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The effect of exercise on the increase of exhaled CO in smokers compared to non-smokers has not been clarified yet. In this study we compared the dynamics of exhaled CO before, during and after exercise between smokers and non-smokers. A group of 8 smokers and a group of 8 non-smokers underwent a bicycle exercise in a ramp fashion to near maximum intensity. Ventilation and gas exchange, and CO exhalation were continuously measured every 30-s before, during and after the exercise. The fraction of CO (F (CO)) in the exhaled air decreased gradually, but the total amount of exhaled CO (V(CO)) increased in a linear manner during the ramp exercise, and F (CO) and returned to the pre-exercise level within several minutes after exercise in all subjects. A linear relationship was observed between V (O(2)) and V (CO) and between V (E) and V (CO) in both the whole period of measurement and during the ramp exercise period in all subjects. However, the at V (CO) 0 W, the peak V (CO) and the slope coefficients in the regression equation between V (CO) and V (O(2)) and between V (CO) and V (E) in the ramp exercise as well as the entire periods of measurement were significantly higher in smokers compared with those in non-smokers, and these were correlated with the number of cigarettes smoked per day. It was concluded that CO exhalation increases linearly with the increase of V (O(2)) and V (E) during exercise, and habitual smoking shifts these relationships upward depending on the number of cigarettes smoked daily.

In order to elucidate the effects of deconditioning (inactivity) on the ventilatory and circulatory responses at the onset of exercise within 20 s, we initiated head-down bed rest and unilateral lower limb suspension experiments, and measured these responses to dynamic voluntary leg exercise and passive movements. Initial ventilatory and heart rate responses to voluntary exercise were attenuated after bed rest but showed no change after suspension or during passive movements, suggesting the minimal role of peripheral neural reflex.

Introduction: This study was designed to elucidate the effect of short-arm centrifuge-induced artificial gravity with exercise training during ground-based simulated spaceflight, i.e., prolonged head-down bed rest (HDBR), on respiratory and cardiovascular responses to upright exercise., Methods: There were 10 healthy men who underwent 20 d of -6 degrees HDBR, and were assigned to either a countermeasure (CM) group (n = 5) or a no countermeasure (No-CM) group (n = 5). The subjects in the CM group performed two sessions (20 min each session, 40 min total) of short-arm centrifuge-induced artificial gravity with exercise training in a supine position on alternate days (10 d total) during HDBR. The first session was set at 0.8-1.4 G load at heart level with a constant exercise intensity (60 W), and the second session began with a 0.3 G load at heart level with an interval exercise protocol (40-80% peak oxygen uptake; VO2peak). The measurements of respiratory and cardiovascular responses to incremental exercise were performed pre- and post-HDBR., Results: The 20 d of HDBR increased minute expired ventilation, heart rate, and respiratory exchange ratio and decreased stroke volume during submaximal exercise in the No-CM group, whereas these parameters were unchanged in the CM group. In the No-CM group, VO2peak decreased significantly (47.0 +/- 8.6 to 34.8 +/- 6.8 ml x kg(-1) x min(-1), p < 0.05), whereas VO2peak in the CM group did not show a significant decrease following 20 d of HDBR (47.7 +/- 10.0 to 43.9 +/- 8.9 ml x kg(-1) x min(-1)). These results suggest that short-arm centrifuge-induced artificial gravity with exercise training is effective in maintaining respiratory and cardiovascular responses to upright exercise.

The purpose of this study was to clarify the characteristics of ventilatory and circulatory responses at the onset of voluntary exercise and passive movement in sprinters. Eleven male university sprinters and 11 male untrained subjects participated in the present study. Voluntary exercise consisted of leg extension-flexion movement for 20 s with weights corresponding to 5% of each subject's body mass attached to each ankle. Passive movement was achieved without weights by the experimenter alternately pulling ropes that were connected to the subject's ankles for the same period and frequency as during voluntary exercise. In the present study, the following results were found: (1) the magnitude of relative changes (gain) of minute ventilation at the onset of passive movement in the sprinters was significantly smaller than that in the untrained subjects [mean (SEM) 33.3 (2.9) vs 61.7 (6.4)%, P<0.05]; (2) the time for reaching one-half of the gain (response time) of heart rate at the onset of voluntary exercise and passive movement in the sprinters was significantly slower than that in the untrained subjects [2.5 (0.2) vs 1.7 (0.2) s in voluntary exercise and 3.4 (0.8) vs 1.5 (0.1) s in passive movement, P<0.05]; (3) the gain and response time of mean blood pressure at the onset of voluntary exercise and passive movement showed no significant differences between the two groups. It is concluded that sprinters show slowed heart rate response at the onset of voluntary exercise, and attenuated ventilatory and slowed heart rate responses at the onset of passive movement as compared with untrained subjects.

