Skeletal Muscle Fatigability in Heart Failure

Abstract

Evidence suggests that heart failure (HF) patients experience skeletal muscle fatigability in the lower extremity during single-limb tasks. The contribution of skeletal muscle fatigability to symptoms of exercise intolerance (perceived fatigue and dyspnea) is relatively unclear. Symptomatic or 'perceived' fatigue is defined by the sensations of exhaustion or tiredness that patients experience either at rest or while performing a motor task. Although factors that contribute to symptoms of fatigue in patients with HF are multifactorial; the skeletal muscle likely plays a major role. Skeletal muscle fatigability, as opposed to symptomatic fatigue, is an objective measure of a reduction in muscle force or power or reduced ability of the muscles to perform over time. Indeed, evidence suggests that patients with HF experience greater skeletal muscle fatigability which may contribute to a diminution in motor performance and the overall symptomatology that is hallmark of exercise intolerance in HF. This review will discuss (1) skeletal muscle fatigability in patients with HF, (2) the mechanisms contributing to locomotor skeletal muscle fatigability in HF and (3) the relationship of fatigability to symptoms of perceived fatigue and exercise intolerance in HF patients. Evidence suggests that cardiac dysfunction alone does not contribute to exercise intolerance. Therefore, mechanisms of skeletal muscle fatigability and their contribution to symptoms of fatigue and exercise intolerance, is an increasingly important consideration as we develop rehabilitative strategies for improving motor performance and functional capacity in patients with HF.

Keywords: exercise intolerance; fatigability; fatigue; heart failure; skeletal muscle.

FIGURE 1

Reduction in Strength after a fatiguing contraction in HF, relative to controls. Each symbol represents the reduction in strength after various fatiguing interventions, normalized to the control group in each respective study. The majority of studies demonstrate a greater fatigability in HF patients compared with controls. When studies used multiple protocols (Buller et al., 1991; Minotti et al., 1991), each protocol was indicated in its own column. CTL, control; HF, heart failure; KE, knee extensors; PF, plantar flexors; AP, adductor pollicis; ES, electrical stimulation.

FIGURE 2

Percent difference in time to task failure in patients with HF. Data in HF is represented as a relative value in comparison with controls. All studies demonstrated a briefer time to failure or greater fatigability in HF. DF, dorsiflexor muscles.

FIGURE 3

Data extracted from Buller et al. (1991). Quadriceps force was strongly associated with fatigue (%) (r = 0.81, P < 0.001). Individuals who were weaker (severe HF patients) had the greatest fatigability (%).

FIGURE 4

Proposed mechanisms of fatigability in HF patients. Mechanisms contributing to muscle fatigability in HF are likely a cascade of events that may be initiated by high sympathetic activity and reduced cardiac output. This review indicates that peripheral factors likely play a large role in fatigability. In particular, skeletal muscle perfusion and altered muscle metabolism appear to be observed as major contributing factors (shown in gray). Although central factors have not yet been shown to contribute to fatigability in HF, more research needs to be conducted to directly measure neural mechanisms of fatigability in these patients. Because greater activation of skeletal muscle (group III/IV) afferents are known to inhibit motor activity (Garland and Kaufman, 1995), the possibility of greater inhibition of the central nervous system by exaggerated activity of group III/IV afferent (outlined in gray boxes) exists.