ABC | Volume 112, Nº6, June 2019

Original Article Fonseca et al Autonomic imbalance, sarcopenia and heart failure Arq Bras Cardiol. 2019; 112(6):739-746 Figure 1 – Muscle sympathetic nerve activity (MSNA) in bursts/min. Values are presented as medians with lower and upper quartiles (CI 95%). Note that sarcopenic patients showed an increase of 18% in MSNA. 80 60 40 20 0 Sarcopenic Non-sarcopenic MSNA (bursts/min) p = 0.028 HF is a complex disease associated with several comorbidities. One of the major co-morbidities observed in patients with advanced chronic HF is sarcopenia, which is associated with poor prognosis. 21 Although the aetiology of sarcopenia is multifactorial, several mechanisms have been suggested to explain this decrease in muscle mass in patients with HF, such as increased inflammatory profile, 22 increased oxidative stress, 23 overactivation of ubiquitin–proteasome system, 24 and increased C-terminal agrin fragment (CAF). 25 These alterations, acting independently or in combination, may lead to excessive muscle protein degradation and reduced muscle protein synthesis. Besides the mechanisms mentioned above, exacerbated sympathetic nerve activity seems to be an important pathophysiological feature in HF leading to the loss of skeletal muscle. 6 In an experimental model of HF, Bacurau and colleagues 6 showed that sympathetic hyperactivity contributes to the development of skeletal myopathy by changing muscle morphology. 6 β 2 -adrenoceptors play a key role in regulating skeletal muscle mass in both anabolic and catabolic state. 26 Figure 2 – Delta heart rate recovery at 1st (∆HRR1) and 2nd (∆HRR2) minutes immediately after maximal exercise testing. Values are presented as medians with lower and upper quartiles (CI 95%). Note that sarcopenic patients showed a lower HRR at 1st (47% difference) and 2nd minutes (40% difference). 0 –20 –40 –60 –80 beats/min (delta) p < 0.001 p = 0.017 ∆HRR1 ∆HRR2 Sarcopenic Non-sarcopenic However, chronic sympathetic hyperactivity may be toxic to skeletal muscle, 27 which favors weight loss and sarcopenia in patients with HF. Moreover, increased sympathetic outflow is associated with higher chance of arrhythmias, 28 and adverse remodeling of the heart. 29 Interestingly, pharmacological treatment of HF is focused on blocking sympathetic activity, mainly by using cardio‑selective and non-selective β -blockers. 30 Treatment with β -blockers can increase total body fat mass and total body fat content in patients with HF, without apparent improvement in muscle mass. 30,31 In this study, we did not observe differences between groups in β -blocker treatment and dosage. In this context, future randomized clinical trials are required to assess the real impact of β -blocker therapy on skeletal muscle mass in patients with HF. Previous studies showed that HRR has an important prognostic value in the general population 12 and in patients with HF. 32 In addition, HRR is a very simple and easy way to indirectly evaluate the reactivation of the parasympathetic 742