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<title><![CDATA[Journal of Orthopaedic & Sports Physical Therapy - Dawn A. Lowe, PhD]]></title>
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<title>Animal Models for Inducing Muscle Hypertrophy: Are They Relevant for Clinical Applications in Humans?</title>
<link>http://www.jospt.org/issues/articleID.168/article_detail.asp</link>
<description><![CDATA[<a href="http://www.jospt.org/rss/author.dawnalowe/author.asp">Dawn A. Lowe</a>, <a href="http://www.jospt.org/rss/author.stephenealway/author.asp">Stephen E. Alway</a><br />Muscle hypertrophy is an adaptive response to overload. Progressive resistance exercise (PRE) is thought to be among the best means to achieve hypertrophy in humans. While functional adaptations to PRE in muscles of humans are made in the clinic, it is difficult to evaluate hypertrophic responses and underlying mechanisms because the adaptations require many weeks or months before they become evident and there is a large variability in response to PRE among humans. In contrast, various animal models have been shown to induce rapid and extensive muscle hypertrophy and some models allow precise control of the exercise parameters. By examining the animal models of muscle hypertrophy and understanding the advantages and disadvantages of each, clinicians may be able to evaluate and use relevant data from these models to design new strategies for modification of PRE in humans. The purpose of this article is to review animal models that are currently used in basic research laboratories, discuss the hypertrophic and functional outcomes, and relate these to PRE used in the clinic. <p>J Orthop Sports Phys Ther. 2002; 32(2):36&ndash;43. </p><p><strong>Key Words:</strong> muscle growth, muscle strength, overload, resistance training, skeletal muscle</p>]]></description>
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<title>What Mechanisms Contribute to the Strength Loss That Occurs During and in the Recovery from Skeletal Muscle Injury?</title>
<link>http://www.jospt.org/issues/articleID.170/article_detail.asp</link>
<description><![CDATA[<a href="http://www.jospt.org/rss/author.gordonlwarren/author.asp">Gordon L. Warren</a>, <a href="http://www.jospt.org/rss/author.christopherpingalls/author.asp">Christopher P. Ingalls</a>, <a href="http://www.jospt.org/rss/author.dawnalowe/author.asp">Dawn A. Lowe</a>, <a href="http://www.jospt.org/rss/author.rbarmstrong/author.asp">R. B. Armstrong</a><br />In the workplace or on the athletic field, muscle strength can be decreased by 50% or more following performance of a relatively few high-force, eccentric contractions. The strength loss can be prolonged, taking a month or more for complete recovery. It is important to understand the cause(s) of the strength loss so we can develop means of preventing or attenuating this loss. The cellular-level mechanisms explaining the loss of strength following contraction-induced muscle injury remain controversial. The traditional thought is that initial strength loss is due solely to damage to force-bearing structures within the muscle, as evidenced by histopathology. In addition, inflammation in the days following injury is commonly thought to exacerbate the strength loss. We present data to the contrary. Recent data show that most of the early strength loss results from a failure of excitation-contraction coupling processes and that a slow loss of contractile protein in the days following injury prolongs the time for recovery. <p>J Orthop Sports Phys Ther. 2002; 32(2):58&ndash;64. </p><p><strong>Key Words:</strong> calcium, eccentric, excitation-contraction coupling, strength</p>]]></description>
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