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The aim of this study was to examine the influence of physical fitness on cardiac autonomic control in passengers prior to, during and following commercial flights. Twenty-two, physically active men (36.4 ± 6.4 years) undertook assessments of physical fitness followed by recordings of 24-h heart rate (HR), heart rate variability (HRV), and blood pressure (BP) on a Control (no flight) and Experimental (flight) day. Recordings were analyzed using a two-way analysis of variance for repeated measures with relationships between variables examined via Pearson product-moment correlation coefficients. Compared to the Control day, 24-h HR was significantly greater (>7%) and HRV measures (5-39%) significantly lower on the Experimental day. During the 1-h flight, HR (24%), and BP (6%) were increased while measures of HRV (26-45%) were reduced. Absolute values of HRV during the Experimental day and relative changes in HRV measures (Control-Experimental) were significantly correlated with measures of aerobic fitness (r = 0.43 to 0.51; -0.53 to -0.52) and body composition (r = -0.63 to -0.43; 0.48-0.61). The current results demonstrated that short-term commercial flying significantly altered cardiovascular function including the reduction of parasympathetic modulations. Further, greater physical fitness and lower body fat composition were associated with greater cardiac autonomic control for passengers during flights. Enhanced physical fitness and leaner body composition may enable passengers to cope better with the cardiovascular stress and high allostatic load associated with air travel for enhanced passenger well-being.

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Recent concerns over the impact of antidepressant medications, including the selective serotonin reuptake inhibitors (SSRIs), on cardiovascular function highlight the importance of research on the moderating effects of specific lifestyle factors such as physical activity. Studies in affective neuroscience have demonstrated robust acute effects of SSRIs, yet the impact of SSRIs on cardiovascular stress responses and the moderating effects of physical activity remain to be determined. This was the goal of the present study, which involved a double-blind, randomized, placebo-controlled, cross-over trial of a single-dose of escitalopram (20 mg) in 44 healthy females; outcomes were heart rate (HR) and its variability. Participants engaging in at least 30 min of vigorous physical activity at least 3 times per week (regular exercisers) showed a more resilient cardiovascular stress response than irregular vigorous exercisers, a finding associated with a moderate effect size (Cohen's d = 0.48). Escitalopram attenuated the cardiovascular stress response in irregular exercisers only (HR decreased: Cohen's d = 0.80; HR variability increased: Cohen's d = 0.33). HR during stress under escitalopram in the irregular exercisers was similar to that during stress under placebo in regular exercisers. These findings highlight that the effects of regular vigorous exercise during stress are comparable to the effects of an acute dose of escitalopram, highlighting the beneficial effects of this particular antidepressant in irregular exercisers. Given that antidepressant drugs alone do not seem to protect patients from cardiovascular disease (CVD), longitudinal studies are needed to evaluate the impact of exercise on cardiovascular stress responses in patients receiving long-term antidepressant treatment.

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Survivors of childhood ALL have been demonstrated to have increased morning cortisol levels compared to healthy controls. Information regarding the response of the HPA axis and the sympathetic nervous system to stress in childhood ALL survivors is not available. The present study aimed at assessing the endocrine and cardiovascular stress response in childhood ALL survivors and healthy controls by evaluating perceived stress on visual analog scales, by determining saliva cortisol, blood pressure and heart rate in response to the Trier Social Stress Test for Children (TSST-C). Fifty survivors who had completed their treatment for childhood ALL 57 (IQR 47.0-72.3) months before and 50 healthy age and sex matched controls were included. Exposure to the TSST-C induced a significant response of perceived stress, saliva cortisol and cardiovascular outcome variables in the total study group. These responses did not significantly differ between survivors of childhood ALL and healthy controls. We conclude that the endocrine and cardiovascular response to social stress are intact in survivors of childhood ALL.

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AIMS: The nucleus of the solitary tract (NTS) is important for cardiovascular regulation and contains angiotensin type 1A (AT1A) receptors. To assess its function, we examined the effect of expressing in AT1A receptors in the NTS of mice lacking these receptors. METHODS AND RESULTS: Bilateral microinjections of lentivirus expressing AT1A receptors (AT1Av mice, n = 6) or green fluorescent protein (GFPv, n = 8, control) under the control of the PRSx8 promotor were made into the NTS of AT1A receptors null mice (AT1A(-/-)). Telemetry devices recorded blood pressure (BP), heart rate (HR), and locomotor activity. Expression of AT1A receptors in the NTS increased BP by 11.2 ± 4 mmHg (P < 0.05) at 2 and 3 weeks, whereas GFPv mice remained at pre-injection BP. Ganglion blockade reduced BP to similar levels pre- and post-transfection in GFPv and AT1Av mice. Greater pressor responses to cage-switch stress were observed following AT1A receptors expression (+18 ± 2 mmHg pre- to +24 ± 2 mmHg post-virus, P < 0.05) with similar stress-induced pressor responses pre- and post-virus in GFPv mice. Pressor responses to restraint stress pre- and post-virus were similar in AT1Av but were 20% less post-GFPv (P < 0.001). The lack of attenuation in BP to restraint was associated with four-fold greater Fos-expression in AT1A receptors mice. AT1A receptors expression in the NTS did not alter baroreflex gain differently between groups. CONCLUSION: The results suggest that transfection of AT1A receptors on neurons in the NTS elevates BP independent of the SNS and pressor responses to aversive stimuli are associated with greater Fos-expression in forebrain regions. This study suggests a novel mechanism by which the NTS may modulate MAP in the long-term via AT1A receptors.

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