Erika Iwamoto

Inspiratory muscle fatigue increases sympathetic vasomotor outflow and blood pressure during submaximal exercise

The purpose of this study was to elucidate the influence of inspiratory muscle fatigue on muscle sympathetic nerve activity (MSNA) and blood pressure (BP) response during submaximal exercise. We hypothesized that inspiratory muscle fatigue would elicit increases in sympathetic vasoconstrictor outflow and BP during dynamic leg exercise. The subjects carried out four submaximal exercise tests: two were maximal inspiratory pressure (PI(max)) tests and two were MSNA tests. In the PI(max) tests, the subjects performed two 10-min exercises at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and with or without inspiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were each set at 0.5 s)]. Before and immediately after exercise, PI(max) was estimated. In MSNA tests, the subjects performed two 15-min exercises (spontaneous breathing for 5 min, with or without inspiratory resistive breathing for 5 min, and spontaneous breathing for 5 min). MSNA was recorded via microneurography of the right median nerve at the elbow. PI(max) decreased following exercise with resistive breathing, whereas no change was found without resistance. The time-dependent increase in MSNA burst frequency (BF) appeared during exercise with inspiratory resistive breathing, accompanied by an augmentation of diastolic BP (DBP) (with resistance: MSNA, BF +83.4%; DBP, +23.8%; without resistance: MSNA BF, +19.2%; DBP, -0.4%, from spontaneous breathing during exercise). These results suggest that inspiratory muscle fatigue induces increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise at mild intensity.

Hypoxia augments muscle sympathetic neural response to leg cycling

It was demonstrated that acute hypoxia increased muscle sympathetic nerve activity (MSNA) by using a microneurographic method at rest, but its effects on dynamic leg exercise are unclear. The purpose of this study was to clarify changes in MSNA during dynamic leg exercise in hypoxia. To estimate peak oxygen uptake (Vo(2 peak)), two maximal exercise tests were conducted using a cycle ergometer in a semirecumbent position in normoxia [inspired oxygen fraction (Fi(O(2)) = 0.209] and hypoxia (Fi(O(2)) = 0.127). The subjects performed four submaximal exercise tests; two were MSNA trials in normoxia and hypoxia, and two were hematological trials under each condition. In the submaximal exercise test, the subjects completed two 15-min exercises at 40% and 60% of their individual Vo(2 peak) in normoxia and hypoxia. During the MSNA trials, MSNA was recorded via microneurography of the right median nerve at the elbow. During the hematological trials, the subjects performed the same exercise protocol as during the MSNA trials, but venous blood samples were obtained from the antecubital vein to assess plasma norepinephrine (NE) concentrations. MSNA increased at 40% Vo(2 peak) exercise in hypoxia, but not in normoxia. Plasma NE concentrations did not increase at 40% Vo(2 peak) exercise in hypoxia. MSNA at 40% and 60% Vo(2 peak) exercise were higher in hypoxia than in normoxia. These results suggest that acute hypoxia augments muscle sympathetic neural activation during dynamic leg exercise at mild and moderate intensities. They also suggest that the MSNA response during dynamic exercise in hypoxia could be different from the change in plasma NE concentrations.

Hypoxic effects on sympathetic vasomotor outflow and blood pressure during exercise with inspiratory resistance

The purpose of the present study was to clarify the influence of inspiratory resistive breathing during exercise under hypoxic conditions on muscle sympathetic nerve activity (MSNA) and blood pressure (BP). Six healthy males completed this study. The subjects performed a submaximal exercise test using a cycle ergometer in a semirecumbent position under normoxic [inspired oxygen fraction (FiO2) = 0.21] and hypoxic (FiO2 = 0.12-0.13) conditions. The subjects carried out two 10-min exercises at 40% peak oxygen uptake [spontaneous breathing for 5 min and voluntary breathing with inspiratory resistance for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were set at 0.5 s each)]. MSNA was recorded via microneurography of the right median nerve at the elbow. A progressive increase in MSNA burst frequency (BF) during leg-cycling exercise with inspiratory resistance in normoxia and hypoxia were accompanied by an augmentation of BP. The increased MSNA BF and mean arterial BP (MBP) during exercise with inspiratory resistive breathing in hypoxia (MSNA BF, 55.7 ± 1.4 bursts/min, MBP, 134.3 ± 6.6 mmHg) were higher than those in normoxia (MSNA BF, 39.2 ± 1.8 bursts/min, MBP, 123.6 ± 4.5 mmHg). These results suggest that an enhancement of inspiratory muscle activity under hypoxic condition leads to large increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise.

Flow-mediated dilation in the inactive limb following acute hypoxic exercise.

