Limitation of Maximal Heart Rate in Hypoxia: Mechanisms and Clinical Importance

Abstract

The use of exercise intervention in hypoxia has grown in popularity amongst patients, with encouraging results compared to similar intervention in normoxia. The prescription of exercise for patients largely rely on heart rate recordings (percentage of maximal heart rate (HRmax) or heart rate reserve). It is known that HRmax decreases with high altitude and the duration of the stay (acclimatization). At an altitude typically chosen for training (2,000-3,500 m) conflicting results have been found. Whether or not this decrease exists or not is of importance since the results of previous studies assessing hypoxic training based on HR may be biased due to improper intensity. By pooling the results of 86 studies, this literature review emphasizes that HRmax decreases progressively with increasing hypoxia. The dose–response is roughly linear and starts at a low altitude, but with large inter-study variabilities. Sex or age does not seem to be a major contributor in the HRmax decline with altitude. Rather, it seems that the greater the reduction in arterial oxygen saturation, the greater the reduction in HRmax, due to an over activity of the parasympathetic nervous system. Only a few studies reported HRmax at sea/low level and altitude with patients. Altogether, due to very different experimental design, it is difficult to draw firm conclusions in these different clinical categories of people. Hence, forthcoming studies in specific groups of patients are required to properly evaluate (1) the HRmax change during acute hypoxia and the contributing factors, and (2) the physiological and clinical effects of exercise training in hypoxia with adequate prescription of exercise training intensity if based on heart rate.

Cardiac Autonomic and Physiological Responses to Moderate- intensity Exercise in Hypoxia

“…At rest, a hypoxic stimulus increases sympathetic activity and reduces parasympathetic regulation [20], elevating HR and decreasing HRV [40]. In addition, during exercise HR is higher at any similar sub-maximal exercise intensity and decreased ad maximal intensities [11,26]. It has been shown that, for sufficiently high exercise intensities ( > 50 % V O 2 max), hypoxia does not exert an additional influence upon HRV [41], due to the already substantial exercise-induced vagal withdrawal and sympathetic activation [42].…”

“…Despite its promise, acute hypoxic exercise can result in altered physiological responses [11][12][13] and in increased exercise-induced homeostatic perturbation [14,15], that must be taken into account when prescribing exercise training. Particularly, both external (e. g. exercise load) and internal (e. g. heart rate) markers, commonly used for setting exercise intensity [16], are affected by acute hypoxia, making exercise prescription more challenging.…”

“…During acute hypoxic exercise arterial oxygen saturation is further decreased [12,23], whilst heart rate (HR) and cardiac output are increased at any same absolute submaximal exercise intensity and reduced at maximal exercise intensities [11,12,24], as well as maximal exercise capacity (i. e. V O 2 max and peak exercise intensity). Similarly, ventilation and blood lactate levels are increased in hypoxia at the same absolute submaximal exercise load [25] due to the greater relative exercise intensity and the increased anaerobic energy contribution [26].…”

Effects of baseline heart rate at sea level on cardiac responses to high-altitude exposure

“…These uniform changes suggest that there must be other reasons that account for the diverse changes in SV for subjects with different levels of baseline HRs after acute HA exposure. The increase in HR was more pronounced in subjects with a low baseline HR than in those with a high baseline HR, which might be attributed to the progressive decrease in maximal heart rate or heart rate reserve with increasing hypoxia [21]; however, the LV myocardial systolic velocity (S′) also increased in these low baseline HR subjects following acute HA exposure, which led to an increased LVEF, and consequently, the SVi was maintained. Moreover, the resting heart rate was positively correlated with LV S′ as well as E′, independent of sex and age [22].…”

Iloprost improves running performance at 5,000 m in Han but not in Tibetans

“…Up to altitudes ~4,000 m the loss of aerobic capacity in hypoxia is determined by a decrease in arterial oxygen saturation (SaO 2 ) and thus arterial oxygen concentration (CaO 2 ) and mass arterial oxygen flux (CaO 2 x cardiac output = QaO 2 ) (Amann & Calbet, 2008;Chapman, Emery, & Stager, 1999;Chapman, Stager, Tanner, Stray-Gundersen, & Levine, 2011;Ferretti, Moia, Thomet, & Kayser, 1997). However, during exercise in more severe hypoxia (above ~4,000 m), when SaO 2 drops below 80 % (Wagner, 2000), there are unexplained reductions in both maximum heart rate and cardiac output (Amann & Kayser, 2009;Boushel et al, 2001;Kayser, Narici, Binzoni, Grassi, & Cerretelli, 1994;Mourot, 2018). The impaired maximal cardiac function at peak exercise in hypoxia is restored rapidly by increasing PiO 2 to normoxic levels, enabling heart rate and cardiac output to further increase with increasing exercise intensity.…”