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Purpose Effort sense has been suggested to be involved in the hyperventilatory response during intense exercise (IE). However, the mechanism by which effort sense induces an increase in ventilation during IE has not been fully elucidated. The aim of this study was to determine the relationship between effort-mediated ventilatory response and corticospinal excitability of lower limb muscle during IE. Eight subjects performed 3 min of cycling exercise at 75-85 % of maximum workload twice (IE1st and IE2nd). IE2nd was performed after 60 min of resting recovery following 45 min of submaximal cycling exercise at the workload corresponding to ventilatory threshold. Vastus lateralis muscle response to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs), effort sense of legs (ESL, Borg 0-10 scale), and ventilatory response were measured during the two IEs. The slope of ventilation (l/min) against CO2 output (l/min) during IE2nd (28.0 +/- 5.6) was significantly greater than that (25.1 +/- 5.5) during IE1st. Mean ESL during IE was significantly higher in IE2nd (5.25 +/- 0.89) than in IE1st (4.67 +/- 0.62). Mean MEP (normalized to maximal M-wave) during IE was significantly lower in IE2nd (66 +/- 22 %) than in IE1st (77 +/- 24 %). The difference in mean ESL between the two IEs was significantly (p < 0.05, r = -0.82) correlated with the difference in mean MEP between the two IEs. The findings suggest that effort-mediated hyperventilatory response to IE may be associated with a decrease in corticospinal excitability of exercising muscle.

The purpose of the present study was to examine how oscillation of tissue oxygen index (TOI) in non-exercising exercise is affected during high-intensity and low-intensity exercises. Three exercises were performed with exercise intensities of 30% and 70% peak oxygen uptake ((V)over doto(2)peak) for 12 min and with exercise intensity of 70% (V)over doto(2)peak for 30 s. TOI in non-exercising muscle (biceps brachii) during the exercises for 12 min was determined by nearinfrared spectroscopy. TOI in the non-exercising muscle during the exercises was analyzed by fast Fourier transform (FFT) to obtain power spectra density (PSD). The frequency at which maximal PSD appeared (Fmax) during the exercise with 70% (V)over doto(2)peak for 12 min (0.00477 +/- 0.00172 Hz) was significantly lower than that during the exercise with 30% (V)over doto(2)peak for 12 min (0.00781 +/- 0.00338 Hz). There were significant differences in blood pH and blood lactate between the exercise with 70% V.o2peak and the exercise with 30% (V)over doto(2)peak. It is concluded that TOI in nonexercising muscle oscillates during low-intensity exercise as well as during high-intensity exercise and that the difference in Fmax between the two exercises is associated with the difference in increase in blood lactate derived from the exercise.

Time delay in the mediation of ventilation (V(.)E) by arterial CO(2) pressure (PaCO(2)) was studied during recovery from short impulse-like exercises with different work loads of recovery. Subjects performed two tests including 10-s impulse like exercise with work load of 200 watts and 15-min recovery with 25 watts in test one and 50 watts in test two. V(.)E, end tidal CO(2) pressure (PETCO(2)) and heart rate (HR) were measured continuously during rest, warming up, exercise and recovery. PaCO(2) was estimated from PETCO(2) and tidal volume (V(T)). Results showed that predicted arterial CO(2) pressure (PaCO(2 pre)) increased during recovery in both tests. In both tests, V(.)E increased and peaked at the end of exercise. V(.)E decreased in the first few seconds of recovery but started to increase again. The highest correlation coefficient between PaCO(2 pre) and V(.)E was obtained in the time delay of 7 s (r=0.854) in test one and in time delays of 6 s (r=0.451) and 31 s (r=0.567) in test two. HR was significantly higher in test two than in test one. These results indicate that PaCO(2 pre) drives V(.)E with a time delay and that higher work intensity induces a shorter time delay.

The aim of the present study was to compare the frequency of oxygenation determined in the vastus lateralis by near-infrared spectroscopy (NIRS) in light exercise with that at rest. A subject rested in a recumbent position for 5 min and changed body position to a sitting position on a cycle ergometer for 9 min. Then exercise with low intensity (work rate of 60% of maximal oxygen uptake) was carried out for 30 min. Total hemoglobin and myoglobin (THb/Mb) suddenly decreased after the start of exercise and gradually increased until 6 min. Oxygenated hemoglobin and myoglobin (Hb/MbO2) suddenly decreased and returned to a steady state after the start of exercise. The difference between Hb/MbO2 and THb/Mb showed a sudden decrease and then a steady state. This difference was analyzed by fast Fourier transform. The peak frequencies of the power spectrum density (PSD) were 0.0169 + 0.0076 Hz at rest and 0.0117 + 0.0042 Hz in exercise. The peak frequency of PSD was significantly decreased in exercise. In exercise, the range of frequencies was expanded. It is concluded that there are oscillations at rest as well as in exercise and that the frequency of peak PSD becomes lower in exercise than at rest.

