Exercise training improves cardiac autonomic control, cardiac function, and arrhythmogenesis in rats with preserved-ejection fraction heart failure

Abstract

Chronic heart failure is characterized by autonomic imbalance, cardiac dysfunction, and arrhythmogenesis. It has been shown that exercise training (ExT) improves central nervous system oxidative stress, autonomic control, and cardiac function in heart failure with reduced ejection fraction; however, to date no comprehensive studies have addressed the effects of ExT, if any, on oxidative stress in brain stem cardiovascular areas, cardiac autonomic balance, arrhythmogenesis, and cardiac function in heart failure with preserved ejection fraction (HFpEF). We hypothesize that ExT reduces brain stem oxidative stress, improves cardiac autonomic control and cardiac function, and reduces arrhythmogenesis in HFpEF rats. Rats underwent sham treatment or volume overload to induce HFpEF. ExT (60 min/day, 25 m/min, 10% inclination) was performed for 6 wk starting at the second week after HFpEF induction. Rats were randomly allocated into Sham+sedentary (Sed) ( = 8), Sham+ExT ( = 6), HFpEF+Sed ( = 8), and HFpEF+ExT ( = 8) groups. Compared with the HFpEF+Sed condition, HFpEF+ExT rats displayed reduced NAD(P)H oxidase activity and oxidative stress in the rostral ventrolateral medulla (RVLM), improved cardiac autonomic balance, and reduced arrhythmogenesis. Furthermore, a threefold improvement in cardiac function was observed in HFpEF+ExT rats. These novel findings suggest that moderate-intensity ExT is an effective means to attenuate the progression of HFpEF through improvement in RVLM redox state, cardiac autonomic control, and cardiac function. In the present study, we found that exercise reduced oxidative stress in key brain stem areas related to autonomic control, improved sympathovagal control of the heart, reduced cardiac arrhythmias, and delayed deterioration of cardiac function in rats with heart failure with preserved ejection fraction (HFpEF). Our results provide strong evidence for the therapeutic efficacy of exercise training in HFpEF.

Rostral ventrolateral medullary catecholaminergic neurones mediate irregular breathing pattern in volume overload heart failure rats

“…In previous studies (Andrade et al . ; Toledo et al . ), we observed that rats with HF induced by volume overload displayed both diastolic and systolic dysfunction, and importantly, decrements in diastolic function were further aggravated by central chemoreflex activation.…”

“…; Andrade et al . ). In addition, systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MABP) and pulse pressure (PP) were calculated from the arterial pressure recordings.…”

“…; Andrade et al . , ). We also calculated EDPVR and ESPVR during hypercapnia ( 7% during 30 s) to estimate the effect of central chemoreflex activation on cardiac function.…”

“…HF was induced by the surgical creation of an arteriovenous (A-V) fistula as previously described (Brodsky et al 1998;Toledo et al 2017;Del Rio et al 2017;Andrade et al 2017;Andrade et al 2019). Briefly, under anaesthesia (isoflurane: 5% for induction, 1.5% for maintenance, balanced with O 2 ), the inferior vena cava and the abdominal aorta were exposed using a midline incision.…”

Cardioprotective effects of high‐intensity interval training are mediated through microRNA regulation of mitochondrial and oxidative stress pathways

“…Abnormal narrowing of vasculature under these conditions can lead to heart failure and cardiac complications that result in functional or structural disorders of this organ. This leads to an autonomic imbalance and creates impaired ventricular filling or ejection of blood to the systemic circulation to meet the metabolic demands of the body and is associated with mortality and diminished vitality (Andrade et al, ; Brito & Cepeda, ). Major causes leading to a higher risk of these issues is physical inactivity and a sedentary lifestyle (Ford & Caspersen, ; Young et al, ).…”