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Exercise Protects against Cancer-induced Cardiac Cachexia

PARRY, TRACI, L.1; HAYWARD, REID2

Medicine & Science in Sports & Exercise: June 2018 - Volume 50 - Issue 6 - p 1169–1176
doi: 10.1249/MSS.0000000000001544
Basic Sciences

Cancer has been shown to negatively stimulate autophagy, leading to a decline in cardiac function. Although exercise is cardioprotective, its influence over autophagy-mediated tumor growth and cardiac function are not well defined.

Purpose This study aimed 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 run tumor bearing (WR + T). Rats remained sedentary or exercised for 6 wk. At week 4, rats in tumor groups were inoculated with MatBIII tumor cells. At week 6, cardiac function was measured.

Results SED + T animals exhibited significantly lower left ventricular developed pressure when compared with SED, WR, and WR + T (P < 0.05). This coincided with a significant increase in cardiac autophagy (increased LC3-II) in SED + T animals when compared with SED, WR, and WR + T (P < 0.05). Furthermore, SED + T hearts showed a significant increase in β-myosin heavy chain expression versus nontumor groups (P < 0.05). Tumor mass was significantly larger (P < 0.001) in SED + T animals when compared with WR + T animals, which was accompanied by a significant increase in tumor LC3-II protein expression (P < 0.05).

Conclusion Nonexercised 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.

1McAllister Heart Institute and Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC; and

2School of Sport and Exercise Science, and the University of Northern Colorado Cancer Rehabilitation Institute, University of Northern Colorado, Greeley, CO

Address for correspondence: Reid Hayward, Ph.D., School of Sport and Exercise Science, University of Northern Colorado Cancer Rehabilitation Institute, Gunter Hall 2780, Campus Box 39, University of Northern Colorado, Greeley, CO 80639; E-mail: reid.hayward@unco.edu.

Submitted for publication September 2017.

Accepted for publication December 2017.

© 2018 American College of Sports Medicine