Breathing patterns and subjective responses to small resistances were investigated in seven subjects during moderate exercise. Inspiratory resistances of 0.15 (Rl), 0.25 (R2) and 0.30 (R3) kPa·l^-1·s were tested against control of 0.06 kPa ·l^-1 s with no added resistance. Subjective responses to small inspiratory resistances were evaluated through whole experiments including periods before and after exercise, herein called SNS. Average SNS significantly increased above the R2 condition. Above the R2 condition, significant changes in the breathing compo-nents of volume, flow and timing were also observed during exercise. SNS grew as a power function of peak inspiratory pressure (P_lmax) measured during exercise within such small range of stimulation less than the R3 condition and individual differences in the relationship between SNS and P_lmax were observed. All subjects felt at least some discomfort below the resistance of R3 and two subjects felt it below around Rl condition. It was suggested that breathing pattern was selected to limit peak pressure at the R3 condition by further increasing inspirator-y work for a breath and this tendency was reinforced in load-sensitive subjects with longer inspiratory time and lower peak flow rate. We concluded that breathing patterns depend mainly on peak work, especially in load-sensitive individuals, which is likely to be one of the primary determinants of a worker's tolerance to respirators

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Departments of Physiology and Anesthesiology. School of Medicine. UCLA. U. S. A. Oxygen uptake (VO₂) kinetics are generally agreed to be first-order for moderate work rates with a time constant (γVO₂) that is thought to reflect the kinetics of intramuscular creatine phosphate depletion. However, when there is a concomitant lactic acidosis, VO₂ is appreciably longer, reflecting an additional, delayed and slowed component that leads to γVO₂s greater than the aerobic equivalent of that work rate and which therefore invalidates current techniques for VO₂ deficit estimation. This "excess" VO₂ is no more than ∼250-300 ml/min at work rates for which [lactate] and [H⁺]a can be stabilized. At higher work rates which demand sustained and progressive increases in [lactate] and [H⁺] a, however, VO₂ also continues to increase progressively, yielding excess VO₂S > 1 l/min at exhaustion. The trajectory of excess VO₂ therefore is to the maximum VO₂ : the resulting exercise limitation becomes progressively more pronounced the higher the work rate, which accounts for the hyperbolic character of the power-duration curve. Factors which speed VO₂ kinetics in this domain reduce the excess VO₂ mechanism and lead to improved exercise performance. We have demonstrated that, in addition to appropriately-designed training regimens, induction of a metabolic acidosis prior to exercise speeds VO₂ kinetics at high work rates, reducing the increase in both [lactate] and [H⁺] a and reducing the CO₂ Ioad to ventilation during the transient phase of the work. The optimum procedure for inducing these improved pulmonary gas-exchange kinetics, however, remains to be determined

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The VO₂ response to a step change in work rate resembles a first order exponential function. This suggests that a single site of the many which link ATP demand to VO₂ is limiting. The location of this site is controversial. Some authors suggest that O₂ delivery regulates the VO₂ response. Others have suggested that peripheral mechanisms within the active muscle regulate O₂ consumption. The evidence supporting each hypothesis is reviewed. It is concluded that O₂ delivery sets the initial parameters and peripheral mechanisms then regulate O₂ utilization within the bounds initially established by delivery mechanisms.

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The behavior of cardiac output (Q) during progressive incremental exercise tests was studied in young healthy men. Q approached a plateau and leveled off at almost the same work rate at which oxygen uptake (VO₂) attained its maxima, while heart rate (HR) still continued to rise. This suggests that the limiting factor for maximal aerobic capacity in healthy subjects is Q. The rate of increase in Q and HR accelerated from a work rate which is close to the ventilatory anaerobic threshold (AT). The prime cause of the progressive augmentation in cardiac activity is probably an accelerated release of plasma catecholamine and/or potassium. There is a possibility that these substances might also affect the AT.

