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This study evaluated the time-to-time aerobic and anaerobic exercise intensities, calculated using the Global Positioning System (GPS), using laboratory measurements of individual physical fitness throughout the game in each female youth football player. In addition, we examine if the anaerobic exercise index calculated by only GPS data presents this evaluation to examine its validity. In the laboratory, the oxygen uptake (V̇O2) matched with moving speed was identified during an incremental exercise test on the treadmill, and the ventilatory (anaerobic) threshold was also analysed to identify individual aerobic and anaerobic exercise intensities. Using these laboratory data, time-to-time changes in individual relative running intensity (aerobic and anaerobic) were visualised from individual GPS data during a football game, and an individual’s sprint output (ability) during the game was evaluated. An index of running intensity and the percentage of anaerobic exercise over the game provided by the GPS software (equivalent distance index [%EDI] and anaerobic index [AI]) did not present the actual individual exercise intensity (ICC(2,1), absolute agreement=−0.031; P=0.596) and percentage of anaerobic exercise (ICC(2,1), absolute agreement=−0.003; P=0.698) values during the game, respectively. These findings suggest that only GPS measurement cannot present the individual actual exercise intensity during a football game because of different individual fitness levels to the same running speed.

What is the central question of this study? Increased work of breathing and the accumulation of metabolites have neural and cardiovascular consequences through a respiratory muscle-induced metaboreflex. The influence of the respiratory muscle-induced metaboreflex on splanchnic blood flow in humans remains unknown. What is the main finding and its importance? Coeliac artery blood flow decreased gradually during inspiratory resistive breathing, accompanied by a progressive increase in arterial blood pressure. It is possible that the respiratory muscle-induced metaboreflex contributes to splanchnic blood flow regulation.The purpose of this study was to clarify the effect of increasing inspiratory muscle work on coeliac artery blood flow. Eleven healthy young males completed the study. The subjects performed voluntary hyperventilation with or without inspiratory resistance (loading or non-loading trial; tidal volume of 40% of vital capacity and breathing frequency of 20 breaths/min). The loading trial was conducted with inspiratory resistance (40% of maximal inspiratory pressure) and was terminated when the subjects could no longer maintain the target tidal volume or breathing frequency. The non-loading trial was conducted without inspiratory resistance and was of the same duration as the loading trial. Arterial blood pressure was recorded using finger photoplethysmography, and coeliac artery blood flow was measured using Doppler ultrasound. Mean arterial blood pressure increased gradually during the loading trial (mean ± SD; from 89.0 ± 10.8 to 103.9 ± 17.3 mmHg) but not in the non-loading trial (from 88.7 ± 5.9 to 90.4 ± 9.9 mmHg). Coeliac artery blood flow and coeliac vascular conductance decreased gradually during the loading trial (from 601.2 ± 155.7 to 482.6 ± 149.5 mL/min and from 6.9 ± 2.2 to 4.8 ± 1.7 mL/min/mmHg, respectively) but were unchanged in the non-loading trial (from 630.7 ± 157.1 to 635.6 ± 195.7 mL/min and from 7.1 ± 1.8 to 7.2 ± 2.9 mL/min/mmHg, respectively). These results show that increasing inspiratory muscle work affects splanchnic blood flow regulation, and we suggest that this might be mediated by the inspiratory muscle-induced metaboreflex.

Respiratory modulation of sympathetic vasomotor outflow to skeletal muscles (muscle sympathetic nerve activity; MSNA) occurs in resting humans. Specifically, MSNA is highest at end-expiration and lowest at end-inspiration during quiet, resting breathing. We tested the hypothesis that within-breath modulation of MSNA would be amplified during graded leg cycling. Thirteen (n = 3 females) healthy young (age: 25.2 ± 4.7 yr) individuals completed all testing. MSNA (right median nerve) was measured at rest (baseline) and during semirecumbent cycle exercise at 40%, 60%, and 80% of maximal workload (Wmax). MSNA burst frequency (BF) was 20.0 ± 4.0 bursts/min at baseline and was not different during exercise at 40%Wmax (21.3 ± 3.7 bursts/min; P = 0.292). Thereafter, MSNA BF increased significantly compared with baseline (60%Wmax: 31.6 ± 5.8 bursts/min; P < 0.001, 80%Wmax: 44.7 ± 5.3 bursts/min; P < 0.001). At baseline and all exercise intensities, MSNA BF was lowest at end-inspiration and greatest at mid-to-end expiration. The within-breath change in MSNA BF (ΔMSNA BF; end-expiration minus end-inspiration) gradually increased from baseline to 60%Wmax leg cycling, but no further increase appeared at 80%Wmax exercise. Our results indicate that within-breath modulation of MSNA is amplified from baseline to moderate intensity during dynamic exercise in young healthy individuals, and that no further potentiation occurs at higher exercise intensities. Our findings provide an important extension of our understanding of respiratory influences on sympathetic vasomotor control., Published online 13 August 2021

What is the central question of this study? Sympathetic vasomotor outflow is reduced during low-intensity dynamic leg exercise in younger individuals: does ageing influence the sympathoinhibitory effect during low-intensity leg cycling? What is the main finding and its importance? Muscle sympathetic nerve activity during low-intensity cycling decreased in older males, as seen in young males. It is possible that cardiopulmonary baroreflex-mediated inhibition of sympathetic vasomotor outflow during dynamic leg exercise is preserved in healthy older males.Muscle sympathetic nerve activity (MSNA) is reduced during low-intensity dynamic leg exercise in young males. It is suggested that this inhibition is mediated by loading of the cardiopulmonary baroreceptors. The purpose of this study was to clarify the impact of age on MSNA during dynamic leg exercise. Nine younger males (YM, mean ± SD, 20 ± 1 years) and nine older males (OM, 72 ± 3 years) completed the study. The subjects performed two 4-min cycling exercises at 10% of their heart rate reserve using a cycle ergometer in a semirecumbent position (MSNA and estimated central venous pressure (eCVP) trials). MSNA was recorded via microneurography of the left radial nerve. The CVP was estimated based on peripheral venous pressure, which was monitored using a cannula in the right large antecubital vein. The magnitude of the increase in mean arterial blood pressure during leg cycling was larger in OM (+9.3 ± 5.5 mmHg) compared with YM (+2.8 ± 4.7 mmHg). MSNA burst frequency was decreased during cycling in both YM (-8.1 ± 3.8 bursts/min) and OM (-10.6 ± 3.3 bursts/min), but no significant difference was found between the two groups. The eCVP increased during exercise in both groups, and there was no difference in the changes in eCVP between YM (+1.1 ± 0.4 mmHg) and OM (+1.2 ± 0.7 mmHg). These data indicate that inhibition of sympathetic vasomotor outflow during low-intensity cycling appears in OM as seen in YM. It is possible that the muscle pump-induced loading of the cardiopulmonary baroreflex is preserved during cycling in healthy older males.

