In the present paper we report the results of a study in which we compared 2 different approaches to the computation of biological age (BA) in a sample of 322 Japanese men (age range 20 to 79 years). In the first approach, 4 commonly used measures of health-related fitness (VO2peak, trunk flexion from a standing position, body fat, and grip strength) were reduced to a single BA score (HRF Age) using principal component analysis. In contrast, in the second approach, 3 commonly used measures of skilled motor performance and agility (vertical jump, stepping side-to-side, and balancing on one leg with eyes closed) were reduced to a single BA score (SMP Age) using similar multivariate procedures. The criterion-related validity of both of the BA measures was examined by assessing each measure's ability to discriminate between healthy and active groups of subjects. This was achieved by classifying the original subject pool into regularly active (ACT; n=108) and healthy (HLTH; n=169) subgroups on the basis of self-reported activity levels. Analyses revealed that HRF Age was a more powerful discriminator between the two activity groups than SMP Age. While HRF Age of HLTH subjects was very close to their chronological age (CA), in the ACT group, HRF Age was on average 15 years less than their CA (P<0.05). In a separate analysis, we assessed the HRF Age of patients with ischemic heart disease, hypertension, obesity, or diabetes (PAT; n=45). The HRF Age of these subjects averaged 10 years above their CA. Our data suggest that commonly used measures of health-related fitness can be usefully employed as indices of BA which differentiate between individuals of similar ages but differing health and physical activity status. In contrast, measures of skilled motor performance were found to be less valuable measures of BA. The implication of our findings for future experimental design in exercise and aging research is discussed.
Subjects who were at intermediate levels of musical performance made equaled interval tapping in several tempos. The temporal fluctuation for the tapping was observed and analysed. The power spectrum of the fluctuation showed a critical phenomenon at around a frequency which corresponds to the period of 20 taps, for all tempos and all subjects, i.e., the slope of the spectrum was flat or had a positive value in the high frequency region above the critical frequency but it increased as the frequency decreased in the low frequency region below the critical frequency. Moreover, auto-regressive models and Akaike's information criterion were introduced to determine the critical tap number. The order of the best auto-regressive model for the temporal fluctuation data was distributed around 20 taps. These results show that the memory capacity of 20 taps governs the control of equaled interval tapping. To interpret the critical phenomenon of 20 taps with the memory capacity of the short term memory, the so called magic number seven, a simple chunking assumption was introduced; subjects might have unconsciously chunked every three taps during the tapping. If the chunking assumption is true, when subjects consciously chunk every seven taps, the memory capacity of taps should shift to about 50 taps. To test if the assumption is true or not, subjects made a three-beat rhythm tapping and a seven-beat rhythm tapping with equaled intervals. As a result, the memory capacity for these accented tappings were also estimated as 20 taps. This suggests that the critical phenomenon cannot be explained by the chunking assumption and the magic number seven, rather this finding suggests that there exists a memory capacity of 20 taps and this is used for equaled interval tapping.
The adaptive response of oxidative enzyme activity in the skeletal muscle to training in normoxic and in normobaric hypoxic training was studied. Forty male Wistar rats were divided into 4 groups: normoxia + sedentary (NS, n=10); hypoxia + sedentary (HS, n=10); normoxia + training (NT, n=10); and hypoxia + training (HT, n=10). Rats in the NT group ran on a treadmill for 30 min a day at 20-30 m·min-1, 4 days a week for 10 weeks in normoxia. Rats in the HT group performed the same training protocol as NT in an ambient FIO2 decreased to 12%. HS rats were exposed to hypoxia in the same degree, duration and frequency as HT without exercise. After the training period, the soleus and the plantaris muscles were removed, and the activities of mitochondrial enzymes, malate dehydrogenase (MDH) and 3-hydroxyacyl-CoA dehydrogenase (HAD) were measured by a spectrophotometer. The normoxic training did not increase MDH or HAD activities, in either the soleus or the plantaris. This absence of change in mitochondrial enzyme activities is considered to be the results of inadequate stimulus of training, including a relatively low amount of exercise. On the other hand, the hypoxie training enhanced the MDH activity in the soleus by 17.5% compared with NS (P<0.01) and by 20.5% compared with HS (P<0.01). Also in the plantaris, the MDH activity in HT was higher than that in HS (15.7%, P<0.05). These findings suggest that even moderate training by which enzyme activity is not increased under normoxic conditions can enhance the oxidative capacity in the skeletal muscle when the training is performed in a hypoxic environment.
We evaluated the time course of alteration in aerobic capacity and coronary risk factors associated with a 36-month exercise program in women with ischemic heart disease (IHD). Twenty-one patients participated in supervised exercise and home-based exercise programs for 36 months. However, of all patients, 11 patients completed the entire program. Oxygen uptake corresponding to lactate threshold (VO2LT), peak oxygen uptake (VO2Peak), percent of body fat (%BF), systolic (BPs) and diastolic (BPd) blood pressure, total cholesterol (TC), low-density lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDLC) and triglycerides (TG) were assessed before and 4, 8, 12, 24, and 36 months after exercise. The intensity of exercise was set at individually determined LT, i.e., 60 to 70% VO2peak. The daily amount of exercise during 36 months averaged 24.0 ± 11.4 minutes per day. During the course of exercise program, VO2LT, VO2peak, BPs, BPd, and TG improved significantly at month 4. Although %BF decreased significantly at month 8 to 12, it tended to return to the initial level at month 36. On the other hand, a significant increase in HDLC was found at month 24 and improved state of HDLC remained unchanged thereafter. No changes were found in TC and LDLC. These results suggest that most of the beneficial effects of exercise on aerobic capacity and coronary risk factors in women with IHD are obtained within 4-8 months, with some further improvement seen with continued exercise up to 24 months.
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