Search

The purpose of this study was to investigate the effects of in vivo creatine monohydrate (Cr) supplementation on doxorubicin (Dox)-induced muscle dysfunction. Male rats were fed a diet supplemented with 3% Cr or a standard chow for 2 wk. After 2 wk of feeding, animals received Dox or saline as a placebo. Five days post-injection, grip strength was measured, and muscle fatigue was analyzed ex vivo. When compared with controls, a significantly lower grip strength was observed with Dox treatment, but no significant handgrip difference was observed with Cr feeding prior to Dox treatment when compared to controls. In the isolated muscle fatigue experiments, solei (primarily type I muscle) from controls produced significantly less force than baseline at 60 s and solei from Dox treated rats produced significantly less force than baseline at 30 s; however, Cr feeding prior to Dox produced significantly less force than baseline at 60 s. In the primarily type II EDL, a decline in force production from baseline was observed at 50 s in controls and Cr + Dox and at 20 s in standard chow + Dox. Cr attenuated the increase in fatigue that accompanies Dox treatment suggesting that Cr supplementation may have use in managing Dox myotoxicity.

Background: Doxorubicin (DOX) is associated with profound skeletal muscle dysfunction. Resistance training (RT) and creatine (Cr) monohydrate have been independently shown to protect against DOX-induced muscle dysfunction. However, no investigation has examined their combined effects on DOX-induced muscle dysfunction. Methods: Male Sprague-Dawley rats were randomly assigned to a RT or sedentary group. After 6 wk of training, the soleus (SOL) and extensor digitorum longus (EDL) were excised and placed in a tissue bath containing Krebs buffer (K) or a K containing Cr (25 mM) for 30 min. The buffers were refreshed with new K or K containing DOX (24 μM) and incubated for 30 min. Muscles were then subjected to maximal twitch and fatigue testing. Results: DOX-induced fatigue occurred at 40 s in the SOL and EDL. RT delayed DOX-induced fatigue by 20 s in the SOL and 10 s in the EDL. Cr treatment delayed the onset of DOX-induced fatigue by 10 s in the EDL. The combination of RT and Cr delayed DOX-induced fatigue by 50 s in the SOL and 20 s in the EDL. Conclusion: This study showed that a combined treatment with RT and Cr minimized DOX-induced fatigue in the SOL and EDL.