PurposePost‐tetanic potentiation (PTP) is the enhancement of twitch force following tetanic stimulation and is an important component when studying skeletal muscle physiology and plasticity. Mechanistically, it is plausible that PTP could be associated with an increase in fiber excitability and/or any event following sarcoplasmic reticulum (SR) calcium release (i.e., at the contractile apparatus). Therefore, the goal of this study was to determine if increased fiber excitability contributes to PTP.MethodsAdult female C57BL/6J mice were chronically implanted with stimulating electrodes on the left common peroneal nerve and electromyographic (EMG) electrodes on the left tibialis anterior (TA) muscle. Following surgical recovery (at least 2 weeks after EMG electrode implantation), in vivo PTP of the anterior crural muscles was performed with simultaneous M‐wave recording from the TA muscle. To measure PTP, baseline twitch torque production was measured using a 0.1‐ms electrical stimulus pulse. Ten seconds later, muscles were stimulated using 0.1‐ms pulses at 100 Hz for 1 s to produce a prolonged, isometric tetanic contraction. Starting 2 s later, two post‐tetanic twitches were elicited with 2 s between the two. Changes in twitch torque (i.e., PTP) and M‐wave amplitude were calculated as percent increases in twitch torque and the corresponding M‐wave from baseline to the highest values following tetanic stimulation. All data were analyzed using paired t‐tests and are reported as means ± SE.ResultsTwitch torque at baseline was 0.45 ± 0.07 mN·m and represented the unpotentiated twitch. Following the tetanic stimulation, twitch torque increased by 34.0 ± 7.3% to 0.60 ± 0.07 mN·m (p=0.01). However, no change was detected in twitch M‐wave amplitude from before to after the tetanic stimulation (0.37 ± 0.03 to 0.39 ± 0.04 mV, p=0.48).ConclusionOn the basis of the disproportionate increase in twitch torque (34%) compared to the corresponding M‐wave amplitude increase (5%) after tetanic stimulation (p=0.02), we suggest that the PTP was not due to an increase in fiber excitability. Instead, it is more likely that PTP was attributable to an enhancement at or distal to SR calcium release such as phosphorylation of myosin regulatory light chain, which is consistent with previously reported mechanisms underlying PTP.Support or Funding InformationSupported by NIH grants R01‐AG031743 and T32‐AR007612, and Metropolitan State University Professional Development Grant.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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