We tested the hypothesis that exercise‐induced changes in plasma composition result in peak stimulation of erythrocyte unidirectional K+ (JK,in) and net K+ (JK,net) transport within the first 120 s. In experimental series 1 (7 men; 2 women), plasma [K+] was continuously measured in vitro (37 °C) after the addition of red blood cells (RBCs) obtained from rested subjects (resting RBCs) into an exercise‐simulated plasma (ESP; increased plasma osmolality, [K+], [H+], [lactate] and [adrenaline] (epinephrine)), and JK,net calculated. In experimental series 2 (7 men; 4 women), resting RBCs were incubated in true exercise plasma (TEP) obtained after two 30 s bouts of high intensity leg cycling exercise to determine JK,net and JK,in (via RBC 86Rb accumulation). JK,net of resting RBCs increased from 0.9 ± 28.7 in resting plasma to 285 ± 164 mmol (l RBCs)−1 h−1 in ESP and to 178 ± 60 mmol (l RBCs)−1 h−1 after 10 s in TEP. Both JK,net and JK,in peaked within 10 s of incubation and decreased rapidly during the initial 120 s. The use of inhibitors for the Na+,K+‐ATPase (ouabain) and the Na+‐K+‐2Cl− cotransporter (NKCC; bumetanide) indicated that rapid increases in JK,in and JK,net upon incubation of resting RBCs in TEP were due primarily to increased Na+,K+‐ATPase activity; the NKCC appeared to be involved only when the Na+,K+‐ATPase was blocked. It is concluded that RBCs rapidly increase JK,in and JK,net in response to exercise‐induced changes in plasma composition.