Abstract-The effects of exercise training on baroreflex control of sympathetic nerve activity in human hypertension are unknown. We hypothesized that exercise training would improve baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) in patients with hypertension and that exercise training would reduce MSNA and blood pressure (BP) in hypertensive patients. Twenty never-treated hypertensive patients were randomly divided into 2 groups: exercise-trained (nϭ11; age: 46Ϯ2 years) and untrained (nϭ9; age: 42Ϯ2 years) patients. An age-matched normotensive exercise-trained group (nϭ12; age: 42Ϯ2 years) was also studied. Key Words: hypertension Ⅲ baroreflex sensitivity Ⅲ sympathetic nerve activity Ⅲ exercise Ⅲ blood pressure T here is accumulated evidence that arterial baroreflex plays an important role in the regulation of the cardiovascular system. During spontaneous variation of blood pressure (BP), stimulation or deactivation of the arterial baroreceptors located in the carotid sinus and aortic arch causes reflex bradycardia and tachycardia, respectively. At the vascular level, stimulation of the arterial baroreceptors results in sympathetic inhibition and, in consequence, reflex vasodilation. In contrast, the deactivation of the arterial baroreceptors elicits sympathetic-mediated vasoconstriction. 1 All of these responses work in concert to maintain the BP levels in the reference range. 1It has been described that arterial baroreflex sensitivity can be profoundly altered in some cardiovascular diseases. 2,3 In hypertension, some investigators, 4 -6 but not all, 7-9 observed that baroreflex control of heart rate (HR) and sympathetic nerve activity is significantly reduced. This autonomic dysfunction seems to correlate with an increase in sympathetic outflow and in BP levels. 10 On the other hand, previous studies have demonstrated that regular exercise causes significant changes in baroreflex control of HR in experimental hypertension. Exercise training improves baroreflex control of HR during the increase and decrease of BP in spontaneously hypertensive rats. 11,12 Furthermore, these studies indicate that the improvement in baroreflex sensitivity is, in part, mediated by the enhancement of the aortic depressor nerve sensitivity. In humans with hypertension, little information exists regarding the effects of exercise training on the baroreflex sensitivity. One of the few studies showed that exercise training caused a modest improvement in baroreflex bradycardia. 13 Thus, the effects of regular exercise on the baroreflex control of sympathetic nerve activity in humans with hypertension are unknown.It has been consistently shown that exercise training is a powerful nonpharmacological strategy to reduce BP levels in humans with hypertension. 14 -16 However, the mechanisms involved in the BP reduction after exercise training are still a matter of discussion. In the present study, we investigated the

Nota: These guidelines are for information purposes and should not replace the clinical judgment of a physician, who must ultimately determine the appropriate treatment for each patient.

These findings suggest an association between hypertension and decreased muscle metaboreflex control of MSNA.

Abstract-Autonomic dysfunction, including baroreceptor attenuation and sympathetic activation, has been reported in patients with myocardial infarction (MI) and has been associated with increased mortality. We tested the hypotheses that exercise training (ET) in post-MI patients would normalize arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA), and long-term ET would maintain the benefits in BRS and MSNA. Twenty-eight patients after 1 month of uncomplicated MI were randomly assigned to 2 groups, ET (MI-ET) and untrained. A normal control group was also studied. ET consisted of three 60-minute exercise sessions per week for 6 months. We evaluated MSNA (microneurography), blood pressure (automatic oscillometric method), heart rate (ECG), and spectral analysis of RR interval, systolic arterial pressure (SAP), and MSNA. Baroreflex gain of SAP-RR interval and SAP-MSNA were calculated using the ␣-index. At 3 to 5 days and 1 month after MI, MSNA and low-frequency SAP were significantly higher and BRS significantly lower in MI patients when compared with the normal control group. ET significantly decreased MSNA (bursts per 100 heartbeats) and the low-frequency component of SAP and significantly increased the low-frequency component of MSNA and BRS of the RR interval and MSNA. These changes were so marked that the differences between patients with MI and the normal control group were no longer observed after ET. MSNA and BRS in the MI-untrained group did not change from baseline over the same time period. ET normalizes BRS, low-frequency SAP, and MSNA in patients with MI. These improvements in autonomic control are maintained by long-term ET. Key Words: myocardial infarction Ⅲ sympathetic nerve activity Ⅲ exercise training Ⅲ autonomic control Ⅲ baroreflex control P revious studies show that myocardial infarction (MI) is linked to increased sympathetic nervous activity 1,2 and impaired arterial baroreflex sensitivity (BRS). 3 These findings of autonomic dysfunction have been associated with increased mortality in patients after MI. 4 -10 La Rovere et al 7 demonstrated that decreased BRS is associated with cardiac mortality risk. A follow-up of 61 months in uncomplicated post-MI patients with preserved left ventricular function showed that depressed BRS discriminated a subgroup at long-term high risk for cardiovascular mortality. 10 Increased muscle sympathetic nerve activity (MSNA) is an independent predictor of poor prognosis in patients with chronic heart failure, including patients with chronic heart failure after MI. 11 Thus, a therapeutic strategy targeted to the improvement in autonomic control in patients with MI represents an important clinical goal.In patients with cardiovascular disease, studies have shown that physical exercise is an important strategy to improve autonomic function. Exercise training has been shown to decrease MSNA 12 and improve BRS 12-14 in patients with MI. It remains unknown whether the magnitude of change in autonomic control actually normalizes BRS and sy...

