Limited Maximal Exercise Capacity in Patients With Chronic Heart Failure Partitioning the Contributors

作者:Esposito Fabio*; Mathieu Costello Odile; Shabetai Ralph; Wagner Peter D; Richardson Russell S
来源:Journal of the American College of Cardiology, 2010, 55(18): 1945-1954.
DOI:10.1016/j.jacc.2009.11.086

摘要

Objectives This study aimed to assess the factors limiting maximal exercise capacity in patients with chronic heart failure (CHF).
Background Maximal exercise capacity, an important index of health in CHF, might be limited by central and/or peripheral factors; however, their contributions remain poorly understood.
Methods We studied oxygen (O-2) transport and metabolism at maximal cycle (centrally taxing) and knee-extensor (KE) (peripherally taxing) exercise in 12 patients with CHF and 8 healthy control subjects in normoxia and hyperoxia (100% O-2).
Results Peak oxygen uptake (VO2) while cycling was 33% lower in CHF patients than in control subjects. By experimental design, peak cardiac output was reduced during KE exercise when compared with cycling (approximately 35%); although muscle mass specific peak leg VO2 was increased equally in both groups (approximately 70%), VO2 in the CHF patients was still 28% lower. Hyperoxia increased O2 carriage in all cases but only facilitated a 7% increase in peak leg VO2 in the CHF patients during cycling, the most likely scenario to benefit from increased O-2 delivery. Several relationships, peak leg VO2 (KE + cycle) to capillary-fiber-ratio and capillaries around a fiber to mitochondrial volume, were similar in both groups (r = 0.6-0.7).
Conclusions Multiple independent observations, including a significant skeletal muscle metabolic reserve, suggest skeletal muscle per se contributes minimally to limiting maximal cycle exercise in CHF or healthy control subjects. However, the consistent attenuation of the convective and diffusive components of O-2 transport (25% to 30%) in patients with CHF during both cycle and even KE exercise compared with control subjects reveals an underlying peripheral O-2 transport limitation from blood to skeletal muscle in this pathology.

  • 出版日期2010-5-4