The purpose of the present study was to clarify the following: (1) whether steady state oxygen uptake (VO(2)) during exercise decreases after short-term intermittent hypoxia during a resting state in trained athletes and (2) whether the change in VO(2) during submaximal exercise is correlated to the change in endurance performance after intermittent hypoxia. Fifteen trained male endurance runners volunteered to participate in this study. Each subject was assigned to either a hypoxic group (n=8) or a control group (n=7). The hypoxic group spent 3 h per day for 14 consecutive days in normobaric hypoxia [12.3 (0.2)% inspired oxygen]. The maximal and submaximal exercise tests, a 3,000-m time trial, and resting hematology assessments at sea level were conducted before and after intermittent normobaric hypoxia. The athletes in both groups continued their normal training in normoxia throughout the experiment. VO(2) during submaximal exercise in the hypoxic group decreased significantly (P<0.05) following intermittent hypoxia. In the hypoxic group, the 3,000-m running time tended to improve (P=0.06) after intermittent hypoxia, but not in the control group. Neither peak VO(2) nor resting hematological parameters were changed in either group. There were significant (P<0.05) relationships between the change in the 3,000-m running time and the change in VO(2) during submaximal exercise after intermittent hypoxia. The results from the present study suggest that the enhanced running economy resulting from intermittent hypoxia could, in part, contribute to improved endurance performance in trained athletes.

To clarify the luteal-follicular and male-female differences in ventilatory and heart rate responses at the onset of exercise, seven women and seven men performed voluntary exercise and passive movement for 20 s (brief voluntary exercise and brief passive movement) and voluntary exercise for 3 min (long voluntary exercise) in a sitting position. Voluntary exercise consisted of alternate flexion-extensions of both lower legs with a weight corresponding to about 2.5% of the subjects' body mass attached to each ankle, at a frequency of about 60 times min(-1). Passive movement was carried out without weights by experimenters pulling ropes attached to both of the subjects' ankles, in the same way as voluntary exercise. During these exercises and movements, minute inspiratory ventilation ( V(I)) and heart rate (HR) were continuously measured by breath-by-breath and beat-to-beat techniques. We calculated relative changes of V(I) and HR (Delta V(I) and DeltaHR). Additionally, we averaged Delta V(I) and DeltaHR obtained during the exercise and movement for each subject, and performed a correlation analysis between the averaged Delta V(I) and DeltaHR. It was clarified that: (1) Delta V(I) and DeltaHR in the follicular phase were almost equal to those in the luteal phase; (2) there were no significant male-female differences in these parameters; (3) significant positive correlations were found in both genders only during brief voluntary exercise. We conclude that ventilatory and HR responses at the onset of voluntary exercise and passive movement are not affected by the menstrual cycle or gender.

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 purpose of the present study was to examine the changes in maximum voluntary isometric contraction (MVC) in the contralateral untrained limb during unilateral resistance training and detraining, and to examine the factors inducing these changes by means of electrophysiological techniques. Nine healthy males trained their plantar flexor muscles unilaterally 4 day-s x week(-1) for 6 weeks using 3 sets of 10-12 repetitions at 70-75% of one-repetition maximum a day, and detrained for 6 weeks. Progressive unilateral resistance training significantly (P < 0.05) increased MVC, integrated electromyogram (iEMG), and voluntary activation in the trained and contralateral untrained limbs. The changes in MVC after training were significantly correlated with the changes in iEMG in both limbs. No significant changes occurred in MVC, voluntary activation, and iEMG in the contralateral limb after detraining. The changes in MVC after detraining did not correlate with the changes in voluntary activation or iEMG in either limb. Training and detraining did not alter twitch and tetanic peak torques in either limb. These results suggest that the mechanisms underlying cross education of muscular strength may be explained by central neural factors during training, but not solely so during detraining.

