Potassium homeostasis during and following exhaustive submaximal static handgrip contractions.

The aim of the present study was to follow local potassium homeostasis during and after exhaustive contractions. Eight subjects performed static handgrip with their right forearm at 10%, 25% and 40% maximal voluntary contraction. Blood flow (venous occlusion plethysmography) and the venous effluent plasma potassium concentration were followed during the contractions and during a 60-min recovery period. Electromyography was registered during exercise (frequency analysis). With all three protocols the blood flow increased significantly during the contractions and the same was true of the effluent plasma potassium concentrations. In the recovery period blood flow and the venous effluent plasma potassium concentration returned to base values within 30 min following 40% maximal voluntary contraction while following 10% and 25% maximal voluntary contraction, venous effluent plasma potassium concentration was still significantly below resting values one hour after the exercise had ceased, indicating a long-lasting uptake of potassium from the blood into the muscles. In line with this a significant potassium deficit was still seen after 1 hour of recovery following 10% and 25% maximal voluntary contraction. It is concluded that the recovery of potassium homeostasis following prolonged low-intensity contractions is a slow process. This may be due to either sequestration of potassium in other tissues with a subsequent slow release and/or insufficient sodium/potassium pump activation. The contraction induced potassium loss may play a major role in muscle performance since it may impair mechanical force production, and it is hypothesized that this may be the origin of low-frequency fatigue.