Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During and after two similar incremental treadmill tests, one with increasing, the other with initially decreasing blood acidosis, plasma potassium was measured in 11 volunteers. Independent of increasing or decreasing hydrogen ion, lactate, or bicarbonate concentrations, plasma potassium rose in relation to muscular stress with nearly equal concentrations for comparable exercise intensities in both tests. During the first 3 min of recovery, plasma potassium fell rapidly in spite of nearly unchanged blood acidosis and significantly decreasing bicarbonate concentration. After the 5th min of recovery, plasma potassium concentration was even slightly below pre-exercise values despite severe metabolic acidosis. It was concluded that there was little or no effect of plasma hydrogen ion, lactate, or bicarbonate on plasma potassium concentration during and after exercise. We propose that plasma potassium is primarily regulated by intracellular effects of inorganic phosphate, pH, and temperature on (Na+-K+)-ATPase. We suggest that these results reflect a model of grand mal seizure-induced lactic acidosis. The noted low blood potassium concentrations despite the presence of severe metabolic acidosis secondary to epileptic seizure is thus suggested to reflect the "normal" post-exercise state of potassium concentration.
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PMID:Effect of consecutive exercise bouts on plasma potassium concentration during exercise and recovery. 269 11