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POINT-COUNTERPOINT COMMENTS

In health and in a normoxic environment, O_{2 max} is/is not limited primarily by cardiac output and locomotor muscle blood flow

¹ACTES Laboratory (EA 3596)
Department of Physiology
University of the French West Indies
Guadeloupe
e-mail: pconnes{at}yahoo.fr ²Department of Physiology
Akdeniz University
Department of Medicine
Antalya, Turkey ³Department of Clinical Physiology
Centre d'Exploration et de Réadaptation des Anomalies du Métabolisme Musculaire (CERAMM)
Academic Hospital Lapeyronie
Montpellier, France ⁴Department of Physiology
Academic Medical Center
University of Amsterdam
Amsterdam, The Netherlands

The following letter is in response to the Point:Counterpoint series "In health and in a normoxic environment, O_2max is/is not limited primarily by cardiac output and locomotor muscle blood flow" that appeared in the February issue (vol 100: 744–748, 2006, http://jap.physiology.org/content/vol100/issue2).

To the Editor:

Among the factors that potentially limit O_{2 max}, hemorheological factors are often neglected by exercise physiologists. However, O_{2 max} and blood viscosity factors are strongly correlated (2), but in a complicated way. At high hematocrit, there is increased oxygen binding capacity; however, the simultaneous increase in blood viscosity may limit the transport capacity. These counteracting effects result in an optimal hematocrit value for maximal oxygen availability to tissues (4). Because the viscosity of blood is shear rate dependent, the optimal hematocrit may differ under different circumstances, e.g., rest, exercise, but also in different parts of the circulation. Blood rheological properties are thus able to influence the cascade of oxygen from lungs to exercising muscles.

Impairment in red blood cell (RBC) deformability can alter the diffusing capacity for oxygen from lungs to blood capillaries that may participate to the occurrence of exercise-induced hypoxemia, which may limit O_{2 max} (3). In the heart, any increase in blood viscosity raises peripheral vascular resistance, which may cause a decrease in maximal stroke volume and, therefore, a decrease in O_{2 max}. In muscular microcirculation, enhanced RBC aggregation causes depressed eNOS activity, resulting in deteriorated NO-mediated relaxation of arterioles (1). This effect of RBC aggregation is explained by the enhanced axial migration of blood cellular elements, reducing the frictional forces affecting on the endothelial cells and downregulating NO synthesis mechanisms.

Although the debate concerning the factors limiting O_{2 max} is far from being closed (5), central mechanisms seem to play an important role, with hemorheology being among the key factors.

REFERENCES

1. Baskurt OK, Yalcin O, Ozdem S, Armstrong JK, and Meiselman HJ. Modulation of endothelial nitric oxide synthase expression by red blood cell aggregation. Am J Physiol Heart Circ Physiol 286: H222–H229, 2004.[Abstract/Free Full Text]
2. Brun JF, Khaled S, Raynaud E, Bouix D, Micallef JP, and Orsetti A. The triphasic effects of exercise on blood rheology: which relevance to physiology and pathophysiology? Clin Hemorheol Microcirc 19: 89–104, 1998.[ISI][Medline]
3. Connes P, Bouix D, Durand F, Kippelen P, Mercier J, Prefaut C, Brun JF, and Caillaud C. Is hemoglobin desaturation related to blood viscosity in athletes during exercise? Int J Sports Med 25: 569–574, 2004.[CrossRef][ISI][Medline]
4. Hardeman MR. Exercise, red cells and blood doping; a conclusive role for LORCA? Biorheology 42: 92–93, 2005.
5. Saltin B and Calbet JA; Wagner PD. Point:Counterpoint: In health and in a normoxic environment, O_{2 max} is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.[Free Full Text]

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This Article Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Connes, P. Articles by Hardeman, M. Search for Related Content PubMed PubMed Citation Articles by Connes, P. Articles by Hardeman, M.