Takuma Arimitsu

Effects of resistive load on performance and surface EMG activity during repeated cycling sprints on a non-isokinetic cycle ergometer

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 (RCSL) and heavy load conditions (RCSH) 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 RCSH than in RCSL. Changes in blood lactate concentration were not different between the two conditions. In RCSL, 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 RCSH. 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.

Oscillation of oxygenation in skeletal muscle at rest and in light exercise

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 for 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.

Effects of awareness of change in load on ventilatory response during moderate exercise

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 1.5kp in steps of 0.1kp every 3min. 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.

Effects of heat exposure in the absence of hyperthermia on power output during repeated cycling sprints

The aim of this study was to investigate the effects of heat exposure in the absence of hyperthermia on power output during repeated cycling sprints. Seven males performed four 10-s cycling sprints interspersed by 30 s of active recovery on a cycle ergometer in hot-dry and thermoneutral environments. Changes in rectal temperature were similar under the two ambient conditions. The mean 2-s power output over the 1st–4th sprints was significantly lower under the hot-dry condition than under the thermoneutral condition. The amplitude of the electromyogram was lower under the hot-dry condition than under the thermoneutral condition during the early phase (0–3 s) of each cycling sprint. No significant difference was observed for blood lactate concentration between the two ambient conditions. Power output at the onset of a cycling sprint during repeated cycling sprints is decreased due to heat exposure in the absence of hyperthermia.

Effects of humoral factors on ventilation kinetics during recovery after impulse-like exercise.

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.

Response of end tidal CO2 pressure to impulse 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.

Effect of arterial carbon dioxide on ventilation during recovery from impulse exercises of various intensities

To determine that whether arterial carbon dioxide (PaCO₂) affects ventilation (VE) during recovery from impulse-like exercises of various intensities, subjects performed four impulse-like tests with different workloads. Each test consisted of a 20-sec impulse-like exercise at 80 rpm and 60-min recovery. Blood samples were collected at rest and during recovery to measure blood ions and gases. VE was measured continuously during rest, exercise and recovery periods. A significant curvilinear relationship was observed between VE and pH during recovery from the 300- and 400-watt tests in all subjects. VE was elevated during recovery from the 100-watt test despite no change in any of the humoral factors. Arterialized carbon dioxide (PaCO₂) kinetics showed fluctuation, being increased at 1 min and decreased at 5 min during recovery, and this fluctuation was more enhanced with increase in exercise intensity. There was a significant relationship between VE and PaCO₂ during recovery from the 300- and 400-watt tests in all subjects. The results of the present study demonstrate that pH and neural factors drive VE during recovery from impulse-like exercise and that fluctuation in PaCO₂ controls VE as a feedback loop and this feedback function is more enhanced as the work intensity increases.

Oscillation in O2 uptake in impulse exercise.

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.

Effects of deception for intensity on surface electromyogram (SEMG) activity and blood lactate concentration during intermittent cycling followed by exhaustive cycling

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.

EFFECTS OF BLOOD LACTATE ON OXYGEN UPTAKE KINETICS DURING RECOVERY AFTER SPRINT IN HUMANS

The purpose of this study was to examine the effects of blood lactate level (La) on oxygen uptake ( · VO2) kinetics during recovery after short-term exercise with maximal effort (sprint). Three sprints were performed on a cycle ergometer with a load of 8% of body weight at maximal rotation rate. · VO2 kinetics and oxygen debt were determined after three sprint tests: one 10-s cycling sprint, five repeated 10-s cycling sprints with 6-min intervals and one 30-s cycling sprint. There was no significant difference between peak power outputs in the 10-s sprint and five sprints. There was no difference in · VO2 kinetics during recovery from one sprint and during recovery after five sprints. La peaked at 5 min. The peak value of La was significantly lower in one sprint (4.41 ± 0.9 mM) than in five sprints (7.01 ± 2.2 mM). Thus, despite a difference in La, there was no difference between · VO2 kinetics during recovery after one sprint and after five sprints. There was a significant difference in · VO2 between the five sprints and 30-s sprint from 70 s to 320 s during recovery, but there were no significant differences in La after 5 min of recovery. There were two phases in · VO2. They consisted of fast oxygen debt and slow oxygen debt. There were also no differences in slow and fast oxygen debts between the two 10-s sprints despite significant differences in blood lactate during recovery. Peak La in the five sprints was not significantly different from that in the 30-s sprint (8.68 ± 1.2 mM). However, slow oxygen debt was significantly greater in the 30-s sprint than in the five sprints. It is concluded that · VO2 kinetics during recovery are not affected by an increase in blood lactate.