This study aimed to elucidate changes in diaphragm and accessory inspiratory muscle (sternocleidomastoid (SCM) muscle and intercostal muscle (IC)) function after a 6-week training program. Nineteen male elite collegiate swimmers were assigned to either a control group (n = 9) or training group (n = 10). The subjects in the training group performed 30 maximum inspirations at a load resistance of 50% of maximum inspiratory mouth pressure (PImax) using an inspiratory muscle training device. These were conducted twice per day and 6 days per week. At baseline and after 6 weeks, PImax, shear modulus of the diaphragm, and electromyograms (EMG) of the SCM and IC during a maximal inspiratory maneuver were evaluated. Relative change in PImax was greater in the training group than in controls. The shear modulus during a PImax maneuver had increased significantly in both groups after 6 weeks. EMG amplitudes of the SCM increased in the training group after 6 weeks, but not in the control group. EMG amplitudes of the IC did not change after 6 weeks in either group. These results suggest that 6-week inspiratory resistive training significantly improves the activation of the SCM, which could be one of the major mechanisms behind increases in inspiratory muscle strength after resistive training. Novelty Six-week inspiratory resistive training increased diaphragm stiffness during maximal inspiration maneuver. Six-week inspiratory resistive training increased electromyogram amplitudes of the sternocleidomastoid during maximal inspiration maneuver.

Muscle sympathetic nerve activity (MSNA) is similar between limbs at rest, although a subset of MSNA bursts do demonstrate limb-specific discharge. Whether limb differences in MSNA synchronicity are present during exercise remains controversial. We concurrently measured MSNA from the radial and fibular nerves at rest and during rhythmic handgrip (RHG), static handgrip (SHG), and post-exercise circulatory occlusion (PECO). MSNA burst frequency and incidence were similar between nerve sites during all conditions. Synchronous bursts resulted in larger increases in sympathetic-blood pressure transduction compared to isolated bursts (∆ + 3.6 ± 2.1 vs. +2.3 ± 2.4 mmHg, P = 0.01). The proportion of bursts firing synchronously between nerves at rest was slightly increased during RHG ([rest vs. exercise; mean ± SD] 45.3 ± 7.1 vs. 61.6 ± 7.2 %) and similar during SHG (56.2 ± 7.2 vs. 54 ± 10.6 %). In contrast, burst firing synchronicity increased during PECO (83.8 ± 12.4 %) alongside larger burst amplitudes. Inter-limb differences in resting MSNA are preserved during handgrip exercise, whereas isolated metaboreflex activation results in greater burst synchronization between limbs.

Change in cardiac output (Q) contributes to cerebral blood flow (CBF) regulation at rest and even during steady-state exercise. At the onset of cycling exercise, Q increases acutely and largely via muscle pump. The purpose of the present study was to examine whether onset exercise-induced a large increase in Q contributes to CBF regulation at the onset of exercise.In 20 young healthy participants (10 males and 10 females), Q, mean arterial pressure (MAP), and mean blood velocities of middle and posterior cerebral arteries (MCA Vm and PCA Vm) were continuously measured during light cycling exercise for 3 min.At the onset of exercise, Q increased acutely to the peak (P 0.001), while the CBF peak responses were not significantly higher than the values during the steady-state exercise (MCA Vm and PCA Vm; P = 0.183 and P = 0.101, respectively). The change in Q was correlated with that of MCA Vm or PCA Vm from resting baseline to the steady-state exercise (r = 0.404, P 0.001 and r = 0.393, P 0.001, respectively). However, the change in Q was not correlated with that of MCA Vm or PCA Vm at the onset of exercise (P = 0.853 and P = 0.893, respectively). Any sex differences in the onset response of peripheral and cerebral hemodynamics to exercise were not observed.These findings suggest that the acute change in Q does not contribute to CBF regulation at the onset of exercise for protecting cerebral vasculature against a large and acute elevation in Q at the onset of exercise.

We hypothesized that, compared with young males, young females have a smaller decrease in blood flow to the inactive limb, accompanied by a smaller increase in arterial blood pressure, during dynamic exercise with increased inspiratory muscle work. Young males and females performed dynamic knee-extension and -flexion exercises for 10 min (spontaneous breathing for 5 min and voluntary hyperpnoea with or without inspiratory resistance for 5 min). Mean arterial blood pressure (MAP) and mean blood flow (MBF) in the brachial artery were continuously measured by means of finger photoplethysmography and Doppler ultrasound, respectively. No sex differences were found in the ΔMAP and ΔMBF (Δ: from baseline) during exercise without inspiratory resistance. In contrast, the ΔMAP during exercise with inspiratory resistive breathing was greater (P0.05) in males (+31.3 ± 2.1 mmHg, mean ± SE) than females (+18.9 ± 3.2 mmHg). The MBF during exercise with inspiratory resistance did not change in males (-4.4 ± 10.6 mL/min), whereas it significantly increased in females (+25.2 ± 15.4 mL/min). These results suggest that an attenuated inspiratory muscle-induced metaboreflex in young females affects blood flow distribution during submaximal dynamic leg exercise.