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Sympathetic nerve activity leading to skin (SSA) and skeletal muscle (MSA) and heart rate were measured before and during two-minute static handgrip (SHG) in seven healthy volun-teers. Two different situations were set before commencement of the exercise ; one was that a preparation time of between 4 and 6 minutes was set prior to SHG while no information of starting time for exercise was given to the subjects (Cond. 1). Another was that after two minutes of control rest, countdown was started two minutes before SHG and then the handgrip was started (Cond. 2). Heart rate for 10-s before SHG in Cond. 2 increased significantly from the control value, while there was no significant change in Cond. l. The magnitude of heart rate response to SHG was the same in either condition. Although SSA for 10 seconds just before the exercise did not show any change from the control value in Cond. 1, it increased in Cond. 2. There was no difference in SSA response patterns during SHG in either condition. Before commencement of SHG, MSA was suppressed at 10·s before exercise from the control value in Cond. 2, but there was no significant change in Cond. l. After onset of contraction, MSA was suppressed in the brief initial period regardless of countdown, thereafter MSA increased time-dependently. The MSA response pattem to SHG was almost identical in both conditions. The increases in SSA and heart rate prior to the commencement of the exercise may be related to the anticipation of the exercise, while suppression of MSA may be, in part, related not only to the central effect but also may be due to involved reflex mechanisms from baroreceptors and cardiac mechanoreceptors

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We studied ³¹P-nuclear magnetic resonance spectroscopy (³¹P-MRS) for repeated non-invasive measurement of changes in the muscle metabolites, i.e., creatine phosphate (PCr) and inorganic phosphate (Pi), and changes in intramuscular pH, during repeated exercise and intervening rest periods. Six healthy male subjects performed 2 min of femoral flexion exercise at 20 kgm/min in a 2.1 Tesla superconducting magnet with a 67 cm bore. This exercise was repeated 4 times with 2-min rest periods between bouts. During this time ³¹P-MRS data was collected with 32 scans per spectrum, requiring 12.8 sec. During exercise, the PCr decreased to 30.3±7.0 % (mean±SD) of the pre-exercise level, and it did not completely recover during the rest period (79.0±1.3 % of the pre-exercise level). Thereafter, when the exercise was repeated, the lowest PCr value during exercise deceased gradually (2nd bout, 22.1±3.9 % ; 3rd bout, 16.7±3.2 %, and 4th bout 14.9±3.5 %). The Pi increased by 705-740 % during exercise and there were no significant differences in maximum Pi among the 4 bouts. During the rest period after the first bout, Pi fell to about 10 % below the pre-exercise level in four of the six subjects. With repeated exercise, this undershoot was less common. The Pi/PCr ratio during exercise increased linearly over time. Furthermore, the maximum Pi/PCr ratio during exercise increased significantly with repeated exercises. We conclude that as exercise is repeated PCr gradually decreases, but there is no cumulative increase in Pi. Thus, the Pi/PCr ratio, an indicator of free ADP, increased with repeated exercise.

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Effect of contraction force on blood flow during the contraction and relaxation phase of rhythmic handgrip exercise was studied on 6 healthy women. Velocity of blood flow in the brachial artery and the diameter of the artery were studied by Dopller-ultrasound method. Both the peak and mean velocity of the blood flow were significantly higher during the relaxation period than during contraction, and the velocity during the relaxation period was significantly higher in 30 % MVC exercise than in 10 % MVC exercise. However, no significant differences were found in the diameter of the artery between resting and exercise conditions, nor between exercises at different intensities. Thus blood flow during the relaxation phase was significantly increased from 135.7±18.2ml·min^-1 (10 % MVC to 182.5±19.6 ml·min^-1(30 % MVC by an increased contraction force, whereas blood flow during the contraction phase was hardly affected by increased contraction force.

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In order to examine the contribution of neuromuscular activity to the slow increase in VO₂ during heavy exercise, integrated electromyogram (iEMG) of dominant working muscle and VO₂, was compared in seven subjects during constant-load cycling exercise at the intensity of l0 % below and 30 % above ventilatory threshold (VT) for seven minutes. VO₂ and iEMG after 4th min in above VT test was significantly correlated (r=0.53, p<0.01) and t02/iEMG was constant after 4th min, indicating coupling of iEMG with VO₂. The results suggested that the slow increase in VO₂ during heavy exercise may result from the changes in the recruitment pattern of motorunits