The purpose of this study was 1) to test the hypothesis that ventilation and arterial oxygen saturation (Sa(O2)) during acute hypoxia may increase during intermittent hypoxia and remain elevated for a week without hypoxic exposure and 2) to clarify whether the changes in ventilation and Sa(O2) during hypoxic exercise are correlated with the change in hypoxic chemosensitivity. Six subjects were exposed to a simulated altitude of 4,500 m altitude for 7 days (1 h/day). Oxygen uptake (VO2), expired minute ventilation (VE), and Sa(O2) were measured during maximal and submaximal exercise at 432 Torr before (Pre), after intermittent hypoxia (Post), and again after a week at sea level (De). Hypoxic ventilatory response (HVR) was also determined. At both Post and De, significant increases from Pre were found in HVR at rest and in ventilatory equivalent for O2 (VE/VO2) and Sa(O2) during submaximal exercise. There were significant correlations among the changes in HVR at rest and in VE/VO2 and Sa(O2) during hypoxic exercise during intermittent hypoxia. We conclude that 1 wk of daily exposure to 1 h of hypoxia significantly improved oxygenation in exercise during subsequent acute hypoxic exposures up to 1 wk after the conditioning, presumably caused by the enhanced hypoxic ventilatory chemosensitivity.

The purpose of this study was to investigate whether or not the ventilatory and circulatory responses at the onset of voluntary exercise and passive movement, especially at the initial stage (phase I), in children are the same as in adults. Ten pre-teenage male children and ten adult men participated in this study. Voluntary exercise and passive movement were performed in a sitting position for about 20 s. Both the exercise and the movement consisted of flexion-extensions of the lower leg from a vertical to horizontal position, either voluntarily or passively, with a frequency of about 60 x min(-1). Inspiratory minute ventilation (V1), tidal volume (VT), respiratory frequency, partial pressure of end-tidal CO2 and O2, heart rate (fc) and mean blood pressure (BP) before, during and after exercise or movement were measured using breath-by-breath and beat-to-beat techniques. Cardiorespiratory responses at the onset of voluntary exercise and passive movement were compared with the relative change (delta), which was estimated from the value at rest (100%). In the present study, it was found that: (1) the V1 during voluntary exercise were significantly lower in the children, mainly due to lower deltaVT; (2) the delta(f)c during voluntary exercise was almost the same in both groups, while deltaf(c) was significantly lower in the children during the last part of passive movement; (3) in the voluntary exercise and passive movement, the BP in the children was increased a little or remained close to the value at rest, while it was significantly decreased in the adults. As a result, there were significant differences in deltaBP between the two groups during voluntary exercise. These results suggest that the cardiorespiratory responses at the onset of voluntary exercise and passive movement may be modified during the growth process.

Background: To clarify 1) how the cross-transfer effect, obtained in a contralateral untrained forearm through a 4-week ipsilateral endurance training regimen, is changed during detraining; and 2) how blood flow to the untrained limb is related to the transfer effect of muscular endurance during training and detraining periods., Methods: Training regimen: hand-grip training by means of a hand-ergometer with a work-load of 1/3 of the maximum handgrip strength 5 times a week for 4 weeks. Blood flow: a mercury-in-rubber strain-gauge for venous occlusion plethysmography., Measures: 1) maximal number of contractions to determine the muscular endurance; 2) reactive hyperaemic blood flow response (RHBF3) to determine whether maximal vasodilatory capacity would be changed in both the forearms post-training and detraining; and 3) maximal work-related blood flow., Results: We found significant increments both in the muscle endurance and the maximal work-related blood flow not only in the trained (+125%, +30%) but also in the untrained (+40%, +19%) forearms. During detraining, we found decreases both in the muscle endurance and the maximal work-related blood flow (-22%, p<0.01; -16%, p=0.053) of the trained forearm. However, in the untrained arm (-3%, NS) the cross-transfer effect of muscular endurance remained unchanged despite a drop in the maximal work-related blood flow (-17%, p<0.05). The RHBF3 did not change in either of the forearms during the whole periods., Conclusions: These findings suggest that the maintenance of the cross transfer effect of muscle endurance during detraining cannot be explained on the basis of changes in forearm blood flow.

To investigate the effects of maximal voluntary exercise on sympathetic nerve activity, contraction force and muscle sympathetic nerve activity (MSNA) were recorded during maximal (MVG) and submaximal voluntary isometric handgrip (SVG) for 2 min in eight healthy subjects. MSNA was determined by a microneurographic technique, and handgrip force, heart rate (HR) and arterial blood pressure (ABP) were measured by a non-invasive method during exercise. Grip force decayed rapidly to 58% of maximal grip force (MGF) at 10 s after commencement of exercise and was almost constant (approximately 30% of MGF) 40 s after exercise. MSNA increase was delayed by 20 s during MVG, followed by a gradual increase. HR was elevated immediately after onset of exercise, while mean ABP rise showed a 20 s lag from initiation of MVG exercise. During SVG increases in MSNA, HR and mean ABP were delayed by 50, 40 and 20 s, respectively, relative to commencement of exercise. Thereafter, these parameters increased time-dependently. These results suggested that the MSNA increase during MVG may be predominantly because of the metaboreflex.

