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Human aerobic performance: too much ado about limits to VO2

S. L. Lindstedt1,* and K. E. Conley2

1 Physiology and Functional Morphology Group, Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640, USA and
2 Departments of Radiology, Physiology and Biophysics, and Bioengineering, University of Washington Medical Center, Seattle, WA 98195-7115, USA



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Fig. 1. (A) Diagram of the human respiratory–locomotory system showing the three stages governing O2 uptake at the lungs (3), O2 delivery by the cardiovascular system (2) and O2 diffusion through the muscle and consumption by the mitochondria (1). (B) Plot of rate of O2 uptake (O2) as a function of leg power output from rest to the aerobic capacity (O2max) in an exercising human. CK, creatine kinase.

 


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Fig. 2. The total volume of skeletal muscle capillaries and mitochondria plotted against maximum rate of oxygen consumption (O2max) for a wide variety of mammals. Both volumes are directly proportional to O2max (data from) (Weibel and Taylor, 1981).

 


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Fig. 3. O2max, rate of oxygen delivery (arterial O2 content times cardiac output) and O2 extraction for elite athletes receiving supplemental blood as the mean hematocrit (Hct) is increased from 45.6 to 50.5%O2max and O2 delivery are shown relative to their control (not blood-doped) values. Oxygen extraction is depicted as the actual percentage O2 extraction. A 29% increase in O2 delivery to the muscles resulted in a 6.7% increase in O2max; hence, O2 extraction dropped from >90% to <75% (data from Spriet et al., 1986).

 


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Fig. 4. O2max at high altitude drops considerably in response to reduced arterial oxygen content. Here, O2max is shown for sea-level sojourners at 3790m altitude and for high-altitude natives at 3600m (filled columns). O2max increases in both groups of subjects when they are given supplemental O2 equal to sea-level normoxia levels (open columns). However, the increase in sojourners (38%) is over four times that of the high-altitude natives (8%) (data from Cymerman et al., 1989; Favier et al., 1995). Values are means + S.E.M., N=8 (Cymerman), N=11 (Favier).

 


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Fig. 5. Mitochondrial O2 increases linearly with intracellular PO2 but only under conditions of hypoxia. When O2 is increased (hyperoxia), the increase in mitochondrial O2 falls considerably below the predicted value (the line on the graph) (data from Richardson et al., 1999). 1mmHg=0.133kPa

 

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© The Company of Biologists Ltd 2001