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J Appl Physiol 106: 911-918, 2009. First published December 18, 2008; doi:10.1152/japplphysiol.91201.2008
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Energetics and mammary carcinogenesis: effects of moderate-intensity running and energy intake on cellular processes and molecular mechanisms in rats

Zongjian Zhu, Weiqin Jiang, John N. McGinley, and Henry J. Thompson

Cancer Prevention Laboratory, Colorado State University, Fort Collins, Colorado

Submitted 8 September 2008 ; accepted in final form 15 December 2008

The objective of this experiment was to determine the effects on mammary carcinogenesis of similar limitations in energy availability either by energy expenditure due to moderate-intensity running (physical activity, PA) or by regulating dietary energy (RE) intake relative to a sedentary control (SC) group that ate ad libitum. A total of 90 female Sprague-Dawley rats were injected with 1-methyl-1-nitrosourea (50 mg/kg) and 7 days thereafter were randomized to either SC, a PA group given free access to a motorized running wheel, or a RE group whose food intake limited growth to the rate observed in PA. Compared with SC, mammary carcinogenesis was inhibited by RE or PA. Cancer incidence, 92.6%, 77.8%, and 66.7% (P = 0.06), and cancer multiplicity, 3.44, 2.11, and 1.62 cancers/rat (P = 0.006), in SC, RE, and PA, respectively, were reduced to a similar extent by RE and PA. Histological and Western blot analyses of mammary carcinomas provided evidence that RE and PA induced apoptosis via the mitochondrial pathway, that cell cycle progression was suppressed at the G1/S transition, and that intratumoral blood vessel density was reduced, although it remains to be determined whether PA and RE exert these effects via the same mechanisms.

energy restriction; physical activity


Address for reprint requests and other correspondence: H. J. Thompson, Cancer Prevention Laboratory, Colorado State Univ., 1173 Campus Delivery, Fort Collins, CO 80523 (e-mail: henry.thompson{at}colostate.edu)






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