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Statin‐associated muscle dysfunction with novel vs. accustomed exercise
Author(s) -
Huey Kimberly,
Meador Benjamin
Publication year - 2011
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.25.1_supplement.1051.7
Subject(s) - statin , medicine , isometric exercise , exacerbation , myopathy , physical therapy , skeletal muscle , cardiology , pharmacology , endocrinology
The most common side effect of statins, skeletal muscle myopathy, is more likely in exercisers. We investigated the interaction of statin treatment with novel vs. accustomed exercise on muscle function, heat shock protein (Hsp) expression, and caspase (CAP) activation and hypothesized that exacerbation of statin‐induced myopathy by exercise is specific to untrained muscle, while prior training is protective against dysfunction. Mice received daily cerivastatin (1/mg/kg) or saline for 2 wks, with/without wheel running (RW) (Novel & Sedentary groups). Accustomed groups completed 2 wks RW before statin treatment. At 4 wks, plantarflexor isometric force and Hsp25, αB‐crystallin, and CAP‐3 & ‐9 protein levels were quantified. Statin treatment did not impact RW, but reduced force in sedentary and novel‐exercise groups compared to saline. The largest statin‐associated force reduction occurred with novel RW, while accustomed RW prevented statin‐associated force loss. Statin treatment did not change Hsp25 or αB‐crystallin muscle protein levels, but both were increased by novel and accustomed RW. Active CAP‐3 was undetectable in all groups. These results suggest that exercise training prior to statin treatment can protect against muscle dysfucntion, rather than exacerbate it, as seen with novel exercise, and exercise‐induced Hsp up‐regulation may contribute to this protective effect. Funded by: AHA 0910107G.