Carbon dioxide pressure-concentration relationship in arterial and mixed venous blood during exercise

To calculate cardiac output by the indirect Fick principle, CO2 concentrations (Cco 2) of mixed venous (Cv̄CO2 ) and arterial blood are commonly estimated from Pco 2, based on the assumption that the CO2 pressure-concentration relationship (Pco 2-Cco 2) is influenced more by changes in Hb concentration and blood oxyhemoglobin saturation than by changes in pH. The purpose of the study was to measure and assess the relative importance of these variables, both in arterial and mixed venous blood, during rest and increasing levels of exercise to maximum (Max) in five healthy men. Although the mean mixed venous Pco 2 rose from 47 Torr at rest to 59 Torr at the lactic acidosis threshold (LAT) and further to 78 Torr at Max, the Cv̄CO2 rose from 22.8 mM at rest to 25.5 mM at LAT but then fell to 23.9 mM at Max. Meanwhile, the mixed venous pH fell from 7.36 at rest to 7.30 at LAT and to 7.13 at Max. Thus, as work rate increases above the LAT , changes in pH, reflecting changes in buffer base, account for the major changes in the Pco 2-Cco 2relationship, causing Cv̄CO2 to decrease, despite increasing mixed venous Pco 2. Furthermore, whereas the increase in the arteriovenous Cco 2 difference of 2.2 mM below LAT is mainly due to the increase in Cv̄CO2 , the further increase in the arteriovenous Cco 2 difference of 4.6 mM above LAT is due to a striking fall in arterial Cco 2 from 21.4 to 15.2 mM. We conclude that changes in buffer base and pH dominate the Pco 2-Cco 2 relationship during exercise, with changes in Hb and blood oxyhemoglobin saturation exerting much less influence.

Aerobically generated CO2stored during early exercise

Previous studies have shown that a metabolic alkalosis develops in the muscle during early exercise. This has been linked to phosphocreatine hydrolysis. Over a similar time frame, the femoral vein blood pH and plasma K+ and[Formula: see text] concentrations increase without an increase in [Formula: see text]. Thus CO2 from aerobic metabolism is converted to [Formula: see text] rather than being eliminated by the lungs. The purpose of this study was to quantify the increase in early CO2 stores and the component due to the exercise-induced metabolic alkalosis (E-I Alk). To avoid masking the increase in CO2 stores by CO2 released as[Formula: see text] buffers lactic acid, the transient increase in CO2 stores was measured only for work rates (WRs) below the lactic acidosis threshold (LAT). The increase in CO2 stores was evident at the airway starting at ∼15 s; the increase reached a peak at ∼60 s and was complete by ∼3 min of exercise. The increase in CO2 stores was greater, but the kinetics were unaffected at the higher WR. Three components of the change in aerobically generated CO2 stores were considered relevant: the carbamate component of the Haldane effect, the increase in CO2 stores due to increase in tissue [Formula: see text], and the E-I Alk. The Haldane effect was calculated to be ∼5%. Physically dissolved CO2 in the tissues was ∼30% of the store increase. The remaining E-I Alk CO2 stores averaged 61 and 68% for 60 and 80% LAT WRs, respectively. The kinetics of O2 uptake correlated with the time course of the increase in CO2stores; the size of the O2 deficit correlated with the size of the E-I Alk component of the CO2 stores. We conclude that a major component of the aerobically generated increase in CO2 stores is the new[Formula: see text] generated as phosphocreatine is converted to creatine.

Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise

Engelen, Marielle, Janos Porszasz, Marshall Riley, Karlman Wasserman, Kazuhira Maehara, and Thomas J. Barstow. Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise. J. Appl. Physiol. 81(6): 2500–2508, 1996.—It is unclear whether hypoxia alters the kinetics of O2 uptake (V˙o 2) during heavy exercise [above the lactic acidosis threshold (LAT)] and how these alterations might be linked to the rise in blood lactate. Eight healthy volunteers performed transitions from unloaded cycling to the same absolute heavy work rate for 8 min while breathing one of three inspired O2 concentrations: 21% (room air), 15% (mild hypoxia), and 12% (moderate hypoxia). Breathing 12% O2 slowed the time constant but did not affect the amplitude of the primary rise inV˙o 2 (period of first 2–3 min of exercise) and had no significant effect on either the time constant or the amplitude of the slowV˙o 2 component (beginning 2–3 min into exercise). Baseline heart rate was elevated in proportion to the severity of the hypoxia, but the amplitude and kinetics of increase during exercise and in recovery were unaffected by level of inspired O2. We conclude that the predominant effect of hypoxia during heavy exercise is on the early energetics as a slowed time constant forV˙o 2 and an additional anaerobic contribution. However, the sum total of the processes representing the slow component ofV˙o 2 is unaffected.

Lactic acidosis as a facilitator of oxyhemoglobin dissociation during exercise

The slow rise in O2 uptake (VO2), which has been shown to be linearly correlated with the increase in lactate concentration during heavy constant work rate exercise, led us to investigate the role of H+ from lactic acid in facilitating oxyhemoglobin (O2Hb) dissociation. We measured femoral venous PO2, O2Hb saturation, pH, PCO2, lactate, and standard HCO3- during increasing work rate and two constant work rate cycle ergometer exercise tests [below and above the lactic acidosis threshold (LAT)] in two groups of five healthy subjects. Mean end-exercise femoral vein blood and VO2 values for the below- and above-LAT square waves and the increasing work rate protocol were, respectively, PO2 of 19.8 +/- 2.1 (SD), 18.8 +/- 4.7, and 19.8 +/- 3.3 Torr; O2 saturation of 22.5 +/- 4.1, 13.8 +/- 4.2, and 18.5 +/- 6.3%; pH of 7.26 +/- 0.01, 7.02 +/- 0.11, and 7.09 +/- 0.07; lactate of 1.9 +/- 0.9, 11.0 +/- 3.8, and 8.3 +/- 2.9 mmol/l; and VO2 of 1.77 +/- 0.24, 3.36 +/- 0.4, and 3.91 +/- 0.68 l/min. End-exercise femoral vein PO2 did not differ statistically for the three protocols, whereas O2Hb saturation continued to decrease for work rates above LAT. We conclude that decreasing capillary PO2 accounted for most of the O2Hb dissociation during below-LAT exercise and that acidification of muscle capillary blood due to lactic acidosis accounted for virtually all of the O2Hb dissociation above LAT.

O2 uptake kinetics above and below the lactic acidosis threshold during sinusoidal exercise

O2 uptake (VO2) kinetics at the onset of a constant work rate exercise are difficult to describe for work rates above the lactic acidosis threshold (LAT), because the steady-state level of VO2 response can usually not be identified. To describe the ability of the O2 transport system to deliver and the cells to utilize O2 above the LAT relative to that below the LAT, we applied a fluctuating (sinusoidal) variation of work rate. After 4 min of constant work at the midpoint of the sinusoidal work rate, a fluctuating work rate, at a period of 4 min, was applied below the LAT for the next 16 min. This was repeated in a range of work rates above the LAT with the same sine-wave amplitude. VO2 response appeared to follow a sinusoidal pattern similar to that of work rate for below- and above-LAT exercise. However, the amplitude of the VO2 response was significantly reduced (5.4 +/- 2.6 vs. 7.6 +/- 1.9 ml.min-1 x W-1, P < 0.01), and the phase lag increased above- compared with below-LAT work rate. VO2/heart rate fluctuations were dramatically reduced, whereas heart rate amplitude decreased and phase lag increased, for above-LAT sinusoidal work rate changes. These results suggest that VO2 kinetics are slowed in the work rate domain above the LAT relative to that below the LAT and that VO2 kinetics could be limited by the O2 transport mechanisms to the exercising muscle.