Normal muscle growth | ScienceGate

Loss of muscle mass occurs with disease, injury, aging, and inactivity. Restoration of normal muscle mass depends on myofiber growth, the regulation of which is incompletely understood. Cyclooxygenase (COX)-2 is one of two isoforms of COX that catalyzes the synthesis of prostaglandins, paracrine hormones that regulate diverse physiological and pathophysiological processes. Previously, we demonstrated that the COX-2 pathway regulates early stages of myofiber growth during muscle regeneration. However, whether the COX-2 pathway plays a common role in adult myofiber growth or functions specifically during muscle regeneration is unknown. Therefore, we examined the role of COX-2 during myofiber growth following atrophy in mice. Muscle atrophy was induced by hindlimb suspension (HS) for 2 wk, followed by a reloading period, during which mice were treated with either the COX-2-selective inhibitor SC-236 (6 mg·kg−1·day−1) or vehicle. COX-2 protein was expressed and SC-236 attenuated myofiber growth during reloading in both soleus and plantaris muscles. Attenuated myofiber growth in the soleus was associated with both decreased myonuclear addition and decreased inflammation, whereas neither of these processes mediated the effects of SC-236 on plantaris growth. In addition, COX-2−/− satellite cells exhibited impaired activation/proliferation in vitro, suggesting direct regulation of muscle cell activity by COX-2. Together, these data suggest that the COX-2 pathway plays a common regulatory role during various types of muscle growth via multiple mechanisms.

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Stretch-induced growth in chicken wing muscles: effects on hereditary muscular dystrophy

AJP Cell Physiology ◽

10.1152/ajpcell.1982.242.3.c178 ◽

1982 ◽

Vol 242 (3) ◽

pp. C178-C183 ◽

Cited By ~ 27

Author(s):

C. R. Ashmore

Keyword(s):

Muscular Dystrophy ◽

Normal Values ◽

Muscle Growth ◽

Cross Sectional Area ◽

Muscle Pathology ◽

Sectional Area ◽

Normal Muscle ◽

Dystrophic Muscle ◽

Cross Sectional ◽

Passive Stretch

Skeletal muscle growth induced by passive stretch was characterized in the Patigialis muscle of chicks with hereditary muscular dystrophy. When the muscle of 6-wk-old chicks was stretched for 1 wk, the effects on muscle growth and on muscle pathology were variable, but in general few differences between stretched and unstretched muscles were observed. However, when the muscle of 1-wk-old chicks was stretched for 6 wk, the effects on muscle growth and on prevention of pathology were dramatic. Similar to results obtained previously when normal chick muscles were stretched [Holly et al., Am. J. Physiol. 238 (Cell Physiol. 7): C62-C71, 1980; Barnett et al., Am. J. Physiol. 239 (Cell Physiol. 8): C39-C46, 1980], stretched dystrophic muscle increased in weight (200%), cross-sectional area (107%), and fiber cross-sectional area (82%). DNA concentration, which is severalfold higher in unstretched dystrophic muscle compared with unstretched normal muscle, fell to values not different from normal values after being stretched. Nuclei per square millimeter also were the same for stretched dystrophic and stretched normal muscle. Histograms indicated that stretching induced a fiber distribution in dystrophic muscle qualitatively similar to that found in stretched normal muscle. Cytochemical observations revealed a dramatic protective effect of stretch against the progressive pathology of dystrophy. It is concluded that stretch of muscle applied to newly hatched dystrophic chicks is a powerful deterrent of symptoms characteristic of hereditary muscular dystrophy. Stretch imposed after the symptoms of dystrophy are apparent provides little, if any, protection.

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Changes in collagen synthesis and degradation during skeletal muscle growth

AJP Cell Physiology ◽

10.1152/ajpcell.1985.249.3.c352 ◽

1985 ◽

Vol 249 (3) ◽

pp. C352-C355 ◽

Cited By ~ 22

Author(s):

G. J. Laurent ◽

R. J. McAnulty ◽

J. Gibson

Keyword(s):

Skeletal Muscle ◽

Muscle Growth ◽

Physiological Role ◽

Synthesis Rate ◽

Normal Muscle ◽

Small Molecular Weight ◽

Adult Chicken ◽

Skeletal Muscle Growth ◽

Anterior Latissimus Dorsi ◽

Synthesis And Degradation

The changes in collagen metabolism during skeletal muscle growth were investigated by measuring rates of synthesis and degradation during stretch-induced hypertrophy of the anterior latissimus dorsi muscle of the adult chicken (Gallus domesticus). Synthesis rates were obtained from the uptake of tritiated proline injected intravenously with a flooding dose of unlabeled proline. Degradation of newly synthesized and "mature" collagen was estimated from the amount of hydroxyproline in the free pool as small molecular weight moieties. In normal muscle, the synthesis rate was 1.1 +/- 0.3%/day, with 49 +/- 7% of the newly produced collagen degraded rapidly after synthesis. During hypertrophy there was an increase of about fivefold in the rate of synthesis (P less than 0.01), a 60% decrease in the rate of degradation of newly synthesized collagen (P less than 0.02), and an increase of about fourfold in the amount of degradation of mature collagen (P less than 0.01). These results suggest an important role for degradative as well as synthetic processes in the regulation of collagen mass. They indicate that enhanced degradation of mature collagen is required for muscle growth and suggest a physiological role for the pathway whereby in normal muscle, a large proportion of newly produced collagen is rapidly degraded.