The aim of the present study was to compare the oscillations of oxygenation in skeletal muscle between early and late phases in prolonged exercise. During prolonged exercise at 60 % of peak oxygen uptake (V o2) for 60 min and at rest, oxygenated hemoglobin/myoglobin (Hb/MbO2) and total Hb/Mb (THb/Mb) were determined by near-infrared spectroscopy in the vastus lateralis. Power spectra density (PSD) for the difference between Hb/MbO2 and THb/Mb (−HHb/MbO2: deoxygenation) was obtained by fast Fourier transform at rest, in the early phase (1-6 min) and in the late phase (55-60 min) in exercise. Peak PSD in the early phase was significantly higher than that at rest. There were at least three peaks of PSD in exercise. The highest peak was a band around 0.01 Hz, the next peak was a band around 0.04 Hz, and the lowest peak was a band around 0.06 Hz. PSD in the early phase was not significantly different from that in the late phase in exercise. Heart rate (HR) showed a continuous significant increase from 3 min in exercise until the end of exercise. Skin blood flow (SBF) around the early phase was significantly lower than that around the late phase. It was concluded that oscillation of oxygenation in the muscle oxygen system in the early phase is not different from that in the late phase in prolonged exercise despite cardiovascular drift.

The purpose of the present study was to determine the effects of deception for exercise intensity on surface electromyogram (SEMG) activity and blood lactate concentration during intermittent cycling exercise (ICE) tests. Sixteen healthy male were randomly assigned to two groups who completed two ICE [three 4-min cycling at 80% peak power output (PPO) with 3-min passive recovery periods followed by exhaustive cycling] tests (ICE-1 and ICE-2). The experimental group (ICED) was deceived of the actual cycling intensity, while the control group (ICEC) was informed of the actual protocol in ICE-2. In ICE-1, both groups were informed of the actual protocol. In ICE-2, root mean square (RMS) calculated from SEMG during submaximal cycling was significantly higher in the ICEC than in the ICED and blood lactate concentration ([La-]) was significantly higher in the ICEC than in the ICED. In particular, the difference in RMS between the groups was also observed during the first 4-min cycling, in which there was no difference in [La-] between the groups. These results suggest that the CNS modulates skeletal muscle recruitment due to the prior deception for exercise intensity.

We investigated ventilation ((V) over dotE) control factors during recovery from light impulse-like exercise (100 watts) with a duration of 20 s. Blood ions and gases were measured at rest and during recovery. (V) over dotE, end tidal CO2 pressure (PETCO2) and respiratory exchange ratio (RER) were measured continuously during rest, exercise and recovery periods. Arterial CO2 pressure (PaCO2 (pre)) was estimated from PETCO2 and tidal volume (V-T). RER at 20 s of exercise and until 50 s during recovery was significantly lower than RER at rest. Despite no change in arterialized blood pH level, PaCO2 (pre) was significantly higher in the last 10 s of exercise and until 70 s during recovery than the resting value. (V) over dotE increased during exercise and then decreased during recovery; however, it was elevated and was significantly higher than the resting value until 155 s (p

To clarify the ventilatory kinetics during recovery after impulse-like exercise, subjects performed one impulse-like exercise test (one-impulse) and a five-times repeated impulse-like exercises test (five-impulse). Duration and intensity of the impulse-like exercise were 20 sec and 400 watts (80 rpm), respectively. Although blood pH during recovery (until 10 min) was significantly lower in the five-impulse test than in the one-impulse test, ventilation (.VE) in the two tests was similar except during the first 30 sec of recovery, in which it was higher in the five-impulse test. In one-impulse, blood CO2 pressure (PCO2) was significantly increased at 1 min during recovery and then returned to the pre-exercise level at 5 min during recovery. In the five-impulse test, PCO2 at 1 min during recovery was similar to the pre-exercise level, and then it decreased to a level lower than the pre-exercise level at 5 min during recovery. Accordingly, PCO2 during recovery (until 30 min) was significantly lower in the five-impulse than in one-impulse test..VE and pH during recovery showed a curvilinear relationship, and at the same pH, ventilation was higher in the one-impulse test. These results suggest that ventilatory kinetics during recovery after impulse-like exercise is attributed partly to pH, but the stimulatory effect of lower pH is diminished by the inhibitory effect of lower PCO2.

The purpose of this study was to examine whether ventilation kinetics are related to blood lactate level after 5 min in recovery after a sprint. Subjects performed two tests, one test consisting of one sprint with maximal effort and the other test consisting of five repeated sprints with time intervals of 6 min. The recovery period from the last sprint was 30 min. Oxygen uptake during recovery from one sprint was the same as that during recovery from five repeated sprints. Ventilation after 50 sec in recovery after one sprint was the same as that in recovery after five repeated sprints despite the significantly higher blood lactate levels during recovery from five repeated sprints than that from a single sprint. There was an exponential relationship between ventilation and blood lactate after 5 min in recovery. The curve shifted to the right in the case of five repeated sprints. End tidal CO[sub]2[/sub] pressure after one sprint was higher than that after five repeated sprints during recovery. From these results, it seems that ventilation control related to blood lactate level is modified by end tidal CO[sub]2[/sub] pressure.

