title: Obese mice incur greater myofiber membrane disruption in response to mechanical load compared with lean mice.
abstract: OBJECTIVE
  Obesity is associated with modified transmembrane signaling events in skeletal muscle, such as insulin signaling and glucose transport. The underlying cause of these obesity-related effects on transmembrane signaling is still unknown. In general, the function of membrane proteins responsible for transmembrane signaling is modulated by the biochemical makeup of the membrane, such as lipid composition, in which they are embedded. Any obesity-related alterations in membrane composition would also be predicted to modify membrane biomechanical properties and membrane susceptibility to mechanical load-induced damage. The primary objective of this study was to investigate whether obesity influences myofiber membrane susceptibility to mechanical damage in skeletal muscle.
  
  
  METHODS
  Myofiber membrane damage was compared between 12-week-old obese, hypercholesterolemic (B6.V Lep(ob) /J) and isogenic, normocholesterolemic control (C57BL6/J) male mice following either normal cage activity or strenuous eccentric exercise (downhill running). Myofiber membrane damage was quantified in perfusion-fixed frozen sections of the gastrocnemius muscle via sarcoplasmic concentration of either albumin (cage activity experiment) or a fluorescent marker that had been injected immediately before activity (eccentric exercise experiment).
  
  
  RESULTS
  Obese mice exhibited evidence of increased myofiber membrane damage compared with lean mice after both normal cage activity and eccentric exercise indicating that myofiber membranes of obese mice are more susceptible to mechanical damage in general and that eccentric exercise exacerbates this effect.
  
  
  CONCLUSIONS
  These observations are consistent with the notion that obesity influences the biochemical and biomechanical properties of myofiber membranes.
authors.affiliation: Department of Health and Human Performance, University of Houston, Houston, Texas, USA. maknoblauch@gmail.com
authors.forename: Mark A
authors.initials: MA
authors.lastname: Knoblauch
authors.forename: Daniel P
authors.initials: DP
authors.lastname: O'Connor
authors.forename: Mark S F
authors.initials: MS
authors.lastname: Clarke
mesh_terms: D000418:Albumins / Q000378:metabolism; D000818:Animals; D001696:Biomechanical Phenomena; D005453:Fluorescence; D006937:Hypercholesterolemia / Q000150:complications; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology* / Q000648:ultrastructure; D009210:Myofibrils / Q000378:metabolism / Q000648:ultrastructure*; D009765:Obesity / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D010805:Physical Conditioning, Animal / Q000502:physiology; D010809:Physical Fitness / Q000502:physiology*; D012016:Reference Values; D012420:Running / Q000502:physiology*; D012508:Sarcolemma / Q000378:metabolism / Q000648:ultrastructure*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D015398:Signal Transduction; D013314:Stress, Mechanical
chemical_list: D000418:Albumins