Hypertrophy and hyperplasia of adult chicken anterior latissimus dorsi muscles following stretch with and without denervation

Sola, Olav M.; Christensen, Dirk L.; Martin, Arthur W.

doi:10.1016/0014-4886(73)90182-9

Cited by 170 publications

(89 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Birds and small mammals have been studied the most extensively. In general, hypertrophic results from the stretch of chicken and quail wing muscles 5,7,16,18,45,59 have been the same as those found in rabbit 21,30,75 and rat 27 hindlimb muscle stretch models. The functional and hypertrophic outcomes of the stretch model are well documented as described below but the mechanism underlying how stretch induces hypertrophy is not known (although it is likely a mechanoreceptor type of response).…”

Section: Chronic Stretch Modelssupporting

confidence: 62%

Animal Models for Inducing Muscle Hypertrophy: Are They Relevant for Clinical Applications in Humans?

Lowe¹

2002

J Orthop Sports Phys Ther

View full text Add to dashboard Cite

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. J Orthop Sports Phys Ther 2002;32:36-43. Key Words: muscle growth, muscle strength, overload, resistance training, skeletal muscle A n increase in muscle strength is a desirable outcome of many rehabilitation therapies. Strength gains are often a result of muscle hypertrophy, and progressive resistance exercise (PRE) is the primary mode of producing muscle hypertrophy in the rehabilitation setting. Several recent reviews have detailed the specifics of PRE in terms of modality, specificity of training, and outcomes, 23,43,44,51,61,62,64 and PRE has been shown to be beneficial as a therapeutic intervention in osteoporosis, 46 65 In this commentary, we will focus on the hypertrophic response of skeletal muscle to PRE.Physiological and cellular mechanisms of muscle hypertrophy have been reviewed extensively, 30,39,43,44 and molecular mechanisms that initiate and regulate muscle hypertrophy is a relatively new and rapidly expanding topic in the field of exercise science. 11,15,19,20,30 However, while the functional outcomes of PRE have been identified largely from human studies, much of the data used in deriving cellular and molecular mechanisms of muscle hypertrophy are drawn from studies using laboratory animals. Several different animal models for inducing muscle hypertrophy are used, and some produce outcomes that are similar to those of PRE in humans. By fully understanding the various animal models used, the clinician will be able to interpret muscle hypertrophy research results generated using laboratory animals. This information can be used by the clinician to evaluate current PRE programs and perhaps design new or modified strategies for implementing PRE. The ultimate goal is to optimize PRE in humans to acquire better functional outcomes in the clinic. The purpose of this article is to review animal models that are currently used in basic science laboratories for investigating skeletal muscle hypertrophy. Examples of recent research us...

show abstract

Section: Chronic Stretch Modelssupporting

confidence: 62%

Animal Models for Inducing Muscle Hypertrophy: Are They Relevant for Clinical Applications in Humans?

Lowe¹

2002

J Orthop Sports Phys Ther

View full text Add to dashboard Cite

show abstract

“…Rapid hypertrophy of the right ALD muscle was induced using the wing-weighting model of Sola et al (1973). Birds were randomly assigned to 1 of 3 experimental groups: baseline (BASE, n = 5), shamweighted (SHAM, n = lo), and wing-weighted (WTED, 1 day, n = 10; 7 days, n = 5).…”

Section: Results and Discussion Hypertrophic Response To Wing-weightingmentioning

confidence: 99%

Role of satellite cells in altering myosin expression during avian skeletal muscle hypertrophy