In order to test our hypothesis that muscle condition has an effect on the cognition of self-motion and consequently on the ventilatory response during exercise, six healthy subjects performed a moderate incremental exercise test (IET) on a cycle ergometer under two conditions [resistance exercise condition (REC) and control condition (CC)]. In the REC, resistance exercise (30 incline leg presses) was conducted during two sessions scheduled at 48 and then 24 h prior to the IET. For the CC, the subjects were instructed to refrain from participating in strenuous exercise for a period of 2 days prior to the IET. In the IET, the workload was increased from 78 to 118 watts in steps of 8 watts every 3 min. Although the ventilatory response during the IET was significantly higher in the REC than in the CC, there were no significant differences in cognitive indexes (RPE and awareness of change in workload) between the two conditions. In addition, the magnitude of muscle soreness was significantly higher in the REC than in the CC. However, the level of soreness in the REC was very low, and there were no significant differences in blood lactate concentration and integrated EMG between the two conditions. These results suggest that a change in peripheral neural reflex is the primary cause of increased ventilatory response to moderate exercise after resistance exercise, although the role of a cognitive element cannot be absolutely excluded.

The purpose of this study was to determine the relationship between oxygen uptake (VO2) kinetics and oxygen supply system during constant-load exercise in the supine position. The main exercises which were carried in supine position were moderate at an intensity corresponding to 80% of ventilatory threshold (VT) and heavy at an intensity corresponding to 20% of the difference between VT and peak VO2. Oxygenation level was obtained from inactive muscle by near-infrared spectroscopy (NIRS). This index is used to express the distribution of oxygen supply to inactive muscle during exercise [19]. After an exponential rise in VO2 (primary component), VO2 during moderate exercise reached a steady state, while during heavy exercise it continued to increase gradually (slow component). The HR kinetics which reflected systemic O2 supply in the supine position was similar to that of VO2 in main exercise tests. However, time constants of primary and slow components in VO2 were not significantly related to those in HR in each exercise mode. Furthermore, oxygenation level decreased after about 0.5 min from the onset of exercise and showed a minimum value at about 2 min and then recovered to the initial level during moderate and heavy exercises. Since there were no significant correlation coefficients in the time constant between VO2 and HR in each component in each exercise mode and since O2 supply to active muscle is affected by systemic O2 supply and distribution of O2 supply to inactive muscle, it is unlikely that VO2 is related to O2 supply to active muscle in supine position.

The aim of this study was to determine whether the increase in blood volume in resting muscle during moderately prolonged exercise is related to heart rate (HR) upward drift. Eight healthy men completed both arm-cranking moderately prolonged exercise (APE) and leg-pedaling moderately prolonged exercise (LPE) for 30 min. Exercise intensity was 120 bpm of HR that was determined by ramp incremental exercise. During both APE and LPE, HR significantly increased from 3 to 30 min (from 108±9.3 to 119±12 bpm and from 112±8.9 to 122±11 bpm, respectively). However, there was no significant difference between HR in APE and that in LPE. Oxygen uptake was maintained throughout the two exercises. Skin blood flow, deep temperature, and total Hb (blood volume) in resting muscle continuously increased for 30 min of exercise during both APE and LPE. During both APE and LPE, there was a significant positive correlation between total Hb and deep temperature in all subjects. Moreover, there was a significant positive correlation between HR and total Hb (in seven out of eight subjects) during LPE. However, during APE, there was no positive correlation between HR and total Hb (r=0.391). These findings suggest that an increase of blood pooling in resting muscle could be proposed as one of the mechanisms underlying HR upward drift during moderately prolonged exercise.

Objectives To determine the effects of resistive load on performance and surface electromyogram (SEMG) activity during repeated cycling sprints (RCS) on a non-isokinetic cycle ergometer. Methods Participants performed two RCS tests (ten 10-second cycling sprints) interspersed with both 30- and 360-second recovery periods under light (RCS L ) and heavy load conditions (RCS H ) in a random counterbalanced order. Recovery periods of 360 seconds were set before the fifth and ninth sprints. Results In the 9th and 10th sprints, the values of peak power output divided by body mass were significantly higher in RCS H than in RCS L . Changes in blood lactate concentration were not different between the two conditions. In RCS L , the root mean square calculated from the SEMG was significantly lower in the ninth sprint than in the first sprint, but there were no differences between the root mean square in the first sprint and that in the ninth sprint in RCS H . Conclusions During RCS on a non-isokinetic cycle ergometer, performance and SEMG activity are influenced by resistive load. It is thought that regulation of skeletal muscle recruitment by the central nervous system is associated with fatigue during RCS with a light resistive load.

The purpose of the present study was to examine the effect of change in blood volume in skin plus active muscle on heart rate drift during moderate exercise and heavy exercise for 30 min. Total hemoglobin concentration (Total Hb) in the vastus lateralis muscle plus its skin was determined by near-infrared spectroscopy. Total Hb significantly increased and remained stable from 20 min in moderate exercise and from 10 min in heavy exercise. Heart rate (HR) rapidly increased until 3 min and showed a steady state in moderate exercise. HR at 30 min was significantly higher than that at 3 min in moderate exercise. HR rapidly increased until 3 min and then gradually but significantly increased in heavy exercise. Increase in total Hb was not significantly related with HR after 3 min of exercise when HR was around 120 beats per min in moderate exercise. Increase in total Hb was significantly related with HR from 3 min to 10 min in the heavy exercise (correlation coefficients ranged from 0.959 to 0.702). It is concluded that an increase in the blood volume in skin plus active muscle is not simply associated with HR drift.

