title: Protective effects of exercise preconditioning on hindlimb unloading-induced atrophy of rat soleus muscle.
abstract: OBJECTIVE
  A chronic decrease in the activation and loading levels of skeletal muscles as occurs with hindlimb unloading (HU) results in a number of detrimental changes. Several proteolytic pathways are involved with an increase in myofibrillar protein degradation associated with HU. Exercise can be used to counter this increase in proteolytic activity and, thus, may be able to protect against some of the detrimental changes associated with chronic decreased use. The purpose of the present study was to determine the potential of a single bout of preconditioning endurance exercise in attenuating the effects of 2 weeks of HU on the mass, phenotype and force-related properties of the soleus muscle in adult rats.
  
  
  METHODS
  Male Wistar rats were subjected to HU for 2 weeks. One half of the rats performed a single bout of treadmill exercise for 25 min immediately prior to the 2 weeks of HU.
  
  
  RESULTS
  Soleus mass, maximum tetanic tension, myofibrillar protein content, fatigue resistance and percentage of type I (slow) myosin heavy chain were decreased in HU rats. In addition, markers for the cathepsin, calpain, caspase and ATP-ubiquitin-proteasome proteolytic pathways were increased. The preconditioning endurance exercise bout attenuated all of the detrimental changes associated with HU, and increased HSP72 mRNA expression and protein levels.
  
  
  CONCLUSIONS
  These findings indicate that exercise preconditioning may be an effective countermeasure to the detrimental effects of chronic decreases in activation and loading levels on skeletal muscles and that an elevation in HSP72 may be one of the mechanisms associated with these responses.
authors.affiliation: Department of Rehabilitation Sciences, Kobe University Graduate School of Health Sciences, Suma-Ku, Kobe, Japan. fujinoh@gmail.com
authors.forename: Hidemi
authors.initials: H
authors.lastname: Fujino
authors.forename: A
authors.initials: A
authors.lastname: Ishihara
authors.forename: S
authors.initials: S
authors.lastname: Murakami
authors.forename: T
authors.initials: T
authors.lastname: Yasuhara
authors.forename: H
authors.initials: H
authors.lastname: Kondo
authors.forename: S
authors.initials: S
authors.lastname: Mohri
authors.forename: I
authors.initials: I
authors.lastname: Takeda
authors.forename: R R
authors.initials: RR
authors.lastname: Roy
mesh_terms: D000375:Aging / Q000473:pathology / Q000502:physiology*; D000818:Animals; D001284:Atrophy / Q000378:metabolism / Q000473:pathology; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism; D006614:Hindlimb / Q000502:physiology; D019417:Hindlimb Suspension / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D016555:Matched-Pair Analysis; D009119:Muscle Contraction / Q000502:physiology; D053580:Muscle Strength / Q000502:physiology*; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D009210:Myofibrils / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D050884:HSP72 Heat-Shock Proteins