Voluntary Exercise and Experimental Mammary Cancer

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Abstract
Both epidemiologic and experimental studies suggest that physical activity may protect against several forms of cancer. Regarding experimental mammary cancer, exercise has been shown to enhance or inhibit tumorigenesis depending on the type of activity employed. Voluntary exercise, consistently inhibited while forced exercise either enhanced or inhibited depending on experimental conditions. The present study explored the protective role of voluntary activity on two different kinds of chemically induced mammary tumors, [Nnitrosomethylurea(NMU) and 7,12-dimethylbenz(a)anthracene (DMBA)], a virally induced mouse mammary tumor (MMTV) and a transplantable metastasizing mammary tumor (R 13672). Its purpose was to determine whether the protective effect of energy expenditure was a species-, strain-, carcinogen-, diet-, or stage-specific phenomenon, or whether it was a general phenomenon affecting all aspects of mammary carcinogenesis. The results of these studies indicate that voluntary exercise inhibits the development of both the NMU- and DMBA-induced mammary tumors and the MMTV-induced mouse mammary tumor under high-fat (HF) 20–23% wt/wt) conditions. The results in the R13762 model study were less clear. Under HF conditions, voluntary exercise exerted a statistically insignificant enhancement of pulmonary metastases in retired breeders, but had the opposite effect in medium-fat (MF, 11.5% wt/wt) conditions. When only the most active half of the HF animals were compared to sedentary controls, a statistically significant enhancement of pulmonary metastases was found. These studies indicate that, with regard to primary prevention, voluntary activity during the post-initiation phase inhibits mammary tumor development whether chemically or virally induced. With regard to secondary prevention, under HF conditions, activity may enhance both the volume and number of lung metastasis, while the converse may occur under MF conditions, indicating that interactions between dietary fat (energy intake) and activity (energy expenditure) may play an important role in determining the effects of physical activity on the metastatic process. Remaining to be clarified are the effects of the degree and amount of exercise, the effects of activity on the initiation and progression phases of carcinogenesis, the nature of the interaction between fat intake, activity and mammary carcinogenesis, and, lastly, the underlying cellular mechanisms responsible for the protective effects of physical exercise.