The purpose of this study was to determine the effect of oral administration of sodium bicarbonate (NaHCO3) on surface electromyogram (SEMG) activity from the vastus lateralis (VL) during repeated cycling sprints (RCS). Subjects performed two RCS tests (ten 10-s sprints) interspersed with both 30-s and 360-s recovery periods 1 h after oral administration of either NaHCO3 (RCSAlk) or CaCO3 (RCSPla) in a random counterbalanced order. Recovery periods of 360 s were set before the 5th and 9th sprints. The rate of decrease in plasma HCO3- concentration during RCS was significantly greater in RCSAlk than in RCSPla, but the rates of decline in blood pH during the two RCS tests were similar. There was no difference between change in plasma lactate concentration in RCSAlk and that in RCSPla. Performance during RCSAlk was similar to that during RCSPla. There were no differences in oxygen uptake immediately before each cycling sprint (preVO2) and in SEMG activity between RCSAlk and RCSPla. In conclusion, oral administration of NaHCO3 did not affect SEMG activity from the VL. This suggests that the muscle recruitment strategy during RCS is not determined by only intramuscular pH.

The purpose of the present study was to examine whether the level of oxygen uptake (V(.)(O2) at the onset of decrement-load exercise (DLE) is lower than that at the onset of constant-load exercise (CLE), since power output, which is the target of V(.)(O2) response, is decreased in DLE. CLE and DLE were performed under the conditions of moderate and heavy exercise intensities. Before and after these main exercises, previous exercise and post exercise were performed at 20 watts. DEL was started at the same power output as that for CLE and power output was decreased at a rate of 15 watts per min. V(.)(O2) in moderate CLE increased at a fast rate and showed a steady state, while V(.)(O2) in moderate DLE increased and decreased linearly. V(.)(O2) at the increasing phase in DLE was at the same level as that in moderate CLE. V(.)(O2) immediately after moderate DLE was higher than that in the previous exercise by 98+/-77.5 ml/min. V(.)(O2) in heavy CLE increased rapidly at first and then slowly increased, while V(.)(O2) in heavy DLE increased rapidly, showing a temporal convexity change, and decreased linearly. V(.)(O2) at the increasing phase of heavy DLE was the same level as that in heavy CLE. V(.)(O2) immediately after heavy DLE was significantly higher than that in the previous exercise by 156+/-131.8 ml/min. Thus, despite the different modes of exercise, V(.)(O2) at the increasing phase in DLE was at the same level as that in CLE due to the effect of the oxygen debt expressed by the higher level of V(.)(O2) at the end of DLE than that in the previous exercise.

The aim of this study was to determine whether excessive oxygen uptake (Vo2) occurs not only during exercise but also during recovery after heavy exercise. After previous exercise at zero watts for 4 min, the main exercise was performed for 10 min. Then recovery exercise at zero watts was performed for 10 min. The main exercises were moderate and heavy exercises at exercise intensities of 40 % and 70 % of peak Vo2, respectively. Vo2 kinetics above zero watts was obtained by subtracting Vo2 at zero watts of previous exercise (DeltaVo2). Delta Vo2 in moderate exercise was multiplied by the ratio of power output performed in moderate and heavy exercises so as to estimate the Delta Vo2 applicable to heavy exercise. The difference between Delta Vo2 in heavy exercise and Delta Vo2 estimated from the value of moderate exercise was obtained. The obtained Vo2 was defined as excessive Vo2. The time constant of excessive Vo2 during exercise (1.88+/-0.70 min) was significantly shorter than that during recovery (9.61+/-6.92 min). Thus, there was excessive Vo2 during recovery from heavy exercise, suggesting that O2/ATP ratio becomes high after a time delay in heavy exercise and the high ratio continues until recovery.

It was hypothesized that an oscillation of tissue oxygen index (TOI) determined by near-infrared spectroscopy during recovery from exercise occurs due to feedback control of adenosine triphosphate and that frequency of the oscillation is affected by blood pH. In order to examine these hypotheses, we aimed 1) to determine whether there is an oscillation of TOI during recovery from exercise and 2) to determine the effect of blood pH on frequency of the oscillation of TOI. Three exercises were performed with exercise intensities of 30 % and 70 % peak oxygen uptake (V(.)o(2)peak) for 12 min and with exercise intensity of 70 % V(.)o(2)peak for 30 s. TOI during recovery from the exercise was analyzed by fast Fourier transform in order to obtain power spectra density (PSD). There was a significant difference in the frequency at which maximal PSD of TOI appeared (Fmax) between the exercises with 70 % V(.)o(2)peak for 12 min (0.0039+/-0 Hz) and for 30 s (0.0061+/-0.0028 Hz). However, there was no significant difference in Fmax between the exercises with 30 % (0.0043+/-0.0013 Hz) and with 70 % V(.)o(2)peak for 12 min despite differences in blood pH and blood lactate from the warmed fingertips. It is concluded that there was an oscillation in TOI during recovery from the three exercises. It was not clearly shown that there was an effect of blood pH on Fmax.

