Keisho Katayama

Intermittent Hypoxia Improves Endurance Performance and Submaximal Exercise Efficiency

The purpose of the present study was to elucidate the influence of intermittent hypobaric hypoxia at rest on endurance performance and cardiorespiratory and hematological adaptations in trained endurance athletes. Twelve trained male endurance runners were assigned to either a hypoxic group (n = 6) or a control group (n = 6). The subjects in the hypoxic group were exposed to a simulated altitude of 4500 m for 90 min, three times a week for 3 weeks. The measurements of 3000 m running time, running time to exhaustion, and cardiorespiratory parameters during maximal exercise test and resting hematological status were performed before (Pre) and after 3 weeks of intermittent hypoxic exposure (Post). These measurements were repeated after the cessation of intermittent hypoxia for 3 weeks (Re). In the control group, the same parameters were determined at Pre, Post, and Re for the subjects not exposed to intermittent hypoxia. The athletes in both groups continued their normal training together at sea level throughout the experiment. In the hypoxic group, the 3000 m running time and running time to exhaustion during maximal exercise test improved. Neither cardiorespiratory parameters to maximal exercise nor resting hematological parameters were changed in either group at Post, whereas oxygen uptake (.V(O2)) during submaximal exercise decreased significantly in the hypoxic group. After cessation of intermittent hypoxia for 3 weeks, the improved 3000 m running time and running time to exhaustion tended to decline, and the decreased .V(O2) during submaximal exercise returned to Pre level. These results suggest that intermittent hypoxia at rest could improve endurance performance and submaximal exercise efficiency at sea level in trained endurance athletes, but these improvements are not maintained after the cessation of intermittent hypoxia for 3 weeks.

The effects of intermittent exposure to hypoxia during endurance exercise training on the ventilatory responses to hypoxia and hypercapnia in humans

Abstract The present study was performed to investigate the effects of a combination of intermittent exposure to hypoxia during exercise training for short periods on ventilatory responses to hypoxia and hypercapnia (HVR and HCVR respectively) in humans. In a hypobaric chamber at a simulated altitude of 4,500 m (barometric pressure 432 mmHg), seven subjects (training group) performed exercise training for 6 consecutive days (30 min · day−1), while six subjects (control group) were inactive during the same period. The HVR, HCVR and maximal oxygen uptake (V˙O2 max) for each subject were measured at sea level before (pre) and after exposure to intermittent hypoxia. The post exposure test was carried out twice, i.e. on the 1st day and 1 week post exposure. It was found that HVR, as an index of peripheral chemosensitivity to hypoxia, was increased significantly (P < 0.05) in the control group after intermittent exposure to hypoxia. In contrast, there was no significant increase in HVR in the training group after exposure. The HCVR in both groups was not changed by intermittent exposure to hypoxia, while V˙O2 max increased significantly in the training group. These results would suggest that endurance training during intermittent exposure to hypoxia depresses the increment of chemosensitivity to hypoxia, and that intermittent exposure to hypoxia in the presence or absence of exercise training does not induce an increase in the chemosensitivity to hypercapnia in humans.

Changes in blood volume and oxygenation level in a working muscle during a crank cycle.

PURPOSE This study examined circulatory and metabolic changes in a working muscle during a crank cycle in a pedaling exercise with near-infrared spectroscopy (NIRS). METHODS NIRS measurements sampled under stable metabolic and cadence conditions during incremental pedaling exercise were reordered according to the crank angles whose signals were obtained in eight male subjects. RESULTS The reordered changes in muscle blood volume during a crank cycle demonstrated a pattern change that corresponded to changes in pedal force and electrical muscle activity for pedal thrust. The top and bottom peaks for muscle blood volume change at work intensities of 180 W and 220 W always preceded (88 +/- 32 and 92 +/- 23 ms, respectively) those for muscle oxygenation changes. Significant differences in the level of NIRS parameters (muscle blood volume and oxygenation level) among work intensities were noted with a common shape in curve changes related to pedal force. In addition, a temporary increase in muscle blood volume following a pedal thrust was detected at work intensities higher than moderate. This temporary increase in muscle blood volume might reflect muscle blood flow restriction caused by pedal thrusts. CONCLUSION The results suggest that circulatory and metabolic conditions of a working muscle can be easily affected during pedaling exercise by work intensity. The present method, reordering of NIRS parameters against crank angle, serves as a useful measure in providing additional findings of circulatory dynamics and metabolic changes in a working muscle during pedaling exercise.

The adaptive responses in several mediators linked with hypertrophy and atrophy of skeletal muscle after lower limb unloading in humans

Aim:  To determine the adaptive changes in several molecules regulating muscle hypertrophy and atrophy after unloading, we examined whether unilateral lower limb suspension changes the mRNA and protein levels of SRF‐linked (RhoA, RhoGDI, STARS and SRF), myostatin‐linked (myostatin, Smad2, Smad3 and FLRG) and Foxo‐linked (P‐Akt, Foxo1, Foxo3a and Atrogin‐1) mediators.

Substrate utilization during exercise and recovery at moderate altitude.

