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 nervous system immediately after maximum effort in cardiopulmonary exercise testing. 11 Several investigators showed that the kinetic of HRR in a 6-min recovery period was reduced in patients with HF 33 and this reduction seems to be independent of β -adrenergic blocker therapy. 34 Ushijima et al. 35 showed an association between norepinephrine and HRR in patients with myocardial infarction, arguing that increased sympathetic excitation at maximum exercise may suppress the parasympathetic reactivation leading to HRR attenuation. 35 Taken together, the sympathovagal impairment in patients with HF is associated with poor outcome, and this autonomic imbalance may worsen the loss of muscle mass in these patients. In fact, we showed greater MSNA and lower decrease in HRR at 1 st and 2 nd minutes post-exercise in sarcopenic patients with HF. Furthermore, reduced appendicular lean muscle mass was correlated with lower HRR1 (r = 0.26), HRR2 (r = 0.25) and greater MSNA (r = -0.29). We recognize limitations in our study. The present study included only male patients, so we are not able to generalize these results to female patients with HF. Further studies are necessary to investigate the influence of sarcopenia on gender‑related differences. The date when HF was diagnosed was not available in patients’ medical records, and to compensate for this missing information, we included only patients with at least one year of diagnosis. We assessed parasympathetic activity using the HRR as a marker of vagal reactivation. Although our study has a clinical applicability, more studies using HR variability should clarify the role of cardiac autonomic control on sarcopenia in patients with HF. Conclusion Sympatho-vagal imbalance seems to be associated with sarcopenia in male patients with HF. These results highlight the importance of a therapeutic approach in patients with muscle wasting and increased peripheral sympathetic outflow. Author contributions Conception and design of the research: Fonseca GWP, dos Santos MR, Alves MJNN; Acquisition of data: Fonseca GWP, dos Santos MR, Souza FR, Costa MJA, Takayama L, Pereira RMR, Alves MJNN; Analysis and interpretation of the data: Fonseca GWP, dos Santos MR, Costa MJA,Souza FR, Pereira RMR, Negrão CE, Alves MJNN; Statistical analysis: Fonseca GWP, dos Santos MR; Obtaining financing: Negrão CE, Alves MJNN; Writing of the manuscript: Fonseca GWP, Souza FR, Alves MJNN; Critical revision of the manuscript for intellectual content: dos Santos MR, von Haehling S, Pereira RMR, Negrão CE, Anker SD, Alves MJNN. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding This study was funded by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP; 2015/22814‑5). Fonseca GWP was supported by Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq; 148758/2016-9); Dos Santos MR by FAPESP (2016/24306-0); Negrão CE by FAPESP (2015/22814-5). All foundations are from São Paulo-SP, Brazil. Study Association This article is part of the thesis of Doctoral submitted by Guilherme Wesley Peixoto da Fonseca, from Universidade Federal de São Paulo. Ethics approval and consent to participate This study was approved by the Ethics Committee of the CAPPesq under the protocol number 0892/07. All the procedures in this study were in accordance with the 1975 Helsinki Declaration, updated in 2013. Informed consent was obtained from all participants included in the study. 1. von Haehling S, Ebner N, Dos Santos MR, Springer J, Anker SD. Muscle wasting and cachexia in heart failure: mechanisms and therapies. Nat Rev Cardiol. 2017;14(6):323-41. 2. Fulster S, TackeM, Sandek A, Ebner N, Tschope C, DoehnerW, et al. 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