The purpose of the present study was to examine 1) whether O(2) uptake (VO(2)) oscillates during light exercise and 2) whether the oscillation is enhanced after impulse exercise. After resting for 1 min on a bicycle seat, subjects performed 5-min pre-exercise with 25 watts work load, 10-s impulse exercise with 200 watts work load and 15-min post exercise with 25 watts work load at 80 rpm. VO(2) during pre-exercise significantly increased during impulse exercise and suddenly decreased and re-increased until 23 s after impulse exercise. In the cross correlation between heart rate (HR) and VO(2) after impulse exercise, VO(2) strongly correlated to HR with a time delay of -4 s. Peak of power spectral density (PSD) in HR appeared at 0.0039 Hz and peak of PSD in VO(2) appeared at 0.019 Hz. The peak of the cross power spectrum between VO(2) and HR appeared at 0.0078 Hz. The results suggested that there is an oscillation in O(2) uptake during light exercise that is associated with the oscillation in O(2) consumption in active muscle. The oscillation is enhanced not only by change in O(2) consumption but also by O(2) content transported from active muscle to the lungs.

In this study, a physiological model to explain the pathway of CO2 output during incremental exercise was examined by referring to experimental data. Since CO2 output (VCO2) shows multiple correlations with mixed venous CO2 pressure (PvCO2) and arterial CO2 pressure (PaCO2), the increase in the difference between PvCO2 and PaCO2 was considered to be involved in the increase in VCO2. In order to better understand the influence of CO2 pressure, VCO2 was divided into the expiratory CO2 phase (non-lactic VCO2), which was unrelated to lactic acid increase and the expiratory CO2 phase (excess VCO2), which was related to lactic acid increase. As a result, the non-lactic VCO2 significantly correlated to PvCO2. When non-lactic VCO2 was zero, the value of PvCO2 was 43.7 mmHg. This was higher than the resting PaCO2 value. On the other hand, as PaCO2 showed an almost constant value in the low load phase and showed a low value in the high load phase, it was believed that the low value of PaCO2 was related to the excess VCO2 that appeared in the high load phase. The CO2 excess, which was obtained by adding excess VCO2 in terms of the lapse of exercise time, correlated significantly with an increase in lactate in the blood. Based on the results, a model was constructed to illustrate the pathway of CO2 output. The key points of the model were as follows: (1) the use of the blood CO2 dissociation curve as the vector to transport CO2 from tissue to lungs, (2) the standard value of PaCO2 was established in order to divide non-lactic VCO2 and excess VCO2, (3) the dextroversion of the blood CO2 dissociation curve due to lactic acid was connected to excess VCO2, and (4) a decrease in PaCO2 was related to excess VCO2 derived from tissue.

The purpose of the present study was to examine the kinetics of mixed venous CO_2 pressure (Pvco_2) in incremental-load exercise. Pvco_2 seemed to indicate a linear increase after a somewhat slow increase. CO_2 Store phase appearing in expiration of CO_2 (stored CO_2) was calculated from the data of 0_2 uptake (VO_2), CO_2 output (Pvco_2) and work rate. The stored CO_2 indicated a linear increase after a time delay. The stored CO_2 also significantly related to Pvco_2. When kinetics of Pvco_2 at light exercise intensity was supposed from stored CO_2, Pvco_2 seemed to indicate a linear increase with a time delay. Excessive expired CO_2 (excess CO_2) was calculated from the data of VO_2 and work rate. The excess CO_2 significantly related to the increase of blood lactate. The blood lactate seemed to start to increase at around 1080 kpm/min. In spite of this change, a linear increase of Pvco_2 was unchanged. This result was considered to be related to the excessive CO_2 expiration corresponding to the increase of blood lactate. Thus, within the present results and assumptions, it seemed that Pvco_2 indicated a linear increase with a time delay without the effect of lactate increase in incremental-load exercise.

The purpose of the present study was to examine how end tidal CO(2) pressure (PETCO(2)) is controlled in impulse exercise. After pre-exercise at 25 watts for 5 min, impulse exercise for 10 sec with 200 watts followed by post exercise at 25 watts was performed. Ventilation (VE) significantly increased until the end of impulse exercise and significantly re-increased after a sudden decrease. Heart rate (HR) significantly increased until the end of impulse exercise and then decreased to the pre-exercise level. PETCO(2) remained constant during impulse exercise. PETCO(2) significantly increased momentarily after impulse exercise and then significantly decreased to the pre-exercise level. PETCO(2) showed oscillation. The average peak frequency of power spectral density in PETCO(2) appeared at 0.0078 Hz. Cross correlations were obtained after impulse exercise. The peak cross correlations between VE and PETCO(2), HR and PETCO(2), and VE and HR were 0.834 with a time delay of -7 sec, 0.813 with a time delay of 7 sec and 0.701 with a time delay of -15 sec, respectively. We demonstrated that PETCO(2) homeodynamics was interactively maintained by PETCO(2) itself, CO(2) transportation (product of cardiac output and mixed venous CO(2) content) into the lungs by heart pumping and CO(2) elimination by ventilation, and it oscillates as a result of their interactions.

