Effects of Fatiguing Stimulation on Intracellular Na+ and K+ in Frog Skeletal Muscle
Format of Original
American Physiological Society
Journal of Applied Physiology
The purpose of this study was to describe the alterations in the intracellular concentrations of sodium ([Na+]i) and potassium ([K+]i) and the membrane potential (Em) as a result of fatiguing stimulation of the frog semitendinosus muscle and to relate these changes to the alterations in the sarcolemma action potential and force-generating ability of the muscle. [Na+]i and [K+]i were measured by using ion-selective microelectrodes. Before stimulation (100-ms trains at 150 Hz, 1 stimulus/s for 5 min), [Na+]i, [K+]i, and Em were 16 ± 1 mM, 142 ± 5 mM, and -83 ± 1 mV, respectively. As a result of stimulation, [Na+]i rose to 49 ± 6 mM and recovered to 16 ± 2 mM with a time constant (τ) of 70 s·[K+]i fell to 97 ± 8 mM as a result of stimulation, then recovered to 148 ± 5 mM with τ= 56 s. Em depolarized to -74 ± 3 mV then recovered to -83 ± 2 mV with τ= 53 s. The Na+/K+ permeability ratio of the resting membrane fell 3%, whereas at the peak of the action potential the permeability ratio fell 38%. A previous study using the same muscle and stimulation protocol showed force to recover with a fast initial phase (~2 min) and a much slower second phase (~50 min). The recovery of [Na+]i, [K+]i, and Em was similar to the fast phase of force recovery; thus the altered Na+ and K+ concentration gradient across the sarcolemma and t-tubular membrane may contribute to this component of fatigue. The possible fatigue mechanisms induced by the altered ionic gradients include 1) complete block of the action potential propagation; 2) depolarization-induced inactivation of t-tubular charge movement; and 3) a reduced magnitude of the t-tubular charge due to the lower action potential spike potential.