It has been demonstrated that oxygen consumption kinetics (V'O_2cin) at the onset of aerobic exercise may be speeded up when preceded by a short bout of heavy exercise (preconditioning heavy exercise, PHE). It was proposed that the mechanism underlying PHE be related to increased muscle blood flow and heart rate after heavy exercise, which would speed up the enhancement of oxygen transport to active muscles after PHE. This phenomenon operates also in patients with chronic heart failure (CHF) has not been determined, yet. 14 CHF male patients (68yy, 77kg, 172cm, Class II NYHA) performed a cycle ergometer incremental to exhaustion test, to determine individual maximal aerobic power (V'O_2max), workload (W_max) and workloads at the first (W_vt1) and the second (W_vt2) ventilator thresholds. V'O_2cin was studied in two moderate load exercises (SW₁, SW₂) at 80% W_vt1, separated by a high intensity exercise (SW_PHE), with load equal to (W_VT2 + (W_max– W_VT2)/2), separated by 6 min sitting rest. Breath by breath oxygen values (V'O_2bxb) were used to calculate oxygen deficit (def_O2=(V'O_2SS*360s–₁S³⁶⁰V'O_2bxb)) and the mean response time (MRT=def_O2*V'O_2SS^-1). Def_O2 was reducted by 14.8% (p=0.007) from SW₁ to SW₂, while VO_2ss did not change at equal workloads. Thus, MRT, was significantly shortened by preconditioning (-18.4%; p=0.001). The metabolic adjustments in CHF patients, although negatively influenced by the heart pathology, may still be modulated by appropriate physiological stimuli.