Comments on Point:Counterpoint Positive effects of intermittent hypoxia (live high:train low) on exercise performance are/are not mediated primarily by augmented red cell volume

ZAOBORNYJ T; VALDEZ LB; BOVERIS A

J Appl Physiol

American Physiological Society

Lugar: Bethesda, Maryland, USA; Año: 2005 vol. 99 p. 2453 - 2454

Concerning the interesting point-counterpoint on the “live high: train low” hypothesis (1), we would like to suggest that during the process of adaptation to hypoxia there would be more things than red cell volume changes. We reported that rats adapted to hypoxia, either by exposure to high altitude (4,340 m, PO2=61.3 kPa) (2) and to life in a hypobaric chamber (PO2=53.8 kPa) (3) showed an increase of about 60% in heart mitochondrial nitric oxide synthase (mtNOS) activity and expression. The effect was selective: cytochrome content and several mitochondrial enzymatic activities were unchanged. The NO produced by mtNOS restricts cytochrome oxidase activity as well as cell and tissue O2 uptake. Under physiological conditions, where heart perfusion and O2 levels become limiting for ATP production and contractility, the NO-inhibited respiration lowers the steepness of the O2 gradient in the normoxic-anoxic transition and extends the oxygenation distance from the blood vessel. The NO-augmented situation would be associated to more areas having enough ATP to sustain a homogeneous and synchronic myofibril contraction. Interestingly, adapted rats showing mtNOS up-regulation exhibited better papillary muscle contractility parameters than their control siblings (3). This property may be associated to higher systolic pressure during the cardiac cycle, useful to counteract the increased blood viscosity due to higher RBCV. Hematocrit and mtNOS activity of rats living at high altitude correlated linearly (r2 = 0.89; p < 0.001) suggesting that both components of the adaptation to hypoxia may have common signaling pathways in which HIF-1a plays a central role (4).