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EHD1 mediates vesicle trafficking required for normal muscle growth and transverse tubule development

Developmental Biology ◽

10.1016/j.ydbio.2014.01.004 ◽

2014 ◽

Vol 387 (2) ◽

pp. 179-190 ◽

Cited By ~ 32

Author(s):

Avery D. Posey ◽

Kaitlin E. Swanson ◽

Manuel G. Alvarez ◽

Swathi Krishnan ◽

Judy U. Earley ◽

...

Keyword(s):

Vesicle Trafficking ◽

Muscle Growth ◽

Normal Muscle ◽

Transverse Tubule

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The role of the myostatin protein in meat quality – a review

Archives Animal Breeding ◽

10.5194/aab-45-159-2002 ◽

2002 ◽

Vol 45 (2) ◽

pp. 159-170 ◽

Cited By ~ 5

Author(s):

J. Kobolák ◽

E. Gócza

Keyword(s):

Muscle Hypertrophy ◽

Muscle Growth ◽

Meat Production ◽

Connective Tissues ◽

Normal Muscle ◽

Partial Dominance ◽

Myostatin Gene ◽

Beef Cattle Production ◽

Better Than

Abstract. The myostatin protein is a regulator factor in the normal muscle that determines the maximum amount of muscle mass that is typical of that species. If the myostatin gene is mutant, the negative regulating function of the gene does not work. This leads to an increased muscle growth resulting in muscle hypertrophy and hyperplasia. That phenomenon occurs in beef cattle production as well, e.g. in Belgian White-Blue breed where the "double-muscled" phenotype is common due to the successful selection. In the view of quality meat production, this is an outstanding trait, since these animals produce not just more, but better: leaner and tenderer meat. Crossing with Belgian White-Blue cattle shows that although the gene is recessive and monofactorial, its effect is apparent even in heterozygotes due to its partial dominance: the meat:bone ratio and meat yield is better than those of the other breed. In animals with a Culard phenotype this trait manifests with others: there are less fat and suet deposited and the amount of connective tissues between muscles are also decreased.

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Influence of corticosteroids on myonuclear domain size in the rat diaphragm muscle

Journal of Applied Physiology ◽

10.1152/japplphysiol.00625.2003 ◽

2004 ◽

Vol 97 (5) ◽

pp. 1715-1722 ◽

Cited By ~ 24

Author(s):

A. Jeroen Verheul ◽

Carlos B. Mantilla ◽

Wen-Zhi Zhan ◽

Miguel Bernal ◽

P. N. Richard Dekhuijzen ◽

...

Keyword(s):

Muscle Growth ◽

Domain Size ◽

Male Rats ◽

Diaphragm Muscle ◽

Gene Products ◽

Sectional Area ◽

Rat Diaphragm ◽

Normal Muscle ◽

Cross Sectional ◽

Myonuclear Domain

Skeletal muscle fibers are multinucleated. Each myonucleus regulates gene products and protein expression in only a restricted portion of the muscle fiber, the myonuclear domain (MND). In the rat diaphragm muscle (DIAm), corticosteroid (CoS) treatment causes atrophy of fibers containing myosin heavy chain (MHC): MHC2X and/or MHC2B. We hypothesized that DIAm fiber MND size is maintained during CoS-induced atrophy. Adult male rats received methylprednisolone for 11 days at 1 (CoS-Low, n = 8) or 8 mg·kg−1·day−1 (CoS-High, n = 8). Age-matched (CTL-AgeM, n = 8), sham-operated (SHAM-AgeM, n = 8), and weight-matched (CTL-WtM, n = 8) animals served as controls. In single DIAm fibers, cross-sectional area (CSA), MND size, and MHC expression were determined. Fiber CSA and MND size were similar in CTL-AgeM and SHAM-AgeM groups. Only fibers containing MHCslow or MHC2A displayed smaller CSA in CTL-WtM than in CTL-AgeM and SHAM-AgeM groups, and MND size was reduced in all fibers. Thus fibers containing MHCslow and MHC2A maintain the number of myonuclei, whereas MHC2X or MHC2B fibers show loss of myonuclei during normal muscle growth. Both CoS groups displayed smaller CSA and MND size than CTL-AgeM and SHAM-AgeM groups. However, compared with CTL-WtM DIAm fibers, only fibers containing MHC2X or MHC2B displayed reduced CSA and MND size after CoS treatment. Thus little, if any, loss of myonuclei was associated with CoS-induced atrophy of MHC2X or MHC2B DIAm fibers. In summary, MND size does not appear to be regulated during CoS-induced DIAm atrophy.

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