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The aim of this study was to evaluate the cardiovascular response to the activation of arterial chemoreceptors during voluntary apnea in snoring subjects. Fifty five men were enrolled in the study: 33 snorers and 22 non-snorers (control group). The majority of snorers were overweight and hypertensive. The experimental session consisted of 20 voluntary inspiratory apneas interspersed with 1 min free breathing periods, and 20 min recovery. The following parameters were recorded noninvasively: blood pressure, ECG, and arterial oxygen saturation. Data analysis was based on the Smietanowski procedure, written in the 4-th generation script language of MATLAB environment, which allows assessing the relative contribution of cardiac and vascular components to blood pressure variability. The results indicate that repetitive apneas led to significantly greater increases in blood pressure in the snorers. In this group, the domination of vascular influences during apnea periods reached 67 ±2.0%, which was greater than the 56 ±1.8% in the non-snorers (P<0.01). In contrast, the contribution of the cardiac component in the blood pressure response to apnea was greater in the non-snorers: 33 ±3% vs. 20 ±2% in the snorers (P<0.01). We conclude that activation of carotid chemoreceptors during voluntary apnea evokes a greater cardiovascular response in snorers, related to the reflex increase in total peripheral vascular resistance, and, consequently, a greater increase in blood pressure.
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The aim of our study was to check the responsiveness the chemoreceptor reflex in 28 young mildly hypertensive men (HTS), aged 18-32 years and 25 normotensive male subjects (NTS) aged 19-32 years, before and after 3-months dynamic exercise training. We tested the hypothesis that dynamic training reduces arterial chemoreceptor drive in mild hypertension. Circulatory response to 3-min hyperoxic inactivation of arterial chemoreceptors induced by 70% oxygen breathing was measured before and after training. Arterial blood pressure (BP) was recorded continuously by Finapres method, stroke volume and arm blood flow were registered by impedance reography, heart rate by ECG. Both groups were submitted to moderate 3-months dynamic exercise training. Before training the hyperoxic breathing caused in HTS a significant decrease in systolic BP by 6±1mmHg p<0.01, in diastolic BP by 2±0.6mmHg p<0.01, and in total peripheral vascular resistance (TPR) by 0.24±0.04 TPRU (p<0.01). After training hyperoxia augmented systolic BP by 2.64±1.9mmHg (NS), diastolic BP by 2±1mmHg p<0.05, and TPR by 0.043±0.05 TPRU (ANOVA). In NTS before training brief hyperoxia produced insignificant change in BP and TPR. In NTS after training hyperoxia increased systolic BP by 4.2 mm Hg±1.23 p<0.01 and diastolic BP by 3.1±0.6mmHg p<0.01 respectively and TPR by 0.053±0.02 TPRU. Our results confirm earlier finding on the enhanced arterial chemoreceptor reflex drive in mild human hypertension. We conclude that normalizing arterial blood pressure in subjects with mild hypertension which occurred after 3-months dynamical exercise training is due to attenuation of the sympathoexcitatory chemoreceptor reflex drive by exercise training. The mechanism of this effect requires further study.
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