Hemodynamic effects of exercise training in heart failure.

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.