Int J Sports Med 2007; 28(3): 186-192
DOI: 10.1055/s-2006-924215
Physiology & Biochemistry

© Georg Thieme Verlag KG Stuttgart · New York

Role of Maximal Heart Rate and Arterial O2 Saturation on the Decrement of V·O2max in Moderate Acute Hypoxia in Trained and Untrained Men

P. Mollard1 , X. Woorons1 , M. Letournel2 , J. Cornolo1 , C. Lamberto1 , 2 , M. Beaudry1 , J.-P. Richalet1 , 2
  • 1Université Paris 13, Laboratoire “Réponses cellulaires et fonctionnelles à l'hypoxie”, EA2363, ARPE, Bobigny, France
  • 2Hôpital Avicenne, AP‐HP, Bobigny, France
Further Information

Publication History

Accepted after revision: March 20, 2006

Publication Date:
06 October 2006 (online)

Abstract

We aimed to evaluate 1) the altitude where maximal heart rate (HRmax) decreases significantly in both trained and untrained subjects in moderate acute hypoxia, and 2) if the HRmax decrease could partly explain the drop of V·O2max. Seventeen healthy males, nine trained endurance athletes (TS) and eight untrained individuals (US) were studied. Subjects performed incremental exercise tests at sea level and at 5 simulated altitudes (1000, 1500, 2500, 3500, 4500 meters). Power output (PO), heart rate (HR), arterial oxygen saturation (SaO2), oxygen uptake (V·O2), arterialized blood pH and lactate were measured. Both groups showed a progressive reduction in V·O2max. The decrement in HRmax (ΔHRmax) was significant from 1000 m for TS and 2500 m for US and more important in TS than US (at 1500 m and 3500 m). At maximal exercise, TS had a greater reduction in SaO2 (ΔSaO2) at each altitude. ΔHRmax observed in TS was correlated with ΔSaO2. When the two groups were pooled, simple regressions showed that ΔV·O2max was correlated with both ΔSaO2 and ΔHRmax. However, a multiple regression analysis demonstrated that ΔSaO2 alone may account for ΔV·O2max. Furthermore, in spite of a greater reduction in SaO2 and HRmax in TS, no difference was evidenced in relative ΔV·O2max between groups. Thus, in moderate acute hypoxia, the reduction in SaO2 is the primary factor to explain the drop of V·O2max in trained and untrained subjects.