ObjectiveTo describe acute/postacute COVID-19 presentations in athletes.DesignSystematic review and meta-analysis.Data sourcesThe search was conducted in four databases (MEDLINE, EMBASE, SCOPUS, SPORTDiscus) and restricted to studies published from 2019 to 6 January 2022.Eligibility criteria for selecting studiesStudies were required to (1) include professional, amateur or collegiate/university athletes with COVID-19; (2) present data on acute/postacute COVID-19 symptoms and (3) have an observational design. Risk of bias was assessed using the Joanna Briggs Institute Critical Appraisal tools.Results43 studies with 11 518 athletes were included. For acute presentation, the pooled event rates for asymptomatic and severe COVID-19 were 25.5% (95% CI: 21.1% to 30.5%) and 1.3% (95% CI: 0.7% to 2.3%), respectively. For postacute presentations, the pooled estimate of persistent symptoms was 8.3% (95% CI: 3.8% to 17.0%). Pooled estimate for myocardial involvement was 5.0% (95% CI: 2.5% to 9.8%) in athletes undergoing any cardiac testing, and 2.5% (95% CI: 1.0% to 5.8%) in athletes undergoing MRI, although clinical symptoms were not characterised. None of the studies with a control group (eg, non-infected athletes) could confirm a causal relationship between COVID-19 and myocardial involvement.ConclusionThis broad characterisation of COVID-19 presentations in athletes indicates that ~94% exhibited mild or no acute symptoms. The available evidence did not confirm a causal relationship between COVID-19 and myocardial involvement. A small proportion of athletes experienced persistent symptoms while recovering from infection, which were mostly mild in nature, but could affect return-to-play decisions and timing.

No abstract

ObjectiveTo examine the SARS-CoV-2 infection rate in a cohort of 6500 professional athletes and staff during the 2020 football (soccer) season in São Paulo, Brazil.MethodsThis retrospective cohort study included 4269 players (87% male, age: 21.7±4.2 years) and 2231 staff (87% male, age: 42.6±11.9 years) from 122 teams (women: n=16) involved in eight leagues (women: n=2), which took place in São Paulo, Brazil. Between 4 July 2020 and 21 December 2020, swab samples were collected weekly (n=29 507) and tested for SARS-Cov-2 via reverse transcription-PCR by an accredited laboratory commissioned by the São Paulo Football Federation. We contacted the medical staff of each team with positive cases to collect information on disease severity.ResultsAmong 662 PCR-confirmed cases, 501 were athletes and 161 were staff. The new infection rate was 11.7% and 7.2% for athletes and staff, respectively. Athletes were more susceptible to infection than staff (OR: 1.71, 95% CI: 1.42, 2.06, p<0.001), although with lower chance for moderate to severe disease (OR: 0.06, 95% CI: 0.01, 0.54, p=0.012). Six teams had ≥20 individuals testing positive for SARS-CoV-2, whereas 19 teams had ≥10 confirmed cases. Twenty-five mass outbreaks were identified (≥5 infections within a team in a 2-week period). The prevalence of SARS-CoV-2 infections was similar in athletes and staff as the general population in São Paulo.ConclusionDespite weekly testing and other preventive measures, we found a high SARS-CoV-2 infection rate in athletes and staff after resuming football, which coincides with the high prevalence of infection in the community during the same period. These data may assist policy-makers and sports federations for determining if and when it is safe to resume competitions.

We investigated the influence of sport modalities in resting bradycardia and its mechanisms of control in highly trained athletes. In addition, the relationships between bradycardia mechanisms and cardiac structural adaptations were tested. Professional male athletes (13 runners, 11 cyclists) were evaluated. Heart rate (HR) was recorded at rest on beat-to-beat basis (ECG). Selective pharmacological blockade was performed with atropine and esmolol. Vagal effect, intrinsic heart rate (IHR), parasympathetic (n) and sympathetic (m) modulations, autonomic influence (AI) and autonomic balance (Abal) were calculated. Plasmatic norepinephrine (high-pressure liquid chromatography) and cardiac structural adaptations (echocardiography) were evaluated. Runners presented lower resting HR, higher vagal effect, parasympathetic modulation (n), AI and IHR than cyclists (P<0.05). Abal, sympathetic modulation (m) and norepinephrine level were similar within athletes regardless of modality. The cardiac chambers were also similar between runners and cyclists (P=0.30). However, cyclists displayed higher septum and posterior wall thickness than runners (P=0.04). Further analysis showed a trend towards inverse correlation between IHR with septum wall thickness and posterior wall thickness (P=0.056). Type of sport influences the resting bradycardia level and its mechanisms of control in professional athletes. Resting bradycardia in runners is mainly dependent on an autonomic mechanism. In contrast, a cyclist's resting bradycardia relies on a non-autonomic mechanism probably associated with combined eccentric and concentric hypertrophy.