Thirty CHF patients were randomized to 3 months of light-to-moderate-intensity AET (CHF-AET) or control (CHF-C). Baseline and end-protocol evaluations included i) one incremental cardiopulmonary exercise test with near infrared spectroscopy analysis of peak deoxygenated hemoglobin + myoglobin concentration changes (¦¤[deoxy(Hb + Mb)]) in vastus lateralis muscle, ii) 8 light-to-moderate-intensity constant-work-rate exercise tests for VO2 on-kinetics phase I duration, phase II ¦Ó, and mean response time (MRT) assessment, and iii) circulating endothelial progenitor cell (EPC) measurement. Reference values were obtained in 7 age-matched normals (N).
At end-protocol, phase I duration, phase II ¦Ó, and MRT were significantly reduced (? 12 % , ? 22 % , and ? 19 % , respectively) and peak VO2, peak ¦¤[deoxy(Hb + Mb)], and EPCs increased (9 % , 20 % , and 98 % , respectively) in CHF-AET, but not in CHF-C. Peak ¦¤[deoxy(Hb + Mb)] and EPCs relative increase correlated significantly to that of peak VO2 (r = 0.61 and 0.64, respectively, p < 0.05).
Light-to-moderate-intensity AET determined a near-normalization of pulmonary VO2 on-kinetics in CHF patients. Such a marked plasticity has important implications for AET intensity prescription, especially in patients more functionally limited and with high exercise-related risk. The AET-induced simultaneous improvement of phase I and phase II, associated with an increase of peak peripheral oxygen extraction and EPCs, supports microcirculatory O2 delivery impairment as a key factor determining exercise intolerance in CHF.