References

  • 1 Benoit H, Busso T, Castells J, Devis C, Geyssant A. Influence of hypoxic ventilatory response on arterial O2 saturation during maximal exercise in acute hypoxia.  Eur J Appl Physiol. 1995;  72 101-105
  • 2 Benoit H, Busso T, Castells J, Geyssant A, Denis C. Decrease in peak heart rate with acute hypoxia in relation to sea level V·O2max.  Eur J Appl Physiol. 2003;  90 514-519
  • 3 Calbet J AL, Boushel R, Radegran G, Sodergaard H, Wagner P D, Saltin B. Determinant of maximal oxygen uptake in severe acute hypoxia.  Am J Appl Physiol. 2003;  284 R291-R303
  • 4 Cerretelli P, Bordoni U, Debijadij R, Saracino F. Respiratory and circulatory factors affecting the maximal aerobic power in hypoxia.  Archivio di fisiologia. 1967;  vol. LXV 344-357
  • 5 Chapman R F, Emery M, Stager J M. Degree of arterial desaturation in normoxia influences V·O2max decline in mild hypoxia.  Med Sci Sports Exerc. 1999;  31 658-663
  • 6 Dempsey J A, Hanson P G, Pegelow D, Claremont A, Rankin J. Limitations to exercise capacity and endurance: pulmonary system.  Can J Appl Sport Sci. 1982;  7 4-13
  • 7 Dill D B, Myhre L G, Phillips E E, Brown D K. Work capacity in acute exposure to altitude.  J Appl Physiol. 1966;  21 1168-1176
  • 8 Favret F, Richalet J P, Henderson K K, Germack R, Gonzalez N C. Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O2 transport in exercise.  Am J Physiol. 2001;  280 R730-R738
  • 9 Ferretti G, Moia C, Thomet J M, Kayser B. The decrease of maximal oxygen consumption during hypoxia in man: a mirror image of the oxygen equilibrium curve.  J Physiol. 1997;  498 231-237
  • 10 Fulco C S, Rock P B, Cymerman A. Maximal and submaximal exercise performance at altitude.  Aviat Space Environ Med. 1998;  69 793-801
  • 11 Gore C J, Hahn A G, Scroop G C, Watson D B, Norton K I, Wood R J, Campbell D P, Emonson D L. Increased arterial desaturation in trained cyclists during maximal exercise at 580 m altitude.  J Appl Physiol. 1996;  80 2204-2210
  • 12 Hopkins S R, McKenzie D C. Hypoxic ventilatory response and arterial desaturation during heavy work.  J Appl Physiol. 1989;  67 1119-1124
  • 13 Kayser B, Narici M, Binzoni T, Grassi B, Cerretelli P. Fatigue and exhaustion in chronic hypobaric hypoxia: influence of exercising muscle mass.  J Appl Physiol. 1994;  76 634-640
  • 14 Kayser B. Exercise starts and ends in the brain.  Eur J Appl Physiol. 2003;  90 411-419
  • 15 Lawler J, Power S K, Thompson D. Linear relationship between V·O2max and V·O2max decrement during exposure to acute hypoxia.  J Appl Physiol. 1988;  64 1486-1492
  • 16 Lundby C, Araoz M, Van Hall G. Peak heart rate decreases with increasing severity of acute hypoxia.  High Alt Med Biol. 2001;  2 369-376
  • 17 Martin D, O'Kroy J. Effects of acute hypoxia on the V·O2max of trained and untrained subjects.  J Sports Sci. 1993;  11 37-42
  • 18 McGuire B J, Secomb T W. Theoretical predictions of maximal oxygen consumption in hypoxia: effect of transport limitations.  Resp Physiol Neurobiol. 2004;  143 87-97
  • 19 Noakes T D, Peltonen J E, Rusko H K. Evidence that central governor regulates exercise performance during acute hypoxia and hyperoxia.  J Exp Biol. 2001;  204 3225-3234
  • 20 Peltonen J E, Rusko H K, Rantamaki J, Sweins K, Niittymaki S, Viitasalo J T. Effects of oxygen fraction in inspired air on force production and electromyogram activity during ergometer rowing.  Eur J Appl Physiol. 1997;  76 495-503
  • 21 Richalet J P. The heart and adrenergic system in hypoxia. Sutton JR, Coates G, Remmers JE Hypoxia: The Adaptations. Philadelphia, PA; BC Dekker 1990: 231-240
  • 22 Richalet J P, Larmignat P, Rathat C, Keromes A, Baud P, Lhoste F. Decreased cardiac response to isoproterenol infusion in acute and chronic hypoxia.  J Appl Physiol. 1988;  65 1957-1961
  • 23 Roach R C, Calbet J A, Olsen N V, Poulsen T D, Vissing S F, Saltin B. Peak exercise heart rate at high altitude.  Med Sci Sport Exerc. 1996;  28 1072
  • 24 Robergs R A, Quintana R, Parker D L, Frankel C C. Multiple variables explain the variability in the decrement in V·O2max during acute hypobaric hypoxia.  Med Sci Sports Exerc. 1998;  30 869-879
  • 25 Roca J, Hogan M C, Story D, Bebout D E, Haab P, Gonzalez R, Ueno O, Wagner P D. Evidence for tissues diffusion limitation of V·O2max in normal humans.  J Appl Physiol. 1989;  67 291-299
  • 26 Roche F, Reynaud C, Pichot V, Duverney D, Costes F, Garet M, Gaspoz J M, Barthelemy J C. Effect of acute hypoxia on QT rate dependence and corrected QT interval in healthy subjects.  Am J Cardiol. 2003;  91 916-919
  • 27 Squires R W, Buskirk E R. Aerobic capacity during acute exposure to simulated altitude, 914 to 2286 meters.  Med Sci Sports Exerc. 1982;  14 36-40
  • 28 Stenberg J, Ekblom B, Messin R. Hemodynamic response to work at simulated altitude, 4000 m.  J Appl Physiol. 1966;  21 1589-1594
  • 29 Wagner P D. Reduced maximal cardiac output at altitude - mechanisms and significance.  Respir Physiol. 2000;  120 1-11
  • 30 Woorons X, Mollard P, Lamberto C, Letournel M, Richalet J P. Effect of acute hypoxia on maximal exercise in trained and sedentary women.  Med Sci Sports Exerc. 2005;  37 147-154

Pascal Mollard

Laboratoire “Réponses cellulaires et fonctionnelles à l'hypoxie”

74 rue Marcel Cachin

93017 Bobigny Cedex

France

Phone: 33 1 48 38 77 57

Fax: 33 1 48 38 77 77

Email: pascal.mollard@laposte.net

    >