Oxygen tension and acid-base equilibria in venous blood of working muscle

Doll, E; Keul, J.; Maiwald, C

doi:10.1152/ajplegacy.1968.215.1.23

Cited by 48 publications

(10 citation statements)

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“…Of note in relation to this discussion may be that Richardson et al . 's P v O 2 values for single‐leg exercise were, in fact, as low as the whole‐body data presented by Doll et al . (1968) and Pirnay et al .…”

Section: Discussioncontrasting

confidence: 80%

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Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise

Pedersen

Kiens

Saltin

1999

Acta Physiologica Scandinavica

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We examined the influence of hyperoxia on peak oxygen uptake (VO2peak) and peripheral gas exchange during exercise with the quadriceps femoris muscle. Young, trained men (n=5) and women (n=3) performed single-leg knee-extension exercise at 70% and 100% of maximum while inspiring normal air (NOX) or 60% O2 (HiOX). Blood was sampled from the femoral vein of the exercising limb and from the contralateral artery. In comparison with NOX, hyperoxic arterial O2 tension (PaO2) increased from 13.5 +/- 0.3 (x +/- SE) to 41.6 +/- 0. 3 kPa, O2 saturation (SaO2) from 98 +/- 0.1 to 100 +/- 0.1%, and O2 concentration (CaO2) from 177 +/- 4 to 186 +/- 4 mL L-1 (all P < 0. 01). Peak exercise femoral venous PO2 (PvO2) was also higher in HiOX (3.68 +/- 0.06 vs. 3.39 +/- 0.7 kPa; P < 0.05), indicating a higher O2 diffusion driving pressure. HiOX femoral venous O2 saturation averaged 36.8 +/- 2.0% as opposed to 33.4 +/- 1.5% in NOX (P < 0.05) and O2 concentration 63 +/- 6 vs. 55 +/- 4 mL L-1 (P < 0.05). Peak exercise quadriceps blood flow (Qleg), measured by the thermo-dilution technique, was lower in HiOX than in NOX, 6.4 +/- 0. 5 vs. 7.3 +/- 0.9 L min-1 (P < 0.05); mean arterial blood pressure at inguinal height was similar in NOX and HiOX at 144 and 142 mmHg, respectively. O2 delivery to the limb (Qleq times CaO2) was not significantly different in HiOX and NOX. VO2peak of the exercising limb averaged 890 mL min-1 in NOX and 801 mL min-1 in HiOX (n.s.) corresponding to 365 and 330 mL min-1 per kg active muscle, respectively. The VO2peak-to-PvO2 ratio was lower (P < 0.05) in HiOX than in NOX suggesting a lower O2 conductance. We conclude that the similar VO2peak values despite higher O2 driving pressure in HiOX indicates a peripheral limitation for VO2peak. This may relate to saturation of the rate of O2 turnover in the mitochondria during exercise with a small muscle group but can also be caused by tissue diffusion limitation related to lower O2 conductance.

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Section: Discussioncontrasting

confidence: 80%

“…Pirnay et al . (1972) and Doll et al . (1968) presented mean values of 2.1 and 2.9 kPa, respectively.…”

Section: Discussionmentioning

confidence: 96%

Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise

Pedersen

Kiens

Saltin

1999

Acta Physiologica Scandinavica

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“…Concomitant small changes in other acids like pyruvic (+0.1 mmol á l )1 , Doll et al 1968) and fatty acids ()0.13 mmol á l )1 , Favier et al 1996) during exercise cancel each other. Possibly the remaining amount is due to scattering of measurements or simpli®cations (e.g., buer curves that are not exactly linear, arterial mixedvenous dierences, non-uniform PCO 2 changes in different tissues, or unequal¯uxes of La ) and H + into the extracellular¯uid).…”

