Plantar Mechanical Stimulation Maintains Slow Myosin Expression in Disused Rat Soleus Muscle via NO-Dependent Signaling

Int J Mol Sci. 2021 Jan 29;22(3):1372. doi: 10.3390/ijms22031372.

Abstract

It was observed that gravitational unloading during space missions and simulated microgravity in ground-based studies leads to both transformation of slow-twitch muscle fibers into fast-twitch fibers and to the elimination of support afferentation, leading to the "switching-off" of postural muscle motor units electrical activity. In recent years, plantar mechanical stimulation (PMS) has been found to maintain the neuromuscular activity of the hindlimb muscles. Nitric oxide (NO) was shown to be one of the mediators of muscle fiber activity, which can also promote slow-type myosin expression. We hypothesized that applying PMS during rat hindlimb unloading would lead to NO production upregulation and prevention of the unloading-induced slow-to-fast fiber-type shift in rat soleus muscles. To test this hypothesis, Wistar rats were hindlimb suspended and subjected to daily PMS, and one group of PMS-subjected animals was also treated with nitric oxide synthase inhibitor (L-NAME). We discovered that PMS led to sustained NO level in soleus muscles of the suspended animals, and NOS inhibitor administration blocked this effect, as well as the positive effects of PMS on myosin I and IIa mRNA transcription and slow-to-fast fiber-type ratio during rat hindlimb unloading. The results of the study indicate that NOS activity is necessary for the PMS-mediated prevention of slow-to-fast fiber-type shift and myosin I and IIa mRNA transcription decreases during rat hindlimb unloading.

Keywords: L-NAME; MyHC; hindlimb unloading; plantar mechanical stimulation; soleus muscle.

MeSH terms

  • Animals
  • Biomechanical Phenomena
  • Down-Regulation
  • Epigenesis, Genetic
  • Foot / physiology*
  • Hindlimb Suspension
  • Male
  • Muscle, Skeletal / physiology*
  • Myosin Heavy Chains / genetics*
  • Myosin Type I / genetics*
  • Nitric Oxide / metabolism*
  • Nonmuscle Myosin Type IIA / genetics*
  • Rats
  • Rats, Wistar
  • Signal Transduction
  • Weightlessness Simulation

Substances

  • Nitric Oxide
  • Myosin Type I
  • Nonmuscle Myosin Type IIA
  • Myosin Heavy Chains