Musculoskeletal fitness, as assessed by SRT, was a significant predictor of mortality in 51-80-year-old subjects. Application of a simple and safe assessment tool such as SRT, which is influenced by muscular strength and flexibility, in general health examinations could add relevant information regarding functional capabilities and outcomes in non-hospitalized adults.

Isolated muscle metaboreflex activation with posthandgrip exercise ischemia (PEI) increases sympathetic nerve activity and partially maintains the exercise-induced increase in blood pressure, but a smaller heart rate (HR) response occurs. The cardiopulmonary baroreceptors, mechanically sensitive receptors that respond to changes in central blood volume and pressure, are strongly associated with changes in body position and upon activation elicit reflex sympathoinhibition. Here, we tested the hypothesis that postural changes modulate the sympathetically mediated cardiac response to PEI in humans. Beat-to-beat HR (electrocardiography) and blood pressure (finger photoplethysmography) were continuously measured, and cardiac function was assessed by echocardiography in 13 healthy men (21 ± 3 yr). After a 15-min rest period, 90-s static handgrip at 40% maximum voluntary contraction was performed followed by 3 min of PEI. Four trials were randomly conducted during either seated or supine position with and without β-adrenergic blockade (25 mg atenolol). During PEI under control conditions, HR remained elevated from baseline in the seated [change (Δ): 4 ± 1 beats/min] but not in the supine (change: -1 ± 1 beats/min) position. Similarly, stroke volume and cardiac output were increased from baseline in the seated (∆13.0 ± 2.4 ml and ∆1.1 ± 0.2 l/min, respectively) but not in the supine (∆2.5 ± 2.9 ml and ∆0.13 ± 0.20 l/min, respectively) position. During β-adrenergic blockade, HR, stroke volume, and cardiac output remained unchanged in both conditions. We conclude that sympathetically mediated cardiac responses to PEI are influenced by changes in body position. These findings indicated that muscle metaboreflex and cardiopulmonary baroreflex have an interactive influence on the neural control of cardiovascular function in humans. NEW & NOTEWORTHY In the present study, we demonstrated that muscle metaboreflex activation increases heart rate, stroke volume, and cardiac output in the seated position but not in the supine position and not after β-adrenergic blockade. These findings indicate that sympathetically mediated cardiac responses to isolated muscle metaboreflex activation after exercise are modulated by central blood volume mobilization.

COP >30, either independently or in combination with low VOmax, is a good predictor of all-cause mortality in community-dwelling adults (healthy or with chronic disease). COP is a submaximal prognostic index that is simple to obtain and adds to CPET assessment, especially for adults unable or unwilling to achieve maximal exercise.

Panic disorder (PD) patients often report respiratory symptoms and tend to perform poorly during maximal cardiopulmonary exercise testing (CPX), at least partially, due to phobic anxiety. Thus, we hypothesized that a submaximal exercise variable, minimum VE/VO2 - hereafter named cardiorespiratory optimal point (COP) -, may be useful in their clinical assessment. Data from 2,338 subjects were retrospectively analyzed and 52 (2.2%) patients diagnosed with PD (PDG) (70% women; aged 48±13 years). PD patients were compared with a healthy control group (CG) precisely matched to number of cases, age and gender profiles. PDG was further divided into two subgroups, based on having achieved a maximal or a submaximal CPX (unwilling to continue until exhaustion). We compared COP, VO2 max, maximum heart rate (HR max) between PDG and CG, and also COP between maximal and submaximal PD subgroups. COP was similar between PDG and CG (21.9±0.5 vs. 23.4±0.6; p = 0.07), as well as, for PD subgroups of maximal and submaximal CPX (22.0±0.5 vs. 21.6±1.3; p = 0.746). Additionally, PD patients completing a maximal CPX obtained VO2 max (mL.kg−1.min−1) (32.9±1.57 vs 29.6±1.48; p = 0.145) and HR max (bpm) similar to controls (173±2.0 vs 168±2.7; p = 0.178). No adverse complications occurred during CPX. Although clinically safe, it is sometimes difficult to obtain a true maximal CPX in PD patients. Normalcy of cardiorespiratory interaction at submaximal effort as assessed by COP may contribute to reassure both patients and physicians that there is no physiological substrate for exercise-related respiratory symptoms often reported by PD patients.

