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Long‐term wheel running improves cardiac function but has negative consequences for diaphragmatic function in the mdx mouse
Author(s) -
Selsby Joshua T.,
Acosta Pedro,
Sleeper Meg M.,
Barton Elisabeth R.,
Lee Sweeney H.
Publication year - 2013
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.27.1_supplement.712.16
Subject(s) - medicine , cardiology , ventricle , cardiac function curve , diaphragm (acoustics) , dystrophin , endocrinology , endurance training , duchenne muscular dystrophy , mdx mouse , heart failure , physics , acoustics , loudspeaker
Dystrophin‐deficient muscles suffer from free radical injury, mitochondrial dysfunction, apoptosis, and inflammation, among other pathologies, which contribute to muscle fiber injury. Endurance exercise has the capacity to counter many of these factors. Indeed, previous work indicates that endurance training decreased disease severity in dystrophic limb muscle. Our purpose was to determine the extent to which long‐term volitional wheel running (VWR) would affect dystrophic diaphragm and cardiac function. This is especially important as the diaphragm most closely recapitulates the human disease. One year of VWR increased cardiac mass by 15% (p<0.05), left ventricle chamber size by 20% (diastole) and 18% (systole) (p<0.05), and stroke volume by 2‐fold (p<0.05) compared to sedentary mdx mice. VWR increased soleus mass by 20% (p<0.05) and tetanic force by 36% (p<0.05) while specific tension was similar between VWR and sedentary mdx mice. Notably, diaphragm specific tension was reduced by 60% (p<0.05) following one year of VWR compared to sedentary mdx mice. These data suggest that the dystrophic heart undergoes beneficial exercise‐induced remodeling. Importantly, however, the severe negative impact on diaphragm function indicates that serious caution should be taken when prescribing exercise to DMD patients. Supported by NIH grants F32AR055005–01 (JTS) and U54AR052646–03 (HLS).