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Purpose: To investigate the effects of an oral glucose tolerance test (OGTT) on baroreflex sensitivity (BRS) in a sample of healthy adolescents, and how acute exercise bouts of different intensities alter the effects of the OGTT on BRS.Methods: Thirteen male adolescents (14.0 ± 0.5 years) completed three conditions on separate days in a counterbalanced order: (1) high-intensity interval exercise (HIIE); (2) moderate-intensity interval exercise (MIIE); and (3) resting control (CON). At ~ 90 min following the conditions, participants performed an OGTT. Supine heart rate and blood pressure were monitored continuously at baseline, 60 min following the conditions, and 60 min following the OGTT. A cross-spectral method (LFgain) was used to determine BRS gain. Arterial compliance (AC) was assessed as the BRS vascular component. LFgain divided by AC (LFgain/AC) was used as the autonomic component.Results: Although non-significant, LFgain moderately decreased post-OGTT when no exercise was performed (pre-OGTT = 24.4 ± 8.2 ms mmHg- 1; post-OGTT = 19.9 ± 5.6 ms mmHg- 1; ES = 0.64, P > 0.05). This was attributed to the decrease in LFgain/AC (pre-OGTT = 1.19 ± 0.5 ms µm- 1; post-OGTT = 0.92 ± 0.24 ms µm- 1; ES = 0.69, P > 0.05). Compared to CON (Δ = - 4.4 ± 8.7 ms mmHg- 1), there were no differences for the pre-post-OGTT delta changes in LF/gain for HIIE (Δ = - 3.5 ± 8.2 ms mmHg- 1) and MIIE (Δ = 1.3 ± 9.9 ms mmHg- 1) had no effects on BRS following the OGTT (all ES < 0.5). Similarly, compared to CON (Δ = - 0.23 ± 0.40 ms µm- 1) there were no differences for the pre-post-OGTT delta changes in LF/gain for HIIE (Δ = - 0.22 ± 0.49 ms µm- 1) and MIIE (Δ = 0.13 ± 0.36 ms µm- 1).Conclusion: A moderate non-significant decrease in BRS was observed in adolescents following a glucose challenge with no apparent effects of exercise. [ABSTRACT FROM AUTHOR]

Purpose: The muscle metaboreflex activation has been shown essential to reach normal hemodynamic response during exercise. It has been demonstrated that patients with multiple sclerosis (MS) have impaired autonomic functions and cardiovascular regulation during exercise. However, to the best of our knowledge, no previous research to date has studied the metaboreflex in MS patients. The purpose of this study was to investigate the hemodynamic response to metaboreflex activation in patients with MS (n = 43) compared to an age-matched, control group (CTL, n = 21).Methods: Cardiovascular response during the metaboreflex was evaluated using the post-exercise muscle ischemia (PEMI) method and during a control exercise recovery (CER) test. The difference in hemodynamics between the PEMI and the CER test was calculated and this procedure allowed for the assessment of the metaboreflex response. Hemodynamics was estimated by impedance cardiography.Results: The MS group showed a normal mean blood pressure (MBP) response as compared to the CTL group (+6.5 ± 6.9 vs. +8 ± 6.8 mmHg, respectively), but this response was achieved with an increase in systemic vascular resistance, that was higher in the MS with respect to the CTL group (+137.6 ± 300.5 vs. -14.3 ± 240 dyne · s(-1) cm(-5), respectively). This was the main consequence of the MS group's incapacity to raise the stroke volume (-0.65 ± 10.6 vs. +6.2 ± 12.8 ml, respectively).Conclusion: It was concluded that MS patients have an impaired capacity to increase stroke volume (SV) in response to low level metaboreflex, even if they could sustain the MBP response by vasoconstriction. This was probably a consequence of their chronic physical de-conditioning. [ABSTRACT FROM AUTHOR]

To define the dynamics of cardiovascular adjustments to apnoea during immersion, beat-to-beat heart rate (HR) and systolic (SBP) and diastolic (DBP) blood pressures were recorded in six divers during and after prolonged apnoeas while resting fully immersed in 27 degrees C water. Apnoeas lasted 215 +/- 35 s. Compared to control values, HR decreased by 20 beats min(-1) and SBP and DBP increased by 23 and 17 mmHg, respectively, in the initial 20 +/- 3 s (phase I). Both HR and BP remained stable during the following 92 +/- 15 s (phase II). Subsequently, during the final 103 +/- 29 s, SBP and DBP increased linearly to values about 60% higher than control, whereas HR remained unchanged (phase III). Cardiac output (Q') decreased by 35% in phase I and did not further change in phases II and III. Compared to control, total peripheral resistances were twice and three times higher than control, respectively, at the end of phases I and III. After resumption of breathing, HR and BP returned to control values in 5 and 30 s, respectively. The time courses of cardiovascular adjustments to immersed breath-holding indicated that cardiac response took place only at the beginning of apnoea. In contrast, vascular responses showed two distinct adjustments. This pattern suggests that the chronotropic control via the baroreflex is modified during apnoea. These cardiovascular changes during immersed static apnoea are in agreement with those already reported for static dry apnoeas. [ABSTRACT FROM AUTHOR]

To define the dynamics of cardiovascular adjustments to apnoea, beat-to-beat heart rate (HR) and blood pressure and arterial oxygen saturation (SaO(2)) were recorded during prolonged breath-holding in air in 20 divers. Apnoea had a mean duration of 210 +/- 70 s. In all subjects, HR attained a value 14 beats min(-1) lower than control within the initial 30 s (phase I). HR did not change for the following 2-2.5 min (phase II). Then, nine subjects interrupted the apnoea (group A), whereas 11 subjects (group B) could prolong the breath-holding for about 100 s, during which HR continuously decreased (phase III). In both groups, mean blood pressure was 8 mmHg above control at the end of phase I; it then further increased by additional 12 mmHg at the end of the apnoea. In both groups, SaO(2) did not change in the initial 100-140 s of apnoea; then, it decreased to 95% at the end of phase II. In group B, SaO(2) further diminished to 84% at the end of phase III. A typical pattern of cardiovascular readjustments was identified during dry apnoea. This pattern was not compatible with a role for baroreflexes in phase I and phase II. Further readjustment in group B may imply a role for both baroreflexes and chemoreflexes. Hypothesis has been made that the end of phase II corresponds to physiological breakpoint. [ABSTRACT FROM AUTHOR]