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investigators find that maximal oxygen uptake is reduced in hot compared to temperate environments (Klausen et al., 1967; Rowell et al., 1969; Saltin et al., 1972; Sen Gupta et al., 1977), but some investigators report no differences (Rowell et al., 1965; Williams et al., 1962). For example, in one study (Sawka et al., 1985) maximal oxygen uptake was 0.25 liter per minute lower in a 49°C, as compared to a 20°C, environment (see Figure 3–3). Clearly, heat stress reduces relative to that achieved in a temperate environment. In addition, the state of heat acclimatization did not alter the approximate 0.25 liter per minute decrement in . The question remains, What physiological mechanism(s) is/are responsible for this reduction in ? It can be theorized that thermal stress might result in a displacement of blood to the cutaneous vasculature, which could (a) reduce the portion of cardiac output perfusing the contracting musculature or (b) result in a decreased effective central blood volume and thus reduce venous return and cardiac output. As skin blood flow can reach 7 liters per minute

FIGURE 3-3 Maximal aerobic power values (liters per minute) for the pre-and postheat acclimatization tests in a moderate (21°C, 30 percent relative humidity) and a hot (49°C, 20 percent relative humidity) environment, r = Pearson product-moment correlation coefficient. SOURCE: Sawka et al. (1985), used with permission.

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