Section: Normoxiamentioning

confidence: 97%

Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition

Böning¹,

Maassen

Thomas

et al. 2001

European Journal of Applied Physiology

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The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios -delta[La].delta pH-1 (where delta[La] is change in lactic acid concentration and delta pH is change in pH) and delta[HCO3-].delta pH-1 (where delta[HCO3-] is change in bicarbonate concentration) in blood plasma. The difference between -delta[La].delta pH-1 and delta[HCO3-].delta pH-1 yields the capacity of available non-bicarbonate buffers (mainly hemoglobin). In turn, delta[HCO3-].delta pH-1 can be separated into a pure bicarbonate buffering (as calculated at constant carbon dioxide tension) and a hyperventilation effect. These quantities were measured in 12 mountaineers during incremental exercise tests before, and 7-8 days (group 1) or 11-12 days (group 2) after their return from a Himalayan expedition (2800-7600 m altitude) under conditions of normoxia and acute hypoxia. In normoxia -delta[La].delta pH-1 amounted to [mean (SEM)] 92 (6) mmol.l-1 before altitude, of which 19 (4), 48 (1) and 25 (3) mmol.l-1 were due to hyperventilation, bicarbonate and non-bicarbonate buffering, respectively. After altitude -delta[La].delta pH-1 was increased to 128 (12) mmol.l-1 (P < 0.01) in group 1 and decreased to 72 (5) mmol.l-1 in group 2 (P < 0.05), resulting mainly from apparent large changes of non-bicarbonate buffer capacity, which amounted to 49 (14) mmol.l-1 in group 1 and to 10 (2) mmol.l-1 in group 2. In acute hypoxia the apparent increase in non-bicarbonate buffers of group 1 was even larger [140 (18) mmol.l-1]. Since the hemoglobin mass was only modestly elevated after descent, other factors must play a role. It is proposed here that the transport of La- and H+ across cell membranes is differently influenced by high-altitude acclimatization.

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“…During a submaximal exercise of about 200 W, the Pot and Pcoz in the mixed venous blood are about 20 and 65 mmHg (base excess -11.05 mEq/liter), respectively, and the pH averages 7.164 [15]. BAYER [7] calculated that in this case the arterio-mixed venous difference in oxygen saturation will be 75 .…”

Section: Molecular Mechanism Of the Bohr Effectmentioning

confidence: 97%

The Bohr effect and the Haldane effect in human hemoglobin.

Tyuma

1984

Jpn.J.Physiol

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In 1904, BOHR, HASSEL$ALCH, and KROGH [11] discovered that increased carbon dioxide pressure (Pcoz) shifts the oxygen equilibrium curve of blood to the right, i.e., the oxygen affinity of blood is inversely proportional to Pcoz. There was much discussion at that time as to whether the shift due to C02 could be explained entirely by the concomitant change in pH, or whether C02 has, in addition, a specific effect. It has now been shown that C02 does exert a specific effect due to its direct combination with hemoglobin to form carbamino compound [27]. Thus, the original observation of Bohr et al., now called "classical Bohr effect" [19,39], is a composite of the specific effects of C02 and Ht The separate effect of pH on the oxygen affinity of hemoglobin has conventionally been referred to as the Bohr effect : between pH 6 and 9 the fall of pH decreases the oxygen affinity (the alkaline Bohr effect) and below pH 6 the oxygen affinity rises with falling pH (the acid or reverse Bohr effect).On the other hand, the reduction of C02 content in blood on oxygenation at constant Pcoz was demonstrated by CHISTIANSEN, DOUGLAS, and HALDANE [13] in 1914. This "classical Haldane effect" [39] is a thermodynamic corollary of the classical Bohr effect and can be explained by the decrease in carbamino binding to hemoglobin and the fall in pH on oxygenation. The release and uptake of protons on oxygenation and deoxygenation of hemoglobin are now defined as the Haldane effect. Sometimes both the Bohr and Haldane effects, including the classical ones, are collectively termed the Bohr effect.It is now well-established that in addition to protons and carbon dioxide, 2, 3-diphosphoglycerate (DPG), the major organic phosphate in mammalian erythrocytes, tremendously decreases the oxygen affinity of hemoglobin by binding to the deoxy form of the protein preferentially [9]. Other salt anions, e.g., chloride and inorganic phosphate, also show a similar but lesser effect [24]. Although the binding sites of these ligands are remote from the heme iron atom, the bindings are related to the oxygenation of the iron atom and have been described as "oxygen-linked" or "oxylabile." The interactions between the oxygen-binding sites and the sites for the non-heme ligands are referred to as the heterotropic allosteric

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Oxygen tension and acid-base equilibria in venous blood of working muscle

Cited by 48 publications

References 0 publications

Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise

Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise

Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition

The Bohr effect and the Haldane effect in human hemoglobin.

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