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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]

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]

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]