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The issue of whether exercise training improves exercise hyperpnea in patients after coronary arterial bypass graft (CABG) surgery has not been fully explored. Effects of short-term physical training on ventilatory response and cardiac output during exercise in patients following coronary arterial bypass grafting surgery is studied. Thirty-four patients underwent exercise training for 2 weeks after the second postoperative week (Ex group); 23 stayed sedentary (Sed group). Ventilatory and cardiac output response during the cardiopulmonary exercise test was measured before and after the training period. The minute ventilation-carbon dioxide output (VE-VCO2) slope decreased from 38.9+/-8.1 to 35.1+/-6.7 (p

To identify and quantify the amount of viable hibernating myocardium in patients with chronic coronary artery disease, resting 201Tl single photon emission computed tomography (SPECT) was compared with 99mTc-methoxy-isobutyl isonitrile (MIBI) SPECT after nitrate infusion (nitrate-99mTc-MIBI) and 201Tl SPECT after 201Tl with glucose-insulin-potassium infusion (201Tl-GIK) in 25 patients. Twenty-one patients also underwent completely left ventriculography beforehand and 5+/-4 months afterwards. SPECT images were divided into 9 segments and scored visually from 0 (normal uptake) to 3 (absent). The defect score was calculated as the summation of the total scores (TDS) in each patient. The TDS of nitrate-99mTc-MIBI images (6.3+/-4.3) and 201Tl-GIK images (5.8+/-4.2) were significantly lower than the 7.4+/-4.3 of resting 201Tl images (p

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.

This study evaluated the reduction in regional work of the left ventricle caused by acute myocardial ischemia during coronary angioplasty, and correlated it with ST-segment elevation. Regional work of the left ventricular myocardium, which is derived from a stress - strain loop, is a useful index of the function of a diseased heart. However, the effects of transient ischemia on the regional work of the myocardium have not been fully elucidated. The subjects consisted of 25 patients who had proximal left anterior descending artery stenosis with normal wall motion and without collateral circulation. The patients were classified as showing ST-segment elevation ≥0.2 mV (group A, 10 patients), or ST-segment elevation

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.

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 AT13 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, p0.01). 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, p0.01). 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, p0.01, CO: 0.2 +/- 0.3 vs 1.1 +/- 0.3 L/min, p0.01). 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.