Staircase but not posttetanic potentiation in rat muscle after spinal cord hemisection

Abstract

Spinal cord hemisection (SCH) results in atrophy of skeletal muscle and altered contractile properties. In this study our purpose was to assess staircase and posttetanic potentiation in the rat gastrocnemius muscle in situ, 1 week after SCH. Tetanic force was reduced by SCH, but twitch amplitude was not. The time course and magnitude of staircase during stimulation at 5 HZ (for 21 s) was similar in the control, sham-operated, and SCH groups. However, posttetanic potentiation observed after 100-, 500-, and 1000-ms tetanic (200 HZ) contractions was absent or drastically reduced after SCH. Twitch force increased 44+/-8.7%, 47+/-7.4%, and 15+/-2.8% for the control, sham, and SCH groups, respectively, after the 1000-ms tetanic contraction. After the 1000-ms tetanic contraction, twitch active force decreased in all groups and was significantly reduced at 5 min relative to pretetanic twitch. In the control and sham groups, but not SCH, the active force recovered to the pretetanic level by 15 min. Resting regulatory light chain (RLC) phosphorylation was 15.4+/-2.5% and 10.97+/-3.3% for the control and SCH groups, respectively. After the 1-s tetanic contraction, values were 41.6+/-2.8% and 9.3+/-2.9%, respectively. The potentiation observed in the SCH animals with 1000-ms contraction apparently occurred without increases in RLC phosphorylation. One week after SCH there were clear changes in the contractile properties typically associated with prior activation. It is concluded that activity-dependent potentiation can occur by a mechanism that is independent of RLC phosphorylation, and accelerated fatigue can mask the potentiating effects of prior activity.

Myosin phosphorylation potentiated steady state work output without altering contractile economy of mouse fast skeletal muscles

“…For example, in mouse lumbrical muscles, isometric twitch potentiation in the absence of RLC phosphorylation has been associated with stimulation-induced elevations in resting myoplasmic Ca 2+ levels . Although this effect was relatively small and dissipated rapidly (≤20 s at 37°C), this mechanism may provide an explanation for the potentiation observed in the present study as well as by others (Macintosh et al, 2008a;Rassier et al, 1999) in the absence of RLC phosphorylation. In the current experiments, the stimulation protocol did not commence until ∼15 s after the PS, perhaps minimizing the ability of this mechanism to contribute.…”

Acute effects of reactive oxygen and nitrogen species on the contractile function of skeletal muscle

“…3. This glutathionylation mechanism causing increased Ca 2+ sensitivity in fast‐twitch fibres may play a role in post‐activation potentiation and counteract the decline in isometric and dynamic performance during fatiguing exercise (Rassier & Macintosh, 2000; MacIntosh et al 2008).…”

“…The overall effect depends on the balance between glutathionylation, oxidation and reversal of oxidation by cytoplasmic GSH, and will change over time particularly if levels of reduced GSH decline. J Physiol 589.9 play a role in post-activation potentiation and counteract the decline in isometric and dynamic performance during fatiguing exercise (Rassier & Macintosh, 2000;MacIntosh et al 2008).…”

Juxtaposition of the changes in intracellular calcium and force during staircase potentiation at 30 and 37°C

“…For example, extensor digitorum longus (EDL) muscles devoid of skeletal myosin light chain kinase, the enzyme responsible for phosphorylating the RLC, exhibit SP in the absence of RLC phosphate incorporation (Zhi et al, 2005; Gittings et al, 2011). Moreover, denervated rat gastrocnemius muscles displaying reduced levels of RLC phosphorylation retain SP (Rassier et al, 1999; MacIntosh et al, 2008). Although an alternative mechanism has not definitively been identified, our recent work has shown that posttetanic potentiation (PTP) of the mouse lumbrical, a muscle without detectable RLC phosphorylation, is associated with elevations in cytosolic Ca 2+ immediately before the onset of an intracellular Ca 2+ transient (ICT), such that baseline Ca 2+ is higher at the onset of potentiated contractions than unpotentiated contractions (Smith et al, 2013).…”