Acetone, which is exhaled with breath, is a by-product of lipolysis and could be used as a simple, useful indicator of lipolysis in the body because, unlike blood sampling, it can be measured non-invasively and repeatedly. Breath acetone concentration, however, is known to be affected by several factors such as exercise and food. We designed the experiments to evaluate the mixed effect on breath acetone of exercise and food ingestion in order to enhance the usefulness of breath acetone for monitoring fat loss. Seven healthy males performed moderate exercise for twice of 45 min with an interval of 15 min then rested for 4 h. Exhaled air was sampled every 15 min throughout the experiment. The subjects took one of four types, sugar-rich, balanced, protein-rich and fat-rich, of food for lunch one hour after the exercises or kept fasting. In the case of fasting, breath acetone kept increasing significantly (p < 0.05) compared with the rest value after the exercises until the end of the experiment. In contrast, in the case of taking any type of food, the change in breath acetone varied according to the food type. In the case of taking sugar-rich food, breath acetone significantly decreased (p < 0.05) compared with the fasting case. This decrease might be due to a suppression of acetone production when carbohydrates such as sugar are supplied to a body in the fasting condition. In contrast, in the case of taking fat-rich food, breath acetone showed the higher level than the fasting case. This additional increase might be attributable to the promotion of ketone bodies production, including acetone, due to the ingestion of medium chain triglycerides contained in the fat-rich food. We should therefore consider exercise and food ingestion in using breath acetone as a non-invasive indicator of lipolysis.

Appropriate cardiovascular adjustment is necessary to meet the metabolic demands of working skeletal muscle during exercise. The sympathetic nervous system plays a crucial role in the regulation of arterial blood pressure and blood flow during exercise, and several important neural mechanisms are responsible for changes in sympathetic vasomotor outflow. Changes in sympathetic vasomotor outflow (i.e., muscle sympathetic nerve activity: MSNA) in inactive muscles during exercise differ depending on the exercise mode (static or dynamic), intensity, duration, and various environmental conditions (e.g., hot and cold environments or hypoxic). In 1991, Seals and Victor [6] reviewed MSNA responses to static and dynamic exercise with small muscle mass. This review provides an updated comprehensive overview on the MSNA response to exercise including large-muscle, dynamic leg exercise, e.g., two-legged cycling, and its regulatory mechanisms in healthy humans.

We hypothesized that respiratory muscle endurance training (RMET) in hypoxia induces greater improvements in respiratory muscle endurance with attenuated respiratory muscle metaboreflex and consequent whole-body performance. We evaluated respiratory muscle endurance and cardiovascular response during hyperpnoea and whole-body running performance before and after RMET in normoxia and hypoxia.Twenty-one collegiate endurance runners were assigned to control (n = 7), normoxic (n = 7), and hypoxic (n = 7) groups. Before and after the 6 wk of RMET, incremental respiratory endurance test and constant exercise tests were performed. The constant exercise test was performed on a treadmill at 95% of the individual's peak oxygen uptake (V˙O2peak). The RMET was isocapnic hyperpnoea under normoxic and hypoxic conditions (30 min·d). The initial target of minute ventilation during RMET was set to 50% of the individual maximal voluntary ventilation, and the target increased progressively during the 6 wk. Target arterial oxygen saturation in the hypoxic group was set to 90% in the first 2 wk, and thereafter it was set to 80%.Respiratory muscle endurance was increased after RMET in the normoxic and hypoxic groups. The time to exhaustion at 95% V˙O2peak exercise also increased after RMET in the normoxic (10.2 ± 2.4 to 11.2 ± 2.6 min) and hypoxic (11.5 ± 2.6 to 12.6 ± 3.0 min) groups, but not in the control group (9.6 ± 3.2 to 9.4 ± 4.0 min). The magnitude of these changes did not differ between the normoxic and the hypoxic groups (P = 0.84).These results suggest that the improvement of respiratory muscle endurance and blunted respiratory muscle metaboreflex could, in part, contribute to improved endurance performance in endurance-trained athletes. However, it is also suggested that there are no additional effects when the RMET is performed in hypoxia.

We aimed to test the hypothesis that the magnitude of differences in muscle activation of the knee and hip extensor muscles between high-intensity interval exercise (HIE) and moderate-intensity constant exercise (CE) would be greater for the gluteus maximus than for the quadriceps femoris muscle. Participants were 11 male middle- or long-distance runners. The HIE (4 sets, 4-min induration, performed at 80–85%VO2peak and followed by a 3-min period of cycling at

Purpose: Inspiratory muscle strength training (IMST) can improve exercise performance. Increased maximal inspiratory mouth pressure (MIP) could be beneficial for swimmers to enhance their performance. This study aimed to clarify the effect of high-intensity IMST for 6 weeks on MIP and swimming performance in highly trained competitive swimmers. Methods: Thirty male highly trained competitive swimmers were assigned to high-intensity IMST (HI; n = 10), moderate-intensity IMST (MOD; n = 10), and control (n = 10) groups. The 6-week IMST intervention comprised twice daily sessions for 6 d/wk at inspiratory pressure threshold loads equivalent to 75% MIP (HI) and 50% MIP (MOD). Before and after the intervention, MIP and swimming performance were assessed. Swimming performance was evaluated in free and controlled frequency breathing 100-m freestyle swimming time trials in a 25-m pool. For controlled frequency breathing, participants took 1 breath every 6 strokes. Results: The MIP values after 2 and 6 weeks of IMST in the HI and MOD groups were significantly higher than those before IMST (P = .0001). The magnitudes of the MIP increases after 6 weeks of IMST did not differ between the HI (13.4% [8.7%]) and MOD (13.1% [10.1%]) groups (P = .44). The 100-m freestyle swimming times under the controlled frequency condition were significantly shorter after IMST than those before IMST in both the HI (P = .046) and MOD (P = .042) groups. Conclusions: Inspiratory pressure threshold load equivalent to 50% MIP could be sufficient to improve MIP and swimming performance under the controlled frequency breathing condition in highly trained competitive swimmers.

