{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T01:34:22Z","timestamp":1648517662813},"reference-count":13,"publisher":"Institute of Physiology of the Czech Academy of Sciences","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiol Res"],"published-print":{"date-parts":[[2017,12,30]]},"abstract":"<jats:p>AT1 receptor (AT1R) blockade prevents physiological cardiac hypertrophy induced by resistance training. Also, our group showed that a single bout of resistance exercise (RE) activates the AKT\/mTOR which was also inhibited by AT1R blocker. Here, we investigated whether IGF1-receptor (IGF1-R) and MAPKs were also activated after a single bout of RE. Wistar rats were divided into Sedentary (Sed), Sedentary treated with losartan (Sed+LOS), Exercise (EX), and Exercise treated with losartan (EX+LOS). Cardiac tissue was obtained 5 and 30 min after 4 sets of 12 repetitions of squat exercise (80 % 1RM). We demonstrated that a single bout of RE did not induce IGF1-R tyrosine phosphorylation. ERK1\/2 and P38 phosphorylation levels were elevated in the EX 5min and EX 30min groups however, only ERK1\/2 was inhibited by losartan treatment (AT1R blocker). Next, we showed that \u03b2-arrestin-2 expression increased 28 % in trained animals compared to sedentary group. Altogether, our results demonstrate that AT1R, but not IGF1-R, may exert the hypertrophic cardiac stimulus RE-induced. Also, activation of AKT\/mTOR and ERK1\/2 pathways may occur through the \u03b2-arrestin-dependent pathway.<\/jats:p>","DOI":"10.33549\/physiolres.933563","type":"journal-article","created":{"date-parts":[[2020,1,19]],"date-time":"2020-01-19T15:41:31Z","timestamp":1579448491000},"page":"1061-1065","source":"Crossref","is-referenced-by-count":0,"title":["Cardiac AT1 Receptor-Dependent and IGF1 Receptor-Independent Signaling Is Activated by a Single Bout of Resistance Exercise"],"prefix":"10.33549","author":[{"given":"S. F. S.","family":"MELO","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"V. G.","family":"BARAUNA","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T.","family":"FERNANDES","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E. C.","family":"CARMO","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. R. O.","family":"CARVALHO","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E. M.","family":"OLIVEIRA","sequence":"additional","affiliation":[{"name":"Laboratory of Biochemistry and Molecular Biology of the Exercise, Department of Human Movement Biodynamics, School of Physical Education and Sport University of S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"19169","published-online":{"date-parts":[[2017,12,16]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"BARAUNA VG, MAGALHAES FC, KRIEGER JE, OLIVEIRA EM: AT1 receptor participates in the cardiac hypertrophy induced by resistance training in rats. 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