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1 Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan; Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Japan
2 Cardiovascular Division, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan; Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Japan
3 Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Japan
4 Graduate School of Medicine, Chiba University, Inohana, Japan
* To whom correspondence should be addressed. E-mail: t-miyauc{at}md.tsukuba.ac.jp.
As exercise training causes cardiac hypertrophy, and a single bout induces mechanical stress to the heart, the present study aimed to characterize the activation patterns of multiple MAPK signaling pathways in the heart after a single bout or chronic exercises. The hearts of untrained rats received 5, 15, and 30 min treadmill running exercise (Ex5 - Ex30) and rested for 0.5, 1, 3, 6, 12, and 24 h (PostEx0.5 - PostEx24) before subjecting them to the following different experiments. Activation of MAPKs (ERK, JNK, and p38) and MAPKKs (MEK1/2, SEK, and MKK3/6) increased immediately after acute exercise in a time-dependent manner, with ERK, JNK, and p38 peaking at Ex15, Ex15, and Ex30, respectively. Expression of immediate early genes (c-fos, c-jun, and c-myc) was augmented and AP-1 DNA binding activity enhanced in un-trained rats, immediately after a single bout of exercise. The elevated levels of MAPKs declined to the resting levels within 24 h after exercise. In another set of experiments, following a 4-, 8-, and 12-week exercise training, the rats exhibited significant cardiac hypertrophy by week 12. Activation of MAPKs in the 4-week trained rats increased after 30-min single bout of exercise, but decreased in the 8-week group. Finally, the activity of MAPKs signaling in the 12-week trained rats exposed to an acute bout of exercise was unaltered. We conclude that exercise induces the activation of multiple MAPK (ERK, JNK, and p38) pathways in the heart, an effect that gradually declines with the development of exercise-induced cardiac hypertrophy.
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