Recent studies have shown that exercise training at moderate altitude or in moderate hypoxia improved glycemic parameters. From these data, it has been supposed that endurance exercise in moderate hypoxia affects substrate utilization and that exposure to moderate hypoxia in combination with exercise may be utilized as part of metabolic or diabetes prevention program. However, the influence of exercise at moderate hypoxia on circulating metabolites and hormones in terms of substrate utilization is unclear. The purpose of this study was to elucidate the influence of exercise in moderate hypoxia on substrate utilization. We determined cardiorespiratory, metabolic, and hormonal parameters during exercise and postexercise recovery at a simulated moderate altitude of 2000 m, and then we compared these variables with values obtained at sea level. Seven men participated in this study; subjects reported to the laboratory on 4 occasions. Two maximal exercise tests were performed to estimate peak oxygen uptake at the simulated 2000-m altitude and sea level on different days. Afterward, submaximal exercise tests were carried out at a simulated altitude of 2000 m or sea level, separated by 1 week. Subjects performed submaximal exercise at the same relative exercise intensity (50% peak oxygen uptake) at a simulated altitude of 2000 m and at sea level for 30 minutes. The tests were performed in random order, and subjects were blinded to the respective altitudes. Venous blood samples and expired gases were obtained before, during exercise (15 and 30 minutes), and during postexercise recovery periods (15, 30, 45, and 60 minutes). The respiratory exchange ratio during exercise and recovery at moderate altitude was greater than at sea level. The epinephrine and norepinephrine concentrations during exercise and recovery were higher (P < .05) at moderate altitude than at sea level. Free fatty acids and glycerol concentrations during recovery were lower (P < .05) at moderate altitude than at sea level. These results suggest that carbohydrate utilization is increased during exercise and postexercise recovery period in moderate hypoxia as compared with normoxia. It is also suggested that moderate hypoxia influences the changes in circulating metabolites and hormones in terms of substrate metabolism during exercise and the recovery.

Effect of intermittent hypoxia on cardiovascular adaptations and response to progressive hypoxia in humans.

The aim of the present study was to elucidate (1) the cardiovascular adaptations and response to hypoxic stimuli during short-term intermittent hypoxia and (2) whether the change in cardiovascular response to hypoxia is correlated to the change in hypoxic ventilatory chemosensitivity. Fourteen subjects were decompressed in a chamber to 432 torr, simulating an altitude of 4500 m, over a period of 30 min and were maintained at that pressure for 1 h daily for 7 days. Ventilatory (DeltaV(I)/DeltaSa(O2); Sa(O2) is arterial oxygen saturation), systolic and diastolic blood pressure (DeltaSBP/DeltaSa(O2) and DeltaDBP/DeltaSa(O2)), and heart rate (DeltaHR/DeltaSa(O2)) responses to progressive isocapnic hypoxia were measured before and after intermittent hypoxia. Resting ventilation, SBP, DBP, and HR did not change after intermittent hypoxia. DeltaSBP/DeltaSa(O2) and DeltaDBP/DeltaSa(O2) increased significantly after intermittent hypoxia accompanied by an enhanced DeltaV(I)/DeltaSa(C2), but there was no change in DeltaHR/DeltaSa(C2). There were significant correlations between the change in DeltaV(I)/DeltaSa(O2) and both the changes in DeltaSBP/DeltaSa(O2) and DeltaDBP/DeltaSa(O2) following intermittent hypoxic exposure. These results suggest that short-term intermittent hypoxia leads to the enhanced arterial BP response to hypoxic stimuli in humans, and that the enhanced peripheral chemosensitivity to hypoxia after intermittent hypoxia may play an important role in the increased arterial BP response.

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.

Electromyographic analysis of hip adductor muscles during incremental fatiguing pedaling exercise

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.

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.

Muscle Deoxygenation during Sustained and Intermittent Isometric Exercise in Hypoxia

PURPOSE It is reported that the rate of locomotor muscle fatigue development during intermittent isometric exercise in hypoxia is accelerated compared with normoxia. In contrast, when sustained isometric contractions are used, some studies do not show any effect of hypoxia on fatigue development. Increased intramuscular pressure during sustained isometric exercise causes substantial and sustained ischemia, even in normoxia. Therefore, we hypothesized that the difference in muscle deoxygenation between normoxia and hypoxia would be small during sustained exercise compared with intermittent exercise and that this may contribute to the inconsistent findings. METHODS Subjects performed sustained and intermittent isometric, unilateral, and submaximal knee-extension exercises (60% maximal voluntary contraction to exhaustion) while breathing normoxic (inspired O2 fraction = 0.21) or hypoxic gas mixtures (inspired O2 fraction = 0.10-0.12). Muscle oxygenation (deoxyhemoglobin/myoglobin and tissue oxygenation index) using near-infrared spectroscopy and surface EMG were measured from the left vastus lateralis. RESULTS During intermittent isometric exercise in hypoxia, increases in deoxyhemoglobin/myoglobin and reductions of tissue oxygenation index were larger (P < 0.05) than those in normoxia. The rate of rise in integrated EMG during intermittent exercise was accelerated (P < 0.05) in hypoxia. In contrast, there were no significant differences in changes in near-infrared spectroscopy variables and integrated EMG during sustained isometric exercise between normoxia and hypoxia. CONCLUSIONS These results suggest that muscle deoxygenation is exaggerated during intermittent isometric exercise in hypoxia compared with normoxia, whereas during sustained isometric exercise, the extent of muscle deoxygenation is the same between normoxia and hypoxia. The different extent of muscle deoxygenation during sustained and intermittent isometric exercise in normoxia and hypoxia could affect muscle fatigability, which results from the varied rate of accumulation of metabolites.