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Very low frequency oscillations in the power spectra of heart rate variability during dry supine immersion and exposure to non-hypoxic hypobaria

机译:仰卧干燥沉浸和暴露于非缺氧性低通气期间心率变异性功率谱中的极低频振荡

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The origin of very low frequency (VLF) oscillations in the power spectra of heart rate variability (HRV) is controversial with possible mechanisms involving thermoregulation and/or renin-angiotensin-aldosterone system. Recently, a major contribution from vagal influences has been suggested. The present study investigated the behaviour of VLF (0.004-0.040 Hz) components of HRV power spectra in a group of healthy male volunteers during their exposure to (1) dry, supine, immersion in thermo-neutral water for 6 h (n = 7) and (2) non-hypoxic hypobaria (breathing 40-60% oxygen at 15 000′ simulated in a decompression chamber) for 5 h (n = 15). The two manoeuvres are established to increase vagal outflow. During both the manoeuvres, all the frequency domain indices of HRV exhibited a significant increase. Increase in HRV was much more than that in the R-R interval. At 6 h of immersion, the R-R interval increased by ~15% but the total power increased ~fourfold. Similarly, at 5 h of exposure to hypobaria, total power increased ~twofold with a very modest increase in an R-R of ~9%. Increase in spectral power was appreciable even after normalization with mean R-R~2. Increase in VLF during immersion was more than reported during enalaprilat blockade of angiotensin convertase enzyme. Plasma renin activity did not vary during hypobaria. There was a significant increase in pNN50, an established marker of cardiac vagal activity. Centre frequencies of the spectra and slope (β) of the relation between log(PSD) and log(frequency) did not change. Results were supportive of the notion that the parasympathetic system is pre-potent to influence slower (than respiratory) frequency components in HRV spectrum. Additionally, such an effect was without a change in the time constant of effector responses or pacemaker frequencies of VLF and LF periodicities and HRV was not a simple linear surrogate for cardiac vagal effects. An invariance of spectral exponent (β) ruled out contamination of VLF and LF spectra from fractal power as an alternate explanation.
机译:心率变异性(HRV)功率谱中的极低频(VLF)振荡的起源与涉及温度调节和/或肾素-血管紧张素-醛固酮系统的可能机制存在争议。最近,已经提出了迷走神经影响的主要贡献。本研究调查了一组健康男性志愿者在暴露于(1)干燥,仰卧,浸入热中性水中6 h(n = 7)时,HRV功率谱的VLF(0.004-0.040 Hz)分量的行为。 )和(2)非低氧性下呼吸道(在减压室中模拟为在15 000'处呼吸40-60%的氧气)5小时(n = 15)。建立这两种操作以增加迷走神经流出。在两次演习中,HRV的所有频域指数均显示出显着增加。 HRV的增加远远超过R-R间隔。浸入6小时后,R-R间隔增加了约15%,但总功率增加了约四倍。同样,在暴露于下半叶的5小时内,总功率增加了约两倍,而R-R却仅增加了约9%。即使在平均R-R〜2归一化之后,光谱功率的增加也是可观的。浸泡过程中VLF的增加超过了对血管紧张素转化酶的依那普利封阻滞期间的报道。低尿期血浆肾素活性无变化。 pNN50显着增加,pNN50是心脏迷走神经活动的既定标志。 log(PSD)和log(frequency)之间关系的频谱中心频率和斜率(β)不变。结果支持以下观点:副交感神经系统会影响HRV频谱中较慢(比呼吸频率)的频率成分。此外,这种效应不会改变效应器反应的时间常数或VLF和LF周期的起搏器频率,并且HRV并不是心脏迷走神经效应的简单线性替代。光谱指数(β)的不变性排除了分形功率对VLF和LF光谱的污染,作为替代解释。

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