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Choir singing is known to promote wellbeing. One reason for this may be that singing demands a slower than normal respiration, which may in turn affect heart activity. Coupling of heart rate variability (HRV) to respiration is called Respiratory sinus arrhythmia (RSA). This coupling has a subjective as well as a biologically soothing effect, and it is beneficial for cardiovascular function. RSA is seen to be more marked during slow-paced breathing and at lower respiration rates (0.1 Hz and below). In this study, we investigate how singing, which is a form of guided breathing, affects HRV and RSA. The study comprises a group of healthy 18 year olds of mixed gender. The subjects are asked to; (1) hum a single tone and breathe whenever they need to; (2) sing a hymn with free, unguided breathing; and (3) sing a slow mantra and breathe solely between phrases. Heart rate (HR) is measured continuously during the study. The study design makes it possible to compare above three levels of song structure. In a separate case study, we examine five individuals performing singing tasks (1–3). We collect data with more advanced equipment, simultaneously recording HR, respiration, skin conductance and finger temperature. We show how song structure, respiration and HR are connected. Unison singing of regular song structures makes the hearts of the singers accelerate and decelerate simultaneously. Implications concerning the effect on wellbeing and health are discussed as well as the question how this inner entrainment may affect perception and behavior.

Arterial stiffness was increased in RA patients. Endothelial dysfunction was implicated and correlated with levels of soluble adhesion molecules. Small vessel resistance correlated with the long-standing inflammatory load in RA.

Objective. To investigate the relationship between endothelium-dependent and endothelium-independent functions and the stiffness of conduit arteries as well as levels of endothelial activation markers in patients with systemic sclerosis (SSc).Methods. Endothelium-dependent (i.e., flowmediated) and endothelium-independent (i.e., nitroglycerin-induced) dilation of the brachial artery was measured as the percentage of change from baseline (FMD% and NTG%, respectively) in 24 SSc patients and 24 age-and sex-matched healthy controls by highresolution ultrasound imaging. The maximum increase in systolic pressure per unit of time (dP/dt max ), as a measure of arterial wall stiffness, was assessed in the radial artery by pulse applanation tonometry. Plasma nitrate, the most important metabolite of nitric oxide, and 24-hour urinary excretion of nitrate were measured by gas chromatography mass spectrometry. Soluble E-selectin and soluble vascular cell adhesion molecule 1 (sVCAM-1) were measured by enzyme-linked immunosorbent assay.Results. Brachial artery FMD% and NTG% did not differ between SSc patients and controls. Radial artery dP/dt max was significantly increased in the patients and correlated significantly with elevated levels of plasma nitrate and sVCAM-1. Twenty-four-hour urinary nitrate excretion tended to be elevated. Brachial artery NTG% was significantly inversely correlated with levels of plasma nitrate and soluble endothelial adhesion molecules.Conclusion. The ability of the brachial arteries to dilate in response to hyperemia and nitroglycerin challenge is preserved in SSc. Stiffness of the radial artery is increased, however. Endothelial activation seems to determine the extent of the brachial artery NTG% and the radial artery dP/dt max . The data are compatible with the hypothesis that nitrate tolerance is present in the vascular smooth muscle cells of the brachial artery wall in SSc.

These data suggest that thioridazine has dose-related effects on ventricular repolarization and that the parent drug causes an important proportion of these effects, although its metabolites may also contribute.

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The effect on work performance of a single oral dose of the cardio-selective beta-adrenoreceptor blocking agent, metoprolol, was compared with an equipotent dose of the non-selective agent, propranolol, in the same subjects. A number of biochemical and physiological variables including heart rate, oxygen consumption, ventilation, lactate, free fatty acid and glucose levels were measured. Following exercise in the presence of both active drugs, subjects complained of excessive leg fatique. For the group there was a significant reduction in the total work performed and the maximum heart rate achieved on both drugs. There was a significant correlation between plasma levels of metoprolol, reduction in total work performed and reduction in maximum heart rate. By contrast, after propranolol, there was a wide variation in work performed at a time when the reduction in maximum heart rate was similar for all subjects. This suggests for propranolol that a reduction in heart rate alone is an inappropriate guide to the impairment of work performance. There was a fail in the circulating level of free fatty acids at the end of exercise in the presence of both drugs and it is possible that this biochemical variable contributed to the decrease in work performance.

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