Search

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 (tau) of 70 s.[K+]i fell to 97 +/- 8 mM as a result of stimulation, then recovered to 148 +/- 5 mM with tau = 56 s. Em depolarized to -74 +/- 3 mV then recovered to -83 +/- 2 mV with tau = 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 (approximately 2 min) and a much slower second phase (approximately 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.

The purposes of this study were to characterize the alterations in the sarcolemma action potential (AP) waveform and sarcolemma excitability as a result of fatiguing stimulation of the frog semitendinosus muscle and to relate these changes to the decrease in the force-generating ability of the muscle. Trains of APs were recorded before and after stimulation (100-ms trains, 150 Hz, 1/s for 5 min). The resting membrane potential (RMP), AP overshoot (OS), and duration at 50% of peak magnitude (DUR) were -84.3 +/- 2.0 mV, 19.5 +/- 1.9 mV, and 1.3 +/- 0.1 ms, respectively, before stimulation. The stimulation protocol caused RMP to depolarize to -75.1 +/- 2.0 mV, OS to fall to 7.3 +/- 1.9 mV, and DUR to increase to 2.5 +/- 0.4 ms. RMP and OS recovered fully in 5 min after the cessation of stimulation, whereas DUR was still prolonged. Before the stimulation protocol, AP frequency matched the stimulation frequency at all stimulation rates < or = 150 Hz. At 200-Hz stimulation, AP frequency was 192 +/- 6 Hz. After 5 min of stimulation, AP frequency matched the stimulation frequency only at < or = 60 Hz. At 100-, 150-, and 200-Hz stimulation, AP frequencies were 89 +/- 8, 84 +/- 17, and 79 +/- 15 Hz, respectively. Because of a decreased fusion frequency at fatigue, the fall in the sarcolemma AP frequency did not contribute to the decreased force. The stimulation-induced alterations in the AP waveform were moderate and unlikely to have caused fatigue. However, the alterations in AP may have been more extreme in the depths of the transverse tubules.