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J Appl Physiol 96: 2249-2256, 2004. First published March 12, 2004; doi:10.1152/japplphysiol.01210.2003
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Exercise delays allogeneic tumor growth and reduces intratumoral inflammation and vascularization

Mark R. Zielinski,1 Melissa Muenchow,1 Matthew A. Wallig,2 Peggy L. Horn,3 and Jeffrey A. Woods1

1Departments of Kinesiology and 2Veterinary Pathobiology, University of Illinois, Urbana-Champaign, Illinois 61801; and 3Canberra University, Canberra, Australia

Submitted 12 November 2003 ; accepted in final form 2 February 2004

This investigation determined whether daily strenuous exercise would alter the progression and regression of an allogeneic lymphoid tumor in mice. We also determined whether exercise would alter the cellular composition and vascularity of the tumor. Female BALB/c mice (age 6–8 wk) were randomly assigned to sedentary control (Con) or daily exercised groups (EXH). EXH mice ran on a treadmill at incremental speeds (20–40 m/min) for 3 h or until fatigue. Each mouse was subcutaneously injected with 20 x 106 EL-4 lymphoma cells immediately after the first exercise bout (day 1) and run daily. Tumor volume was measured daily with calipers. In some experiments, mice were euthanized on days 5–10, 12, and 14. Tumors were excised and stained with hematoxylin and eosin or for Factor VIII-associated antigen using immunohistochemistry and analyzed in a blinded fashion under a light microscope. There was no significant treatment main effect found for tumor volumes. Interestingly, a significant treatment x time interaction was found, such that there was a 2-day delay in peak tumor volume and a more rapid tumor regression in EXH. Tumors isolated from Con exhibited significantly higher numbers of apoptotic bodies, blood vessels, macrophages, and neutrophils when compared with EXH. Intratumoral lymphocytes were higher in Con early in tumor growth but higher in EXH at peak tumor size. These data indicate that daily strenuous exercise may influence tumor growth by affecting the microenvironment of the tumor, resulting in a delay in tumor growth and a more rapid regression.

angiogenesis; cancer; transplant; mice



Address for reprint requests and other correspondence: J. A. Woods, 348 Freer Hall, 906 S. Goodwin Ave., Univ. of Illinois, Urbana, IL 61801 (E-mail: Woods1{at}uiuc.edu).




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