Hemodynamic effects of exercise training in heart failure.

ABSTRACT

BACKGROUND: Exercise performance improvement after training in heart failure (HF) can be due to central or peripheral changes. METHODS AND RESULTS: In 70 HF stable patients we measured peak VO(2) and cardiac output (CO, inert gas rebreathing technique) and calculated arteriovenous O(2) differences (a-v O(2)diff) before and after an 8-week training program. Peak VO(2) 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 O(2)diff from 17.5 ± 5.1 mL/100 mL to 16.6 ± 4.1 (P = .081). Changes in peak CO and a-v O(2)diff allowed to identify 4 behaviors group 1 (n = 15) reduction in peak CO and increase in a-v O(2)diff (peak VO(2) unchanged, peak workload +9.5%); group 2 (n = 16) both peak CO and a-v O(2)diff increased as well as peak VO(2) (23%) and workload (18%); group 3 (n = 4) peak CO and a-v O(2)diff reduced as well as peak VO(2) (-18%) and workload (-5%); group 4 (n = 35) peak CO increased with a-v O(2)diff reduced (increase in peak VO(2) by 5.5 and workload by 8.4%). CONCLUSIONS: Exercise training improves peakVO(2) by increasing CO with unchanged a-v O(2)diff. A reduction after training of a-v O(2)diff 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.