title: Effect of ischemic preconditioning in skeletal muscle measured by functional magnetic resonance imaging and spectroscopy: a randomized crossover trial.
abstract: BACKGROUND
  Nuclear magnetic resonance (NMR) imaging and spectroscopy have been applied to assess skeletal muscle oxidative metabolism. Therefore, in-vivo NMR may enable the characterization of ischemia-reperfusion injury. The goal of this study was to evaluate whether NMR could detect the effects of ischemic preconditioning (IPC) in healthy subjects.
  
  
  METHODS
  Twenty-three participants were included in two randomized crossover protocols in which the effects of IPC were measured by NMR and muscle force assessments. Leg ischemia was administered for 20 minutes with or without a subsequent impaired reperfusion for 5 minutes (stenosis model). IPC was administered 4 or 48 hours prior to ischemia. Changes in 31phosphate NMR spectroscopy and blood oxygen level-dependent (BOLD) signals were recorded. 3-Tesla NMR data were compared to those obtained for isometric muscular strength.
  
  
  RESULTS
  The phosphocreatine (PCr) signal decreased robustly during ischemia and recovered rapidly during reperfusion. In contrast to PCr, the recovery of muscular strength was slow. During post-ischemic stenosis, PCr increased only slightly. The BOLD signal intensity decreased during ischemia, ischemic exercise and post-ischemic stenosis but increased during hyperemic reperfusion. IPC 4 hours prior to ischemia significantly increased the maximal PCr reperfusion signal and mitigated the peak BOLD signal during reperfusion.
  
  
  CONCLUSIONS
  Ischemic preconditioning positively influenced muscle metabolism during reperfusion; this resulted in an increase in PCr production and higher oxygen consumption, thereby mitigating the peak BOLD signal. In addition, an impairment of energy replenishment during the low-flow reperfusion was detected in this model. Thus, functional NMR is capable of characterizing changes in reperfusion and in therapeutic interventions in vivo.
  
  
  BACKGROUND
  ClinicalTrials.gov: NCT00883467.
authors: Department of Clinical Pharmacology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
authors: Martin
authors: M
authors: Andreas
authors: Albrecht I
authors: AI
authors: Schmid
authors: Mohammad
authors: M
authors: Keilani
authors: Daniel
authors: D
authors: Doberer
authors: Johann
authors: J
authors: Bartko
authors: Richard
authors: R
authors: Crevenna
authors: Ewald
authors: E
authors: Moser
authors: Michael
authors: M
authors: Wolzt
mesh_terms: D000328:Adult; D001317:Austria; D018592:Cross-Over Studies; D006801:Humans; D019194:Ischemic Preconditioning / Q000379:methods*; D007537:Isometric Contraction; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D053580:Muscle Strength; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000378:metabolism; D012039:Regional Blood Flow; D015427:Reperfusion Injury / Q000175:diagnosis* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D013997:Time Factors; D055815:Young Adult
chemical_list: D010725:Phosphocreatine; D010100:Oxygen