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 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%).

Conclusions

Exercise 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.