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Low-frequency stimulation regulates metabolic gene expression in paralyzed muscle
Journal article   Open access   Peer reviewed

Low-frequency stimulation regulates metabolic gene expression in paralyzed muscle

Michael Petrie, Manish Suneja and Richard K Shields
Journal of applied physiology (1985), Vol.118(6), pp.723-731
03/15/2015
DOI: 10.1152/japplphysiol.00628.2014
PMCID: PMC4360022
PMID: 25635001
url
https://doi.org/10.1152/japplphysiol.00628.2014View
Published (Version of record) Open Access

Abstract

The altered metabolic state after a spinal cord injury compromises systemic glucose regulation. Skeletal muscle atrophies and transforms into fast, glycolytic, and insulin-resistant tissue. Osteoporosis is common after spinal cord injury and limits the ability to exercise paralyzed muscle. We used a novel approach to study the acute effect of two frequencies of stimulation (20 and 5 Hz) on muscle fatigue and gene regulation in people with chronic paralysis. Twelve subjects with chronic (>1 yr) and motor complete spinal cord injury (ASIA A) participated in the study. We assessed the twitch force before and after a single session of electrical stimulation (5 or 20 Hz). We controlled the total number of pulses delivered for each protocol (10,000 pulses). Three hours after the completion of the electrical stimulation (5 or 20 Hz), we sampled the vastus lateralis muscle and examined genes involved with metabolic transcription, glycolysis, oxidative phosphorylation, and mitochondria remodeling. We discovered that the 5-Hz stimulation session induced a similar amount of fatigue and a five- to sixfold increase (P < 0.05) in key metabolic transcription factors, including PGC-1α, NR4A3, and ABRA as the 20-Hz session. Neither session showed a robust regulation of genes for glycolysis, oxidative phosphorylation, or mitochondria remodeling. We conclude that a low-force and low-frequency stimulation session is effective at inducing fatigue and regulating key metabolic transcription factors in human paralyzed muscle. This strategy may be an acceptable intervention to improve systemic metabolism in people with chronic paralysis.
Spinal Cord Injuries - metabolism Humans Oxidative Phosphorylation Muscle, Skeletal - metabolism Mitochondria - metabolism Paralysis - metabolism Glycolysis - physiology Electric Stimulation Therapy - methods Gene Expression - physiology Muscle, Skeletal - physiopathology Paralysis - physiopathology Spinal Cord Injuries - physiopathology Mitochondria - physiology Muscle Fatigue - physiology Electric Stimulation - methods

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