Heart failure(HF) is characterized by decreased exercise capacity, attributable to neurocirculatory and skeletal muscle factors. Cardiac resynchronization therapy(CRT) and exercise training have each been shown to decrease muscle sympathetic nerve activity(MSNA) and increase exercise capacity in patients with HF. We hypothesized that exercise training in the setting of CRT would further reduce MSNA and vasoconstriction and would increase Ca2+ handling gene expression in skeletal muscle in chronic systolic HF patients. Thirty HF patients, EF<35% and CRT for 1 month, were randomized into two groups: Exercise-trained(ET, n=14) and untrained(NoET, n=16). The following parameters were compared at baseline and after 4 months in each group: peak VO2, MSNA (microneurography), forearm blood flow, and Ca2+ handling gene expression in vastus lateralis muscle. After four months, exercise duration and peak VO2 were significantly increased in the ET group(p=0.04 and p=0.01, respectively), but not in the NoET group. MSNA was significantly reduced in the ET(p=0.001), but not in NoET group. Similarly, forearm vascular conductance significantly increased in the ET(p= 0.0004), but not in the NoET. The expression of the Na+/Ca2+ exchanger(p =0.01) was increased and ryanodine receptor expression was preserved in ET compared to NoET. In conclusion, the exercise training in the setting of CRT improves exercise tolerance and neurovascular control and alters Ca2+ handling gene expression in the skeletal muscle of systolic HF patients. These findings highlight the importance of including exercise training in the treatment of HF patients even following CRT.
- heart failure
- cardiac resynchronization
- neurovascular control
- skeletal muscle
- Copyright © 2016, American Journal of Physiology-Heart and Circulatory Physiology