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The generation of reactive oxygen and nitrogen species (RONS) is not different during injurious lengthening contractions and non‐damaging isometric contractions
Author(s) -
Sloboda Darcee,
Brooks Susan V.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1075.9
Subject(s) - isometric exercise , chemistry , skeletal muscle , contraction (grammar) , biophysics , muscle contraction , anatomy , medicine , endocrinology , biology
Neither isometric contractions (IC) nor stretches without activation (passive stretches, PS) cause injury to skeletal muscle. In contrast, when muscles are activated and stretched (lengthening contractions, LC), structural damage occurs that leads to the degeneration of damaged muscle fibers by unknown mechanisms. RONS may contribute to fiber degeneration by damaging proteins and lipids or by initiating signaling pathways, but RONS generation during LC has not been examined. We hypothesized that RONS generation would be greater during LC than IC. Whole lumbrical muscles dissected from mice were subjected to a series of IC or PS that did not injure the muscle or damaging LC that caused a 28 ± 9% deficit in isometric force. RONS were monitored during the protocols with CM‐H 2 DCF‐DA. CM‐DCF fluorescence increased 6‐fold during IC. CM‐DCF fluorescence also increased during LC, but the increase was not different from that during IC, despite greater force generation during LC (29 ± 2 mN vs 19 ± 2 mN, P < 0.001) and the resultant force deficit. CM‐DCF fluorescence did not increase with PS. We conclude that RONS generation by muscle is associated primarily with activation rather than force and does not change as muscle is damaged by LC. Since RONS generation was not different during contractions whether or not the muscle was damaged, RONS may not be required for the initiation of injury following LC. This work is supported by AG020591.