatively prepared and used in the reaction with 4-chloroquinazoline. The present study reveals that the intermediates having benzimidazole moiety serve as acylating agents for the introduction of straight-chain alkanoyl groups. Natural bond orbital analysis indicates that the reactivity of intermediates partly correlates to the occupancy of the π C-C bonds of the hydroxyl enamine moieties. The putative rate-determining step of the acylation reaction has been theoretically investigated. Several new 4-alkanoylquinazolines are synthesized using the BI precursors. [ABSTRACT FROM AUTHOR]

• Whole-body thermal sensation score declined as core temperature decreased. • Whole-body thermal sensation of hypothermia was blunted by exercise compared to rest. • Local skin thermal sensation did not differ between rest and exercise. Thermal sensation, a key component of behavioral thermoregulation, is modulated by the changes in both skin and core temperatures. Although cutaneous thermal sensation to local cold is blunted during exercise as compared to rest in normothermic humans, it remains to be determined whether this holds true during core cooling. Furthermore, when local skin thermal sensation is diminished during exercise, it remains unclear whether whole-body thermal sensation is also attenuated. We therefore tested whether low-intensity exercise (VO 2 : ~1300 ml min−1) attenuates local skin and/or whole-body thermal sensation in hypothermic young males. Eleven healthy young males (24 ± 2 years) were cooled through cold water immersion (18 °C) up to their lower abdomen while resting (rest trial) and during low-intensity cycling (30–60 W, 30 rpm) (exercise trial). Body temperature, cardiorespiratory variables, and whole-body (9-point scale: 0, unbearably cold; 4, neutral; 8, unbearably hot) and local skin thermal sensation were measured at baseline on land and before the esophageal temperature (T es) began to decrease (defined as -0.0 T es) and after 0.5 and 1.0 °C decrements in T es from baseline during the immersion period. Local skin thermal sensation was measured using a thermostimulator with Peltier element that was attached to the chest. The temperature of the probe was initially equilibrated to the chest skin temperature, then gradually decreased at a constant rate (0.1 °C s -1) until the participants felt coolness. The difference between the initial skin temperature and the local skin temperature that felt cool was assessed as an index of local skin thermal sensation. Throughout the immersions, esophageal and mean skin temperatures did not differ between the rest and exercise trials. Local skin thermal sensation also did not differ between the two trials or at any core temperature level. By contrast, the whole-body thermal sensation score was higher (participants felt less cold) in the exercise than in the rest trial at esophageal temperature of -1.0 °C (1.25 ± 0.46 vs. 0.63 ± 0.35 units, P = 0.035). These results suggest that local skin thermal sensation during low-intensity exercise is not affected by a decrease in core temperature. However, whole-body thermal sensation mediated by a decrease in core temperature (-1.0 °C) is blunted by low-intensity exercise during cold water immersion. [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]