NEW FINDINGS What is the central question of this study? Increased respiratory muscle activation is associated with neural and cardiovascular consequences via the respiratory muscle-induced metaboreflex. Does ageing and/or sex influence the arterial blood pressure response during voluntary normocapnic incremental hyperpnoea? What is the main finding and its importance? The increase in blood pressure during hyperpnoea was smaller in younger females than in older females, whereas no difference was found between older males and older females. The blunted respiratory muscle-induced metaboreflex in younger females is normalized with advancing age, whereas ageing has no such effect in males. ABSTRACT We hypothesized that older females (OF) have a greater arterial blood pressure response to increased respiratory muscle work compared with younger females (YF) and that no such difference exists between older males (OM) and younger males (YM). To test these hypotheses, cardiovascular responses during voluntary normocapnic incremental hyperpnoea were evaluated and compared between older and younger subjects. An incremental respiratory endurance test (IRET) was performed as follows: target minute ventilation was initially set at 30% of the maximal voluntary ventilation (MVV12) and was increased by 10% of MVV12 every 3 min. The test was terminated when the subject could not maintain the target percentage of MVV12. Heart rate and mean arterial blood pressure (MAP) were recorded continuously. The increase in MAP from baseline (ΔMAP) during the IRET in OM (+24.0 ± 14.7 mmHg, mean ± SD) did not differ (P = 0.144) from that in YM (+24.3 ± 13.4 mmHg), but it was greater (P = 0.004) in OF (+31.2 ± 11.6 mmHg) than in YF (+10.3 ± 5.5 mmHg). No significant difference in ΔMAP during the IRET was observed between OM and OF (P = 0.975). These results suggest that the respiratory muscle-induced metaboreflex is blunted in YF, but it could be normalized with advancing age. In males, ageing has little effect on the respiratory muscle-induced metaboreflex. These results show no sex difference in the respiratory muscle-induced metaboreflex in older adults.

We hypothesized that the trained distance runners, who have a relatively high respiratory muscle endurance, but not high respiratory muscle strength, have lower dyspneic sensations during submaximal running. Twenty-one male collegiate distance runners participated. Incremental respiratory endurance tests (IRET) and maximal inspiratory mouth pressure (PImax) measurements were performed under resting conditions. A submaximal exercise test was also performed on a treadmill at two different speeds (16 and 18 km/h) for 4 min each, and the subjects reported the rate of dyspnea (range: 0–10). The time to endpoint during the IRET, an index of respiratory muscle endurance, ranged from 9.4 to 18.8 min, and PImax, as an index of inspiratory muscle strength, ranged from 74.1 to 137.0 cmH2O. The dyspnea rating during running at 16 and 18 km/h ranged from 1 to 6 and from 4 to 8, respectively. The relative exercise intensity was approximately 80 % of peak oxygen uptake (VO2peak) at 16 km/h and 90 %VO2peak at 18 km/h. The time to endpoint during the IRET was significantly negatively correlated with dyspnea during running at 18 km/h (r = -0.459, P = 0.040), but not at 16 km/h (r = -0.161, P = 0.470). There was no significant correlation between PImax and dyspnea during running at 16 km/h (r = -0.003, P = 0.989) or 18 km/h (r = 0.070, P = 0.755). These results suggest that dyspneic sensations during high-intensity running are related to respiratory muscle endurance, but not inspiratory muscle strength, in trained distance runners.

New findings What is the topic of this review? Elevated demand is placed on the respiratory muscles during whole-body exercise-induced hyperpnoea. What is the role of elevated demand in neural modulation of cardiovascular control in respiratory and locomotor skeletal muscle, and what are the mechanisms involved? What advances does it highlight? There is a sympathetic restraint of blood flow to locomotor muscles during near-maximal exercise, which might function to maintain blood pressure. During submaximal exercise, respiratory muscle blood flow might be also be reduced if ventilatory load is sufficiently high. Methodological advances (near-infrared spectroscopy with indocyanine green) confirm that blood flow is diverted away from respiratory muscles when the work of breathing is alleviated. Abstract It is known that the respiratory muscles have a significant increasing oxygen demand in line with hyperpnoea during whole-body endurance exercise and are susceptible to fatigue, in much the same way as locomotor muscles. The act of ventilation can itself be considered a form of exercise. The manipulation of respiratory load at near-maximal exercise alters leg blood flow significantly, demonstrating a competitive relationship between different skeletal muscle vascular beds to perfuse both sets of muscles adequately with a finite cardiac output. In recent years, the question has moved towards whether this effect exists during submaximal exercise, and the use of more direct measurements of respiratory muscle blood flow itself to confirm assumptions that uphold the concept. Evidence thus far has shown that there is a reciprocal effect on blood flow redistribution during ventilatory load manipulation observed at the respiratory muscles themselves and that the effect is observable during submaximal exercise, where active limb blood flow was reduced in conditions that simulated a high work of breathing. This has clinical applications for populations with respiratory disease and heart failure, where the work of breathing is remarkably high, even during submaximal efforts.

This study assessed the shear modulus of the diaphragm at various submaximal inspiratory mouth pressure levels by ultrasound shear wave elastography. In 14 healthy male subjects, diaphragmatic shear moduli were assessed at end expiration during resting breathing and at submaximal inspiratory tasks at 15, 30, 45, 60, and 75% of the maximal inspiratory mouth pressure. The shear modulus increased along with mouth pressure, and the mouth-pressure–shear-modulus relationship fit the second-order polynomial regression equation (r2 = 0.99 ± 0.01; all subjects, r2 ≥ 0.95) better than it did the simple linear regression equation (r2 = 0.94 ± 0.05; 8/14 subjects, r2 ≥ 0.95). The second regression coefficient in the second-order polynomial equation was a negative value in 10 of 14 subjects, which indicates that the second-order polynomial regression equation opened downwards. These findings suggest that the diaphragmatic shear modulus increases along with inspiratory mouth pressure, but the rate of increase slows when the pressure reaches higher levels.

