A study was conducted to examine the recovery of vagal activity after strenuous exercise based on changes in the magnitude of respiratory cardiac cycle variability, changes in the phase of this variability and the mechanism of the change. Six healthy male university students were studied for 5 h after exhaustive treadmill running. For cardiac cycle (RR) and blood pressure, the magnitude of respiratory variability and phase difference between respira-tory variability and respiration were measured. Respiratory period and tidal volume were maintained at 6 s and 21, respectively.
1. The amplitude of respiratory RR variability decreased markedly after exercise and returned almost to normal after 2 h of recrvery. The phase of RR delayed with exercise, proceeded rapidly 2 h after exercise and progressively after that.
2. The amplitude and phase of respiratory systolic blood pressure variability were almost stable before and after exercise.
Based on these results, we conclude that vagal activity inhibited by strenuous exercise recovers about 2 h after the end of exercise. The delay in the phase of respiratory cardiac cycle variability with exercise may reflect inhibition of vagal activity.

To investigate the responses of heart rate and plasma catecholamines to exercise at various intensities, seven healthy adult males performed 6-min bouts of cycling exercise at 30, 50, 70 and 90% of maximal oxygen consumption (VO₂max) . Heart rate (HR), plasma noradrenaline (NA), plasma adrenaline (A), blood lactate (La) and coefficient of variation of R-R intervals (CVRR) were determined i n each case.
The following results were obtained:
1) CVRR showed a sharp decline to the extent of 50%VO₂max, then fell more slightly for heavier exercise.
2) NA and A significantly increased from resting value at 50%VO₂max, and followed by further increase with exercise intensity. NA/A increasd in proportion to exercise intensity.
3) The results of multiple regression analysis of HR (dependent variable) and NA, A and CVRR (independent variables) indicated the greatest standardized partial regression coefficient for CVRR in the case of low intensity exercise, and for NA with high intensity exercise.
4) La increased abruptly at 70%VO₂max, whereas NA and A rose drastically at 90%VO₂max.
The conclusion based on these results is as follows: HR is mainly influenced by change in parasympathetic tone to the extent of 50%VO₂max, whereas sympathetic and adrenomedullary activity are the main factors controlling HR in heavier exercise. Within the submaximal level of exercise, sympathetic activity increases more markedly than that of adrenomedullary activity. Abrupt increase in La may be independent of catecholamines.

This study was designed to evaluate the effect of exercise duration on the relation between sympathetic and adrenomedullary activities. Six trained subjects completed the following two exercise protocols ; six 2-min exercise sessions at 100% maximal O₂uptake (VO₂max) interspersed with 10-min recovery periods, and three 10-min exercise sessions at 80%VO₂max interspersed with 10-min recovery periods. Plasma noradrenaline (NA), plasma adrenaline (A), NA/A ratio (NA/A), heart rate (HR), coefficient of variation of R-R intervals (CVRR) and blood lactate (La) were measured. With repetition of exercise sessions in both protocols, HR, NA and A gradually increased. CVRR rapidly decreased at the first exercise session and remained unchanged thereafter. NA/A increased by the first exercise session, but decreased by the following exercise sessions. NA in the second exercise session at 100%VO₂max was significantly lower than that in the first. We conclude that, at the beginning of exercise, the increase of sympathetic activity is more dominant than that of adrenomedullary activity, whereas, with prolongation of exercise duration, the increase of adrenomedullary activity becomes more dominant than that of sympathetic activity,

Using near-infrared spectroscopy, we monitored changes of oxygenated hemoglobin and myoglobin contents [oxy (Hb+Mb) ], deoxygenated hemoglobin and myoglobin contents [deoxy (Hb+Mb) ], and total hemoglobin and myoglobin contents [total (Hb+Mb) ] of the thigh muscle at rest and during incremental bicycle exercise and recovery in 10 healthy male volnuteers. Gas exchange parameters were also measured in breath-by-breath mode.
The following results were obtained :
1) During low-intensity exercise (216 kpm/min), oxy (Hb+Mb) increased, while deoxy (Hb+Mb) and total (Hb+Mb) decreased. These changes are thought to reflect an increase in arterial blood flow to the exercising muscle and an increase in venous return.
2) During high-intensity exercise (above 972 kpm/min), oxy (Hb+Mb) decreased, while deoxy (Hb+Mb) increased. These findings probably reflect increased O₂extraction.
3) Upon cessation of exercise, oxy (Hb+Mb) and total (Hb+Mb) increased, and deoxy (Hb+Mb) decreased abruptly. These changes probably reflect post-exercise hyperemia with decreased O₂extraction.
4) Oxy (Hb+Mb) level at ventilatory threshold (VT) was the same as or higher than that of resting condition, indicating that VT occurs when the level of O₂in the vessels of the thigh muscle is relatively high.
5) Spontaneous fluctuation of oxy (Hb+Mb) with frequency of 7-10 cycles/min was observed. This fluctuation was more marked during exercise than during rest or recovery.
These findings suggest that the influence of increased blood flow and venous return on oxy (Hb+Mb), deoxy (Hb+Mb) and total (Hb+Mb) are greater than that of O₂extraction during low intensity exercise, whereas the influence of O₂extraction increases with exercise intensity.
Near-infrared spectroscopy provides valuable information with regard to O₂transport and O₂extraction in the exercising muscle.

This study was undertaken to clarify the relationship between respiratory period and respiratory arrhythmia. Five healthy male university students voluntarily changed the respiratory period over a range of 3-30 seconds while maintaining tidal volume constant (; 21) . Maximum and minimum cardiac cycles (RRmax and RRmin) and amplitude of cardiac cycle variability (ΔRR), the difference between RRmax and RRmin, were measured from electrocardiogram and respiratory curve.
1. Amplitude of cardiac cycle variability was small for shorter respiratory periods and increased with respiratory period, attaining maximum at respiratory periods of 8-14 seconds followed by decrease at longer respiratory periods.
2. The time from the onset of inspiration to the minimum cardiac cycle was the same for respiratory periods of 8-14 seconds (about 3.6 seconds) .
3. Phase difference between cardiac cycle variability and respiration was determined at each respiratory period. When the minimum or maximum cardiac cycle coincided with the onset of inspiration, this situation being defined as 0°, RRmin was delayed by 180°, 90°, and 0° at respiratory periods of 2.3, 14.4, and 26.5 seconds, respectively and by 360°, 270°, and 180° at respiratory periods of 2.7, 15.0, and 27.3 seconds, respectively.
Based on these results, respiratory arrhythmia is concluded to be quite stable at respiratory periods of 8-14 seconds. At short respiratory periods, tachycardia was found to occur during inspiration and bradycardia during expiration. During long respiratory periods, bradycardia was noted during inspiration and tachycardia during expiration.