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The role of haemoglobin mass on VO2max following normobaric ‘live high–train low’ in endurance-trained athletes
  1. Paul Robach1,
  2. Christoph Siebenmann2,
  3. Robert A Jacobs2,3,
  4. Peter Rasmussen2,
  5. Nikolai Nordsborg4,
  6. Dominik Pesta5,
  7. Erich Gnaiger5,
  8. Víctor Díaz3,
  9. Andreas Christ6,
  10. Julia Fiedler7,
  11. Nadine Crivelli7,
  12. Niels H Secher8,
  13. Aurélien Pichon9,
  14. Marco Maggiorini6,
  15. Carsten Lundby2
  1. 1Département Médical, Ecole Nationale de Ski et d'Alpinisme, site de l'Ecole Nationale des Sports de Montagne, Chamonix, France
  2. 2Zurich Center for Integrative Human Physiology (ZIPH), University of Zurich, Zurich, Switzerland
  3. 3Institute of Veterinary Physiology, University of Zurich, Zurich, Switzerland
  4. 4Department of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark
  5. 5Department of Transplant Surgery, D. Swarovski Research Laboratory, Innsbruck Medical University, Innsbruck, Austria
  6. 6Intensive Care Unit DIM, University Hospital Zurich, Zurich, Switzerland
  7. 7Hôpital La Vallée, Le Sentier, Switzerland
  8. 8Department of Anaesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
  9. 9Université Paris 13, Sorbonne Paris Cité, Laboratoire Réponses Cellulaires et Fonctionnelles à l'Hypoxie, Bobigny, France
  1. Correspondence to Professor Carsten Lundby, Center for Integrative Human Physiology (ZIHP), University of Zurich, Institute of Physiology, Office 23 H 6, Winterthurerstr. 190, Zurich 8057, Switzerland; carsten.lundby{at}access.uzh.ch

Abstract

It remains unclear by which mechanism ‘live high–train low’ (LHTL) altitude training increases exercise performance. Haematological and skeletal muscle adaptations have both been proposed. To test the hypotheses that (i) LHTL improves maximal oxygen uptake (VO2max) and (ii) this improvement is related to hypoxia-induced increases in total haemoglobin mass (Hbmass) and not to improved maximal oxidative capacity of skeletal muscle, we determined VO2max before LHTL and after LHTL, before and after the altitude-induced increases in Hbmass (measured by carbon-monoxide rebreathing) had been abolished by isovolumic haemodilution. We obtained skeletal muscle biopsies to quantify mitochondrial oxidative capacity and efficiency. Sixteen endurance-trained athletes were assigned (double-blinded, placebo controlled) to ≥16 h/day over 4 weeks to normoxia (placebo, n=6) or normobaric hypoxia equivalent to 3000 m altitude (LHTL, n=10). Four-week LHTL did not increase VO2max, irrespective of treatment (LHTL: 1.5%; placebo: 2.0%). Hbmass was slightly increased (4.6%) in 5 (of 10) LHTL subjects but this was not accompanied by a concurrent increase in VO2max. In the subjects demonstrating an increase in Hbmass, isovolumic haemodilution elicited a 5.8% decrease in VO2max. Cycling efficiency was altered neither with time nor by LHTL. Neither maximal capacity of oxidative phosphorylation nor mitochondrial efficiency was modified by time or LHTL. The present results suggest that LHTL has no positive effect on VO2max in endurance-trained athletes because (i) muscle maximal oxidative capacity is not improved following LHTL and (ii) erythrocyte volume expansion after LHTL, if any, is too small to alter O2 transport.

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Footnotes

  • Funding This study was funded through grants obtained from the Bundes Amt für Sport (BASPO, Switzerland), Team Danmark (Denmark) and Ministère des Sports/Institut National du Sport, de l'Expertise et de la Performance (France).

  • Ethics approval Ethics Committee of Zurich (2010-066/0) and Vaud (215/10) (Switzerland).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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