NEW FINDINGS What is the central question of this study? Premenopausal women have an attenuated inspiratory muscle metaboreflex-induced increase in arterial blood pressure compared with men. It is unclear whether sympathetic vasomotor outflow during dynamic exercise with increased inspiratory muscle activation is less in young women than in men. What is the main finding and its importance? The magnitude of increased sympathetic vasomotor outflow during leg cycling with inspiratory resistance was smaller in women than in men. Less sympathetic vasomotor outflow with inspiratory muscle metaboreflex activation could be one of the mechanisms for the attenuated inspiratory muscle-induced metaboreflex during exercise in young women. ABSTRACT We compared changes in muscle sympathetic nerve activity (MSNA) and cardiovascular variables during leg cycle exercise with increased inspiratory muscle resistance in men and women. We hypothesized that sympathetic vasomotor outflow during exercise with increased inspiratory resistance would be attenuated in young women compared with age-matched men. Eight women and seven men completed the study. The subjects performed two 10 min exercise bouts at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and voluntary hyperventilation with or without inspiratory resistive breathing for 5 min (breathing frequency 50 breaths min-1 with a 50% duty cycle; inspiratory resistance 30% of maximal inspiratory pressure)]. Mean arterial blood pressure (MAP) was acquired using finger photoplethysmography. The MSNA was recorded via microneurography of the right median nerve at the cubital fossa. During leg cycle exercise with inspiratory resistive breathing, MSNA burst frequency was increased, accompanied by an increase in MAP in both men and women. Women, compared with men, had less of an increase in MAP (women +22.8 ± 12.3 mmHg versus men +32.2 ± 5.4 mmHg; P

Acute exercise has been demonstrated to improve cognitive function. In contrast, severe hypoxia can impair cognitive function. Hence, cognitive function during exercise under severe hypoxia may be determined by the balance between the beneficial effects of exercise and the detrimental effects of severe hypoxia. However, the physiological factors that determine cognitive function during exercise under hypoxia remain unclear. Here, we examined the combined effects of acute exercise and severe hypoxia on cognitive function and identified physiological factors that determine cognitive function during exercise under severe hypoxia. The participants completed cognitive tasks at rest and during moderate exercise under either normoxic or severe hypoxic conditions. Peripheral oxygen saturation, cerebral oxygenation, and middle cerebral artery velocity were continuously monitored. Cerebral oxygen delivery was calculated as the product of estimated arterial oxygen content and cerebral blood flow. On average, cognitive performance improved during exercise under both normoxia and hypoxia, without sacrificing accuracy. However, under hypoxia, cognitive improvements were attenuated for individuals exhibiting a greater decrease in peripheral oxygen saturation. Cognitive performance was not associated with other physiological parameters. Taken together, the present results suggest that arterial desaturation attenuates cognitive improvements during exercise under hypoxia.

Acute moderate intensity exercise has been shown to improve cognitive performance. In contrast, hypoxia is believed to impair cognitive performance. The detrimental effects of hypoxia on cognitive performance are primarily dependent on the severity and duration of exposure. In this review, we describe how acute exercise under hypoxia alters cognitive performance, and propose that the combined effects of acute exercise and hypoxia on cognitive performance are mainly determined by interaction among exercise intensity and duration, the severity of hypoxia, and duration of exposure to hypoxia. We discuss the physiological mechanism(s) of the interaction and suggest that alterations in neurotransmitter function, cerebral blood flow, and possibly cerebral metabolism are the primary candidates that determine cognitive performance when acute exercise is combined with hypoxia. Furthermore, acclimatization appears to counteract impaired cognitive performance during prolonged exposure to hypoxia although the precise physiological mechanism(s) responsible for this amelioration remain to be elucidated. This review has implications for sporting, occupational, and recreational activities at terrestrial high altitude where cognitive performance is essential. Further studies are required to understand physiological mechanisms that determine cognitive performance when acute exercise is performed in hypoxia.

The purpose of this study was to elucidate the effects of hypoxia on deoxygenation and neuromuscular activation in synergistic quadriceps femoris (QF) muscles (i.e., the rectus femoris, vastus medialis, vastus intermedius, and vastus lateralis) during submaximal intermittent knee extension. Ten healthy men performed isometric intermittent knee extension exercises with the right leg at 50% of maximal voluntary contraction for 3 min while inhaling a normoxic [inspired oxygen (O2) fraction = 0.21] or hypoxic (inspired O2 fraction = 0.10–0.12) gas mixture. Muscle deoxygenation was measured by tissue O2 saturation (StO2), and neuromuscular activation by root mean square (RMS) of the surface electromyographic signals, from individual muscles of the QF using near-infrared spectroscopy and surface electromyography. StO2 was decreased more in hypoxia than normoxia during the exercises, and there was a greater increase in RMS during intermittent knee extension in hypoxia than normoxia in individual muscles of the QF. There were no differences in the ratios of StO2 and RMS in hypoxia compared with normoxia between individual muscles of the QF. These findings suggest that submaximal, isometric, and intermittent exercises in hypoxic conditions enhanced muscle oxygen consumption and muscle activity similarly for synergistic muscles.

