Predominance of Intrinsic Mechanism of Resting Heart Rate Control and Preserved Baroreflex Sensitivity in Professional Cyclists after Competitive Training.

Different season trainings may influence autonomic and non-autonomic cardiac control of heart rate and provokes specific adaptations on heart's structure in athletes. We investigated the influence of transition training (TT) and competitive training (CT) on resting heart rate, its mechanisms of control, spontaneous baroreflex sensitivity (BRS) and relationships between heart rate mechanisms and cardiac structure in professional cyclists (N = 10). Heart rate (ECG) and arterial blood pressure (Pulse Tonometry) were recorded continuously. Autonomic blockade was performed (atropine-0.04 mg.kg-1; esmolol-500 µg.kg-1 = 0.5 mg). Vagal effect, intrinsic heart rate, parasympathetic (n) and sympathetic (m) modulations, autonomic influence, autonomic balance and BRS were calculated. Plasma norepinephrine (high-pressure liquid chromatography) and cardiac structure (echocardiography) were evaluated. Resting heart rate was similar in TT and CT. However, vagal effect, intrinsic heart rate, autonomic influence and parasympathetic modulation (higher n value) decreased in CT (P≤0.05). Sympathetic modulation was similar in both trainings. The autonomic balance increased in CT but still showed parasympathetic predominance. Cardiac diameter, septum and posterior wall thickness and left ventricular mass also increased in CT (P<0.05) as well as diastolic function. We observed an inverse correlation between left ventricular diastolic diameter, septum and posterior wall thickness and left ventricular mass with intrinsic heart rate. Blood pressure and BRS were similar in both trainings. Intrinsic heart rate mechanism is predominant over vagal effect during CT, despite similar resting heart rate. Preserved blood pressure levels and BRS during CT are probably due to similar sympathetic modulation in both trainings.

Neurovascular Control and Cardiac Structure in Amateur Runners with Hypertension.

PURPOSE: The neurovascular mechanisms underlying hypertension are minimized by exercise training. However, it is not known whether previously trained individuals with hypertension would have deleterious repercussion of this disease. Our aim was to investigate the neurovascular control and the cardiac structure of athletes with hypertension. METHODS: Muscle sympathetic nerve activity (MSNA) (microneurography), baroreflex sensitivity (intravenous infusion of phenylephrine and nitroprusside), arterial stiffness (pulse wave velocity and echotracking), and cardiac structure (echocardiography) were evaluated in 17 runners with hypertension (42 ± 1 yr) and 20 normotensive (43 ± 1 yr) amateur runners. RESULTS: Runners with hypertension had higher MSNA (+24% burst frequency, P = 0.02; +24%, burst incidence, P < 0.01), left ventricular mass (+22%, P < 0.01), septum wall thickness (+9%, P = 0.04), posterior wall thickness (+11%, P = 0.04), and left atrium (+11%, P < 0.001) compared with normotensive runners. Baroreflex control of heart rate was lower in runners with hypertension during increase (P = 0.05) but not during decrease (P = 0.11) of systolic blood pressure when compared with normotensive runners. There was no difference between groups in baroreflex control of MSNA during increase (P = 0.38) and decrease (P = 0.36) of diastolic blood pressure. Pulse wave velocity (P = 0.71) and carotid variables: intima media thickness (P = 0.18), diameter (P = 0.09), and distension (P = 0.79) were similar between groups. CONCLUSIONS: Sympathetic overactivity seems to be involved in the underlying mechanisms of hypertension in amateur runners. Alterations in cardiac structure and decreased baroreflex control of heart rate suggest limited protection from exercise training. However, baroreflex control of MSNA and elastic properties of artery are preserved in this population.

Effects of exercise training on circulating and skeletal muscle renin-angiotensin system in chronic heart failure rats.

BACKGROUND: Accumulated evidence shows that the ACE-AngII-AT1 axis of the renin-angiotensin system (RAS) is markedly activated in chronic heart failure (CHF). Recent studies provide information that Angiotensin (Ang)-(1-7), a metabolite of AngII, counteracts the effects of AngII. However, this balance between AngII and Ang-(1-7) is still little understood in CHF. We investigated the effects of exercise training on circulating and skeletal muscle RAS in the ischemic model of CHF. METHODS/MAIN RESULTS: Male Wistar rats underwent left coronary artery ligation or a Sham operation. They were divided into four groups: 1) Sedentary Sham (Sham-S), 2) exercise-trained Sham (Sham-Ex), sedentary CHF (CHF-S), and exercise-trained CHF (CHF-Ex). Angiotensin concentrations and ACE and ACE2 activity in the circulation and skeletal muscle (soleus and plantaris) were quantified. Skeletal muscle ACE and ACE2 protein expression, and AT1, AT2, and Mas receptor gene expression were also evaluated. CHF reduced ACE2 serum activity. Exercise training restored ACE2 and reduced ACE activity in CHF. Exercise training reduced plasma AngII concentration in both Sham and CHF rats and increased the Ang-(1-7)/AngII ratio in CHF rats. CHF and exercise training did not change skeletal muscle ACE and ACE2 activity and protein expression. CHF increased AngII levels in both soleus and plantaris muscle, and exercise training normalized them. Exercise training increased Ang-(1-7) in the plantaris muscle of CHF rats. The AT1 receptor was only increased in the soleus muscle of CHF rats, and exercise training normalized it. Exercise training increased the expression of the Mas receptor in the soleus muscle of both exercise-trained groups, and normalized it in plantaris muscle. CONCLUSIONS: Exercise training causes a shift in RAS towards the Ang-(1-7)-Mas axis in skeletal muscle, which can be influenced by skeletal muscle metabolic characteristics. The changes in RAS circulation do not necessarily reflect the changes occurring in the RAS of skeletal muscle.