The purpose of this study was to elucidate the effect of acute aerobic exercise performed under hypoxic conditions on flow‐mediated dilation (FMD) in the inactive limb. Seven males participated in the study. The subjects performed two submaximal leg cycling on a semirecumbent ergometer at the same relative intensity (60% peak oxygen uptake) in normoxia [inspired oxygen fraction (FIO2) = 0·21] and hypoxia (FIO2 = 0·12–0·13) for 30 min. The brachial artery diameter and blood velocity during exercise were measured via ultrasound, and the antegrade and retrograde shear rates were calculated. Before and 5, 30 and 60 min after exercise, brachial artery FMD was measured in normoxia. FMD was estimated as the percentage increase in peak diameter from the baseline diameter at prior occlusion (%FMD) and as the controlling changes in baseline diameter (the corrected‐%FMD). No difference in antegrade shear rate during exercise was detected between the normoxic and hypoxic conditions, whereas the retrograde shear rate was larger during hypoxic exercise. The %FMD decreased significantly at 5 min after exercise in both normoxia and hypoxia, and it returned to pre‐exercise levels within 60 min of recovery. Significant decreases in FMD at 5 min after exercise had disappeared when the baseline diameter was controlled using an analysis of covariance (the corrected‐%FMD). No significant differences were observed between the normoxic and hypoxic trials in the %FMD and corrected‐%FMD following exercise. These results suggest that hypoxia has no impact on endothelial function in the inactive limb following acute aerobic exercise.

Hypoxia augments oscillatory blood flow in brachial artery during leg cycling.

PURPOSE The purpose of the present study was to elucidate changes in mean blood flow and oscillatory blood flow patterns to the inactive limb during leg cycle exercise in hypoxia. We hypothesized that oscillatory antegrade and retrograde blood flows to the nonworking limb would increase during incremental cycle exercise under hypoxic condition. METHODS Eight males participated in this study. Two maximal exercise tests were conducted on a semirecumbent cycle ergometer while subjects inhaled a normoxic (inspired oxygen fraction [FIO2] = 0.21) or hypoxic gas mixture (FIO2 = 0.12). The exercise began at an initial power output of 30 W, and workload was increased by 30 W every 2 min until exhaustion. Brachial artery blood velocity and diameter were simultaneously recorded during exercise using Doppler ultrasonography. Blood flow was calculated using the cross-sectional area of the brachial artery and time-averaged mean blood velocity. RESULTS Mean blood flow decreased until 120 W in both trials (P < 0.05), and the magnitude of the reduction in mean blood flow was not different between two trials. However, the extent of changes in antegrade and retrograde blood flows during submaximal exercise in hypoxia was greater than that in normoxia (normoxia vs hypoxia: antegrade blood flow at 120 W = 145.4 ± 10.3 vs 172.4 ± 9.0 mL·min and retrograde blood flow at 120 W = -89.1 ± 4.9 vs -118.1 ± 6.2 mL·min, P < 0.05). CONCLUSIONS These results indicate that hypoxia has a significant effect on oscillatory antegrade/retrograde blood flow patterns in nonworking limb during cycling exercise.

Blunted blood pressure response during hyperpnoea in endurance runners

UNLABELLED The purpose of this study was to elucidate the cardiovascular response during hyperpnoea in endurance-trained runners compared to sedentary controls. Twelve runners and ten sedentary individuals participated in this study. A maximal respiratory endurance test (MRET) was performed as follows: target minute ventilation was initially set at 30% of maximal voluntary ventilation (MVV12) and was increased by 10% MVV12 every 3min. The test was terminated when the subject could no longer maintain the target ventilation. Heart rate and mean arterial blood pressure (MBP) were continuously measured. Respiratory endurance time during the MRET was longer in the runners than the controls. The change in MBP during the MRET was lower in the runners compared to the sedentary controls (runners: 100.2±2.4mmHg vs. CONTROLS 109.1±3.0mmHg at 6min of hyperpnoea). Therefore, the blood pressure response during hyperpnoea is blunted in endurance runners, suggesting that whole-body endurance exercise training attenuates the respiratory muscle-induced metaboreflex.

The neural influence on the occurrence of locomotor–respiratory coordination

This study focused on the neurogenic mechanisms of coordination between locomotor and respiratory rhythms. The aim of the present study was to investigate the influence of peripheral neurogenic drive from moving limbs, and the level of consciousness, on locomotor-respiratory coordination. Subjects performed movement for 20 min in a supine position using a bicycle ergometer. The movement comprised three types of leg movements: active (loadless) movement, passive movement while awake and passive movement during sleep. We found no difference between active and passive movement in the degree of coordination. However, the degree of coordination during sleep was significantly lower than that while awake (p<0.05). We conclude that peripheral neurogenic drive from moving limbs is able to generate locomotor-respiratory coordination, and that the level of consciousness may influence the degree of coordination.