McCormick

Schultz

1994

Developmental Dynamics

View full text Add to dashboard Cite

This study examined whether satellite cells express an embryonic isoform of myosin upon fusion with hypertrophying muscle fibers. Anterior latissimus dorsi (ALD) muscle hypertrophy was induced in adult chickens by weighting one wing. One and 7 days of wingweighting produced significant increases in ALD muscle wet weight and in the number of mature fibers expressing ventricular-like embryonic (V-EMB) myosin. V-EMB myosin expression could be an event during regeneration of fibers injured by overload or part of the hypertrophy process itself. Although there was an increase in both the number of damaged fibers and the number of mature fibers expressing embryonic myosin after wingweighting, results from this study suggest that these two events were not necessarily related. The apparent health of fibers expressing V-EMB myosin and the lack of correlation between the numbers of damaged and V-EMB myosin positive fibers (r = 0.20) suggest that embryonic myosin expression in mature fibers was likely a feature of the hypertrophy process itself. The appearance of V-EMB myosin in mature fibers 1 day after wing weighting suggests that the change in myosin expression did not involve satellite cells since 24 hr is too short a time to permit more than limited satellite cell fusion. The relationship between satellite cells and embryonic myosin expression was examined more closely by labeling dividing satellite cells and their progeny with 5-bromo-2-deoxyuridine, and then colocalizing labeled myofiber nuclei and embryonic myosin in consecutive transverse sections of hypertrophied ALD muscle. One week of wingweighting resulted in marked increases in myofiber nuclear labeling index and myofiber nuclear density compared to contralatera1 control. V-EMB myosin was not expressed uniformly throughout individual fibers, but rather in discrete regions of varying length. Many V-EMB myosin positive regions had a higher labeled nuclear density than V-EMB myosin negative regions indicating that V-EMB myosin expression was associated with an accumulation of satellite cell progeny in a restricted area. However, it was also clear that satellite cell progeny were not the sole source of V-EMB myosin since labeled nuclei were completely absent from 41% of the V-EMB positive regions. Furthermore, the 0 1994 WILEY-LISS, INC.presence of new nuclei did not result in obligatory expression of embryonic myosin because many V-EMB negative regions had a high labeled nuclear density. Thus, recently incorporated nuclei arising by satellite cell division are implicated as one, but not the sole source of embryonic myosin in hypertrophying muscle. These observations suggest that the non-uniform pattern of embryonic myosin expression in hypertrophying muscle resulted from differences in nuclear activity, not necessarily the addition of new nuclei.

show abstract

“…Type I1 muscle fibers in cachectic atrophy differ from denervation atrophy by a slower rate of fiber mass loss [ 12,19,29,34,43], and by the brief period of hypertrophy which interrupts atrophy. Fiber atrophy patterns are different as well [ 10,431. Evidence presented here on the sternocephalicus muscle of sheep suggests that the interruption of the atrophic process takes the form of a slowed rate of atrophy only; in contrast, the Type 11-dominant sternocephalicus muscle showed a marked Type I1 fiber hypertrophy at the same point.…”

Section: Discussionmentioning

confidence: 99%

“…Although there may be a size differential in neurogenic atrophy between fiber types, with Type I fibers atrophy-resistant for a while [ 12,291, that condition is characterized by relatively rapid progressive atrophy only. Attempts at reproducing hypertrophy of muscle fibers have indicated that increased stretch may be a stimulus in innervated fibers [2,34]. Resistance to disuse atrophy can be seen in intact, innervated muscle by maintaining or by strengthening antagonistic muscles [29].…”

Section: Discussionmentioning

confidence: 99%

“…The obligatory hypertrophy in postural muscles that is evident particularly in Type I fibers could be a product of increased stretch [34] or stimulation [27] as Type I1 fibers decrease in size and the muscles become weaker. Because muscle volume probably reduces at a rate more rapid than, and disproportionate to, the reduction of body weight [7,16,261, there may well be increased tension and stretch.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Histochemical and Morphometric Evaluation of Skeletal Muscle of Cachectic Sheep

Hulland

1981

Vet Pathol

View full text Add to dashboard Cite

Abstract. Skeletal muscle of sheep was examined histochemically in an attempt to define muscle fiber populations capable of distinctive biological behavior. ATPase at alkaline and acid pH, NADH-TR, and succinic dehydrogenase showed at least 12 fiber types, but only three often enough to be considered biologically important muscle fiber populations. The proportions of the three major types altered during early life, but not perceptibly during adult life. Proportions of Type I and Type I1 fibers were different, sometimes significantly, from breed to breed.Histochemical techniques and morphometric analyses of fiber cross-sectional area were used to study muscle fiber changes in moderate to marked cachectic atrophy. Progressive reduction of gross muscle volume was attended by complex interrelationships between the two major muscle fiber types, including alternate episodes of atrophy and hypertrophy, resulting in marked inequality of mean fiber size between the fiber types. The patterns appeared to be different but characteristic for each muscle. The usual pattern of cachectic atrophy shows atrophy resistance of Type I fibers, but here a Type 11-dominant atrophy also was seen. It is concluded that the large muscle fibers often seen in advanced cachectic atrophy are those Type I fibers that are more labile in both atrophy and hypertrophy than most.

show abstract

Hypertrophy and hyperplasia of adult chicken anterior latissimus dorsi muscles following stretch with and without denervation

Cited by 170 publications

References 22 publications

Animal Models for Inducing Muscle Hypertrophy: Are They Relevant for Clinical Applications in Humans?

Animal Models for Inducing Muscle Hypertrophy: Are They Relevant for Clinical Applications in Humans?

Role of satellite cells in altering myosin expression during avian skeletal muscle hypertrophy

Histochemical and Morphometric Evaluation of Skeletal Muscle of Cachectic Sheep

Contact Info

Product

Resources

About