Training in hypoxia vs training in normoxia in high altitude
natives.
Favier, R., H. Spielvogel, D. Desplanches, G. Ferretti, B. Kayser, A.
Grunenfelder, M. Leuenberger, L. Tuscher, E. Caceres, and H. Hoppeler.
Instituto Boliviano de Biologia de Altura, La Paz-Bolivia, URA 1341
CNRS, Laboratoire de Physiologie, Universit[acute]e Claude Bernard,
Lyon-France, Laboratoire de Physiologie, Centre M[acute]edical
Universitaire, Gen[grave]eve-Switzerland, Anatomisches Institut,
Universit[umlaut]at Bern, Bern, Switzerland
APStracts 2:0108A, 1995.
To determine the interactions between endurance training and hypoxia
on maximal exercise performance, we performed a study on sedentary
high altitude natives who were trained in normoxia at the same
relative (N-rel, n=10) or at the same absolute (N-abs, n=10)
intensity of work as hypoxia-trained subjects (H, n=10). The
training-induced improvement of maximal oxygen uptake (VO2max) in H
subjects was similar to that obtained in normoxia-trained sea-level
natives submitted to the same training protocol (Hoppeler et al.J.
Appl. Physiol., 59: 320-327, 1985). Training at the same absolute
work intensity (group N-abs) in presence of an increased oxygen
delivery failed to provide a further increase in VO2max. VO2max was
not improved to a greater extent by increasing simultaneously
absolute work intensity and O2 delivery during the training sessions
(group N-rel). In addition, training in normoxia is accompanied by an
increased blood lactate accumulation during maximal exercise, leading
to greater drops in arterial pH, bicarbonates concentration [HCO3-]
and base Excess (BE). We conclude that, in high altitude natives, 1/
training at altitude does not provide any advantage over training at
sea level for maximal aerobic capacity whether assessed in chronic
hypoxia or in acute normoxia; 2/ VO2max improvement with training
cannot be further enhanced by increasing O2 availability alone or in
combination with an increased work intensity during the exercising
sessions ; and 3/ training in normoxia in these subjects results in a
reduced buffer capacity.
Received 18 November 1994; accepted in final form 9 February
1995.
APS Manuscript Number A1181-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 21 March 1995.