O2 transport during exercise following blood reinfusion.

Reasons for an increase in maximal O2 consumption (VO2max) following blood reinfusion remain unclear; thus the present investigation was undertaken to examine the arterial and femoral venous blood gases during submaximal and maximal exercise. Four untrained males (22-25 yr) performed modified Balke work capacity tests under control conditions (Hct = 42.4 +/- 0.8%; Hb = 14.7 +/- 0.5 g X 100 ml-1) and following autologous blood reinfusion (Hct = 46.2 +/- 1.3%; Hb = 16.4 +/- 0.9 g X 100 ml-1). VO2 was determined by open-circuit spirometry and cardiac output by the N2O method; radial arterial and deep femoral venous blood were sampled at each work load throughout the incremental work tests. Following blood reinfusion, subjects' VO2max increased (P less than 0.05) from 4.0 (in control) to 4.5 1 X min-1. Throughout submaximal exercise arterial PO2 remained relatively constant (between 80.1 +/- 4.4 and 89.1 +/- 5.0 Torr) and cardiac output unchanged, comparing the two experimental conditions. Femoral venous PO2 values were almost identical throughout the work capacity tests, declining at exhaustion to 15.7 +/- 1.5 Torr in control and to 13.8 +/- 3.3 Torr postreinfusion. It appeared that the subjects' increase in VO2max postreinfusion was due to an increased O2 supplied to the tissue [i.e., cardiac output (Q) X arterial O2 content (CaO2)] by the central circulation. This resulted from a small (10%) increase in Q and a constant elevation in CaO2 of 1.7-2.2 ml X 100 ml-1, since virtually no changes were observed in the femoral venous blood postreinfusion and the acid-base status and temperature, important determinant of O2 dissociation, were (almost) identical, comparing the two experimental conditions.