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 x day(-1)), while six subjects (control group) were inactive during the same period. The HVR, HCVR and maximal oxygen uptake (VO2max) 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 VO2max 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.

In order to examine the origin and role of nitric oxide (NO) in exhaled air during exercise, exhaled NO outputs of 8 healthy human subjects were compared using different breathing methods, through the mouth or nose, at two intensities of bicycle exercise. The concentration of NO in the exhaled air and ventilatory gas exchange variables were measured by a chemiluminescence analyzer and a mixing chamber method, respectively. The concentration and total output of NO in the expired air was significantly higher under nasal breathing than under oral breathing for both exercise intensities, whereas no significant difference was observed in cardiorespiratory variables between them. NO output increased significantly when exercise intensity was increased from unloaded (0 W) to 60 W under nasal breathing, but not under oral breathing. A negative correlation among subjects was found between NO output and minute ventilation in both breathing methods only for unloaded exercise. Data indicate that nasal airways have a large contribution, at least 50% of total NO output in the exhaled air during nasal breathing, but this nasal NO may have no further modulation on respiratory function during submaximal exercise by healthy humans.

To elucidate whether combined adrenergic and parasympathetic blockade would affect the ventilatory response to exercise, especially at the initial stage (phase I), six healthy subjects performed a brief and light voluntary bilateral leg extension exercise and passive movements under the conditions of control (before the blockade) and after intravenous administration of combined beta-adrenergic (propranolol, 0.2 mg.kg-1) and muscarinic (atropine, 0.04 mg.kg-1) receptor antagonists. The movements were continued only within two breaths after the onset of the motion. Ventilation increased immediately and significantly (P < 0.05) within the first breath at the onset of voluntary exercise in all conditions as compared with at rest. However, the magnitude of increase in mean ventilation within two breaths at the start of exercise as against the resting value (delta ventilation) was significantly less (P < 0.05) after the combined blockades (2.5 l.min-1) than in the control condition (3.7 l.min-1). Passive movements showed a similar but smaller change as compared with voluntary exercise. The heart rate response to exercise was attenuated by the combined blockade while cardiac output showed a slight change at the onset of exercise. It is concluded that phase I should occur despite the inhibited activity of the beta-adrenergic and the cholinergic systems; nevertheless, the response was attenuated by the combined blockade. These results suggest a possible role of the beta-adrenergic and/or cholinergic systems in the rapid increase in ventilation that occurs at the start of exercise.

The present study was performed to examine whether or not the ventilatory response at the onset of voluntary exercise and passive movement in endurance runners is the same as in untrained subjects. Twelve long-distance runners belonging to the varsity athletic club and 13 untrained subjects of our university participated as subjects in this study. Maximum oxygen uptake was significantly higher in the endurance runner group [mean (SD) 70.8 (4.7) ml.kg-1.min-1] than in the untrained group [49.8 (6.3) ml.kg-1.min-1]. Cardiorespiratory responses during voluntary exercise and passive movement of alternate flexion-extension of the right and left legs for about 15 s at a frequency of about 60 rpm, were determined by means of breath-by-breath techniques. Minute inspiratory ventilation (VI), tidal volume (VT), respiratory frequency (fb), cardiac output (Qc), stroke volume (SV) and heart rate (HR) increased significantly immediately at the onset of voluntary exercise and passive movement. The incremental rate for VI was greater than that for Qc. Average values and standard deviations of changes in VI were calculated as the difference between the mean of the first and second breath and the mean of five breaths preceding the exercise or movement. The rates obtained in voluntary exercise and passive movement in the endurance runner group [2.34 (0.82) and 1.72 (0.71 l.min-1), respectively] were significantly (P < 0.05) lower than those in the untrained group [4.16 (2.66) and 2.71 (1.56 l.min-1), respectively]. Also changes in VT and HR were significantly lower in the endurance group than in the untrained group with regard to both voluntary exercise and passive movement. The results suggest that the magnitude of cardiorespiratory responses at the onset of voluntary exercise and passive movement in humans is influenced by chronic endurance training for long periods.