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Recent evidence suggested that exercise-induced arterial O₂ desaturation may occur in highly trained endurance athletes. So, Dempsey brought the hypothesis that the pulmonary capacity for oxygen transport cannot meet superior demands imposed by cardiovascular system in highly trained endurance athletes, and endurance training primarily causes adapta-tion in the skeletal muscles and in the systemic cardiovascular system, with little change in the pulmonary system. In the present study, we determined the propriety of the hypothesis due to measure the ventilatory capacity of endurance athletes. Sixteen highly trained endurance athletes (ET) and thirteen untrained subjects (UT) volunteered to participate in these experi-ments. All subjects performed the four experiments, 1) the highest oxygen uptake (peak VO₂) during incremental cycle exercise and ventilation (V_E), ventilatory equivalent for O₂ (V_E/VO₂) and arterial O₂, saturation (SaO₂) at which peak VO₂ was observed, 2) the maximal voluntary ventilation for 30 sec at rest (MVV), 3) the pulmonary diffusing capacity for CO (DLCO) and expressed per unit of alveolar lung volume (KCO) at rest by the single breath inethod, and 4) the ventilatory response to hypercapnia (S) at rest by rebreathing method, were measured. The peak VO₂ of ET (66.7ml·min^-1·kg^-1) was significantly (30.8 %) higher than UT (52.4 ml·min^-1·kg^-1), and V_E/VO₂ and SaO₂ of ET (29.3 and 93.7 %, respectively) were significantly lower than UT (34.6 and 95.8 %). There were no differences in V_E, MVV, DLCO, and S between two groups. Although, KCO of ET (6.02 ml·min^-1·mmHg^-11^-1) was significantly higher than UT (5.45ml·min^-1·mmHg^-11^-1), the relative difference was only 10.5 %· Therefore, the arterial oxygen desaturation and less hyperventilation during maximal exercise were observed in ET, and the ventilatory capacity of ET may not be so much superior to that of untrained subjects. These findings supported the hypothesis of Dempsey.

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Swimming takes place in a medium, that presents different gravitational and resistive forces, respiratory conditions and thermal stress compared to air. The energy cost of propulsion in swimming is high, but a considerable reduction occurs at a given velocity as result of regular swim training. In medley swimmers the energy cost is lowest for front crawl, followed by backstroke, butterfly and breaststroke. Cardiac output is probably not limiting for performance since swimmers easily achieve higher values during running. Maximal heart rate, however, is lowered by approx. 10 beats/min during swimming compared to running. Most likely active muscle mass is smaller and rate of power production lesser in swimming. Local factors, such as peripheral circulation, capillary density, perfusion pressure and metabolic capacity of active muscles, are important determinants of the power production capacity and emphasize the role of swirn specific training movements. Improved swimming technique and efficiency are likely to explain much of the continuous progress in performance. Rational principles based on improved understanding of the biomechanics and physiology of swimming should be guidelines for swimmers and coaches in their efforts to explore the limits of human perf ormance.

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The validity of ratings of perceived exertion (RPE), proposed by Borg (1962), as an index of exercise intensity in swimming training was discussed based on the following four experi-ments. Experiment I : to, and heart rate (HR) were measured and RPE was asked in ten female and seven male physical education students with different levels of swimming skill performing submaximal and maximal work in tethered swimming. The increases in HR and RPE with increase in %Vo, ₂max were fitted well by straight lines with high correlation coefficients of r=0.957-0.999 and r=0.893-0.988, respectively. RPE was increased in a linear fashion with increase in HR except for a few subjects. The correlation coefficients for linear regression for individuals were 0.862-0.987. Experiment 11 : Swimming velocity and HR were measured in four groups with different levels of swimming skill. The breast stroke in a 50-m pool for 5 min at three RPE ratings, i. e., very light (RPE 9), somewhat hard (RPE 13) and very hard (RPE 17) was requested of these groups. In good skilled well trained college swimmers, %HRmax was fairly higher than the RPE at the RPE 9 and RPE 13 Ievels but coincided with the RPE at the RPE 17 Ievel. In skilled trained physical education -students, the HR increased with a corresponding increase in RPE. But in the group with low or lower levels of swimming skill, the HR kept about the same values in spite of the increase in RPE. Experiment 111 : Two male and six female low skilled physical education students took the swimming training in the swimming pool for 2.0-2.5 hours a day, 6 days a week, for 2 weeks. The students also received the swimming training in the sea which lasted for 2 hours each in the moming and in the afternoon for 6 days. The same RPE test, as mentioned in Experiment II, was done before, during and after swimming training. Mean swimming velocity during and after training was slightly higher than that before training at the RPE 9 and RPE 13 Ievels, and was much higher at the RPE 17 Ievel. Before training, the HR was fairly higher than the RPE at the RPE 9 and RPE 13 Ievels. But during and after training, the HR was much closer to the RPE at the RPE 9 and RPE 13 Ievels.

