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1 The Copenhagen Muscle Research Center, Department of Anesthesia, Rigshospitalet, and 2 Department of Biochemistry and Genetics, The Panum Institute, University of Copenhagen, DK-2100 Copenhagen, Denmark
The contribution of pH to exercise-induced arterial O2 desaturation was evaluated by intravenous infusion of sodium bicarbonate (Bic, 1 M; 200-350 ml) or an equal volume of saline (Sal; 1 M) at a constant infusion rate during a "2,000-m" maximal ergometer row in five male oarsmen. Blood-gas variables were corrected to the increase in blood temperature from 36.5 ± 0.3 to 38.9 ± 0.1°C (P < 0.05; means ± SE), which was established in a pilot study. During Sal exercise, pH decreased from 7.42 ± 0.01 at rest to 7.07 ± 0.02 but only to 7.34 ± 0.02 (P < 0.05) during the Bic trial. Arterial PO2 was reduced from 103.1 ± 0.7 to 88.2 ± 1.3 Torr during exercise with Sal, and this reduction was not significantly affected by Bic. Arterial O2 saturation was 97.5 ± 0.2% at rest and decreased to 89.0 ± 0.7% during Sal exercise but only to 94.1 ± 1% with Bic (P < 0.05). Arterial PCO2 was not significantly changed from resting values in the last minute of Sal exercise, but in the Bic trial it increased from 40.5 ± 0.5 to 45.9 ± 2.0 Torr (P < 0.05). Pulmonary ventilation was lowered during exercise with Bic (155 ± 14 vs. 142 ± 13 l/min; P < 0.05), but the exercise-induced increase in the difference between the end-tidal O2 pressure and arterial PO2 was similar in the two trials. Also, pulmonary O2 uptake and changes in muscle oxygenation as determined by near-infrared spectrophotometry during exercise were similar. The enlarged blood-buffering capacity after infusion of Bic attenuated acidosis and in turn arterial desaturation during maximal exercise.
arterial O2 pressure; lactate; pH; rowing; ventilation
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