Cardiac autonomic control, influenced by thermoregulatory changes in humans

It is known that autonomic cardiac control and thermoregulation are connected. Heart rate variability (HRV) is an analysis which refers to the regulation of the sinoatrial node of the heart by the sympathetic and parasympathetic branches of the autonomic nervous system (ANS). Publications that investigate HRV under changed thermoregulatory states lack certain information e.g. time of day or measures for both, skin and core body temperature (CBT). Thus, the main focus of the present thesis is to broaden the basic physiological and chronobiological knowledge about the interaction between autonomic cardiac control and thermoregulation. To examine this subjects’ thermoregulatory state was modified either by passive body heating or was investigated in subjects with endogenous dysregulation of distal vessels, leading to thermal discomfort from cold extremities.
In chapter 2 both physiological and chronobiological aspects of a thermal load in the evening on CBT, melatonin, heart rate (HR) and HRV measures were addressed in healthy young men within a stringent controlled 40-h ‘constant routine’ (CR) protocol. Passive body heating for 30 minutes was able to induce a phase shift of output rhythms of the suprachiasmatic nuclei (SCN), the origin of the endogenous circadian rhythm. HR, CBT and melatonin were phase advanced by ~2h, whereas no shift was analysed for HRV measures. These findings indicate either no influence of the SCN to measures for HRV or only peripheral clocks were shifted by the evening heat load without a contribution from the SCN. Further, the acute implication of heat to the cardiovascular system was of great interest. Not only was an increase in CBT, HR and a global vasodilated body state found, but also an increase of sympathetic and decrease of the vagal activity, and an overall reduced HRV.
In chapter 3, HR and HRV analyses were assessed in a group of women including a different physiological thermoregulatory state and compared with the results derived from a control group of women during a stringent controlled 40-h CR protocol. Spectral analysis of RR-intervals during 3-minutes paced breathing episodes every 2-h revealed lower activity in the high-frequency band but not in the low-frequency (LF) band. This is leading to an elevated sympathovagal balance in women with an endogenous dysregulation of distal vessels. These findings indicate an autonomic imbalance in this study sample. From a chronobiological point of view a circadian rhythm for power in the LF band and for HR occurred. The power for the LF band was low in the afternoon and high at the end of the subjective night. Further, a correlation was found between sleepiness and sympathovagal balance in both groups. These findings suggest active regulation of the ANS against fatigue in women, regardless of their thermoregulatory state.
In chapter 4, HR and HRV were analysed in young healthy women during the sleep initiation period. This period is especially characterised by striking changes in HR, body temperature and electroencephalogram wave amplitude and frequency. Skin temperature, especially the gradient between distal and proximal skin temperature, is known to be an easily measurable variable for distal vasodilatation, which is controlled by the ANS. The relationship between skin temperature and cardiac autonomic control during sleep initiation was investigated. Furthermore, changes in sleep, temperature or cardiac regulation after constant posture conditions without prolonged wakefulness were analysed. Thus, the pattern of CBT and skin temperature, HR and its variability was elucidated during the sleep initiation period, examined on two subsequent nights in the chronobiological laboratory. To prolong the period from lights out to sleep onset and hence to a vasodilated body state, data derived from subjects that had thermal discomfort from cold extremities and difficulties initiating sleep was used. Sleep onset latency was longer in the first night compared to the second. Hence, the faster decline of arousals in the second night compared to the first allowed a faster build-up of sleep stage 2, slow wave sleep and delta power. Both, proximal and distal skin temperatures showed an increase after lights out. The distal-proximal skin temperature gradient, used as a measure for distal vasodilatation, started with a lower level after lights out in the first night, compared to the second. To summarise, different dynamics and differences between the two nights in skin temperature and sleep variables (but not in HR and HRV variables) were examined.