title: Resistance training reduces subclinical inflammation in obese, postmenopausal women.
abstract: OBJECTIVE
  Aerobic exercise is frequently prescribed to reduce inflammatory-related disease (cardiovascular disease and diabetes) risk. Resistance training (RT), however, may be key to maximizing anti-inflammatory benefits of consistent exercise. We examined the influence of RT on inflammatory biomarkers in obese, postmenopausal women.
  
  
  METHODS
  Twenty-three women (65.6 ± 2.6 yr; body mass index, 33 kg·m) underwent 12 wk of RT (3 sets, 10 exercises, 3× per week, 8-12 repetition maximum (RM), resistance exercise (EX), N = 11) or social interaction intervention (SI, stretching, knitting, health lectures, 2× per week, control group (CON), N = 12). Both before (BT) and after (AT) RT or SI, blood was collected before (PR), immediately (PO), 2 h (2H), and 24 h (24H) after a single resistance exercise bout (RE) in EX and at the same time points in nonexercise, resting CON. For all time points, blood was analyzed for IL-6, leptin, and lipopolysaccharide (LPS)-stimulated tumor necrosis factor-α (TNF-α) (LPS-TNF) and IL-10 (LPS-IL10). PR samples were also examined for C-reactive protein, TNF-α, and adiponectin, and mRNA expression of toll-like receptor 4 (TLR4) and MC1R. Subcutaneous adipose tissue was extracted BT and AT and analyzed for mRNA expression of monocyte chemotactic protein-1, leptin, CD68, and TLR4.
  
  
  RESULTS
  RT improved strength (44%) and reduced circulating C-reactive protein (-33%), leptin (-18%) and TNF-α (-29%) with no change in body composition. IL-6 decreased after SI in CON (-17%). LPS-TNF increased after SI or RT (CON +26%, EX +67%, respectively), whereas LPS-IL10 decreased in CON (-28%) but increased in EX (+20%). RT did not influence inflammatory biomarker gene expression in whole blood or subcutaneous adipose tissue. A single RE bout augmented LPS-TNF and LPS-IL10 at 24H in EX, particularly AT.
  
  
  CONCLUSIONS
  RT reduced markers of subclinical inflammation in circulation in obese, postmenopausal women in the absence of changes in body composition. Chronic RT also enhanced response to endotoxin challenge both at rest (PR) and 24 h after an acute RE bout (24H).
authors.affiliation: Exercise Physiology Laboratory, Texas Christian University, Fort Worth, TX, USA. m.phillips@tcu.edu
authors.forename: Melody D
authors.initials: MD
authors.lastname: Phillips
authors.forename: Robert M
authors.initials: RM
authors.lastname: Patrizi
authors.forename: Dennis J
authors.initials: DJ
authors.lastname: Cheek
authors.forename: Joshua S
authors.initials: JS
authors.lastname: Wooten
authors.forename: James J
authors.initials: JJ
authors.lastname: Barbee
authors.forename: Joel B
authors.initials: JB
authors.lastname: Mitchell
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001824:Body Constitution; D002097:C-Reactive Protein; D018932:Chemokine CCL2 / Q000097:blood; D005260:Female; D015870:Gene Expression; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008070:Lipopolysaccharides / Q000097:blood; D008875:Middle Aged; D053580:Muscle Strength; D009765:Obesity / Q000097:blood*; D017698:Postmenopause / Q000097:blood*; D055070:Resistance Training; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D018932:Chemokine CCL2; D018836:Inflammation Mediators; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D002097:C-Reactive Protein