This study was undertaken to elucidate whether phase I appeared at the onset of voluntary and passive arm movements and to compare these results with those of similar leg movements. Instead of the conventional cranking exercise, seven male subjects performed alternately flexion-relaxation of both arms, extension-relaxation of both legs, and combined arm and leg exercise at the rate of about 60 min-1 for four breaths in a sitting position. Similar movements were accomplished passively by the experimenters. In all experiments, minute ventilation increased rapidly within the first breath after the onset of exercise. The difference of ventilation (delta value) between the mean of the first two breaths at the onset of voluntary exercise and that of five breaths during rest was significantly (P < 0.05) greater in arm (7.75 l min-1) than in leg (5.19 l min-1). Passive movement showed a similar tendency. Arm delta ventilation correlated highly (r = 0.74-0.91) with leg delta ventilation and the slope of the regression lines was about 1.2. Heart rate increased abruptly while cardiac output did not always increase rapidly at the onset of locomotion. Oxygen uptake in the voluntary leg exercise continued for 3 min was slightly but nonsignificantly higher than in the arm exercise, indicating the equality of the exercise intensity. In conclusion, ventilatory responses at the onset of the arm exercise are larger than those of the leg in both voluntary and passive conditions regardless of the muscle mass, suggesting the different neurogenic mechanism between arm and leg.

Ventilatory responses at the onset of passive and active exercise with different amount of exercising muscle mass were studied in 10 healthy male subjects. Four exercise tests were performed for each subject with appropriate intervals on the same day, i.e., two voluntary exercises of one leg or both legs and two passive exercises of one leg or both legs. Inspiratory minute volume (VI), end-tidal CO2 and O2 partial pressures (PETCO2, PETO2) were measured breath-by-breath using a hot-wire flowmeter, infrared CO2 analyzer, and a rapid O2 analyzer. Average values of VI were obtained from 5 breaths at rest preceding exercise and the first and second breaths after the onset of exercise. The ventilatory response to exercise was calculated as the difference (delta) between the mean of exercise VI and mean of resting VI. In this study, the PETCO2 decreased by about 0.5 Torr in four exercise tests, though the decrement of PETCO2 was not statistically significant. The average values and standard deviation of delta VI were 4.22 +/- 1.63 l/min for the one leg and 6.46 +/- 1.80 l/min for the two legs in the active exercise, and were 2.46 +/- 1.12 l/min for the one leg and 3.44 +/- 1.55 l/min for the two legs in the passive exercise, respectively. These results suggest that in awake conditions, the ventilatory response at the onset of passive or active exercise does not increase additively with the increasing amount of muscle mass being exercised.

Changes in the time courses of VO2 during constant-load exercise were examined in connection with other cardiorespiratory and blood chemical parameters. Eleven healthy male subjects performed a ramp exercise and three to six constant-load exercises at varying degrees of load using an electro-braked bicycle ergometer. Heart rate, ventilation, and gas exchange were measured during both types of exercise, and chemical parameters of the subject's blood (blood gas, pH, lactate, and electrolytes) were determined during two intensities of constant-load exercise. The time courses of cardiorespiratory and blood chemical data 3 min after the onset of constant-load exercise were fitted by linear regressions to see whether these parameters had reached the steady state or not. Heart rate increased significantly at a lower intensity of constant-load exercise than VE, VO2, and VCO2. While the increase in VCO2 was slower than that of VO2, a definite difference in time courses was not found between VE and VO2. The time courses of changes in blood gas, pH, bicarbonate, and lactate were not correlated with those of VO2. However, changes in blood potassium concentration were closely correlated with those of VO2 in terms of time courses and magnitude. This suggests the possibility that blood potassium may play an important role in the control of VO2 time course during constant-load exercise.

In order to investigate the effects of acute hypoxia and accompanying hypocapnia on the ventilatory response at the onset of dynamic exercise, four healthy adult men performed 50W rectangular loads on a cycle-ergometer in normoxic (FIO2 = 0.21) and hypoxic (FIO2 = 0.11) conditions. No statistically significant differences in the initial ventilatory responses to exercise (both delta VI and delta VE assessed on a breath-by-breath basis) were found between eucapnic normoxia (PETO2 approximately 95, PETCO2 approximately 42 Torr) and hypocapnic hypoxia (PETO2 approximately 45, PETCO2 approximately 35 Torr). The present findings support the contention that the neurogenic ventilatory drive at the onset of early exercise is independent from PO2 and PCO2.

In the untrained subjects, inhalation of 4.5-6.0% CO2 prior to maximal treadmill exercise does not affect physical performance and maximum oxygen uptake, while blood lactate levels during recovery have a tendency to greater decrease in CO2 breathing than that in the room-air breathing. It was suggested that CO2 inhalation immediately prior to maximal exercise as applied here is not a useful tool in increasing physical performance.