Central arterial distensibility decreases with age-related changes in the arterial wall, and as a result, systolic blood pressure and/or pulse pressure (difference of systolic pressure and diastolic pressure) may increase in the elderly. Systolic hypertension and increased pulse pressure are known to be independent risk factors of cardiovascular and cerebrovascular diseases. Decreased distensibility of the central arteries may also cause the deterioration of circulatory function and physical ability in the elderly. Several studies have shown that central arterial distensibility is increased in athletes, and that daily physical activity is positively related to central arterial distensi bility in not only young but also elderly people. It has also been shown that relatively short-term and low-intensity exercise training could improve central arterial distensibility even in the elderly. Thus, physical exercise may have an effect on retarding age-related changes of the central arteries. To establish higher quality of life by preventing cardiovascular and cerebrovascular diseases and by improving circulatory function and physical ability in the elderly, further studies are needed to investigate the detailed mechanism and the appropriate amount and or intensity of exercise in improving central arterial distensibility.

We have been proceeding with studies on the effects of water immersion on autonomic nerve activity using the power spectral analysis of heart rate variability. The results obtained so far suggest that cardiac parasympathetic nerve activity is enhanced and sympathetic nerve activity is suppressed during immersion at temperatures between 25°C and 34°C and that parasympathetic nerve activity is suppressed and sympathetic nerve activity is enhanced during immersion at temperatures around 38°C. However, water immersion affects the respiration rate and tidal volume, and though the change in the respiration rate does not affect the real cardiac autonomic nerve activity, it affects the index of autonomic nerve activity as assessed by the power spectral analysis of heart rate variability. Therefore, this study examined the changes in cardiac autonomic nerve activity during water immersion with the tidal volume measured and its changes considered while controlling the respiration to a certain level. Eight healthy young males (ages: 19 to 28) sat calmly for 20 minutes before immersion and then soaked in water at the subaxillary level in sitting position for 15 minutes while controlling their respiration rate to 15cycles/min. Autonomic nerve activity was estimated by the power spectral analysis of the heart rate together with the Fast Fourier Transformation. Integral values of power were obtained in the high frequency (HF; 0.15 to 0.50Hz) and low frequency (LF; 0.04 to 0.15Hz) component areas. HF was used as the index of cardiac parasympathetic nerve activity, and the ratio of LF to HF (LF/HF), as the index of cardiac sympathetic nerve activity. During immersion at 34°C, HF increased significantly and the heart rate and LF/HF decreased slightly though not at a statistically significant level. During immersion at 27°C, HF increased significantly and the heart rate and LF/HF decreased significantly. During immersion at 38°C, the heart rate increased significantly while HF decreased and LF/HF varied slightly with no statistical significance. The tidal volume increased significantly during immersion at 27°C and 34°C, and it increased during immersion at 38°C though it was not statistically significant.
These results suggest that cardiac parasympathetic nerve activity is enhanced while sympathetic nerve activity is suppressed during immersion at 27°C, because the remarkable increase in HF that occurred during immersion cannot be accounted for by the increase in the tidal volume per breathing cycle alone. However, it is possible that the increase in the tidal volume enhanced the increase in HF. It was suggested, however, that autonomic nerve activities did not change significantly during water immersion at 38°C though there is possibility that the changes in HF were underestimated due to the increase in the tidal volume.

