A Minimal Dose of Electrically Induced Muscle Activity Regulates Distinct Gene Signaling Pathways in Humans with Spinal Cord Injury

Paralysis due to spinal cord injury leads to reduced muscle activity, affecting glucose utilization and metabolic control. Electrically induced muscle activity can potentially regulate genes that improve oxidative metabolism in paralyzed muscle. This study explores how short-term and long-term electrically induced exercise impacts mRNA expression in paralyzed human muscle. The exercise dose involved activating the muscle for only 0.6% of the day. The research found that a single dose of exercise regulated more biological pathways than a year of training. Acute stimulation increased mRNA expression related to metabolism, while chronic training increased mRNA expression of specific metabolic pathway genes, mitochondrial genes, and slow muscle fiber genes.

• 1
  Acute stimulation of paralyzed muscle regulates over 100 biological pathways as compared to less than 30 in chronically trained muscle.
• 2
  Acute electrically induced exercise up regulates transcriptional, translational, and enzyme regulators of metabolic pathways that shift muscle toward an oxidative phenotype (PGC-1a, NR4A3, IFRD1, ABRA, PDK4).
• 3
  Long term electrically induced exercise increased oxidative muscle fiber (MYH6, MYH7 MYL3, and MYL2) and mitochondrial fission/fusion (MFF, OA1, MFN1, MFN2) genes, but repressed glycolytic muscle (ACTN3, MYLK2, and MYL5) and muscle atrophy (MSTN) genes.