Emerging data indicate a substantial decrease in global physical activity levels during the period of social isolation adopted worldwide to contain the spread of the coronavirus disease 2019 (COVID-19). Confinement-induced decreases in physical activity levels and increases in sedentary behavior may provoke a rapid deterioration of cardiovascular health and premature deaths among populations with increased cardiovascular risk. Even short-term (1–4 wk) inactivity has been linked with detrimental effects in cardiovascular function and structure and increased cardiovascular risk factors. In this unprecedented and critical scenario, home-based physical activity programs arise as a clinically relevant intervention to promote health benefits to cardiac patients. Many studies have demonstrated the feasibility, safety, and efficacy of different models of home-based exercise programs in the primary and secondary prevention of cardiovascular diseases and major cardiovascular events among different populations. This body of knowledge can inform evidence-based policies to be urgently implemented to counteract the impact of increased physical inactivity and sedentary behavior during the COVID-19 outbreak, thereby alleviating the global burden of cardiovascular disease.

Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise - known as heart rate recovery (HRR) - is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR.

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Introduction:The acute blood pressure (BP) decrease is greater after evening than morning exercise, suggesting that evening training may have a greater hypotensive effect. Objective:To compare the hypotensive effect of aerobic training performed in the morning versus evening in treated hypertensives. Methods: Fifty treated hypertensive men were randomly allocated to 3 groups: morning training (MT); evening training (ET); and control (C). Training groups cycled for 45min at moderate-intensity (progressing from the heart rate of the anaerobic threshold to 10% below the heart rate of the respiratory compensation point), while C stretched for 30 min. Interventions were conducted 3 times/week for 10 weeks. Clinic and ambulatory BP, hemodynamic, and autonomic mechanisms were evaluate d before and after the interventions. Clinic assessments were performed in the morning (7-9a.m.) and evening (6-8p.m.). Between-within ANOVAs were used (P≤0.05). Results: Only ET decreased clinic systolic BP differently from C and MT (morning assessment -5±6 mmHg and evening assessment -8±7 mmHg, P<0.05). Only ET reduced 24h and asleep diastolic BP differently from C and MT (-3±5 and -3±4 mmHg, respectively, P<0.05). Systemic vascular resistance (SVR) decreased from C only in ET (P=0.03). Vasomotor sympathetic modulation decreased (P=0.001) and baroreflex sensitivity (P<0.02) increased from C in both training groups with greater changes in ET than MT. Conclusions: In treated hypertensive men, aerobic training performed in the evening decreased clinic and ambulatory BP, due to reductions in SVR and vasomotor sympathetic modulation. Aerobic training conducted at both times of day increases baroreflex sensitivity, but with greater after ET.