Activation pattern of MAPK signaling in the hearts of trained and untrained rats following a single bout of exercise.
Since 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 of exercise or chronic exercises. The hearts of untrained rats received 5, 15, and 30 min of treadmill running exercise (Ex5 to Ex30) and rested for 0.5, 1, 3, 6, 12, and 24 h (PostEx0.5 to 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 activator protein-1 DNA binding activity was enhanced in untrained 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 4, 8, and 12 wk of exercise training, the rats exhibited significant cardiac hypertrophy by week 12. Activation of MAPKs in the 4-wk-trained rats increased after a 30-min single bout of exercise but decreased in the 8-wk group. Finally, the activity of MAPKs signaling in the 12-wk-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.
Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
Motoyuki
M
Iemitsu
Seiji
S
Maeda
Subrina
S
Jesmin
Takeshi
T
Otsuki
Yoshitoshi
Y
Kasuya
Takashi
T
Miyauchi
D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D019332:Endothelin-1 / Q000032:analysis / Q000235:genetics / Q000502:physiology; D005786:Gene Expression Regulation / Q000502:physiology; D006321:Heart / Q000502:physiology*; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D009206:Myocardium / Q000737:chemistry / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000032:analysis / Q000235:genetics / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000502:physiology*; D013997:Time Factors; D018808:Transcription Factor AP-1 / Q000032:analysis / Q000235:genetics / Q000502:physiology
D019332:Endothelin-1; D012333:RNA, Messenger; D018808:Transcription Factor AP-1; D020097:Natriuretic Peptide, Brain; D020928:Mitogen-Activated Protein Kinases