Is the Soleus a Sentinel Muscle for Impaired Aerobic Capacity in Heart Failure?

Purpose: Skeletal muscle wasting is well documented in chronic heart failure (CHF). This article provides a more detailed understanding of the morphology behind this muscle wasting and the relation between muscle morphology, strength, and exercise capacity in CHF. We investigated the effect of CHF on lower limb lean mass, detailed muscle–tendon architecture of the individual triceps surae muscles (soleus (SOL), medial gastrocnemius, and lateral gastrocnemius) and how these parameters relate to exercise capacity and strength. Methods: Eleven patients with CHF and 15 age-matched controls were recruited. Lower limb lean mass was assessed by dual energy x-ray absorptiometry and the architecture of skeletal muscle and tendon properties by ultrasound. Plantarflexor strength was assessed by dynamometry. Results: Patients with CHF exhibited approximately 25% lower combined triceps surae volume and physiological cross-sectional area (PCSA) compared with those of control subjects (P < 0.05), driven in large part by reductions in the SOL. Only the SOL volume and the SOL and medial gastrocnemius physiological cross-sectional area were statistically different between groups after normalizing to lean body mass and body surface area, respectively. Total lower limb lean mass did not differ between CHF and control subjects, further highlighting the SOL specificity of muscle wasting in CHF. Moreover, the volume of the SOL and plantarflexor strength correlated strongly with peak oxygen uptake (V˙O2peak) in patients with CHF. Conclusions: These findings suggest that the SOL may be a sentinel skeletal muscle in CHF and provide a rationale for including plantarflexor muscle training in CHF care

Conference report on contractures in musculoskeletal and neurological conditions

Limb contractures are debilitating complications associated with various muscle and nervous system disorders. This report summarizes a conference at the Shirley Ryan AbilityLab in Chicago, IL on April 19–20, 2018 involving researchers and physicians from diverse disciplines convened to discuss current clinical and preclinical understanding of contractures in Duchenne muscular dystrophy, stroke, cerebral palsy and other conditions. Presenters described changes in muscle architecture, activation, extracellular matrix, satellite cells and muscle fiber sarcomeric structure that accompany or predispose muscles to contracture. Participants identified ongoing and future research directions that may lead to understanding of the intersecting factors that trigger contractures. These include additional studies of changes in muscle, tendon, joint and neuronal tissues during contracture development using imaging, molecular and physiologic approaches. Participants identified the need for improved biomarkers and outcome measures to identify patients likely to develop contractures and to accurately measure efficacy of treatments currently available and under development