The autonomic nervous system at high altitude

Abstract

IntroductionHigh altitude places are amongst the most inhospitable on earth. According to WHO [70] in 1966 there were approximately 140 million people living at altitudes over 2,500 m and there are several areas of permanent habitation at over 4,000 m. These are in three main regions of the world: the Andes of South America, the highlands of Eastern Africa, and the Himalayas of South-Central Asia. This review is concerned with the effects of the altitude on visitors and the ways by which the permanent high altitude dwellers have adapted to their environment.The two main challenges to life at high altitude come from hypobaric hypoxia and the low ambient temperatures. Temperature decreases about 1°C for each 150 m elevation, so that at 4,500 m temperature is roughly 30°C lower than at sea level. Barometric pressure falls progressively with increasing altitude. Up to about 2,500 m there are few if any effects of hypoxia. Above 3,000 m some effects of hypoxia are likely to be experienced and above 4,000 m adverse effects would be experienced by most unacclimatized visitors. However, many people live and work at altitude with no apparent adverse effects. One such example is Cerro de Pasco a busy mining town of Roger Hainsworth Mark J. Drinkhill Maria Rivera-ChiraThe autonomic nervous system at high altitude j Abstract The effects of hypobaric hypoxia in visitors depend not only on the actual elevation but also on the rate of ascent. Sympathetic activity increases and there are increases in blood pressure and heart rate. Pulmonary vasoconstriction leads to pulmonary hypertension, particularly during exercise. The sympathetic excitation results from hypoxia, partly through chemoreceptor reflexes and partly through altered baroreceptor function. High pulmonary arterial pressures may also cause reflex systemic vasoconstriction. Most permanent high altitude dwellers show excellent adaptation although there are differences between populations in the extent of the ventilatory drive and the erythropoiesis. Some altitude dwellers, particularly Andeans, may develop chronic mountain sickness, the most prominent characteristic of which being excessive polycythaemia. Excessive hypoxia due to peripheral chemoreceptor dysfunction has been suggested as a cause. The hyperviscous blood leads to pulmonary hypertension, symptoms of cerebral hypoperfusion, and eventually right heart failure and death. j

Cardiorespiratory parameters during submaximal exercise under acute exposure to normobaric and hypobaric hypoxia

“…The other way is through stimulation of pulmonary arterial baroreceptors in order to reduce the pulmonary hypertension elicited by the hypoxic stimulus. 41 As mentioned above, this sympathetic activation is reflected in changes in some HRV parameters under HH. An inverse relationship between sympathetic nerve activity and arterial SpO 2 in subjects with and without history of high altitude pulmonary oedema has been observed.…”

Upward Shift and Steepening of the Blood Pressure Response to Exercise in Hypertensive Subjects at High Altitude

“…This exaggerated BP rise could be a consequence of altitude‐induced reflex activation. We previously described that during exercise the ventilatory equivalents for oxygen and CO 2 were both higher at altitude compared to sea level,2 likely as a consequence of augmented peripheral chemoreflex input6, 22 and fluid accumulation along the alveolar capillary membrane 23…”

“…In previous articles, we demonstrated that acute exposure to high‐altitude hypobaric hypoxia induces a blood pressure (BP) rise in subjects with hypertension, both at rest over the 24 hours and during exercise,1, 2, 3 likely through chemoreflex‐induced sympathetic activation 4, 5, 6. Moreover, we also showed that the combination treatment with telmisartan and sustained‐release formulation of nifedipine gastrointestinal therapeutic system formulation (GITS) is able to lower BP levels during exercise not only at sea level but also at high altitude, as compared with placebo.…”

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats

“…The reductions in HR in the T. violacea -treated andcaptopril treated rats may also be partly due the animals becoming better accustomed to the small space, being more relaxed, and consequently, reducing sympathetic nervous system activation, which normally would increase HR and BP, as part of the 'fight', 'fright' or 'flight' response (Kurtz et al, 2005;Freeman et al, 2006;Fox et al, 2007;Hainsworth et al, 2007;McCorry, 2007;Reil & Bohm, 2007;Craven, 2008).…”