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ACE GENE
IN DOUBT
Will
G Hopkins PhD, Physiology and Physical Education, University of Otago,
Dunedin 9001, New Zealand. Email: will.hopkins=AT=otago.ac.nz.
Sportscience 3(3), sportsci.org/jour/9903/inbrief.html#gene, 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
HYPOXIC-MUSCLE UPDATE
Will
G Hopkins PhD, Physiology and Physical Education, University of Otago,
Dunedin 9001, New Zealand. Email: will.hopkins=AT=otago.ac.nz.
Sportscience 3(3), sportsci.org/jour/9903/inbrief.html#hypoxic, 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
©1999
Published December 1999
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