2003
DOI: 10.1007/s00421-003-0928-x
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Acid?base balance at exercise in normoxia and in chronic hypoxia. Revisiting the "lactate paradox"

Abstract: Transitions between rest and work, in either direction, and heavy exercise loads are characterized by changes of muscle pH depending on the buffer power and capacity of the tissues and on the metabolic processes involved. Among the latter, in chronological sequence: (1). aerobic glycolysis generates sizeable amounts of lactate and H(+) by way of the recently described, extremely fast (20-100 ms) "glycogen shunt" and of the excess of glycolytic pyruvate supply; (2). hydrolysis of phosphocreatine, tightly couple… Show more

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Cited by 58 publications
(58 citation statements)
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“…Although the respiratory alkalosis that develops on immediate HA ascent (e.g. Tables 2 and 3) would be expected to temper the deleterious consequences of developing acidosis in the exercising muscles, subsequent renal compensation compromises the bicarbonate-related buffer capacity (Cerretelli and Samaja, 2003). However, the extent to which whole-body buffer capacity might be affected in our study is uncertain.…”
Section: Decreased Wcontrasting
confidence: 46%
See 1 more Smart Citation
“…Although the respiratory alkalosis that develops on immediate HA ascent (e.g. Tables 2 and 3) would be expected to temper the deleterious consequences of developing acidosis in the exercising muscles, subsequent renal compensation compromises the bicarbonate-related buffer capacity (Cerretelli and Samaja, 2003). However, the extent to which whole-body buffer capacity might be affected in our study is uncertain.…”
Section: Decreased Wcontrasting
confidence: 46%
“…Resting and peak exercise muscle [ATP] and [PCr] levels have been reported to be essentially unaffected by ascent to HA (van Hall et al, 2009). Likewise, maximum blood [L − ] has been reported to be similar to SL values on immediate ascent (despite the lowerV O 2 max ), and although this is widely reported to decline as acclimatization proceeds (the "lactate paradox") (Cerretelli and Samaja, 2003;Reeves et al, 1992;West, 1986), no blunting was evident in arterial [L − ], muscle [L − ] or leg net lactate release during incremental exercise for moderate HA exposure (i.e. two weeks at 4100 m) compared to acute hypoxia at SL (van Hall et al, 2009).…”
Section: Introductionmentioning
confidence: 99%
“…6 Since haemoglobin is an excellent buffer, an increase in the circulating haemoglobin mass helps improve the blood buffering capacity. 7 A higher blood buffering capacity could facilitate lactate 8 and proton release from the active muscle and increase the capacity to produce energy via the anaerobic pathways.…”
mentioning
confidence: 99%
“…The most serious effects of high altitude on human physiology are due to the low oxygen partial pressure of the inspired air; consequently, different adjustments are needed to improve the tissue oxygen availability. Hypobaric hypoxia causes an increase in ventilation (see West, 1993), increases in arteriovenous O 2 difference, hemoglobin concentration, and hematocrit (Ferretti et al, 1990a), profound effects on the structure and function of skeletal muscle tissue (Ferretti et al, 1990b;Hoppeler et al, 1990), acid-base alterations with an important incidence in the affinity of hemoglobin to oxygen (Cerretelli and Samaja, 2003), and elevated erythropoietin levels (Eckardt et al, 1989). Moreover, prolonged exposure to hypobaric hypoxia also induces a degree of physical deterioration, which increases with altitude (Kayser, 1994).…”
Section: Introductionmentioning
confidence: 99%