The purpose of the present study was to examine the effects of muscle glycogen reduction on surface electromyogram (EMG) activity and effort sense and ventilatory responses to intense exercise (IE). Eight subjects performed an IE test in which IE [100–105% of peak O2 uptake (\( \dot{V}{\text{O}}_{{2{\text{peak}}}} \)), 2 min] was repeated three times (IE1st, IE2nd and IE3rd) at 100–120-min intervals. Each interval consisted of 20-min passive recovery, 40-min submaximal exercise at ventilatory threshold intensity (51.5 ± 2.7% of \( \dot{V}{\text{O}}_{{2{\text{peak}}}} \)), and a further resting recovery for 40–60 min. Blood pH during IE and subsequent 20-min recovery was significantly higher in the IE3rd than in the IE1st (P < 0.05). Effort sense of legs during IE was significantly higher in the IE3rd than in the IE1st and IE2nd. Integrated EMG (IEMG) measured in the vastus lateralis during IE was significantly lower in the IE3rd than in the IE1st. In contrast, mean power frequency of the EMG was significantly higher in the IE2nd and the IE3rd than in the IE1st. Ventilation (\( \dot{V}{\text{E}} \)) in the IE3rd was significantly higher than that in the IE1st during IE and the first 60 s after the end of IE. These results suggest that ventilatory response to IE is independent of metabolic acidosis and at least partly associated with effort sense elicited by recruitment of type II fibers.

To determine whether post-exercise ventilation is related to decrease in blood pH and also whether post-exercise ventilation, associated or not with decreased blood pH, involves an increase in central motor command during exercise, we examined the effects of NaHCO3 ingestion on the ventilatory response (\( {\dot{\text{V}}} \)E), integrated electromyogram (iEMG) and effort sense of legs (ESL) during intense exercise (IE) and subsequent active recovery. Subjects performed two IE tests (105–110% of maximal work rate, 2 min) after ingestion of NaHCO3 or CaCO3. Subjects performed light load exercise (20 W) before and after IE for 6 min and 30 min, respectively. Although there was a significant difference in blood pH between the two conditions during and after IE, \( {\dot{\text{V}}} \)E, iEMG and ESL were similar. iEMG returned to the pre-IE level immediately after the end of IE, while ESL showed slow recovery. \( {\dot{\text{V}}} \)E decreased rapidly until about 50 s after the end of IE (fast phase) and then showed a slow recovery kinetics (slow phase). The ventilatory responses during the fast phase and during the slow phase were correlated with ESL at the end of IE and from 3 min after the end of IE, respectively. Moreover, there was no significant difference in the slopes and intercepts of regression lines between \( {\dot{\text{V}}} \)E and ESL under the two conditions in both phases. These results suggest that the ventilatory response after IE is associated with effort sense indirectly-elicited by central motor command, but the effort sense-mediated response is not affected by blood pH.

This study was designed to determine whether awareness of change in load alters ventilatory response during moderate exercise. Subjects performed two incremental exercise protocols on a cycle ergometer. The load was increased from 1.0 to 1.5 kp in steps of 0.1 kp every 3 min. Subjects were provided true information about the load in the control protocol and untrue information that the load would remain constant in the deception protocol. Slope of ventilation against CO2 output was significantly lower in the deception protocol than control protocol. Integrated EMG (iEMG) and ratings of perceived exertion (RPE) were similar between the two protocols, but awareness of change in load was significantly attenuated by the deception protocol. However, there was no temporal coincidence between awareness and actual change in load. These results suggest that ventilatory response during moderate exercise depends not so much on RPE but mainly on awareness or attention that is closely connected to information detection.

The purpose of the present study was to examine whether excessive CO2 output (VCO2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (DeltaLa) were 11.17+/-2.57 mM from rest to 5.5 min during first recovery and 2.07+/-1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (VCO2) was significantly higher than O2 uptake (VO2) during both recovery periods. This difference was defined as VCO2excess. VCO2excess was significantly higher during first recovery than during second recovery. VCO2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). DeltaLa was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETCO2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETCO2 during first recovery was significantly higher than that during second recovery. It is concluded that VCO2excess is not simply determined by ventilation during recovery from repeated cycle sprints.

To determine the relationship between hyperventilation and recovery of blood pH during recovery from a heavy exercise, short-term intense exercise (STIE) tests were performed after human subjects ingested 0.3 g · kg-1 body mass of either NaHCO3 (Alk) or CaCO3 (Pla). Ventilation (VE) - CO2 output (V.co2) slopes during recovery following STIE were significantly lower in Alk than in Pla, indicating that hyperventilation is attenuated under the alkalotic condition. However, this reduction of the slope was the result of unchanged VE and a small increase in V.co2. A significant correlation between VE and blood pH was found during recovery in both conditions. While there was no difference between the VE - pH slopes in the two conditions, VE at the same pH was higher in Alk than in Pla. Furthermore, the values of pH during recovery in both conditions increased toward the preexercise levels of each condition. Thus, although VE - V.co2 slope was decreased under the alkalotic condition, this could not be explained by the ventilatory depression attributed to increase in blood pH. We speculate that hyperventilation after the end of STIE is determined by the VE - pH relationship that was set before STIE or the intensity of the exercise performed.

