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Low force contractions induce fatigue consistent with muscle mRNA expression in people with spinal cord injury
Journal article   Open access   Peer reviewed

Low force contractions induce fatigue consistent with muscle mRNA expression in people with spinal cord injury

Michael A Petrie, Manish Suneja, Elizabeth Faidley and Richard K Shields
Physiological reports, Vol.2(2), pp.e00248-n/a
02/2014
DOI: 10.1002/phy2.248
PMCID: PMC3966256
PMID: 24744911
url
https://doi.org/10.1002/phy2.248View
Published (Version of record) Open Access

Abstract

Spinal cord injury (SCI) is associated with muscle atrophy, transformation of muscle fibers to a fast fatigable phenotype, metabolic inflexibility (diabetes), and neurogenic osteoporosis. Electrical stimulation of paralyzed muscle may mitigate muscle metabolic abnormalities after SCI, but there is a risk for a fracture to the osteoporotic skeletal system. The goal of this study was to determine if low force stimulation (3 Hz) causes fatigue of chronically paralyzed muscle consistent with selected muscle gene expression profiles. We tested 29 subjects, nine with a SCI and 20 without and SCI, during low force fatigue protocol. Three SCI and three non‐SCI subjects were muscle biopsied for gene and protein expression analysis. The fatigue index (FI) was 0.21 ± 0.27 and 0.91 ± 0.01 for the SCI and non‐SCI groups, respectively, supporting that the low force protocol physiologically fatigued the chronically paralyzed muscle. The post fatigue potentiation index (PI) for the SCI group was increased to 1.60 ± 0.06 (P < 0.001), while the non‐SCI group was 1.26 ± 0.02 supporting that calcium handling was compromised with the low force stimulation. The mRNA expression from genes that regulate atrophy and fast properties (MSTN, ANKRD1, MYH8, and MYCBP2) was up regulated, while genes that regulate oxidative and slow muscle properties (MYL3, SDHB, PDK2, and RyR1) were repressed in the chronic SCI muscle. MSTN, ANKRD1, MYH8, MYCBP2 gene expression was also repressed 3 h after the low force stimulation protocol. Taken together, these findings support that a low force single twitch activation protocol induces paralyzed muscle fatigue and subsequent gene regulation. These findings suggest that training with a low force protocol may elicit skeletal muscle adaptations in people with SCI. e00248 People with spinal cord injury develop severe osteoporosis and diabetes because of decreased muscle activity. We developed a low force muscle activation protocol that challenges the muscle and is suitable to apply in those with bone demineralization. This is the first study that illustrates the magnitude of muscle fatigue and the associated molecular adaptations associated with key genes known to regulate proteins associated with muscle fatigue.
 phenotype Electrical stimulation paralysis potentiation genotype

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