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The purpose of this study was to examine the limiting factor for swimming by measuring peak oxygen uptake (peak⁰²) during front crawl (C) and arm stroke (A) under a hypobaric hypoxic condition. Seven-trained swimmers (age ; 19-21 yrs, 100 m free style event ; 57.2±2.5 secs) were measured twice under a normal (N) (751 mmHg) and a hypobaric hypoxic (H) (602 mmHg) condition in a chamber where atmospheric pressure was regulated. Water flow rate started at 0.80m·sec^-1 and was increased by 0.05m·sec^-1 every 2 min up to 1.00m·sec^-1. Subsequently, flow rate was increased by 0.05 m·sec^-1 every minute until exhaustion. VO₂ was measured with an automatic analyzer. The peak heart rate under N was not significantly different from that under H in both C (N ; 190±9, H ; 184±6 beats·min^-1) and A (N ; 180±6, H ; 181±6 beats ·min^-1). PeakVO₂ values during A (N ; 3.42±0.27, H ; 3.08±0.19 1·min^-1) were significantly lower by 15-20 % than those during C (N ; 4.18±0.18, H ; 3.65±0.11 1·min^-1) for both N and H (p<0.01). PeakVO₂ Values under H were significantly lower than those under N during both C and A (p<0.01). There was no significant difference in the magnitude of decrease in peak VO₂ between C (12.0±3.4 %) and A (9.8±3.8 %) under H. This ratio of decrease agrees with previous investigations that studied centrally limited exercise, such as running and cycling, under similar levels of hypoxia. The results in this study suggest that the peakVO₂ during arm stroke, which is an upper body exercise, may be limited by central circulation rather than the extraction of O₂ in active muscles.

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The purpose of this research is to investigate the range of response to the treadmill running and swimming. Cardiovascular changes and substrates changes in blood were examined before and after healthy male subjects (swimming group (SG) has swimming habits and running group (RG) has practiced basketball or baseball or running more than four days a week) swam and ran for 10 to 15 minutes voluntarily. Average heart rate was recovered more quickly in case of running than swimming in the RG, but in the SG there was no difference. Diastolic blood pressure recovered to the rest condition faster in the SG than RG. In case that subjects have done familiar exercise, free fatty acids increased a little more after 10 minutes than in case of unfamiliar exercise. These results suggest that response of habitual exercise showed lesser change of diastolic blood pressure and more increase of free fatty acids. There might be a difference in physiological responses between usual sports and other kinds, so that we had to be careful when we apply different styles of activity to use training.

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The purpose of this investigation was to determine whether the critical velocity (CV) as the swimming speed which can be theoretically maintained for a very long time without exhaustion could be applied to estimate the swimmer's endurance performance. CV was based on the concept of critical power originality established by Monod and Scherrer (1965) and extended by Moritani et al. (1981), and expressed as the slope of a regression line between swimming distance (D) at each velocity and its sustained time (T). Seventeen highly trained swimmers were instructed to swim the four different swimming distances (50 m, 100 m, 200 m and 400 m) at maximal effort using the swimming pool. In the results of CV, the regression relations between D and T were expressed in the general form, D=a+bxT, with r² showing higher than 0.997 (p<0.001). These results indicate extremely good lineality. Furthermore, VO_2max during incremental exercise test, swimming speed corre-sponding 4 mM of blood lactate concentration (V-OBLA) and mean velocity in the 200 m and 400 m freestyle (V-200 and V-400) were measured on nine subjects. Significant correlations were found between CV and V-OBLA (r = 0.862, p < 0.01), CV and V-200 (r = 0.781, p < 0.01), CV and V-400 (r = 0.999, p < 0.001), V-OBLA and V-400 (r = 0.869, p < 0.01) and V-200 and V-400 (r = 0.776, p < 0.01). These data suggest that CV can be determined by performing several maximal effort swimming (50m, 100m, 200m and 400m events) and a stopwatch only, and CV can be adopted as an index for assessing the physical performance without blood sampling and employing highly expensive equipments

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The maximal average power output (W_max) and capacity (W_cap) of the short-term (anaerobic) energy processes are examined in cyclists and young adults with respect to body size and muscularity. The results show that when W_max and W_cap are standardized for muscle size the power and capacity of the anaerobic mechanisms are similar between trained sprint and pursuit cyclists and untrained young healthy adults. Thus the efficiency of anaerobiosis appears to a function of muscularity in man over the range of subjects studies. From the data it is estimated that the probable efficiency of supra maximal cycling is of the same order (0.22) as found for steady state submaximal (aerobic) exercise.

