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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]

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]

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]

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]

• 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]

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 chemoreceptors activity, mitigate hyperthermia-induced hyperventilation. We also assessed that the effect of sodium bicarbonate ingestion on cerebral blood flow responses, which are associated with hyperthermia-induced hyperventilation. Twelve healthy men ingested a 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 (V E ) during the heating were similar in the two trials. Moreover, when V E is expressed as a function of esophageal temperature, there were no between-trial differences in the core temperature threshold for hyperventilation (37.9 ± 0.3 vs. 38.0 ± 0.4°C, P = 0.338), and sensitivity of hyperthermia-induced hyperventilation as assessed by the slope of the core temperature-V E relation (13.7 ± 14.9 vs. 15.8 ± 15.6 L/min/°C, P = 0.748). 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.

Purpose: We investigated the effects of pre-exercise voluntary hyperventilation and the resultant hypocapnia on metabolic and cardiovascular responses during and after high-intensity exercise. Methods : Ten healthy participants performed a 60-s cycling exercise at a workload of 120% peak oxygen uptake in control (spontaneous breathing), hypocapnia and normocapnia trials. Hypocapnia was induced through 20-min pre-exercise voluntary hyperventilation. In the normocapnia trial, voluntary hyperpnea was performed with CO 2 inhalation to prevent hypocapnia. Results : Pre-exercise end-tidal CO 2 partial pressure was lower in the hypocapnia trial than the control or normocapnia trial, with similar levels in the control and normocapnia trials. Average V ˙ O 2 during the entire exercise was lower in both the hypocapnia and normocapnia trials than in the control trial (1491 ± 252vs.1662 ± 169vs.1806 ± 149 mL min -1 ), with the hypocapnia trial exhibiting a greater reduction than the normocapnia trial. Minute ventilation during exercise was lower in the hypocapnia trial than the normocapnia trial. In addition, minute ventilation during the first 10s of the exercise was lower in the normocapnia than the control trial. Pre-exercise hypocapnia also reduced heart rates and arterial blood pressures during the exercise relative to the normocapnia trial, a response that lasted through the subsequent early recovery periods, though end-tidal CO 2 partial pressure was similar in the two trials. Conclusions : Our results suggest that pre-exercise hyperpnea and the resultant hypocapnia reduce V ˙ O 2 during high-intensity exercise. Moreover, hypocapnia may contribute to voluntary hyperventilation-mediated cardiovascular responses during the exercise, and this response can persist into the subsequent recovery period, despite the return of arterial CO 2 pressure to the normocapnic level.

Hyperthermia stimulates ventilation (hyperthermia-induced hyperventilation). In exercising humans, once the core temperature reaches ∼37°C, minute ventilation (V̇e) increases linearly with rising core temperature, and the slope of the relation between V̇e and core temperature reflects the sensitivity of the response. We previously reported that sodium bicarbonate ingestion reduces V̇e during prolonged exercise in the heat without affecting the sensitivity of hyperthermia-induced hyperventilation. Here, we hypothesized that reductions in V̇e associated with sodium bicarbonate ingestion reflect elevation of the core temperature threshold for hyperthermia-induced hyperventilation. Thirteen healthy young males ingested sodium bicarbonate (0.3 g/kg body wt) (NaHCO 3 trial) or sodium chloride (0.208 g/kg body wt) (NaCl trial), after which they performed a cycle exercise at 50% of peak oxygen uptake in the heat (35°C and 50% relative humidity) following a pre-cooling. The pre-cooling enabled detection of an esophageal temperature (T es : an index of core temperature) threshold for hyperthermia-induced hyperventilation. The T es thresholds for increases in V̇e were similar between the two trials ( P = 0.514). The slopes relating V̇ E to T es also did not differ between trials ( P = 0.131). However, V̇e was lower in the NaHCO 3 than in the NaCl trial in the range of T es = 36.8-38.4°C ( P = 0.007, main effect of trial). These results suggest that sodium bicarbonate ingestion does not alter the core temperature threshold or sensitivity of hyperthermia-induced hyperventilation during prolonged exercise in the heat; instead, it downshifts the exercise hyperpnea.

When one is exposed to a stressful situation in their daily life, a common response is hyperventilation. Although the physiological significance of stress-induced hyperventilation remains uncertain, this response may blunt perception of the stress-inducing stimulus. This study examined the effects of voluntary hyperventilation and resultant hypocapnia on the local skin thermal detection threshold in normothermic resting humans. Local skin thermal detection thresholds were measured in 15 young adults (three females) under three breathing conditions: 1 ) spontaneous breathing (Control trial), 2 ) voluntary hypocapnic hyperventilation (HH trial), and 3 ) voluntary normocapnic hyperventilation (NH trial). Local skin thermal detection thresholds were measured using thermostimulators containing a Peltier element that were attached to the forearm and forehead. The temperature of the probe was initially equilibrated to the skin temperature, then gradually increased or decreased at a constant rate (±0.1 °C/s) until the participants felt warmth or coolness. The difference between the initial skin temperature and the local skin temperature at which the participant noticed warmth/coolness was assessed as an index of the local skin warm/cool detection threshold. Local detection of warm and cool stimuli did not differ between the Control and NH trials, but it was blunted in the HH trial as compared with the Control and NH trials, except for detection of warm stimuli on the forearm. These findings suggest that hyperventilation-induced hypocapnia, not hyperventilation per se, attenuates local skin thermal perception, though changes in responses to warm stimuli may not be clearly perceived at some skin areas (e.g., forearm).

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.

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.