Stretch and force generation induce rapid hypertrophy and myosin isoform gene switching in adult skeletal muscle

Goldspink, Geoffrey; Scutt, Andrew; Martindale, J. G.; Jaenicke, Thomas; Turay, Lucien; Gerlach, Gerald-F.

doi:10.1042/bst0190368

Cited by 88 publications

(53 citation statements)

References 4 publications

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“…For example, chronic immobilization of the rabbit ankle in plantar flexion resulted in a 20% increase in the dorsiflexor muscles after only three to four days. 29,32 Casting muscles in lengthened positions results in similar hypertrophic and functional changes seen in avian stretch and rodent ablation and tenotomy overload models. 75 It is interesting to note that studies have also shown that combinations of muscle stretch and muscle activity induced by electrical stimulation result in a 10% greater increase in muscle mass compared to stretch alone.…”

Section: Chronic Stretch Modelsmentioning

confidence: 99%

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

Lowe¹

2002

J Orthop Sports Phys Ther

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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...

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Section: Chronic Stretch Modelsmentioning

confidence: 99%

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

Lowe¹

2002

J Orthop Sports Phys Ther

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“…Similar findings were observed after general sprint training (3), as expressed by a decrease in the number of individual fibers that expressed MHC-IIB. Indeed, it has been suggested that MHC-IIB is the ''default'' gene (21), the expression of which is increased with disuse and ''switches'' to MHC-IIA when activity is increased (5). In the present study MHC-IIB was detected in the vastus lateralis in only four of the subjects, an observation that possibly reflects a relatively high level of habitual physical activity in our subjects, although none was sprint trained or strength trained.…”

mentioning

confidence: 99%

Sprint training, in vitro and in vivo muscle function, and myosin heavy chain expression

Harridge

Bottinelli

Canepari

et al. 1998

Journal of Applied Physiology

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. Sprint training, in vitro and in vivo muscle function, and myosin heavy chain expression. J. Appl. Physiol. 84(2): 442-449, 1998.-Sprint training represents the condition in which increases in muscle shortening speed, as well as in strength, might play a significant role in improving power generation. This study therefore aimed to determine the effects of sprint training on 1) the coupling between myosin heavy chain (MHC) isoform expression and function in single fibers, 2) the distribution of MHC isoforms across a whole muscle, and 3) in vivo muscle function. Seven young male subjects completed 6 wk of training (3-s sprints) on a cycle ergometer. Training was without effect on maximum shortening velocity in single fibers or in the relative distribution of MHC isoforms in either the soleus or the vastus lateralis muscles. Electrically evoked and voluntary isometric torque generation increased (P Ͻ 0.05) after training in both the plantar flexors (ϩ8% at 50 Hz and ϩ16% maximal voluntary contraction) and knee extensors (ϩ8% at 50 Hz and ϩ7% maximal voluntary contraction). With the shortening potential of the muscles apparently unchanged, the increased strength of the major lower limb muscles is likely to have contributed to the 7% increase (P Ͻ 0.05) in peak pedal frequency during cycling. contraction; exercise THE INCREASE IN MUSCLE POWER generation that results from training could be brought about by at least two different mechanisms. First, it can be brought about by an increase in the force-producing capability of the muscle, either through increased activation or through an increase in muscle size. Second, it can occur by increasing the speed at which a muscle can shorten against a given load.A close coupling exists between the speed of muscle shortening and the expression of the different myosin heavy chain (MHC) isoforms. Muscle fibers that express the MHC-I isoform exhibit significantly slower maximal velocities of shortening (V o ) (24, 28) and power outputs (11) compared with fibers expressing the two fast MHC isoforms. Within the subgroups of fast isoforms, fibers that express the MHC-IIB isoform [which has recently been shown to be homologous to the MHC-IIX isoform found in small mammals (18,34)] are significantly faster (24, 28) and can generate higher power outputs than fibers containing the MHC-IIA isoform (11,36). Muscle speed of movement could be increased either by altering the relative expression of the fast and slow isoforms or by changing the coupling between isoform expression and function.

