Effect of acute and established anemia on O2 transport at rest, submaximal and maximal work

Abstract

Effects of acute and maintained isovolemic anemia on oxygen transport was studied during rest and exercise in normal males. Following 34% reduction in hemoglobin concentration (Hb), supine and standing Q rose acutely by 56% and 20%, respectively, but returned nearly to the control value by 10-14 days, producing a decrease in PVO2. Redistribution of blood flow appeared to compensate significantly for the decrease in systemic oxygen transport. 2,3-Diphosphoglycerate rose by 18%, in vivo PO2 at half-saturation of hemoglobin (P50) rose by approximately 2 mm over 7-9 days and probably afforded some compensation. The relationship between VO2 and external work intensity was independent of Hb. During exercise, Q/VO2 and VE/VO2 were increased in acute anemia, but PVO2, for a given VO2, decreased below control levels. After 10-14 days the relative increase in VE with exercise persisted; the increase in Q was less pronounced; and PVO2 was further decreased. With both acute and extablished anemia maximal exercise capacity and maximal VO2 (VO2 max) decreased in proportion to the Hb reduction.

Intravenous iron and recombinant erythropoietin for the treatment of postoperative anemia

“…Although in these patients acute anemia may not necessarily lead to overt organ dysfunction, it may lead to debilitating symptoms of anemia that include reduced exercise capacity, fatigue, dizziness, disorientation, indigestion, and loss of appetite. [3][4][5][6] Moreover, owing to the slow recovery from postoperative anemia, 7-9 these patients may have longer hospital stays and delayed postoperative recovery. Treatment modalities that accelerate recovery from severe postoperative anemia may therefore hasten patient recovery, improve quality of life, and decrease duration and cost of hospitalization.…”

Exercise Performance Falls over Time in Patients with Chronic Kidney Disease Despite Maintenance of Hemoglobin Concentration

“…Anemia per se is well established as a factor that limits exercise in the normal population (25,26), and a direct relationship between Hb and VO 2 also has been demonstrated in patients with CKD (5,6). Furthermore, when anemic patients with CKD are treated with erythropoietin to increase [Hb], exercise capacity (12) and VO 2peak (27) have been shown to improve, although only modestly compared with the increase in [Hb].…”

Energetics of Muscular Exercise

“…Also the effects of acute manipulations of the cardiovascular oxygen transport system on _ V O 2max were widely investigated. _ V O 2max was found to be lower in acute anaemia than in normaemia (Celsing et al 1987;Krip et al 1997;Woodson et al 1978) and higher in acute polycythaemia than in normaemia (Buick et al 1980;Celsing et al 1987;Ekblom et al 1975Ekblom et al , 1976Spriet et al 1986;Turner et al 1993), and after erythropoietin administration (Russell et al 2002;Thomsen et al 2007). _ V O 2max is reduced also when small quantities of carbon monoxide are added to inspired air (Ekblom and Huot 1972;Pirnay et al 1971;Vogel and Gleser 1972).…”

“…This explains, in Wagner's model, the effects of acute polycythaemia and anaemia on _ V O 2max Woodson et al 1978): the convective curve is displaced upwards and becomes steeper. The intercept on the x-axis of the convective curve corresponds to the P a O 2 point, i.e.…”

“…2.14b coincides with a specific CaO 2 isopleth because CaO 2 is fairly invariant. Anaemic individuals (Roach et al 1999;Woodson et al 1978), whose CaO 2 is reduced because of [Hb] loss in the …”