Exercise Protects against Cancer-induced Cardiac Cachexia

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Abstract

Cancer has been shown to negatively stimulate autophagy, leading to declines in cardiac function. While exercise is cardioprotective, its influence over autophagy-mediated tumor growth and cardiac function are not well defined. Purpose: To determine the effect of exercise on tumor morphology and cardiac function. Methods: Fisher 344 rats (n=28) were assigned to one of four groups: 1) sedentary non tumor-bearing (SED), 2) sedentary tumor-bearing (SED+T), 3) wheel run non-tumor bearing (WR), or 4) wheel running tumor bearing (WR+T). Rats remained sedentary or exercised for 6 weeks. At week 4, rats in tumor groups were inoculated with MatBIII tumor cells (flank). At week 6, cardiac function was measured. Results: SED+T animals exhibited significantly lower left ventricular developed pressure when compared to SED, WR, and WR+T (P < 0.05). This coincided with a significant increase in cardiac autophagic flux (increased LC3-II) in SED+T animals when compared to SED, WR, and WR+T (P < 0.05). Furthermore, SED+T hearts showed a significant increase in β-MHC expression vs NT groups (P < 0.05). Tumor mass was significantly larger (P < 0.001) in SED+T animals when compared to WR+T animals, which was accompanied by a significant increase in tumor LC3-II protein expression (P < 0.05). Conclusion: Non-exercised tumor-bearing rats showed severe cardiac dysfunction and excessive, maladaptive autophagy in the heart and tumors. Voluntary exercise preserved cardiac function and attenuated the autophagic response in heart and tumor tissues. This preservation may be related to the reduced tumor growth in aerobically exercised rats, to the improved regulation of autophagy by exercise, or both.

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