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Experimental Physiology 91.2 pp 413-421
DOI: 10.1113/expphysiol.2005.032490
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AT1 receptors are necessary for eccentric training-induced hypertrophy and strength gains in rat skeletal muscle

Todd A. McBride1

1 Department of Biology, California State University, Bakersfield, Bakersfield, CA 93311, USA

This study was undertaken to measure the response of skeletal muscle to eccentric contractions (EC) in the presence of the angiotensin type 1 (AT1) receptor blocker, losartan. It was hypothesized that blocking AT1 receptors prior to an initial bout of EC would prevent the muscle from developing the normal adaptation to EC as demonstrated by the repeated bout effect. It was also hypothesized that continuous AT1 receptor blockade during EC training would significantly reduce muscle hypertrophy and strength gains that occur with repeated EC. Rats received losartan in their drinking water at either a low dose (20 mg (kg body weight)–1 day–1) or a high dose (40 mg (kg body weight)–1 day–1). Each bout of EC consisted of a total of 24 contractions. Rats were assigned to four groups: a single acute bout of EC (n= 6); two bouts of EC separated by 14 days (n= 8); and 4 weeks of training twice a week on the low dose (n= 5) or the high dose (n= 9). There was no effect of AT1 receptor blockade on the initial loss of function following a single acute bout of EC, or on the repeated bout effect following a second exposure to EC. AT1 receptor blockade did alter the results of EC training, in both the low and high dose groups. Losartan treatments prevented EC training-induced increases in muscle wet and dry weights compared to untreated rats. Finally, the low and high dose losartan treatments also prevented an increase in muscle contractile force following EC training compared to the untreated group. Functional AT1 receptors are therefore not necessary for an acute adaptation to EC as demonstrated by the repeated bout effect, but are necessary for muscle hypertrophy and increased contractile force associated with EC training.

(Received 10 October 2005; accepted after revision 25 November 2005; first published online 29 November 2005)
Corresponding author T. A. McBride: California State University, Bakersfield, Bakersfield, CA 93311, USA. Email: tmcbride{at}csub.edu







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