The purpose of this study was to assess an alteration of cardiac autonomic nerve activity during water immersion. Ten healthy young males (age : 21-28 yr.) were immersed in water at the temperatures of 25°C, 30°C and 34°C. Subjects sat calmly for 20 minutes in sitting position before water immersion, and then were immersed in water at subaxillary level in sitting position for 15 minutes, performing controlled breathing (15 cycle/min.) . Electrocardiograms were recorded continuously. Autonomic nerve activity was estimated with the analysis of power spectral by using the Fast Fourier Transformation (FFT) . High (HF ; 0.15-0.50 Hz) and low (LF ; 0.04-0.15 Hz) frequency areas and the ratio of LF to HF (LF/HF) were calculated as the indices of cardiac parasympathetic nerve activity, sympathetic nerve activity with parasympathetic modulation, and sympathetic nerve activity, respectively. During the water immersion at 25°C, 30°C and 34°C, HF was significantly increased, while the heart rate and LF/HF were significantly decreased. There were no statistically significant differences among both of HF and LF/HF during the immersion at 25°C, 30°C and 34°C, although the rate of change in HF at the temperature of 25°C appeared to be prominent compared to those at 30°C and 34°C and some subjects showed an exaggerated change in HF immediately after immersion. These results suggest that cardiac parasympathetic nerve activity is enhanced and cardiac sympathetic nerve activity is suppressed during a short time water immersion at the thermo-neutral temperature (34°C) and the temperatures of 25°C and 30°C, which are the usual temperatures found in indoor pools.

A study was carried out to examine the effects of water replacement on cardiovascular function during kendo practice in a hot environment. Five male college kendoists performed moderately severe 30-min kendo practice at a WBGT index of about 27°C with and without water intake. For water replacement, the subjects ingested 700 ml water (500 ml before exercise and 200 ml at 15 min after the start of exercise) . Under both conditions, body weight was decreased significantly, and hematocrit and serum total protein concentration were increased significantly after the exercise. With water replacement, the body weight loss induced by the exercise was similar to that under water deprivation. However, the decrease in body weight from the basal body weight, i. e. body weight measured before water intake, was significantly less with water replacement than under water deprivation. There were no significant differences in the percentage increases of hematocrit and serum total protein concentration between the two conditions, although the percentage change in plasma vasopressin concentration was significantly lower with water replacement than without. In the subjects deprived of water, the left ventricular end-diastolic dimension and left atrial dimension were significantly reduced after the exercise, and stroke volume, ejection fraction, and fractional shortening were also decreased significantly. The ratio of left ventricular end-systolic wall stress to left ventricular end-systolic volume index was increased significantly after the exercise without water intake. With water replacement, however, the percentage decreases in cardiac dimensions, stroke volume, ejection fraction, and fractional shortening were significantly lower than those under water deprivation. There was no significant change in the ratio of left ventricular end-systolic wall stress to left ventricular end-systolic volume index before and after the exercise with water intake. It is suggested that 700 ml water replacement before and during kendo exercise in a hot environment prevents depletion of stroke volume and deterioration of cardiovascular function, although it might not improve significantly the plasma volume loss after exercise.

Although it has been established that exercise is useful for health promotion, physical exercise may induce oxidative stress in humans. Our previous study showed that the concentration of plasma protein-bound sulfhydryl groups (p-SHs) was significantly decreased after strenuous exercise, i. e. full-marathon running and participation in an athletic training camp. Reactive oxygen species may cause oxidation of plasma proteins in vitro. To study whether moderate exercise for health promotion, e. g. jogging or walking, induces oxidative stress in human circulating blood, the authors examined the change in plasma p-SHs concentration following ergometric exercise at moderate intensity and of relatively short duration {Exercise 1: 80% ventilatory threshold (VT), 100% VT, and 110% VT; 30 min, Exercise 2 : 90% VT; 120 min} in 8 (23-28 yr; Exercise 1) and 6 males (23-28 yr; Exercise 2) respectively. The plasma p-SHs concentration did not changed significantly after Exercise 1 or 2. The data indicated that the exercise did not cause significant modification of plasma proteins, suggesting that it did not induce significant oxidative stress in the circulating blood.

