Exercise training in chronic heart failure: improving skeletal muscle O₂transport and utilization

Abstract

Hirai DM, Musch TI, Poole DC. Exercise training in chronic heart failure: improving skeletal muscle O 2 transport and utilization. Am J Physiol Heart Circ Physiol 309: H1419 -H1439, 2015. First published August 28, 2015; doi:10.1152/ajpheart.00469.2015.-Chronic heart failure (CHF) impairs critical structural and functional components of the O 2 transport pathway resulting in exercise intolerance and, consequently, reduced quality of life. In contrast, exercise training is capable of combating many of the CHF-induced impairments and enhancing the matching between skeletal muscle O 2 delivery and utilization (Q mO 2 and V mO 2 , respectively). The Q mO 2 /V mO 2 ratio determines the microvascular O2 partial pressure (PmvO 2 ), which represents the ultimate force driving blood-myocyte O 2 flux (see Fig. 1). Improvements in perfusive and diffusive O2 conductances are essential to support faster rates of oxidative phosphorylation (reflected as faster V mO 2 kinetics during transitions in metabolic demand) and reduce the reliance on anaerobic glycolysis and utilization of finite energy sources (thus lowering the magnitude of the O 2 deficit) in trained CHF muscle. These adaptations contribute to attenuated muscle metabolic perturbations (e.g., changes in [PCr], [Cr], [ADP], and pH) and improved physical capacity (i.e., elevated critical power and maximal V mO 2 ). Preservation of such plasticity in response to exercise training is crucial considering the dominant role of skeletal muscle dysfunction in the pathophysiology and increased morbidity/mortality of the CHF patient. This brief review focuses on the mechanistic bases for improved Q mO 2 /V mO 2 matching (and enhanced PmvO 2 ) with exercise training in CHF with both preserved and reduced ejection fraction (HFpEF and HFrEF, respectively). Specifically, O 2 convection within the skeletal muscle microcirculation, O 2 diffusion from the red blood cell to the mitochondria, and muscle metabolic control are particularly susceptive to exercise training adaptations in CHF. Alternatives to traditional whole body endurance exercise training programs such as small muscle mass and inspiratory muscle training, pharmacological treatment (e.g., sildenafil and pentoxifylline), and dietary nitrate supplementation are also presented in light of their therapeutic potential. Adaptations within the skeletal muscle O 2 transport and utilization system underlie improvements in physical capacity and quality of life in CHF and thus take center stage in the therapeutic management of these patients.

A Combined and Intensive Exercise Model Improves Physical Capacity in Cardiac Patients

“…Endurance training has been recommended for cardiac patients [42]. In our study we found that the maximal oxygen uptake increased equally in both groups.…”

Frailty and sarcopenia as the basis for the phenotypic manifestation of chronic diseases in older adults

“…Moreover, in obese older patients with chronic heart failure with preserved ejection fraction, 20 weeks of diet and exercise had additive effect in increasing peak oxygen consumption, a functional recovery that positively correlated with the increase in lean body mass and with the improvement in thigh muscle quality (muscle/intermuscular fat ratio) (Kitzman et al, 2016). In this sense, beneficial effects of exercise in chronic heart failure patients seem to be related to the improvement in skeletal muscle oxygen delivery and utilization (Hirai et al, 2015). The positive impact of exercise is not restricted to heart failure since exercise training in patients with chronic pulmonary hypertension is associated with a significant improvement in physical performance, pulmonary arterial pressure and quality of life (Pandey et al, 2015).…”

Diaphragm abnormalities in heart failure and aging: mechanisms and integration of cardiovascular and respiratory pathophysiology

“…Endurance exercise training promotes several cardiovascular and muscular benefits in CHF and aging [184,185], including improvements in inspiratory muscle function in CHF [186]. Endurance training prevents the loss of diaphragm specific force in animals with CHF with preserved ejection fraction or after injection of TNF-α [187,149].…”