The aim of this study was to determine whether a 350-s recovery period allows recovery of peak power output (PPO) to its initial value under the condition of a blood lactate (La) concentration higher than 10 mmol·L-1 during repeated cycling sprints (RCS). RCS (10×10-s cycling sprints) were performed under two conditions. Under one condition, the recovery period of RCS was fixed at 35 s (RCS35), and under the other condition, a 350-s recovery period was set before the 5th and 9th sets, and a 35-s recovery period was set before the other sets (RCScomb). In RCScomb, PPO in the 5th set recovered to that in the 1st set, but PPO in the 9th set did not. Under both conditions, blood La concentration progressively increased and reached approximately 14 mmol·L-1 at the end of the RCS. In RCScomb, VO2 immediately before the 5th set was not significantly different from that immediately before the 9th set. Mean power frequency (MPF) values estimated by a surface electromyogram from the vastus lateralis in the 5th and 9th sets were significantly higher in RCScomb than in RCS35. In conclusion, a 350-s recovery period does not allow recovery of PPO to its initial value under the condition of a blood La concentration of 14 mmol·L-1 during RCS.

平成18年度日本生理人類学会奨励賞受賞, The purpose of this study was to determine whether neuromuscular activation is affected by blood lactate concentration (La) and the level of oxygen uptake immediately before a cycling sprint (preVO2). The tests consisted of ten repeated cycling sprints for 10 sec with 35-sec (RCS35) and 350-sec recovery periods (RCS350). Peak power output (PPO) was not significantly changed despite an increase in La concentration up to 12 mmol/L in RCS350. Mean power frequency (MPF) of the power spectrum calculated from a surface electromyogram on the vastus lateralis showed a significantly higher level in RCS350. In RCS35, preVO2 level and La were higher than those in RCS350 in the initial stage of the RCS and in the last half of the RCS, respectively. Thus, neuromuscular activation during exercise with maximal effort is affected by blood lactate concentration and the level of oxygen uptake immediately before exercise, suggesting a cyclic system between muscle recruitment pattern and muscle metabolites.

The purpose of this study was to compare the kinetics of oxygen uptake (VO(2)) during arm cranking with the legs inactive or exercising. Each subject (n = 8) performed three exercise protocols: 6-min arm cranking at an intensity of 60% of peak oxygen uptake (VO(2peak), AC(60)) and 6-min combined arm cranking and leg cycling in which AC(60) was added to on-going leg cycling at an intensity of 20% or 40% of VO(2peak) (LC(20) and LC(40): AC(60)LC(20) and AC(60)LC(40), respectively). After the onset of arm cranking, VO(2) tended to increase until the end of arm cranking in all of the three exercise modes. The amplitudes of this increase in VO(2) were 0.98 (0.18), 0.93 (0.16) and 0.84 (0.12) l.min(-1) during AC(60), AC(60)LC(20) and AC(60)LC(40), respectively, and there were significant differences between values for each exercise. The data are presented as means and standard deviations. There were no significant differences in the effective VO(2) time constant, partial O(2) deficit, and the difference between the values of VO(2) measured at 3 and 6 min in the three exercise modes. The present results indicate that the amplitude of the increase in VO(2) is reduced during arm cranking with the legs exercising, that this reduction becomes greater with increases in the intensity of leg cycling, and that the rate of increase in VO(2) is not affected by the additional muscle mass of the legs exercising below moderate intensities. The decrease in the amplitude of increase in VO(2) might be caused by reduction in oxygen supply to the exercising arms due to large muscle mass and/or overlaps of activity of stabilizing muscles during combined arm and leg exercise.

This study was carried out to determine whether hemodynamics in inactive forearm muscle during ramp leg cycling is affected from the ventilatory threshold (VT) and respiratory compensation point (RCP), at which the rate of increase in ventilation (VE) against power output begins to increase abruptly. Change in hemodynamics was evaluated by change in oxygenation index (difference between concentrations of oxygenated hemoglobin and deoxygenated hemoglobin, HbD) measured using near-infrared spectrometry (NIRS). Each subject (n=9) performed 4-min constant-work-rate leg cycling and subsequent ramp leg cycling at an increasing rate of 10 watts.min(-1) in power output. The work rates at VT, RCP and peak oxygen uptake (VO(2 peak)) were 107 +/- 11, 172 +/- 21 and 206 +/- 20 watts, respectively. The rates of increase in VE between 10-watt leg cycling, VT, RCP and VO(2 peak) were 0.19 +/- 0.03, 0.44 +/- 0.07 and 1.32 +/- 0.47 l.min(-1).watts(-1), respectively. In one subject, HbD started to decrease during ramp exercise from the VT, and the rate of decrease increased at a high intensity of exercise. In eight subjects, although no decrease in HbD from the VT was observed, HbD showed a sudden drop at a high intensity of exercise. The work rate at which HbD began to decrease at a high intensity of exercise was 174 +/- 23 watts. This work rate was not significantly different from that at the RCP and was significantly correlated with that at the RCP (r=0.72, P0.05). The results suggest that the abrupt increase in VE from the RCP affects hemodynamics, resulting in a decrease in HbD in inactive forearm muscle.

