Biomedical subjects

M Tanehata

Publications and source records attributed to M Tanehata.

4 recordsLinked to original sources

PubMed2000

Effect of long-term exercise training on blood viscosity during endurance exercise at an anaerobic threshold intensity.

Blood viscosity (etaB) is low in athletes, but the effect of exercise training on etaB during endurance exercise at an anaerobic threshold (AT) intensity in non-athletes is not well known, although it is known that exercise training sometimes induces the hyperviscosity syndrome. Fourteen subjects were recruited and divided into 2 groups: those who trained at an AT intensity for 30 min/day, 3 times weekly for 1 year (Group T, n=8), and sedentary subjects (Group C, n=6). The test protocol consisted of a single 30-min treadmill exercise at each individual's AT intensity, which was determined in advance. The etaB, plasma viscosity (etaP), and hematocrit were measured just before and at the end of the treadmill exercise. The subjects were not allowed to drink any water before exercise. In the Group C subjects, the hematocrit and etaP increased significantly and the etaB tended to increase. However, in the Group T subjects, the hematocrit and etaP did not increase and the etaB decreased significantly. These data indicate that long-term exercise training attenuates the increase in blood viscosity during exercise.

Adult↗

PubMed1999

The time from anaerobic threshold (AT) to respiratory compensation point reflects the rate of aerobic and anaerobic metabolism after the AT in chronic heart failure patients.

The significance of the time from anaerobic threshold to respiratory compensation point (RCP-AT time) in patients with chronic heart failure was investigated. Thirty-seven patients with chronic heart failure (New York Heart Association class II or III) were enrolled into the study. Cardiopulmonary exercise testing was performed using breath-by-breath gas sampling. A bicycle ergometer was used, and incremental exercise testing was carried out. Anaerobic threshold, respiratory compensation point (RCP), and the slope of oxygen uptake (VO2) as a function of work rate (deltaVO2/deltaWR) were measured. A positive correlation (r=0.53) between RCP-AT time and deltaVO2/deltaWR was found. RCP-AT time was corrected for the whole exercise period (ramp exercise-RCP point), and the correlation between corrected RCP-AT time and deltaVO2/deltaWR was still present (r=0.46). There was no correlation between RCP-AT time and anaerobic threshold. These findings suggest that RCP-AT time is a new parameter that reflects the rate of the aerobic and anaerobic metabolism after AT.

Anaerobic Threshold↗

PubMed1999

[Effect of exercise therapy on oxygen consumption in patients with chronic heart failure].

The effect of exercise training on delta Vo2/delta WR was studied in 12 patients(11 men, one woman, mean age 62 +/- 9 yr)with chronic heart failure(old myocardial infarction, dilated cardiomyopathy, patients after coronary arterial bypass graft surgery and patients after aortic valve replacement). Cardiopulmonary exercise testing was performed to decide the exercise tolerance and assess the delta Vo2/delta WR. Patients underwent physical training at the anaerobic threshold for 3 months. Cardiopulmonary exercise testing was performed after the second week and after the third month. The anaerobic threshold increased at the third month compared with before exercise testing and the second week(p < 0.05, respectively) (before exercise testing: 13.6 +/- 2.0 ml/min/kg, the second week: 14.7 +/- 2.5 ml/min/kg, the third month: 16.2 +/- 2.1 ml/min/kg). The delta Vo2/delta WR increased at the second week compared with before exercise testing(before exercise testing: 8.9 +/- 1.9 ml/min/W, the second week: 10.6 +/- 1.9 ml/min/W, p < 0.05), but significantly decreased at the third month compared with the second week(the third month: 9.4 +/- 1.7 ml/min/W, p < 0.05). Serial increase of the anaerobic threshold and the peak Vo2/heart rate suggests that the exercise tolerance and cardiac function of the patients improved significantly. The increase of the delta Vo2/delta WR after the first 2 weeks seemed to depend on the luxury blood supply to both working and non-working muscles. The decrease of delta Vo2/delta WR at the third month may be due to the redistribution of the blood flow to the working muscles.

Chronic Disease↗

PubMed1998

Improved oxygen utilization during mild exercise in heart failure.

In heart failure with low cardiac output, exercise tolerance is reduced despite modulated regional blood distribution and oxygen extraction. However, low cardiac output does not necessarily lead to reduced exercise tolerance especially during mild exercise. In the present study, in order to understand the mechanisms regulating exercise tolerance in heart failure, we measured oxygen consumption (VO2) and cardiac output (CO) during both mild and intense exercise. Patients with heart failure were divided into 2 groups; group L (n = 8) consists of patients with low anaerobic threshold (AT) < 13 ml/min per kg and group H (n = 7) consisting of patients with AT > 13 ml/min per kg. At rest, VO2 was similar between groups L and H, whereas CO was lower in group L than in group H (3.5 + 0.3 vs 4.8 + 1.4 ml/min, p < 0.01). Increase in VO2 during warm-up exercise was not significant between the 2 groups (7.4 +/- 0.5 (group L) vs 6.2 +/- 0.3 ml/min per kg (group H), ns), but increase in CO was lower in group L than in group H (2.5 +/- 0.6 vs 3.4 +/- 0.4 ml/min, p < 0.01). After warm-up to the AT point, however, the increase in not only VO2 but also CO was markedly reduced in group L than in group H (VO2: 0.5 +/- 0.4 vs 3.7 +/- 0.8 ml/min per kg, p < 0.01, CO: 0.2 +/- 0.3 vs 1.1 +/- 0.3 L/min, p < 0.01). Based on these measurements, we calculated the arteriovenous oxygen difference (c(A-V)O2 difference) during exercise in individual patients using Fick's equation. The c(A-V)O2 difference was markedly increased in severe heart failure during the warm-up stage, but between the end of warm-up and the AT point, it remained at the same level as that of group H. These results suggest the presence of a unique mechanism regulating the c(A-V)O2 difference in severe heart failure patients, activation of which may, at least during mild exercise, contribute to efficient oxygen delivery to the peripheral tissues thus compensating for the jeopardized exercise tolerance in those patients.

Aged↗