TY - JOUR
T1 - Role of hemoglobin P50 in O2 transport during normoxic and hypoxic exercise in the dog
AU - Schumacker, P. T.
AU - Suggett, A. J.
AU - Wagner, P. D.
AU - West, J. B.
PY - 1985
Y1 - 1985
N2 - High hemoglobin affinity for O2 [low PO2 at 50% saturation of hemoglobin (P50)] could degrade exercise performance in normoxia by lowering mean tissue PO2 but could enhance O2 transport in hypoxic exercise by increasing arterial O2 saturation. We measured O2 transport at rest and at graded levels of steady-state exercise in tracheostomized dogs with normal P50 (28.8 ± 1.8 Torr) and again after P50 was lowered (19.5 ± 0.7 Torr) by sodium cyanate infusions. Measurements were made during ventilation with room air (RA), 12% O2 in N2, or 10% O2 in N2. Cardiac output (Q̇T) as a function of O2 consumption (V̇O2) was not altered by low P50 at any inspired O2 fraction (P>0.05). With RA exercise, arterial content (Ca(O2)) and O2 delivery (Q̇T x Ca(O2)) were unchanged at low P50, whereas mixed venous PO2 was reduced at each level of V̇O2. With exercise in hypoxia, Ca(O2) and O2 delivery were significantly improved at low P50 (P<0.05). Mixed venous PO2 was lower than control during 12% O2 (P<0.05) but not different from control during 10% O2 exercise at low P50. Despite a presumed decrease in tissue PO2 during RA and 12% O2 exercise, exercise performance and base excess decline were not significantly worse than control levels. We conclude that, in canine steady-state exercise, hemoglobin P50 is not an important determinant of tissue O2-extraction capacity during normoxia or moderate hypoxia. In extreme hypoxia, low P50 may help to maintain tissue PO2 by enhancing systemic O2 delivery at each level of Q̇T.
AB - High hemoglobin affinity for O2 [low PO2 at 50% saturation of hemoglobin (P50)] could degrade exercise performance in normoxia by lowering mean tissue PO2 but could enhance O2 transport in hypoxic exercise by increasing arterial O2 saturation. We measured O2 transport at rest and at graded levels of steady-state exercise in tracheostomized dogs with normal P50 (28.8 ± 1.8 Torr) and again after P50 was lowered (19.5 ± 0.7 Torr) by sodium cyanate infusions. Measurements were made during ventilation with room air (RA), 12% O2 in N2, or 10% O2 in N2. Cardiac output (Q̇T) as a function of O2 consumption (V̇O2) was not altered by low P50 at any inspired O2 fraction (P>0.05). With RA exercise, arterial content (Ca(O2)) and O2 delivery (Q̇T x Ca(O2)) were unchanged at low P50, whereas mixed venous PO2 was reduced at each level of V̇O2. With exercise in hypoxia, Ca(O2) and O2 delivery were significantly improved at low P50 (P<0.05). Mixed venous PO2 was lower than control during 12% O2 (P<0.05) but not different from control during 10% O2 exercise at low P50. Despite a presumed decrease in tissue PO2 during RA and 12% O2 exercise, exercise performance and base excess decline were not significantly worse than control levels. We conclude that, in canine steady-state exercise, hemoglobin P50 is not an important determinant of tissue O2-extraction capacity during normoxia or moderate hypoxia. In extreme hypoxia, low P50 may help to maintain tissue PO2 by enhancing systemic O2 delivery at each level of Q̇T.
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U2 - 10.1152/jappl.1985.59.3.749
DO - 10.1152/jappl.1985.59.3.749
M3 - Article
C2 - 4055564
AN - SCOPUS:0022270766
SN - 8750-7587
VL - 59
SP - 749
EP - 757
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 3
ER -