Oxygen consumption (V’O2) at the onset of a constant-load exercise rises progressively to an enhanced steady state level, with typical kinetics, that can be altered by aerobic training or by disease (cardiovascular, diabetes). Kinetics is typically studied by fitting procedures, including a time delay and a one, two or three component exponential model. Alternatively, mean response time (MRT) is calculated, as the ratio between the integral of V’O2 deficit during the transient phase and V’O2 at steady state. We sought to verify whether MRT can be reduced during a bout of constant load exercise preceded by an identical exercise, in chronic heart failure (CHF) patients, in which V’O2 kinetics is known to be typically slowed with respect to healthy subjects. Twenty patients (mean±SD: 67±5 yy, 78¬±12 kg, 173±7 cm; V’O2peak 17.35±5 ml kg-1 min-1; peak work 96±23 W) with NYHA class II/III chronic heart failure (Pardee H et al (1953)), all wearing an automatic implanted defibrillator for safety reasons, performed two bouts of 6 min cycle ergometer exercise, separated by 6 min sitting rest, while connected to a QUARK b2 (COSMED, Italy) metabolimeter for breath by breath recording of respiratory variables. After two min stabilisation, the subjects started pedalling at 60-70 strokes/min against a load corresponding to the individual first ventilatory threshold (Wasserman (1999)), previously determined in an incremental trial. The steady state values of V’O2 during the first and the second exercise bouts were unchanged (1026±150 and 1035±175 ml min-1, ns, t-test), while the MRT decreased from 42.2 ±14.3 s to 34.7±13.8 s (p<0.01). Thus, a bout of constant load exercise sped up V’O2 kinetics by significantly decreasing MRT by about 18%. It may be suggested that the first exercise bout exerts a sort of preconditioning on active muscles, as previously described by others (Gurd et al. (2005)) in normal subjects, albeit with a substantial difference, consisting in the use of a much higher-load preconditioning exercise. Although the precise mechanism cannot be determined at present, we believe that CHF patients suffer for a specific skeletal muscle deconditioning status deriving from their chronic cardiac disease, which can be quickly attenuated by a short aerobic exercise.