Hemodynamic Effects of Exercise Training in Heart Failure

BackgroundExercise performance improvement after training in heart failure (HF) can be due to central or peripheral changes.Methods and ResultsIn 70 HF stable patients we measured peak VO2 and cardiac output (CO, inert gas rebreathing technique) and calculated arteriovenous O2 differences (a-v O2diff) before and after an 8-week training program. Peak VO2 changed from 1111 ± 403 mL/minute to 1191 ± 441 (P < .001), peak workload from 68 ± 29 watts to 76 ± 32 (P < .0001), peakCO from 6.6 ± 2.2 L/minute to 7.3 ± 2.5 (P < .0001), and peak a-v O2diff from 17.5 ± 5.1 mL/100 mL to 16.6 ± 4.1 (P = .081). Changes in peak CO and a-v O2diff allowed to identify 4 behaviors: group 1: (n = 15) reduction in peak CO and increase in a-v O2diff (peak VO2 unchanged, peak workload +9.5%); group 2: (n = 16) both peak CO and a-v O2diff increased as well as peak VO2 (23%) and workload (18%); group 3: (n = 4) peak CO and a-v O2diff reduced as well as peak VO2 (-18%) and workload (-5%); group 4: (n = 35) peak CO increased with a-v O2diff reduced (increase in peak VO2 by 5.5 and workload by 8.4%).ConclusionsExercise training improves peakVO2 by increasing CO with unchanged a-v O2diff. A reduction after training of a-v O2diff with an increase in CO is frequent (50% of cases), is suggestive of blood flow redistribution and, per se, not a sign of reduced muscle performance been associated with improved exercise capacity.