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Previous studies have shown that a decrease in muscle tension is not proportional to decrease in the ATP concentration and free energy for ATP degradation but is proportional to the decrease in ATP consumption during muscle contraction, and that the free ADP concentration in the cell can be estimated using the Pi/PCr ratio obtained by ³¹P NMR. From this view, we discuss findings on muscle energetics during exercise that have been clarified by ³¹P NMR and its future problems.

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Blood lactate level begins to increase at a certain work load or oxygen consumption which is called as anaerobic threshold (AT). However, numerous studies showed that anaerobic glycolysis is not the cause of the enhanced accumulation of blood lactate during exercise. Increased lactate production is seen even in fully aerobic muscles. Some studies suggest that elevation of lactate is due to a temporary imbalance between the rates of pyruvate formation by aerobic glycolysis and pyruvate utilization in the Krebs cycle. These results clearly suggest

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To investigate the role of the peripheral effector for the generation of heart rate variability, the relationship among the P-P, R-R. P-R, and R-P intervals were compared on five healthy male subject in the supine position. During supine rest, electrocardiogram was monitored, and P-P, R-R, P-R, and R-P intervals were measured. Power spectral densities (PSD) were esti-mated by using direct method for successive 256 intervals. PSDS were integrated at the low (PSD_LF ; 0.05-0.15 cycle/beat) and high (PSD_HF ; 0.20-0.40 cycle/beat) frequency bands. Mean interval times of P-P, R-R. R-P, and P-R intervals were 827±40, 827±40, 657±34, 170±19 msec, respectively. PSD_LFS of P-P, R-R, R-P, and P-R intervals were 15677±2771, 15566±2815, 15345±2767, 1491±255 msec²/c/b, respectively. PSD_HFS of P-P, R-R, R-P, and P-R intervals were 13289±3602, 12918±3897, 12558±3630, 2758±517 msec²/c/b, respectively. The PSD of P-R intervals showed white noise. These results might suggest that the periodic fluctuation would be formed at or above the sinoatrial node.

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The purpose of this study was to investigate the recovery kinetics of cardiac autonomic regulation after acute exercises related to exercise intensity. Firstly, eight healthy subjects performed two kinds of constant load exercises at the work rate corresponding to 20 % and 100 % of the individual ventilatory threshold (VT) in addition to the exhaustive incremental exercise using a cycle ergometer. Blood pressure (BP) and oxygen uptake (VO₂) were measured during 9 to 10 min after the exercises as well as the beat-by-beat recording of R-R intervals. Coarse graining spectral analysis (CGSA) was applied to heart rate variability (HRV) data sets of 5 min before exercise, Iast 5 min during exercise, and 8 to 10 min after exercise. The low frequency (O - 0.15 Hz ; LO) and the high frequency (0.15-0.5 Hz : HI) areas under power spectra were calculated for evaluating sympathetic (LO/HI) and vagal (HI) activities. The recovery for 10 min was sufficient to settle both VO₂ and BP even after the exhaustion. Comparing to the pre-exercise value, however, HI was still suppres-sed until 10 min after the 100 % VT exercise (522±300 vs. 122±63 msec², p<0.05) while it was recovered at 10 min after the 20 % VT one (353±122 vs. 487±159 msec²). Secondly, six healthy subjects performed an incremental cycle exercise until exhaustion. The R-R intervals were monitored beat-by-beat during 30 min after exercise. The CGSA was applied to every five min data set of HRV during recovery phase. Comparing to pre-exercise value, the R-R interval was not recovered at 30 min after the exercise (827±44 vs. 597±17 msec). The HI value was still significantly lower (367±154 vs. 24±14 msec²) and the LO/HI was also higher (3.8±0.9 vs. 16.8±5.1, p<0.05) during 25 to 30 min after the exercise. These results suggest that the recovery of the cardiac autonomic regulation especially after a moderate to high intensity exercise was later than those of the peripheral circulation as well as the oxygen uptake.

