Lack of influence of potassium or osmolality on steady-state exercise hyperemia.

Abstract

Hyperkalemia, hyperosmolality, and hypoxia are known to have synergistic vasodilatory effects on resting skeletal muscle. The purpose of this study was to determine the importance of hyperkalemia and hyperosmolality in the hyperemia accompanying steady-state muscle exercise. Denervated dog gastrocnemius-plantaris muscles were perfused at constant pressure. Blood flow (Q), oxygen consumption (VO2), and venous potassium ion concentration ([K+]), osmolarity (OSM), and oxygen tension (PO2) were measured during steady-state exercise at rates between rest and 6 Hz. In control experiments the transition from rest to 6-Hz exercise resulted in large increases in VO2 and Q but modest increases in venous [K+] (+0.7 +/- 0.2 meq/l) and OSM (+6.1 +/- 1.2 mosmol/kg). Increasing venous [K+] by 2.3 meq/l by intra-arterial infusion of isotonic KCl had no steady-state effect on resting Q, nor did it alter the relationship of Q to VO2 or PO2 during exercise. Similarly, increasing venous OSM by 13 mosmol/kg by hypertonic saline infusion produced no alterations in steady-state exercise hyperemia. These findings indicate that neither local hyperkalemia nor hyperosmolality plays a significant role in sustaining the hyperemia of steady-state exercise.