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144                                Biobehavioral Resilience to Stress

                             The Physiological Basis of Performance Limits and Injury


                             Hochachka, Gunga, and Kirsch (1998) have suggested that the human
                             ancestral phenotype arose under conditions that favored endurance per-
                             formance under increasingly cold, hypoxic, and arid conditions. In their
                             analysis, Hochachka et al. proposed that physiological responses, which
                             developed originally through oxygen sensing to mitigate hypobaric
                             hypoxia in Andean and Tibetan natives (Figure 7.1), are now common to
                             an up- regulated version of the human phenotype that enhances endurance
                             performance. For example, vascular endothelial growth factor (VEGF)
                             stimulates angiogenesis to better accommodate the need for oxygen trans-
                             port at altitude. Intramuscular VEGF response to the demands of physi-
                             cal training must also be important to the angiogenic responses that occur
                             in endurance-trained athletes. Ultimately, the key physiological predictor
                             of human performance is mitochondrial activity, which refl ects all other
                             critical functions (Hochachka et al., 1998; Hoyt & Friedl, 2006). In practi-
                             cal terms, sustained endurance activity in land-living mammals is limited
                             by mitochondrial/respiratory function to approximately five times resting

                             energy expenditure.*


                             High Altitude
                             As elevation increases, the partial pressure of oxygen decreases. In functional
                             terms, reduced oxygen pressure makes less oxygen available to the body. Th is
                             has profound consequences for the human body at altitudes of 8000 ft . and
                             above. Hypobaric hypoxia is detrimental to physical and cognitive functions.
                             However, hundreds of studies have demonstrated that the human body can
                             acclimatize quite well to hypobaric hypoxia. Initial ascent to high altitude


                             provokes a series of physiological changes that reflect an effort by the body to

                             maintain maximum oxygen saturation to bodily tissues. These changes are
                                                                                               †
                             observable as increases in heart rate, cardiac output, and ventilation rate.
                             Following acclimatization, heart rate and cardiac output return gradually
                             to their near baseline (sea level) values, and stroke volume decreases. Res-
                             piration rate remains elevated, however. Neuroendocrine and metabolic
                             processes support acclimatization to high altitude. During the first 4 days of

                             exposure to altitude, norepinephrine (NE) levels (found in urine) rise, and



                             * This is quite different than factors that determine performance and survival limits for
                              diving mammals (Hochachka et al., 1998).
                             †  On initial ascent, an increase in hematocrit is also observed due to a loss of plasma
                              volume. This initial hematocrit increase is not related to an increase in the number of
                              red blood cells, which occurs more slowly over the course of several weeks or months in
                              response to erythropoeitin.






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