Endotoxemia stimulates skeletal muscle Na+-K+-ATPase and raises blood lactate under aerobic conditions in humans

Author:

Bundgaard Henning1,Kjeldsen Keld1,Suarez Krabbe Karen2,van Hall Gerrit3,Simonsen Lene4,Qvist Jesper2,Hansen Christian Muff2,Møller Kirsten2,Fonsmark Lise2,Madsen Per Lav2,Pedersen Bente Klarlund23

Affiliation:

1. Department of Medicine,

2. Department of Infectious Diseases,

3. The Copenhagen Muscle Research Center Rigshospitalet, and

4. National University Hospital and Department of Clinical Physiology, Bispebjerg Hospital, University of Copenhagen, 2100 Copenhagen, Denmark

Abstract

We assessed the hypothesis that the epinephrine surge present during sepsis accelerates aerobic glycolysis and lactate production by increasing activity of skeletal muscle Na+-K+-ATPase. Healthy volunteers received an intravenous bolus of endotoxin or placebo in a randomized order on two different days. Endotoxemia induced a response resembling sepsis. Endotoxemia increased plasma epinephrine to a maximum at t = 2 h of 0.7 ± 0.1 vs. 0.3 ± 0.1 nmol/l ( P < 0.05, n = 6–7). Endotoxemia reduced plasma K+reaching a nadir at t = 5 h of 3.3 ± 0.1 vs. 3.8 ± 0.1 mmol/l ( P < 0.01, n = 6–7), followed by an increase to placebo level at t = 7–8 h. During the declining plasma K+, a relative accumulation of K+was seen reaching a maximum at t = 6 h of 8.7 ± 3.8 mmol/leg ( P < 0.05). Plasma lactate increased to a maximum at t = 1 h of 2.5 ± 0.5 vs. 0.9 ± 0.1 mmol/l ( P < 0.05, n = 8) in association with increased release of lactate from the legs. These changes were not associated with hypoperfusion or hypoxia. During the first 24 h after endotoxin infusion, renal K+excretion was 27 ± 7 mmol, i.e., 58% higher than after placebo. Combination of the well-known stimulatory effect of catecholamines on skeletal muscle Na+-K+-ATPase activity, with the present confirmation of an expected Na+-K+- ATPase-induced decline in plasma K+, suggests that the increased lactate release was due to increased Na+-K+-ATPase activity, supporting our hypothesis. Thus increased lactate levels in acutely and severely ill patients should not be managed only from the point of view that it reflects hypoxia.

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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