Air Force Station, Jamnagar-361 003, Gujarat, India.
Physiol Meas. 2011 Jun;32(6):717-29. doi: 10.1088/0967-3334/32/6/008. Epub 2011 May 23.
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.
心率变异性(HRV)的功率谱中极低频(VLF)振荡的起源存在争议,可能的机制涉及体温调节和/或肾素-血管紧张素-醛固酮系统。最近,有人提出迷走神经影响是一个主要贡献。本研究在一组健康男性志愿者中,观察了他们在(1)干燥、仰卧、在热中性水中浸泡 6 小时(n = 7)和(2)非缺氧性低气压(在减压室中模拟呼吸 40-60%氧气,15000')5 小时(n = 15)期间,HRV 功率谱的 VLF(0.004-0.040 Hz)成分的行为。这两种操作都被证明可以增加迷走神经输出。在这两种操作中,所有的 HRV 频域指标都显示出显著的增加。HRV 的增加比 R-R 间隔的增加还要多。在 6 小时的浸泡中,R-R 间隔增加了约 15%,但总功率增加了约四倍。同样,在 5 小时的低气压暴露中,总功率增加了约两倍,R-R 仅增加了约 9%。即使在与平均 R-R(2)归一化后,频谱功率的增加也是可观的。在浸泡期间,VLF 的增加超过了依那普利阻断血管紧张素转换酶时的增加。低气压期间,血浆肾素活性没有变化。pNN50 显著增加,pNN50 是心脏迷走神经活动的一个既定标志物。频谱的中心频率和对数(PSD)与对数(频率)之间关系的斜率(β)没有变化。结果支持这样一种观点,即副交感神经系统预先准备好影响 HRV 频谱中较慢(比呼吸慢)的频率成分。此外,这种影响不会改变效应器反应的时间常数或 VLF 和 LF 周期性的起搏器频率,并且 HRV 不是心脏迷走神经效应的简单线性替代物。频谱指数(β)的不变性排除了 VLF 和 LF 频谱中分数幂的污染作为替代解释。