Endurance training restores peritoneal macrophage function in post-MI congestive heart failure rats.
Congestive heart failure (CHF) induces a state of immune activation, and peritoneal macrophages (M phi s) may play an important role in the development and progression of one such condition. Moderate endurance training modulates peritoneal M phi function. We evaluated the effect of endurance training on different stages of the phagocytic process and in the production of interleukin-6 (IL-6), interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) after LPS stimulation. Either ligation of the left coronary artery or Sham operations were performed in adult Wistar rats. After 4 wk, control (Sham operated) and MI (ligation of the left coronary artery) animals were randomly assigned to either a sedentary (Sham-operated sedentary, n = 7 and MI sedentary, n = 10) or a trained group (Sham-operated trained, n = 8 and MI trained, n = 8). Trained rats ran on a treadmill (0% grade at 13-20 m/min) for 60 min/day, 5 days/wk, for 8-10 wk, whereas sedentary rats had only limited activity. Training increased maximal oxygen uptake normalized for body weight (ml.kg(-1).min(-1)), as well as skeletal muscle citrate synthase maximal activity, when compared with sedentary groups. The resident and total cell number, the chemotaxis index, and the production of TNF-alpha stimulated by LPS were significantly higher in the MI sedentary group when compared with the Sham sedentary group. Moderate endurance training reversed these alterations promoted by post-MI. These results demonstrate that moderate intensity exercise training modulates peritoneal M phi function and induces beneficial metabolic effects in rats with post-MI CHF.
Batista
M L
ML
University of São Paulo, SP, Brazil. migueljr@usp.br
Santos
R V T
RV
Oliveira
E M
EM
Seelaender
M C L
MC
Costa Rosa
L F B P
LF
D000818:Animals; D002950:Citrate (si)-Synthase / Q000378:metabolism; D003331:Coronary Vessels / Q000601:surgery; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008026:Ligation; D008070:Lipopolysaccharides / Q000494:pharmacology; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism / Q000503:physiopathology; D009203:Myocardial Infarction / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D010101:Oxygen Consumption; D010587:Phagocytosis / Q000187:drug effects; D010807:Physical Endurance; D005082:Physical Exertion; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D002950:Citrate (si)-Synthase