What is the central question of this study? The cardiopulmonary baroreflex inhibits adjustment of sympathetic vasomotor outflow during mild-intensity dynamic exercise. However, it is unclear how suppression of sympathetic vasomotor outflow by the cardiopulmonary baroreflex is modulated by a powerful sympatho-excitatory drive from the exercise pressor reflex, central command and/or the arterial chemoreflex. What is the main finding and its importance? Hypoxia-induced heightened sympathetic nerve activity during dynamic exercise attenuated cardiopulmonary baroreflex control of sympathetic vasomotor outflow. This could facilitate the redistribution of blood flow to the active muscles by sympathetically mediated vasoconstriction of inactive muscles. Muscle sympathetic nerve activity (MSNA) does not increase during mild-intensity dynamic leg exercise in normoxic conditions, despite activation of central command and the exercise pressor reflex. Suppression of MSNA could be caused by muscle pump-induced loading of cardiopulmonary baroreceptors. In contrast, MSNA increases during mild dynamic leg exercise in hypoxic conditions. We hypothesized that hypoxic exercise, which induces a powerful sympatho-excitatory drive from the exercise pressor reflex, central command and/or arterial chemoreflex, attenuates cardiopulmonary reflex control of sympathetic vasomotor outflow. To test this hypothesis, MSNA was recorded during leg cycling in hypoxic conditions and with increased central blood volume by increasing the pedalling frequency to change the cardiopulmonary baroreflex. Subjects performed two leg cycle exercises at different pedal cadences of 60 and 80 r.p.m. (60EX and 80EX trials, respectively) in two (haemodynamic and MSNA) measurement conditions while breathing a hypoxic gas mixture (inspired oxygen fraction = 0.12). Thoracic impedance, stroke volume and cardiac output were measured non-invasively using impedance cardiography. During the MSNA test, MSNA was recorded via microneurography at the right median nerve at the elbow. Changes in thoracic impedance, stroke volume and cardiac output during the 80EX trial were greater than those during the 60EX trial. The MSNA burst frequency during hypoxic exercise in the 80EX trial (39 ± 4 bursts min(-1)) did not differ from that during the 60EX trial (39 ± 3 bursts min(-1)). These results suggest that the cardiopulmonary baroreflex of sympathetic vasomotor outflow during dynamic exercise is modulated by heightened hypoxia-induced sympathetic nerve activity.

Previous studies have shown that acute exercise elevates sex steroid hormone concentrations in rodents and that sprint exercise increases circulating testosterone in healthy young men. However, the effect of different exercise intensities on sex steroid hormone responses at different levels of physical fitness is still unclear. In this study, we compared circulating sex steroid hormone responses at different exercise intensities in athletes and non-athletes. Eight male endurance athletes and 11 non-athletes performed two 15 min sessions of submaximal exercise at 40 and 70% peak oxygen uptake (V(O2peak)), respectively, and exercised at 90% V(O2peak) until exhaustion. Venous blood samples were collected during the last minute of each submaximal exercise session and immediately after exhaustion. Acute exercise at 40, 70 and 90% V(O2peak) induced significant increases in serum dehydroepiandrosterone (DHEA) and free testosterone concentrations in non-athletes. On the contrary, only 90% VO2 peak exercise led to an increase in serum DHEA and free testosterone concentrations in athletes. Serum 5α-dihydrotestosterone concentrations increased with 90% V(O2peak) exercise in both athletes and non-athletes. Additionally, serum estradiol concentrations were significantly increased at moderate and high exercise intensities in both athletes and non-athletes. These results indicate that in endurance athletes, serum sex steroid hormone concentrations, especially serum DHEA and 5α-dihydrotestosterone concentrations, increased only with high-intensity exercise, suggesting that different responses of sex steroid hormone secretion are induced by different exercise intensities in individuals with low and high levels of physical fitness. In athletes, therefore, high-intensity exercise may be required to increase circulating sex steroid hormone concentrations.

New findings What is the central question of this study? Increased respiratory muscle activation is associated with neural and cardiovascular consequences via the respiratory muscle metaboreflex. Does increased sympathetic vasoconstriction originating from the respiratory musculature elicit a reduction in blood flow to an inactive limb in order to maintain blood flow to an active limb? What is the main finding and its importance? Arm blood flow was reduced whereas leg blood flow was preserved during mild leg exercise with inspiratory resistance. Blood flow to the active limb is maintained via sympathetic control of blood flow redistribution when the respiratory muscle-induced metaboreflex is activated. Abstract The purpose of this study was to elucidate the effect of increasing inspiratory muscle work on blood flow to inactive and active limbs. Healthy young men (n = 10, 20 ± 2 years of age) performed two bilateral dynamic knee-extension and knee-flexion exercise tests at 40% peak oxygen uptake for 10 min. The trials consisted of spontaneous breathing for 5 min followed by voluntary hyperventilation either with or without inspiratory resistance for 5 min (40% of maximal inspiratory mouth pressure, inspiratory duty cycle of 50% and a breathing frequency of 40 breaths min-1 ). Mean arterial blood pressure was acquired using finger photoplethysmography. Blood flow in the brachial artery (inactive limb) and in the femoral artery (active limb) were monitored using Doppler ultrasound. Mean arterial blood pressure during exercise was higher (P 0.05). These results suggest that sympathetic control of blood redistribution to active limbs is facilitated, in part, by the respiratory muscle-induced metaboreflex.

Previous studies have shown that muscle sympathetic nerve activity (MSNA) is reduced during low- and mild-intensity dynamic leg exercise. It has been suggested that such inhibition is mediated by loading of the cardiopulmonary baroreceptors and that this effect is overridden by muscle metaboreflex activation with higher-intensity exercise. However, limited data are available regarding the interaction between the cardiopulmonary baroreflex and the muscle metaboreflex. Therefore, we tested the hypothesis that cardiopulmonary baroreflex-mediated inhibition of MSNA is attenuated during high-intensity muscle metaboreflex activation. In nine young men, MSNA (right peroneal nerve), mean arterial pressure (MAP), and thoracic impedance were recorded. Graded isolation of muscle metaboreflex activation was achieved via postexercise ischemia (PEI) following low (PEI-L)-, moderate (PEI-M)-, and high (PEI-H)-intensity isometric handgrip performed at 20, 30, and 40% maximum voluntary contraction, respectively. Lower-body positive pressure (LBPP, +10 Torr) was applied at rest and during PEI, to load the cardiopulmonary baroreceptors. Handgrip exercise elicited intensity-dependent increases in MSNA and MAP that were maintained during PEI, indicating a graded muscle metaboreflex activation. LBPP at rest significantly decreased MSNA burst frequency (BF: −36.7 ± 4.7%, mean ± SE, P < 0.05), whereas MAP was unchanged. When LBPP was applied during PEI, MSNA BF decreased significantly at PEI-L (−40.0 ± 9.2%, P < 0.05) and PEI-M (−27.0 ± 6.3%, P < 0.05), but not at PEI-H (+1.9 ± 7.1%, P > 0.05). These results suggest that low- and moderate-intensity muscle metaboreflex activation does not modulate the inhibition of MSNA by cardiopulmonary baroreceptor loading, whereas high-intensity metaboreflex activation can override cardiopulmonary baroreflex-mediated inhibition of sympathetic vasomotor outflow. NEW & NOTEWORTHY The interaction between the sympathoinhibitory influence of cardiopulmonary baroreflex and sympathoexcitatory effect of skeletal muscle metaboreflex is not completely understood. In the current study, light- to moderate-intensity muscle metaboreflex activation did not modulate the suppression of muscle sympathetic nerve activity by cardiopulmonary baroreceptor loading, whereas high-intensity muscle metaboreflex activation attenuated the cardiopulmonary baroreflex-mediated inhibition of muscle sympathetic nerve activity. These results provide important information concerning the neural reflex mechanisms regulating sympathetic vasomotor outflow during exercise.