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“…A factor that should also be considered is the duration of the stimulus required for transformation [96]. In adult animals, changes have been observed even after extremely short periods of stimulation [48].…”

Section: Series 'Cell Biology Of Respiratory Muscles' Edited By M Dementioning

confidence: 99%

“…It is believed that the expression is regulated fundamentally by mechanical signals, particularly by changes in the tension generated by the muscle during the effort [47]. The stretch (active tension) as well as electrical stimulation (passive tension) provoke the repression of the fast-type genes, with activation of the slow-type genes [2,48]. This implies a progressive transformation in the type of fibres [49][50][51][52].…”

Section: Series 'Cell Biology Of Respiratory Muscles' Edited By M Dementioning

confidence: 99%

Myosin gene expression in the respiratory muscles

Jg¹

1997

Eur Respir J

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The muscle phenotype is the product of genome plus environmental stimuli. The family of genes that codifies the MyHC isoforms is located in two different clusters, each isoform being encoded by a separate gene. The gene corresponding to slow MyHC is located in chromosome 14, both in humans and in mice. The other genes are positioned in chromosome 17 in humans, and in chromosome 11 in mice. The transcriptional and translational mechanisms that control the expression of MyHC isoforms are not well known, although it is believed that the main regulation is dependent on mechanical signals. These signals are probably mediated by a biochemical messenger. As a general rule, fast MyHC genes seem to be expressed "by default", whereas the slow MyHC gene would be expressed as a response to changes in load.So far, few studies have analysed the in vivo regulation of MyHC gene expression in respiratory muscles. It has recently been reported that breathing against moderate levels of inspiratory resistance quickly induces an increase in the genetic expression of slow MyHC in the diaphragm. This suggests the possibility of eliciting a phenotypic adaptation of respiratory muscles using specific training protocols. Eur Respir J 1997; 10: 2404-2410 Muscles are extremely plastic, and are capable of modifying their structure to the activity they develop [1][2][3][4]. At the molecular level, muscles are composed of different structural and enzymatic elements, whose genetic expression is modulated by such activity. Myosin is one of the main structural components of the skeletal muscles, which include respiratory muscles. This myofibrillar protein ( fig. 1), essential for muscle contraction, is composed of two heavy (MyHC) and two light chains (MyLC). The MyHC (molecular weight 220 kDa) has a globular portion at one of its ends (amino-terminal part). This site is called the "head" (or S 1 ) of the molecule, and is the site of interaction with actin. This is also the site of action for the actomyosin adenosine triphosphatase (ATPase). The two MyLC (molecular weights, 17-23 kDa) are located very close to this portion, in the "neck" of the molecule. On the other side, there is an alphahelicoidal structure (carboxy-terminal part) called the "tail". Both MyHC and MyLC present different isoforms. The presence of one or another isoform conditions the acti-vity of the myosinic ATPase [5], and these two factors determine the maximum velocity of shortening, the predominant metabolism of the fibre and its resistance to fatigue [1,[6][7][8][9][10]. In this regard, those fibres containing slow MyHC isoforms present a smaller contraction velocity but higher metabolic efficiency for maintaining similar levels of tension [11]. The relationship between the MyHC composition and fibrillar function has been evidenced, not only in skeletal limb muscles but also in the diaphragm [12]. The MyLC isoforms are involved in force transduction, and, thus, in the mechanical efficiency and economy of different kinds of contraction [13]. SERIES 'CELL BIOLOGY OF RESPIRA...

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Stretch and force generation induce rapid hypertrophy and myosin isoform gene switching in adult skeletal muscle

Cited by 88 publications

References 4 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?

Sprint training, in vitro and in vivo muscle function, and myosin heavy chain expression

Myosin gene expression in the respiratory muscles

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