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PPARδ preserves a high resistance to fatigue in the mouse medial gastrocnemius after spinal cord transection
Author(s) -
Kim Jung A.,
Roy Roland R.,
Zhong Hui,
Alaynick William A.,
Embler Emi,
Jang Claire,
Gomez Gabriel,
Sonoda Takuma,
Evans Ronald M.,
Edgerton V. Reggie
Publication year - 2016
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.24723
Subject(s) - endocrinology , medicine , spinal cord , gastrocnemius muscle , peroxisome proliferator activated receptor , spinal cord injury , oxidative stress , skeletal muscle , receptor , chemistry , biology , neuroscience
: Skeletal muscle oxidative capacity decreases and fatigability increases after spinal cord injury. Transcription factor peroxisome proliferator‐activated receptor δ (PPARδ) promotes a more oxidative phenotype. Methods : We asked whether PPARδ overexpression could ameliorate these deficits in the medial gastrocnemius of spinal cord transected (ST) adult mice. Results : Time‐to‐peak tension and half‐relaxation times were longer in PPARδ‐Con and PPARδ‐ST compared with littermate wild‐type (WT) controls. Fatigue index was 50% higher in PPARδ‐Con than WT‐Con and 70% higher in the PPARδ‐ST than WT‐ST. There was an overall higher percent of darkly stained fibers for succinate dehydrogenase in both PPARδ groups. Conclusions : The results indicate a conversion toward slower, more oxidative, and less fatigable muscle properties with overexpression of PPARδ. Importantly, the elevated fatigue resistance was maintained after ST, suggesting that enhanced PPARδ expression, and possibly small molecule agonists, could ameliorate the increased fatigability routinely observed in chronically paralyzed muscles. Muscle Nerve 53: 287–296, 2016