Orthostatic intolerance is the development of disabling symptoms upon assuming an upright posture that are relieved partially by resuming the supine position. Postural tachycardia syndrome (POTS) is an orthostatic intolerance syndrome characterized by palpitations because of excessive orthostatic sinus tachycardia, lightheadedness, tremor, and near-syncope. Patients usually undergo extensive medical, cardiac, endocrine, neurologic, and psychiatric evaluation, which usually fails to identify a specific abnormality. The authors investigated the autonomic and hemodynamic profile of patients with POTS and the effectiveness of bisoprolol and fludrocortisone. The authors evaluated 11 female patients with POTS before and after medical treatment with a cardioselective bisoprolol beta-blocker or fludrocortisone, or both, and 11 age-matched control patients. Variability of heart rate and systolic blood pressure was assessed by fast Fourier transform, and spontaneous baroreceptor gain was assessed by use of the temporal sequences slope and alpha index. Modelflow was used to quantify hemodynamics. Symptoms in all patients improved greatly after medication. The autonomic and hemodynamic impairment observed in patients with POTS, particularly after orthostatic stress, is treated effectively with bisoprolol or fludrocortisone or both. These results need further confirmation in a controlled double-blind study. Proper medical treatment improves dramatically the clinical and autonomic-hemodynamic disturbances observed in patients with POTS. The data support the hypothesis that POTS is the result of a hyperadrenergic activation or hypovolemia during orthostasis.

This study provides descriptive data on injuries developed in a subpopulation of Portuguese amateur youth football players that could represent a focus for future prevention.

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Purpose: To analyze whether exercise training conducted at night disturbs sleep and affects nocturnal cardiac autonomic control in high-level female athletes. Methods: A total of 18 high-level female soccer players (mean [SD] age 20.4 [2.1] y) wore actigraphs and heart-rate (HR) monitors during night sleep throughout night training days (n = 8) and resting days (n = 8), for 3 consecutive weeks. This was a longitudinal study that measured internal training load, sleep, nocturnal cardiac autonomic activity, and well-being ratings prior to training sessions. Results: Training load varied across training days (eg, training impulse range, mean [SD]; effect size, ES [95% confidence interval]: 72.9 [18.8] to 138.4 [29.6] a.u.; F4,62 = 32.331; [.001–.16], large effect; P < .001). However, no differences in subjective well-being ratings were observed, although ES was large. Total sleep time (training days vs resting days: 07:17 [00:47] h vs 07:51 [00:42] h; ES = 0.742 [0.59–0.92], P = .005; moderate effect) and sleep-onset time (00:58 [00:19] h vs 00:44 [00:16] h; ES = 0.802 [0.68–0.94], P = .001; moderate effect) were negatively affected after night training. In addition, small effects were detected for wake-up time, time in bed, and sleep latency (P > .05). No differences were detected in HR variability during sleep (range of lnRMSSD: 4.3 [0.4] to 4.5 [0.4] ln[ms] vs 4.6 [0.3] to 4.5 [0.4] ln[ms]; F3,52 = 2.148; P > .05; [.01–.25], medium effect), but HR during sleep was significantly higher after training days (range of HR: 56 [4] to 63 [7] beats/min vs 54 [4] to 57 [6] beats/min; F2,32 = 15.956; P < .001; [.20–.63], large effect). Conclusion: Overall, the results indicate that exercise training conducted at night may disturb sleep and affect HR, whereas limited effects can be expected in HR variability assessed during sleep in high-level female soccer players.

Autonomic dysfunction seems to play a central role in the pathophysiology of neurocardiogenic syncope (NCS) but conflicting data have recently become available. We evaluated autonomic nervous system (ANS) function (heart rate variability (HRV), systolic blood pressure variability (SBPV) and baroreceptor gain (BRG)) and non-invasive haemodynamics (cardiac output and total peripheral resistance) in patients with neurocardiogenic syncope. Retrospectively, we evaluated 12 NCS patients (positive head-up tilt without pharmacological provocation) in the basal state and at initial tilt, 12 non-NCS patients with tilt-negative syncope and 12 aged-matched normal controls. Prospectively, we evaluated 16 NCS patients to analyse the haemodynamics and ANS activity throughout the tilt test (beginning of tilt and before syncope occurs). HRV and SBPV were accessed by fast Fourier transforms (FFT) and spontaneous BRG by temporal sequences, slope and a index. Modelflow was used to quantify the non-invasive haemodynamics. None of the autonomic and haemodynamic parameters at baseline or in the first 10 min of tilt was different among the respective NCS, non-NCS syncope and normal control groups, except for SBP, which was higher at baseline in controls. Throughout the tilt test in the prospective NCS group, the heart rate increased (88-95 beats x min(-1), P<0.05), systolic blood pressure decreased (123-109 mmHg, P<0.01), and arterial baroreceptor gain was reduced (7.6 to 5.5 ms mmHg(-1), P<0.01) and the absolute high frequency component of HRV (HF HRV) decreased (150-80 ms(-2), P<0.05), before syncope occurred. There was no change in the low frequency component of HRV (LF HRV), SBPV, cardiac output (CO) or total peripheral resistance (TPR). Tilt-induced syncope could not be predicted by non-invasive haemodynamic or autonomic parameters at rest or in the initial minutes of tilt. The decrease in arterial baroreceptor gain could be a precocious expression of the transient autonomic dysfunction that characterizes the occurrence of neurocardiogenic syncope.