SUMMARY1. Methods were developed and described for partitioning the total daily energy expenditure of rats into compartments attributable to rest, total spontaneous motor activity and feeding activity.2. In terms of energy expenditure feeding appeared as a form of motor activity which was at least as costly as other spontaneous activity.3. The compartment attributable to total spontaneous activity within a 24 hr period was about 25 % of total energy expenditure and was not altered by body weight, food intake or feeding mode (e.g. solid or liquid food). 4. The compartment attributable to feeding activity varied with food intake and with feeding mode in such a way that non-feeding activity varied inversely with feeding activity. By a given feeding mode non-feeding activity varied inversely with food intake.5. It is concluded (a) that food deprivation does not induce increased total activity by the rat, but does produce a complementary increase in non-feeding activity; (b) that measurement of a specific motor activity does not give a valid estimate of change in total activity; and (c) that the complementary relationship between the energy expended on feeding activity and that expended on non-feeding activity is responsible for the decline in food intake with increasing non-feeding activity that has been shown to occur at low habitual levels of spontaneous activity.

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Cancer cachexia is a complex syndrome that includes host tissue wasting, anorexia, asthenia, and abnormal host intermediary metabolism. It is present in approximately 50% of cancer patients during treatment and nearly 100% of treated cancer patients at death. Cachexia has a detrimental impact on cancer therapy. The central problem of cancer cachexia is that energy balance is not maintained, and the host has a relative hypophagia which results in host tissue wasting. The tumor by its nature and obligate growth can continue to consume glucose, amino acids, and lipids at the expense of the host. This produces abnormal host intermediary metabolism including elevated glucose production and recycling, decreased muscle protein synthesis, and increased muscle and fat breakdown. The exact mechanisms of cancer cachexia have been only partially elucidated. The identification of signal molecules like cachectin which mediate these changes may be on the horizon. Nutritional support can reverse some of the derangements seen with cachexia, and there is evidence that functional lean body mass or body cell mass can be restored in some (but not all) patients. However, nutritional support has not yet improved response to chemotherapy or radiation therapy, nor has it improved host tolerance of chemotherapy. It has improved operative mortality and morbidity in cachectic cancer patients undergoing major surgical procedures. Optimum host nutritional support appears to be dependent on high insulin concentrations in both humans and rats. Insulin and exercise may be methods to preserve host lean tissue and feed the host rather than the tumor. Future studies depend on better definition of tumor-bearing host metabolism, altering the relationship between neoplasm and host to preferentially feed the host, and making the neoplasm more susceptible to effective treatment.

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