Attenuation of myosin light chain phosphorylation and posttetanic potentiation in atrophied skeletal muscle.

Previously we have demonstrated that the absence of staircase potentiation in atrophied rat gastrocnemius muscle is accompanied by a virtual absence of phosphorylation of the regulatory light chains (R-LC) of myosin. It was our purpose in the present study to determine if posttetanic potentiation and corresponding R-LC phosphorylation were also attenuated in disuse-atrophied muscles. Two weeks after a spinal hemisection (T12), twitch and tetanic contractile characteristics were measured in situ in control, sham-treated and atrophied (hemisected) muscles. Posttetanic potentiation 20 s after a 2 s tetanic contraction (200 Hz) was depressed in atrophied muscles (128.7 +/- 2.6%; mean +/- SEM) when compared to sham-treated (149.9 +/- 2.4%) and control (142.9 +/- 2. 7%) muscles. Atrophied muscles demonstrated a significant increase in R-LC phosphorylation from rest (0.05 +/- 0.04 moles of phosphate/mole of R-LC) to posttetanic conditions (0.21 +/- 0.03 moles of phosphate/mole of R-LC), and less phosphorylation than control and sham-treated muscles (0.43 +/- 0.06 and 0.49 +/- 0.03 moles of phosphate/mole of R-LC, respectively) after tetanic stimulation. The preservation of the potentiation-phosphorylation relationship in atrophied muscles is consistent with the hypothesis that R-LC phosphorylation may be the principal mechanism for twitch potentiation.