Modeling the oxygen transport to the myocardium at maximal exercise at high altitude

Figures

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  FIGURE 1. Model of oxygen handling in the myocyte. Tissue PO2 (PtO2) depends on the balance between O2 availability after diffusion from the capillary and O2 consumption by the myocyte. O2 consumption is determined by cardiac mechanical power, which mainly depends on three factors: Heart rate (HR), stroke volume (SV), and mean ejection pressure (Pej)

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  FIGURE 2. Values of arterial O2 saturation at maximal exercise (Samh) and its corresponding HR (expressed as the percentage of maximal HR at sea level), in subjects acclimated to hypoxia, as a function of altitude. Data extracted from literature (references in Table 1). There is a significant linear decrease in Samh and in HRmh with increasing altitude

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  FIGURE 3. Calculated values of myocardial venous O2 saturation (SvO2) at maximal exercise as a function of altitude in prolonged exposure to hypoxia. In open squares, values are calculated using data from the literature (Table 1) with the actual value of maximal heart rate (decreasing from sea level). In black triangles, values are re‐calculated using the same data but with a value of maximal heart rate at altitude identical to the sea‐level value. Note that with the actual values, SvO2 stays over 10% (minimal value compatible with normal myocardial oxygenation), while if we suppose that maximal heart rate does not decrease with altitude, SvO2 plunges below 10% over 6200 m and becomes negative above 8000 m, values incompatible with life. Negative values of SvO2 are physiologically impossible in the case of the absence of regulation

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  FIGURE 4. Calculated values of myocardial venous PO2 (PvO2) in the same conditions as in Figure 3. Pv at maximal exercise stays almost constant, whatever the altitude, thanks to the autoregulation of maximal heart rate (see text for explanations). Negative values of PvO2 are physiologically impossible in the case of the absence of regulation

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  FIGURE 5. Maximal reachable altitude compatible with normal myocardial oxygenation (myocardial venous O2 saturation above 10%) as a function of an expected increase in coronary reserve at maximal exercise from sea level to high altitude, if we suppose that maximal heart rate does not decrease with altitude (no autoregulation). Note that if we consider that coronary reserve at maximal exercise is already maximal at sea level, the maximal tolerated altitude would be 6200 m. If we hypothesize a 20% increase in coronary reserve, the maximal altitude would be 7600 m. To reach the summit of Mount Everest (8848 m), the coronary reserve would have to increase by 44.5%