News & Comment / In Brief

Ace Gene in Doubt
Hypoxic-Muscle Update


Will G Hopkins PhD, Physiology and Physical Education, University of Otago, Dunedin 9001, New Zealand. Email: Sportscience 3(3),, 1999 (223 words)
     Last year it looked like the gene coding for angiotensin converting enzyme--the ACE gene--was a human-performance gene. In a short item summarizing recent research, I described how army recruits who had the I form of this gene appeared to benefit more from training than those with the D form. Top mountaineers and top athletes were also more likely to have the I form. But anyone planning to identify future Olympians by typing their ACE genes had better wait a while. At this year's ACSM meeting there was a poster with evidence that, if anything, the D form was better (see my report). And now in a recently published study from an Australian lab (Taylor et al. 1999), there appears to be little difference in frequency of the I form between athletes and the general population. I emailed one of the authors for more information, but he was unable to explain the disparity between this study and the earlier study of athletes, which had come from another Australian lab.
Taylor RR, Mamotte CDS, Fallon K, van Bockxmeer FM (1999). Elite athletes and the gene for angiotensin converting enzyme. Journal of Applied Physiology 87, 1035-1037

Will G Hopkins PhD, Physiology and Physical Education, University of Otago, Dunedin 9001, New Zealand. Email: Sportscience 3(3),, 1999 (480 words)
    Do muscles run short of oxygen in hard exercise? In a great debate at this year's ACSM meeting, Tim Noakes cited recent research by Russell Richardson as direct evidence that muscles do not become hypoxic at any intensity of exercise. I took Tim's word for it in my report on the debate, but having read the recent paper by Richardson et al. (1999), I am reasonably certain that muscles do indeed go hypoxic when you push them hard.
     Tim was apparently referring to the state of oxygen in the cytoplasm of muscle cells. In their groundbreaking work, Richardson and coworkers used magnetic resonance spectroscopy to measure cytoplasmic oxygen in active muscle of cyclists exercising one leg hard. They found that the partial pressure (aka tension or concentration) of oxygen in the cytoplasm is a few millimeters of mercury. You have to get down to a fraction of a millimeter in mitochondria before energy production falls--which is what hypoxia means. That's a fraction of a millimeter in mitochondria, not the cytoplasm. As yet no-one has managed to measure mitochondrial oxygen tension in a human exercising hard, but Richardson et al. argued that it is likely to be hypoxic. They cited good evidence of hypoxia in electrically stimulated muscles of anaesthetized dogs. In other recent work they showed that cytoplasmic oxygen tension stays constant whatever the exercise, so to get more oxygen into mitochondria the oxygen tension inside mitochondria has to drop. Does it drop to hypoxic levels in hard exercise? Someone should find out by modeling oxygen transport in muscle using the basic physics of diffusion. We will still need confirmation by direct measurement, when someone can figure out how to do it in exercising humans.
     Tim would like muscles not to be hypoxic in hard exercise, because he has a theory that hard exercise is limited by a protective reflex arising in the heart. His idea is that the reflex acts like a governor to limit drive to muscles before their oxygen demand exceeds their supply. Fair enough. And even if muscles do go hypoxic, there could still be a governor limiting drive--it's just that the limit isn't enough to prevent hypoxia. But surely the feelings of fatigue and pain we get in our legs during hard exercise are evidence for a reflex arising in the legs? A reflex arising in the heart would be more likely to give us angina.
     Bottom line for athletes: if a governor limits drive to the extent that muscles aren't hypoxic, training the mind/brain to overcome the limit might enhance performance. But don't neglect strategies that enhance oxygen transport, because there's plenty of evidence that they enhance performance regardless of any governor.
Richardson RS, Leigh JS, Wagner PD, Noyszewski EA (1999). Cellular PO2 as a determinant of maximal mitochondrial O2 consumption in trained human skeletal muscle. Journal of Applied Physiology 87, 325-331

Published December 1999