Air to Muscle O₂Delivery during Exercise at Altitude

Abstract

Calbet, José, and Carsten Lundby. High Alt. Med. & Biol. 10.123-134, 2009.-Hypoxia-induced hyperventilation is critical to improve blood oxygenation, particularly when the arterial Po 2 lies in the steep region of the O 2 dissociation curve of the hemoglobin (ODC). Hyperventilation increases alveolar Po 2 and, by increasing pH, left shifts the ODC, increasing arterial saturation (Sao 2 ) 6 to 12 percentage units. Pulmonary gas exchange (PGE) is efficient at rest and, hence, the alveolar-arterial Po 2 difference (Pao 2 ÀPao 2 ) remains close to 0 to 5 mm Hg. The (Pao 2 ÀPao 2 ) increases with exercise duration and intensity and the level of hypoxia. During exercise in hypoxia, diffusion limitation explains most of the additional Pao 2 ÀPao 2 . With altitude, acclimatization exercise (Pao 2 ÀPao 2 ) is reduced, but does not reach the low values observed in high altitude natives, who possess an exceptionally high DLo 2 . Convective O 2 transport depends on arterial O 2 content (Cao 2 ), cardiac output (Q), and muscle blood flow (LBF). During whole-body exercise in severe acute hypoxia and in chronic hypoxia, peak Q and LBF are blunted, contributing to the limitation of maximal oxygen uptake (Vo 2max ). During small-muscle exercise in hypoxia, PGE is less perturbed, Cao 2 is higher, and peak Q and LBF achieve values similar to normoxia. Although the Po 2 gradient driving O 2 diffusion into the muscles is reduced in hypoxia, similar levels of muscle O 2 diffusion are observed during small-mass exercise in chronic hypoxia and in normoxia, indicating that humans have a functional reserve in muscle O 2 diffusing capacity, which is likely utilized during exercise in hypoxia. In summary, hypoxia reduces Vo 2max because it limits O 2 diffusion in the lung.

Assessment of oxidative stress biomarkers – neuroprostanes and dihomo-isoprostanes – in the urine of elite triathletes after two weeks of moderate-altitude training

“…In addition, the neuronal membranes are rich in polyunsaturated fatty acids (PUFA), which are particularly vulnerable to free radical attack [2]. When exercising at altitude the body responds to the fall in the barometric pressure as well as physical exercise, other factor that contribute to increased oxidative stress (OS) according to literature [3,4]. The OS seems to be linearly related to the altitude: higher altitude leads to greater oxidative challenge to the body [5].…”

Muscle Activation During Exercise in Severe Acute Hypoxia: Role of Absolute and Relative Intensity

“…Interestingly, hypoxia has, if any, a small effect on muscle metabolism and exercise capacity when the muscle mass recruited is small (Roach et al, 1999; or the impairment in exercise capacity is only observed in severe hypoxia (Goodall et al, 2010). Moreover, during exercise with a small muscle mass in severe acute hypoxia, pulmonary gas exchange is less perturbed and consequently, brain oxygenation is less altered than during exercise with a large muscle mass (Amann and Calbet, 2008;Calbet and Lundby, 2009;). The energy charge of the cell is less reduced during submaximal cycling at the same relative intensity in hypoxia (F I o 2 = 0.115; 72% of Vo 2 max) than in normoxia (73% of Vo 2 max) (Wadley et al, 2006), implying a similar or milder alteration of muscle metabolism in hypoxia.…”

AltitudeOmics: The Basic Biology of Human Acclimatization to High Altitude

“…Specifically, various compensatory mechanisms, including increases in cardiac output and muscle O 2 delivery and extraction, could have reduced the hypoxia-induced impact on the development of fatigue. Such an effective compensation might not-or only to a much smaller degree-be possible during intense, whole-body exercise, performed close to a human's maximal circulatory and ventilatory capacity (14,15).…”

“…Regulation of large cerebral arteries and cerebral 522 microvascular pressure. Circ Res 66: [8][9][10][11][12][13][14][15][16][17]1990. 523…”