Background: At the maximal Cardiopulmonary Exercise Testing (CPET), several ventilatory variables are analyzed, including the ventilatory equivalent for oxygen (VE/VO2). The minimum VE/VO2 value reflects the best integration between the respiratory and cardiovascular systems and may be called "Cardiorespiratory Optimal Point (COP)".

BackgroundPhysiological reflexes modulated primarily by the vagus nerve allow the heart to decelerate and accelerate rapidly after a deep inspiration followed by rapid movement of the limbs. This is the physiological and pharmacologically validated basis for the 4-s exercise test (4sET) used to assess the vagal modulation of cardiac chronotropism.ObjectiveTo present reference data for 4sET in healthy adults.MethodsAfter applying strict clinical inclusion/exclusion criteria, 1,605 healthy adults (61% men) aged between 18 and 81 years subjected to 4sET were evaluated between 1994 and 2014. Using 4sET, the cardiac vagal index (CVI) was obtained by calculating the ratio between the duration of two RR intervals in the electrocardiogram: 1) after a 4-s rapid and deep breath and immediately before pedaling and 2) at the end of a rapid and resistance-free 4-s pedaling exercise.ResultsCVI varied inversely with age (r = -0.33, p < 0.01), and the intercepts and slopes of the linear regressions between CVI and age were similar for men and women (p > 0.05). Considering the heteroscedasticity and the asymmetry of the distribution of the CVI values according to age, we chose to express the reference values in percentiles for eight age groups (years): 18–30, 31–40, 41–45, 46–50, 51–55, 56–60, 61–65, and 66+, obtaining progressively lower median CVI values ranging from 1.63 to 1.24.ConclusionThe availability of CVI percentiles for different age groups should promote the clinical use of 4sET, which is a simple and safe procedure for the evaluation of vagal modulation of cardiac chronotropism.

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Previous studies have indicated that central GABAergic mechanisms are involved in the heart rate (HR) responses at the onset of exercise. On the basis of previous research that showed similar increases in HR during passive and active cycling, we reasoned that the GABAergic mechanisms involved in the HR responses at the exercise onset are primarily mediated by muscle mechanoreceptor afferents. Therefore, in this study, we sought to determine whether central GABA mechanisms are involved in the muscle mechanoreflex-mediated HR responses at the onset of exercise in humans. Twenty-eight healthy subjects (14 men and 14 women) aged between 18 and 35 yr randomly performed three bouts of 5-s passive and active cycling under placebo and after oral administration of diazepam (10 mg), a benzodiazepine that produces an enhancement in GABA activity. Beat-to-beat HR (electrocardiography) and arterial blood pressure (finger photopletysmography) were continuously measured. Electromyography of the vastus lateralis was obtained to confirm no electrical activity during passive trials. HR increased from rest under placebo and further increased after administration of diazepam in both passive (change: 12 ± 1 vs. 17 ± 1 beats/min, P < 0.01) and active (change: 14 ± 1 vs. 18 ± 1 beats/min, P < 0.01) cycling. Arterial blood pressure increased from rest similarly during all conditions ( P > 0.05). Importantly, no sex-related differences were found in any variables during experiments. These findings demonstrate, for the first time, that the GABAergic mechanisms significantly contribute to the muscle mechanoreflex-mediated HR responses at the onset of exercise in humans. NEW & NOTEWORTHY We found that passive and voluntary cycling evokes similar increases in heart rate and that these responses were enhanced after diazepam administration, a benzodiazepine that enhances GABA activity. These findings suggest that the GABAergic system may contribute to the muscle mechanoreflex-mediated vagal withdrawal at the onset of exercise in humans.