Received October 10, 2005
Revised November 1, 2005
Accepted after revision November 25, 2005
AT1 receptors are necessary for eccentric training induced hypertrophy and strength gains in rat skeletal muscle
Todd McBride 1*
1 California State University, Bakersfield
* To whom correspondence should be addressed. E-mail: tmcbride{at}csub.edu.
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Abstract |
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This study was undertaken to measure the response of skeletal muscle to eccentric contractions (EC) in the presence of the angiotensin type one (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 in either a low dose (20 mg/kgBW/day) or high dose (40mg/kg/BW). Each bout of EC consisted of 24 total contractions performed in four different groups of rats. A single acute bout (n=6), two bouts separated by 14 days (n=8) and four weeks of training twice a week low dose (n=5) and 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 the repeated bout effect following a second exposure to EC. AT1 receptor blockade did alter the results of EC training, in both the low dose and high dose groups. Losartan treatments prevented EC training induced increases in muscle wet and dry weights compared to non-treated rats. Finally, the low dose and high dose Losartan treatments also prevented an increase in muscle contractile force following EC training compared to the non-treated group. Functional AT1 receptors therefore are 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.
Key Words:
Angiotensin, Exercise, Muscle contraction