The authors hypothesized that habitual physical exercise and aortic distensibility would be the major factors which influence systolic blood pressure. This study was designed to analyze the relationships among systolic blood pressure (SBP) and parameters determined at medical checks, including age, diastolic blood pressure (DBP), aortic pulse wave velocity (APWV) index (APWVI : APWV standardized by the diastolic blood pressure), plasma lipid profiles (IC, TG), plasma glucose during an oral glucose tolerance test (2 h-OGTT), percentage body fat (%Fat), cigarette smoking habit (Cigarettes), alcohol consumption (Alcohol), and physical activity index (PAI) using a questionnaire, in 678 males aged 30 to 69 years, who visited a hospital for a thorough medical check-up. For analysis of factorial structure in the subjects, principal factor analysis was applied to the correlation matrix which was calculated with 12 variables. Correlational analysis and path analysis were applied to confirm the hypothetical model. The results demonstrated that DBP and APWVI were the major factors which significantly affected the SBP. The PAI was significantly and inversely correlated not only with the APWVI, but also with %Fat, which was significantly and positively correlated with the DBP. In conclusion, aortic wall stiffness may be an independent factor in the manifestation of systolic hypertension, and habitual physical exercise may decrease the SBP through direct reduction of aortic wall stiffness and indirectly decreasing the DBP.

It has been shown that the time constant of heart rate decline for the first 30 sec (T₃₀) after exercise, at an intensity lower than the ventilatory threshold (VT), can serve as a specific index to assess post-exercise vagal reactivation. The purpose of this study was to validate the use of a simpler alternative index, i. e. %Δ HR₃₀ (the ratio of heart rate decrement for the first 30 sec after exercise) for the evaluation of parasympathetic nervous reactivation, and to examine whether it would be a useful index in the conditioning of athletes. Eighteen college students performed 4 minutes cycle ergometer exercise routines at intensities of 40%, 80%, and 120% VT to compare the %Δ HR₃₀ and the T₃₀. In addition, the %Δ HR₃₀ was obtained by a field test (4 minutes jogging) in 15 college middle and long distance runners, every morning during summer camp training to assess the state of athletic conditioning. The %Δ HR₃₀ at 80% VT was similar to the value at 40% VT, but significantly different from the value at 120% VT, as was the T₃₀ at 80% VT.
The %Δ HR₃₀ significantly correlated with the T₃₀ and VO₂max. During the camp, the %Δ HR₃₀ was higher on mornings following light training days than on mornings following hard training days. These results suggest that the %Δ HR₃₀, at an exercise intensity lower than the VT, could be a simple and useful index to evaluate post-exercise parasympathetic nervous reactivation in the conditioning of athletes.

This study was conducted to assess the effects of bathing in still water and in flowing water on the heart rate variability. Eight healthy young males (age 20 to 28) bathed in still water at temperatures of 34°C, 38°C, and 41°C for 20 minutes each. The other eight healthy young males (age 22 to 28) bathed in flowing water at a temperature of 36°C for 30 minutes. Electrocardiograms were recorded before, during, and after the bathing. Subjects sat still for 20 minutes before bathing, and then bathed in water to the axilla in a sitting position. Subjects breathed freely during the experiment. Heart rate variability was estimated with the power spectral analysis using FFT. The power densities in the high frequency (0.15 to 0.50Hz) and low frequency (0.04 to 0.15Hz) areas as obtained from this frequency analysis (HF and LF) as well as the ratio of LF/HF were calculated, and HF was used as index of cardiac parasympathetic activity, LF as index of sympathetic activity with parasympathetic modulation, and LF/HF as index of sympathetic activity.
During bathing in still water at 34°C and 36°C, no significant change from the value before the bathing was found in heart rate, HF, LF, or LF/HF. HF and LF significantly decreased during the bathing in still water at 38°C and 41°C, LF/HF significantly increased during the bathing in still water at 38°C, During the bathing in still water at 41°C, we could not calculate LF/HF for many subjects because HF disappeared. During the bathing in water flowing at a moderate speed (1.0m/sec), LF/HF increased significantly. During the bathing in water flowing at a high speed (2.0m/sec), heart rate and LF/HF increased significantly while LF decreased significantly.
These results suggest that parasympathetic nervous activities are suppressed and sympathetic nervous activities are enhanced during bathing in still water at temperatures higher than the neutral temperature (34°C), and sympathetic nervous activity is enhanced during the bathing in flowing water at 36°C, However, the effects of respiration rate and tidal-volume on HF, and the validity of the HR variabilities as an index of autonomic nervous activities should be examined in further detail.