The purpose of the present study was to examine the response of excess CO(2) output to short-term intensive exercise in sprinters (SPR) and long-distance runners (LDR). End-tidal CO(2) pressure (PETCO(2)) increased up to about 20 s postexercise and then returned to the resting level at about 2-3 min postexercise. Thereafter, PETCO(2) remained below the resting level. VCO(2) excess, defined as the difference between VCO(2) and VO(2) was integrated from the start of exercise until PETCO(2) returned to the resting level. This integrated VCO(2) excess was defined as the first phase of CO(2) excess (1st CO(2) excess). The subsequent integrated VCO(2) excess until 10 min postexercise was defined as the second phase of CO(2) excess (2nd CO(2) excess). The ratio of 1st CO(2) excess to the lactate rise from rest to the peak value was significantly lower in SPR than in LDR, whereas 2nd CO(2) excess was significantly greater in SPR than in LDR. The decrease in PETCO(2) at 10 min postexercise was significantly larger in SPR than in LDR. The 2nd CO(2) excess was closely related to the decrease in PETCO(2). The results in the second phase suggest that the difference in the response of excess CO(2) output is derived from the difference in the respiratory chemosensitivity to lactic acid rise.

In order to clarify the kinetics of excess CO2 output during and after intensive exercise, six male subjects were each instructed to perform 40-, 60- and 80-s cycle ergometer exercises (282 +/- 9 W, 90 rpm). Ventilation and gas exchange parameters were recorded breath-by-breath, and lactate concentration (La) was repeatedly measured with blood samples from a finger tip. The increase in La from the resting value to peak value and the duration of exercise showed a significant linear relationship (r = 0.91, p

Cerretelli et al. (1982) proposed a model to estimate pH changes due to lactate production in exercise. This model was modified in the present study so as to express the relationship between CO2 excess and lactate production. The modified model fitted to the data reported on endurance-trained men.

The purpose of this study was to investigate the differences in kinetics of CO2 output (VCO2) during incremental exercise in sprinters (S), middle (MD), and long distance runners (LD). In the steady state exercise, the VCO2 was linearly related to the O2 uptake (VO2). In the incremental exercise below anaerobic threshold (AT), the VCO2 was also linearly related to the VO2. The difference between the VCO2 estimates from the regression lines obtained in steady state and incremental exercise was added from the start of exercise up to a given time. The added values were defined as CO2 stores. The CO2 stores per body weight were significantly related to mixed venous CO2 pressure (PVCO2) determined by the CO2 rebreathing method. The slopes of the regression lines between PVCO2 and CO2 stores per body weight were not different among three groups. If VCO2 above AT is estimated from the VO2 using the regression line obtained in incremental exercise below AT, the estimated VCO2 is lower than the measured VCO2. The sum of the differences in VCO2 up to a given time was defined as CO2 excess. The CO2 excess per body weight was significantly related to delta LA (the difference between blood lactates at 5 min after exercise and at rest). The ratios of CO2 excess per body weight to delta LA were 3.30 +/- 1.49, 4.16 +/- 2.33, and 5.55 +/- 2.05 for sprinters, middle, and long distance runners, respectively. This ratio obtained in sprinters was significantly lower than that in long distance runners (p less than 0.01).

The purpose of the present study was to obtain the immediate CO2 storage capacity at the onset of exercise. The CO2 stores at the onset of the exercise were calculated from the difference between the respiratory gas exchange ratio (R) and the metabolic gas exchange ratio (RQ: R obtained at 5.5 min of exercise). The CO2 stores per body weight (CO2 stores/w) were linearly related to the CO2 pressure (P'vCO2) determined by the CO2 rebreathing method (r = 0.713, p less than 0.001), the slope being 0.330 ml/(mmHg X kg). The CO2 stores were then corrected for change in O2 stores with exercise, that defined as total CO2 stores. P'vCO2 was also corrected for the effect of lung-bag volume shrinkage and Haldane effect during CO2 rebreathing, that defined as true PvCO2. The total CO2 stores/w were also related linearly to the true PvCO2 (r = 0.725, p less than 0.001), the slope of the regression line defined as the immediate CO2 storage capacity being 0.650 ml/(mmHg X kg).

The purpose of this study was to elucidate the effect of lung-bag volume shrinkage on P'VCO2 estimated by the CO2 rebreathing method and to correct its effect in calculation of cardiac output. The P'VCO2 was extrapolated with the linear relationship between dPACO2/dt and PACO2 during rebreathing. The P'VCO2 was higher than real mixed PCO2 by 0.82 mmHg at rest, by 1.35 mmHg at 50W, 1.57 mmHg at 100W, and 3.06 mmHg at 150W considering the effect of lung-bag volume shrinkage detected by argon concentration. The cardiac output obtained by the CO2 rebreathing method with correction of above differences was in good agreement with that determined by the acetylene method (r = 0.930, p less than 0.001). When the cardiac output was plotted against O2 uptake, our results and the regression line were fairly close to the reported regression lines.

The differences between VO2 at the 5th min in steady state exercise and VO2 in incremental exercise were consecutively added from start of incremental exercise to a given time. These added values were defined as oxygen deficit. Anaerobic threshold was determined as the breakpoint of blood lactate during incremental exercise. The oxygen deficit at the anaerobic threshold in normoxia was almost identical to that in hypoxia.