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The purpose of this study was to investigate the effect of the activation of tissue oxidative capacity by dichloroacetate (DCA) administration or endurance training on oxidative removal of lactate, which is the major pathway of lactate metabolism, in mice during prolonged exercise and after supramaximal exercise. DCA administration significantly decreased the blood lactate concentration and activated the oxidative removal of lactate during prolonged exercise. DCA administration did not change lactate metabolism in mice after supramaximal exercise. Endurance training significantly decreased the blood lactate concentration during prolonged exercise and also activated the oxidative removal of lactate. Endurance training signiiicantly increased the recovery of the blood lactate concentration after supramaximal exercise, while it did not activate the oxidative removal of lactate. These results suggest that the activation of the tissue oxidative capacity decreases the blood lactate concentration and also can activate the oxidative removal of lactate during prolonged exercise, while it does not activate the oxidative removal of lactate after supramaximal exercise.

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This study has measured the pattern of elevated serum enzyme activity (ESEA) during extended daily training in a dose-response manner and compared ESEA to the pattern of accumulated fitness and fatigue predicted from a mathematical model previously described. Blood samples were taken regularly during the study from each subject and the activity of lactate dehydrogenase (LDH), creatine kinase (CK), and aspartate aminotransferase (AST) in the serum was measured. Although no single physiological/biochemical correlate of the hypothesized fatigue compart-ment of performance is firmly identified it is significant that the pattern of variation of model fatigue and ESEA throughout training were similar although slightly out of phase. With continued hard training, model fatigue began to plateau and concomitantly ESEA declined exponentially from its initial high value in early training. During relative rest throughout a tapering period following training both ESEA and fatigue reverted quickly towards baseline and follow the similar but earlier time course in blood of a degradative membrane enzyme phospholipase A2 observed in clinical studies.

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The purpose of this study was to determine the effect of strength training in prepubescent boys and girls on muscle strength and cross-sectional area of upper arm. Subjects were ninety-nine healthy elementary school children who belonged to 1st, 3rd and 5th grades and they were assigned to two groups of training (N = 52) and control (N = 47). Training group participated in strength training program for 12 weeks which consisted of maximum sustained isometric contraction of elbow flexion for ten sec, whereas control group did not participate in special training program in this period. In orger to determine the changes due to training, cross-sectional areas of the tissues in upper arm, such as muscle, fat and bone, were measured by the ultrasonic method. Maximum isometric and isokinetic muscle strength of elbow flexion and extension were measured by means of isokinetic cybex dynamometer. In order to assess the development of physiological maturity, TW2 method was used to estimate the skeletal age in each subject by taking the hand-wrist X-ray photograph. After 12-week training period, the whole cross-sectional areas increased in both training and control groups. This increment was due to significant increases in muscle and bone area in the training group and, on the other hand, due to the increase in fat area in the control. The increment of muscle area of training group was about 50 % of that derived from the study on adults (Fukunaga, T., 1978). The increment in cross-sectional area of muscle with training was significantly correlated with the skeletal age. Isometric strength of elbow extension showed significant increase and for 5th grade males this increase was about 40 % of that obtained from adults, whereas isokinetic strength unchanged with training. Muscle strength per cross-sectional area did not show a significnat increase except for the training group of 5th grade boys. In conclusion, the effects of strength training on cross-sectional muscle area and strength for prepubescent were similar in its direction but different in its magnitude from those found in adults.

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This presentation addressed the researches concerning the effects of the low intensity training on health promotion done in our laboratory. Supervised physical training performed at 50 % to, max or lactate threshold for 60 minutes, 3 or 5 times a week for 30 sessions could induce the improvement in to, max, Iipid profiles, and augment in cardio-pulmonary barore-flex. This training was also applied for patients in ischemic heart disease, hypertension, and obesity. These patients could improve their aerobic work capacity. Hypertensive patients could reduce their blood pressure in association with modulating in humoral factors without changes in body weight and diet. The obese patients succeeded in significant body reduction with mild food reduction. We also found the existence of break-point of double product (BPDP) during graded exercise test corresponding to lactate threshold. BPDP will be able to use for estimating lactate threshold. This low intensity training, which is easier and safer, can be recommended to the wide-variety of persons including older person to promote health.

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In this paper, previous studies regarding the effect of physical training on the disappearance rate of blood La during recovery after strenuous exercise have been briefly summarized. The results of our own recent study of this problem have also been added. It may be concluded that there is some evidence for an improved lactate metabolic clearance rate resulting from physical training in human subjects, when the degradation rate is estimated from serial blood samples taken during a standard ramp ergometer test to exhaustion during each week of a training/detraining sequence. This beneficial effect of training, however, may also be influen-ced by the initial physical status of the subject and the nature of the training program.

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