Exercise intensity modulates brachial artery retrograde blood flow and shear rate during leg cycling in hypoxia

The purpose of this study was to elucidate the effect of exercise intensity on retrograde blood flow and shear rate (SR) in an inactive limb during exercise under normoxic and hypoxic conditions. The subjects performed two maximal exercise tests on a semi‐recumbent cycle ergometer to estimate peak oxygen uptake ( V˙ O2peak) while breathing normoxic (inspired oxygen fraction [FIO2 = 0.21]) and hypoxic (FIO2 = 0.12 or 0.13) gas mixtures. Subjects then performed four exercise bouts at the same relative intensities (30 and 60% V˙ O2peak) for 30 min under normoxic or hypoxic conditions. Brachial artery diameter and blood velocity were simultaneously recorded, using Doppler ultrasonography. Retrograde SR was enhanced with increasing exercise intensity under both conditions at 10 min of exercise. Thereafter, retrograde blood flow and SR in normoxia returned to pre‐exercise levels, with no significant differences between the two exercise intensities. In contrast, retrograde blood flow and SR in hypoxia remained significantly elevated above baseline and was significantly greater at 60% than at 30% V˙ O2peak. We conclude that differences in exercise intensity affect brachial artery retrograde blood flow and SR during prolonged exercise under hypoxic conditions.

High-intensity Exercise Enhances Conduit Artery Vascular Function in Older Adults

Purpose Modulation of vascular function follows an exercise intensity–dependent pattern in young adults. This study aimed to investigate the potential intensity–dependent effects of an acute bout of exercise on conduit and resistance artery function in healthy older adults. Methods Eleven healthy older adults (five males/six females, 66 ± 1 yr) completed 30 min of recumbent cycling at 50%–55% (low intensity) and 75%–80% (high intensity) of their age-predicted HRmax on two separate study visits. Doppler ultrasound measures of brachial artery flow-mediated dilation (FMD) and reactive hyperemia were taken at baseline, 10 min postexercise, and 1 h postexercise. In addition, cardiovascular hemodynamics and brachial shear rate were measured every 5 min during exercise. Results Brachial artery FMD was enhanced 10 min after high-intensity exercise (4.8% ± 0.2% to 9.1% ± 0.3%, P < 0.01), but not low-intensity (4.7% ± 0.2% to 6.2% ± 0.3%, P = 0.54) exercise. Peak and total (area under the curve) blood flow during reactive hyperemia (measures of resistance artery function) were enhanced 10 min postexercise for both intensities (peak low intensity, 372 ± 31 to 444 ± 37 mL·min−1; peak high intensity, 391 ± 30 to 455 ± 28 mL·min−1; total low intensity, 142 ± 16 to 205 ± 20 mL; total high intensity, 158 ± 14 to 240 ± 25 mL; main effect of time for both, P < 0.05). However, the magnitude of change in peak and the total blood flow were not different between exercise intensities (interaction effect; P = 0.56 and P = 0.97, respectively). Independent of exercise intensity, FMD returned to baseline 1 h after exercise (high, 5.9% ± 0.3%; low, 5.1% ± 0.1%; both P > 0.05). Conclusion Our data indicate that high-intensity exercise acutely enhances conduit artery function in healthy older adults. In addition, an acute bout of exercise enhances resistance artery function independent of intensity.

Acute vascular effects of carbonated warm water lower leg immersion in healthy young adults

Endothelial dysfunction is associated with increased cardiovascular mortality and morbidity; however, this dysfunction may be ameliorated by several therapies. For example, it has been reported that heat‐induced increases in blood flow and shear stress enhance endothelium‐mediated vasodilator function. Under these backgrounds, we expect that carbon dioxide (CO2)‐rich water‐induced increase in skin blood flow improves endothelium‐mediated vasodilation with less heat stress. To test our hypothesis, we measured flow‐mediated dilation (FMD) before and after acute immersion of the lower legs and feet in mild warm (38°C) normal or CO2‐rich tap water (1000 ppm) for 20 min in 12 subjects. Acute immersion of the lower legs and feet in mild warm CO2‐rich water increased FMD (P < 0.01) despite the lack of change in this parameter upon mild warm normal water immersion. In addition, FMD was positively correlated with change in skin blood flow regardless of conditions (P < 0.01), indicating that an increase in skin blood flow improves endothelial‐mediated vasodilator function. Importantly, the temperature of normal tap water must reach approximately 43°C to achieve the same skin blood flow level as that obtained during mild warm CO2‐rich water immersion (38°C). These findings suggest that CO2‐rich water‐induced large increases in skin blood flow may improve endothelial‐mediated vasodilator function while causing less heat stress.