The purpose of this study was to elucidate inspiratory accessory muscle deoxygenation and myoelectric activity during isolated volitional hyperpnoea under hypoxic conditions. Subjects performed voluntary isocapnic hyperpnoea (tidal volume=30-40% of forced vital capacity, breathing frequency=60 breaths/min) in normoxia [inspired gas fraction (FIO₂)=0.21] and hypoxia (FIO₂). Muscle deoxyhemoglobin/myoglobin (Deoxy-Hb/Mb) and muscle oxygen saturation (SMO₂) using near-infrared spectroscopy and surface electromyography were measured from sternocleidomastoid (SCM) and intercostal (IC) muscles. During hyperpnoea, increases in Deoxy-Hb/Mb and reductions of SMO₂ in the SCM and IC muscles were larger (P

We hypothesized that young women have a lower arterial blood pressure (BP) response to high inspiratory and expiratory muscle contractions with normocapnic hyperpnoea compared to age-matched men. To test this hypothesis, the cardiovascular response during voluntary normocapnic incremental hyperpnoea was evaluated in young women and compared to that of young men. An incremental respiratory endurance test (IRET) was performed as follows: target minute ventilation was initially set to 30% of the maximal voluntary ventilation (MVV12) and was increased by 10% MVV12 every 3min. The test was terminated when the subject could not maintain the target%MVV. Heart rate and mean arterial BP (MBP) were continuously recorded. The increase in MBP from the baseline (ΔMBP) during the IRET was lower in women than in men (ΔMBP, men: +32.1±4.6mmHg vs. women: +14.9±3.5mmHg at 8min during IRET). This result suggests that young women exhibit a blunted arterial BP response during high-speed inspiratory and expiratory muscle contractions with normocapnic hyperpnoea compared to young men.

In the present study, a tandem-bicycle ergometer was developed, because it is believed that such an ergometer can be used to eliminate differences in signaling between single- and tandem-exercise in cardiorespiratory responses, and is able to quantify interdependence in one load. It is necessary to verify whether cardiorespiratory responses to submaximal exercise are the same between single and tandem-bicycle ergometers. Accordingly, we compared cardiorespiratory variables during exercise in three conditions: 1) with a general bicycle single saddle using a general bicycle ergometer, 2) with a tandem bicycle front saddle using a tandem ergometer, and 3) with a tandem bicycle rear saddle using a tandem ergometer. Eleven healthy males participated in this study. The subjects exercised for 15 min at three intensities (1.5, 2.0 and 2.5 kp) in each condition. The pedaling rate was constantly kept at 60 rpm. Heart rate (HR), oxygen uptake (VO2), and the rating of perceived exertion (RPE) were measured during the last minute of each intensity. There were no significant differences in the variables HR, VO2, and RPE at each load among the three conditions. The ranges of coefficient of variation (CV) values were 3.0 - 4.8%: HR and 4.2 - 5.1%: VO2. It was reported that between-day CV for HR and VO2 during treadmill running was 1.0 - 10.7% and 1.9 - 11.6%. Given these CV values of present and previous studies, it can be seen that physiological response is stable during developed tandem-bicycle ergometer exercise. These results suggest that cardiorespiratory responses to exercise are at comparable levels between a normal bicycle ergometer and the newly developed tandem-bicycle ergometer.

The purpose of this study was to clarify the effect of acute exercise in hypoxia on flow-mediated vasodilation (FMD). Eight males participated in this study. Two maximal exercise tests were performed using arm cycle ergometry to estimate peak oxygen uptake [Formula: see text] while breathing normoxic [inspired O(2) fraction (FIO(2)) = 0.21] or hypoxic (FIO(2) = 0.12) gas mixtures. Next, subjects performed submaximal exercise at the same relative exercise intensity [Formula: see text] in normoxia or hypoxia for 30 min. Before (Pre) and after exercise (Post 5, 30, and 60 min), brachial artery FMD was measured during reactive hyperemia by ultrasound under normoxic conditions. FMD was estimated as the percent (%) rise in the peak diameter from the baseline value at prior occlusion at each FMD measurement (%FMD). The area under the curve for the shear rate stimulus (SR(AUC)) was calculated in each measurement, and each %FMD value was normalized to SR(AUC) (normalized FMD). %FMD and normalized FMD decreased significantly (P

This is a brief review of recent evidence concerning the influences of respiratory muscle fatigue on the circulatory response to exercise, endurance exercise performance and associated peripheral locomotor muscle fatigue. Inspiratory muscle fatigue enhances muscle sympathetic vasomotor outflow and blood pressure during exercise. As a consequence, blood flow and oxygen transport to the working limbs are reduced, and this exacerbates the develop- ment of peripheral muscle fatigue and compromises endurance performance. These effects are relevant for healthy humans performing high intensity endurance, and, even at mild intensities, for patients with pulmonary disease and heart failure.

