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 (V̇O2) 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) &lt
13 ml/min per kg and group H (n=7) consisting of patients with AT &gt
13 ml/min per kg. At rest, V̇O2 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+1.4ml/min, p&lt
0.01). Increase in V̇O2 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&lt
0.01). After warm-up to the AT point, however, the increase in not only V̇O2 but also CO was markedly reduced in group L than in group H (V̇O2:0.5±0.4 vs 3.7±0.8 ml/min per kg, p&lt
0.01, CO: 0.2±0.3 vs 1.1±0.3 L/min, p&lt
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.