We investigated whether intense interval training on a cycle ergometer would prevent loss of muscle strength and atrophy in the human calf during unilateral lower limb suspension (ULLS). The present study involved 11 healthy men. We defined unloading leg and contralateral leg as ULLS-leg and CONT-leg, respectively. The subjects were divided into 2 groups: one with single-leg cycling training (Tr-UL, n=6); the other as a control (UL, n=5). The Tr-UL group performed an intense 25-min interval cycling training up to 80% of peak oxygen uptake on alternate days during 20-d ULLS. It was found that: 1) in maximal voluntary contraction (MVC) and the cross-sectional area of the planter flexor, there was a significant time- (pre-ULLS and post-ULLS) by-leg (ULLS-leg and CONT-leg) interaction; 2) in voluntary activation during MVC evaluated by the twitch interpolation technique, no significant time-by-leg interaction was detected but the trend of change from before to after ULLS tended to be different between ULLS-leg and CONT-leg; and 3) regarding ULLS-leg, the change in any parameters was not significantly different between the Tr-UL and UL groups. These results suggest that unloading induces dysfunction and atrophy in the human calf and that high-intensity interval training on a cycle ergometer cannot significantly prevent unloading-induced deconditioning in the human calf.

Reducing the work of breathing during exercise improves locomotor muscle blood flow and reduces diaphragm and locomotor muscle fatigue and is thought to be the result of a sympathetically mediated reflex. AIM The aim of this study was to assess muscle sympathetic nerve activity (MSNA) when the work of breathing is experimentally lowered during dynamic exercise. METHODS Healthy subjects (n = 12; age = 29 ± 9 years) performed semi-recumbent cycling trials at 40%, 60%, and 80% of peak workload. Exercise trials consisted of spontaneous breathing, reduced work of breathing (proportional assist ventilator), followed by further spontaneous breathing (post-ventilator). MSNA was recorded from the median nerve. RESULTS There was no difference in work of breathing between PAV and post-PAV at 40% peak work. At 60% peak work, the ventilator significantly (P V ˙ O 2 (2.4 ± 0.5 vs 2.6 ± 0.5 L min-1 ) without influencing ventilation (86 ± 9 vs 82 ± 10 L min-1 ; P > 0.05), for PAV and post-PAV respectively. During 80% peak work (n = 8), the ventilator significantly (P V ˙ O 2 (2.9 ± 0.6 vs 3.2 ± 0.7 L min-1 ) but not ventilation (121 ± 20 vs 123 ± 20 L min-1 ; P > 0.05), for PAV and post-PAV respectively. There was a significant relationship between MSNA and V ˙ O 2 (P

The mechanism(s) for the increased occurrence of a grayout or blackout, syncope, immediately after heavy resistance exercise are unclear. It is well‐known that orthostatic stress increases the occurrence of postexercise syncope. In addition, previous findings have suggested that hypo‐perfusion, especially in the posterior cerebral circulation rather than anterior cerebral circulation, may be associated with the occurrence of syncope. Herein, we hypothesized that the postexercise decrease in posterior, but not anterior, cerebral blood flow (CBF) would be greater during orthostatic stress. Nine healthy subjects performed 3‐min isometric handgrip (HG) at 30% maximum voluntary contraction without (CONTROL) and during lower body negative pressure (LBNP; −40 Torr) while vertebral artery (VA) blood flow, as an index of posterior CBF, and middle cerebral artery blood velocity (MCAv), as an index of anterior CBF, were measured. Immediately after HG (0 to 15 sec of recovery phase), mean arterial pressure decreased but there was no difference in this reduction between CONTROL and LBNP conditions (−15.4 ± 4.0% and −17.0 ± 6.2%, P = 0.42). Similarly, MCAv decreased following exercise and was unaffected by the application of LBNP (P = 0.22). In contrast, decreases in VA blood flow immediately following HG during LBNP were significantly greater compared to CONTROL condition (−24.2 ± 9.5% and ‐13.4 ± 6.6%, P = 0.005). These findings suggest that the decrease in posterior CBF immediately following exercise was augmented by LBNP, whereas anterior CBF appeared unaffected. Thus, the posterior cerebral circulation may be more sensitive to orthostatic stress during the postexercise period.

Introduction: Atrophy of the leg muscles is a serious consequence of disuse and occurs with prolonged exposure to microgravity. We investigated whether intense interval training on a cycle ergometer would prevent muscle changes during unilateral lower limb suspension (ULLS). Methods: This study involved 11 healthy men who were divided into 2 groups, one with training on a cycle ergometer (TRN, N = 6) and the other a control group (CON, N = 5). TRN performed intense interval training (up to 90% of maximum heart rate) on alternate days during 20 d of unloading. Maximum voluntary contraction (MVC) of the quadriceps femoris and volume of the thigh muscle were measured before and after unloading. Muscle functional magnetic resonance imaging (mfMRI), which reflects the contractile activity of the activating muscle, were acquired during submaximal dynamic knee extension exercises. Results: The MVC was significantly decreased in TRN (―11.1%) and CON (―18.7%). The total volume of the thigh muscles was maintained in TRN (―0.2%); however, a significant decrease was found in CON (―6.9%). The mfMRI signal increase for submaximal exercise did not change for TRN; however, it significantly increased for CON. Conclusions: Although the power of this study was limited, these results suggest that training on a cycle ergometer counteracts some of the effects of unloading and merits further study as a potential countermeasure for muscle changes in microgravity.

The purpose of this study was to investigate activity of hip adductor muscles over time and during a representative crank cycle in fatiguing pedaling. Sixteen healthy men performed incremental pedaling exercise until exhaustion. During the exercise, surface electromyogram (EMG) was detected from adductor magnus (AM), adductor longus (AL), and selected thigh muscles. Temporal changes to normalized EMG in AM muscle resembled those in vastus lateralis (VL) muscle, whereas those in AL muscle showed later onset of increase from baseline compared with AM and VL muscles. During a representative crank cycle, the same level of normalized EMG was found between propulsive and pulling phases for AM muscle, whereas muscle activation of AL muscle during the pulling phase was statistically significant higher than that during the propulsive phase. We concluded that AM and AL muscles were gradually recruited over time during fatiguing pedaling exercise, but their temporal change and activation phases were not completely the same.