Effects of Distraction on Muscle Length: Mechanisms Involved in Sarcomerogenesis

Caiozzo, Vincent J.; Utkan, Ali; Chou, Richard C.; Khalafi, Afshin; Chandra, Heena; Baker, Michael; Rourke, Bryan C.; Adams, Greg; Baldwin, K. M.; Green, Stuart

doi:10.1097/00003086-200210001-00016

Cited by 50 publications

(44 citation statements)

References 29 publications

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“…Removing sarcomeres in series requires increased protein degradation and possibly myonuclear apoptosis, whereas sarcomerogenesis is believed to occur through migration of satellite cells, fusion, development of mini-sarcomeres, and production of new nuclear domains (8). Although the latter is thought to occur near the myotendinous junctions (17), there is little evidence for a localized site for chronic shortening adaptations, nor are the signaling mechanisms clearly understood.…”

Section: Length Plasticitymentioning

confidence: 99%

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Clanton¹,

Levine²

2009

Journal of Applied Physiology

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Clanton TL, Levine S. Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation? J Appl Physiol 107: 324 -335, 2009. First published April 9, 2009 doi:10.1152/japplphysiol.00173.2009.-The diaphragm and other respiratory muscles undergo extensive remodeling in both animal models of emphysema and in human chronic obstructive pulmonary disease, but the nature of the remodeling is different in many respects. One common feature is a shift toward improved endurance characteristics and increased oxidative capacity. Furthermore, both animals and humans respond to chronic hyperinflation by diaphragm shortening. Although in rodent models this clearly arises by deletion of sarcomeres in series, the mechanism has not been proven conclusively in human chronic obstructive pulmonary disease. Unique characteristics of the adaptation in human diaphragms include shifts to more predominant slow, type I fibers, expressing slower myosin heavy chain isoforms, and type I and type II fiber atrophy. Although some laboratories report reductions in specific force, this may be accounted for by decreases in myosin heavy chain content as the muscles become more oxidative and more efficient. More recent findings have reported reductions in Ca 2ϩ sensitivity and reduced myofibrillar elastic recoil. In contrast, in rodent models of disease, there is no consistent evidence for loss of specific force, no consistent shift in fiber populations, and atrophy is predominantly seen only in fast, type IIX fibers. This review challenges the hypothesis that the adaptations in human diaphragm represent a form of dysfunction, secondary to systemic disease, and suggest that most findings can as well be attributed to adaptive processes of a complex muscle responding to unique alterations in its working environment. diaphragm; fiber type; sarcomere; skeletal muscle; emphysema THIS REVIEW IS INTENDED TO bring readers up to date with accumulating evidence that the diaphragm undergoes remarkable adaptations to chronic hyperinflation and chronic lung obstruction. Some of these adaptations are expected, based on well known responses of limb muscle to chronic changes in length and mechanical load, but others appear to be surprisingly unique, revealing aspects of muscle plasticity and pathology that are not anticipated from known basic science concepts. We will concentrate this review on what has been observed, primarily at the muscle fiber level in both animals and humans, with primary emphasis on the diaphragm. There have been several excellent previous reviews of this area, and the reader is encouraged to refer to these (13,41,58,65,66). Where possible, we will attempt to complement, update, and at times challenge current concepts with the purpose of furthering dialogue and promoting further inquiry. LENGTH PLASTICITYThe diaphragm, like all other muscles, exhibits a characteristic length-tension relationship analogous to the Frank-Starling curve for the heart. As length is increased in the relaxed muscle, a passive length-tension cu...

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Section: Length Plasticitymentioning

confidence: 99%

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Clanton¹,

Levine²

2009

Journal of Applied Physiology

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“…This finding might explain the tendency to relapse of congenital clubfoot during this period of time, regardless of the conservative and surgical procedures performed to either prevent or manage recurrence of the deformity [11]. Very few studies have been done so far on the mechanisms regulating muscle-tendon unit growth [12][13][14][15]. An increase in muscular thickness and length expresses the amount of muscle growth [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

“…Very few studies have been done so far on the mechanisms regulating muscle-tendon unit growth [12][13][14][15]. An increase in muscular thickness and length expresses the amount of muscle growth [12][13][14]. In normal conditions, physical activity stimulates radial muscle growth, whereas stretching stimulates longitudinal muscle growth, as in limb-lengthening procedures [11,[13][14][15][16].…”

Section: Discussionmentioning

confidence: 99%

An MRI volumetric study for leg muscles in congenital clubfoot

Ippolito

Dragoni

Antonicoli

et al. 2012

Journal of Children's Orthopaedics

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Purpose To investigate both volume and length of the three muscle compartments of the normal and the affected leg in unilateral congenital clubfoot. Methods Volumetric magnetic resonance imaging (VMRI) of the anterior, lateral and postero-medial muscular compartments of both the normal and the clubfoot leg was obtained in three groups of seven patients each, whose mean age was, respectively, 4.8 months, 11.1 months and 4.7 years. At diagnosis, all the unilateral congenital clubfeet had a Pirani score ranging from 4.5 to 5.5 points, and all of them had been treated according to a strict Ponseti protocol. All the feet had percutaneous lengthening of the Achilles tendon. Results A mean difference in both volume and length was found between the three muscular compartments of the leg, with the muscles of the clubfoot side being thinner and shorter than those of the normal side. The distal tendon of the tibialis anterior, peroneus longus and triceps surae (Achilles tendon) were longer than normal on the clubfoot side. Conclusions Our study shows that the three muscle compartments of the clubfoot leg are thinner and shorter than normal in the patients of the three groups. The difference in the musculature volume of the postero-medial compartment between the normal and the affected side increased nine-fold from age group 2 to 3, while the difference in length increased by 20 %, thus, showing that the muscles of the postero-medial compartment tend to grow in both thickness and length much less than the muscles of the other leg compartments.

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“…Investigators have reported that distraction osteogenesis promotes muscle regeneration, including increased sarcomerogenesis, higher numbers of proliferating nuclei, and increased muscle weight. [8][9][10][11][12] In addition, Olfert et al 23 showed that VEGF produced by myocytes was required for regulating muscle capillarity. These results suggest that VEGF in the satellite cells, induced by mechanical tension-stress, also affect myogenesis and angiogenesis.…”

Section: Angiogenesis and Myogenesis In Lengthened Skeletal Musclesmentioning

confidence: 99%

“…[4][5][6][7] Similar results have been reported for myogenesis in the surrounding skeletal muscles following distraction osteogenesis. [8][9][10][11][12] However, the cellular and molecular mechanisms underlying angiogenesis and myogenesis in the skeletal muscles which are induced by mechanical tension-stress during distraction osteogenesis has not yet been elucidated.…”

mentioning

confidence: 99%

Angiogenesis and myogenesis in mouse tibialis anterior muscles during distraction osteogenesis: VEGF, its receptors, and myogenin genes expression

Nishisho

Yukata

Matsui

et al. 2012

Journal Orthopaedic Research

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Angiogenesis and myogenesis occur in the surrounding skeletal muscles following distraction osteogenesis, but their molecular mechanisms remain unclear. The present study investigated morphological features of lengthened muscles and the time course change of vascular endothelial growth factor (VEGF), its receptors (VEGFR-1 and VEGFR-2) and myogenin gene expression profiles related to angiogenesis and myogenesis in tibialis anterior (TA) muscles with a mouse model of distraction osteogenesis, which involves 1 week of waiting period (latency phase), 2 weeks of intermittent distraction (distraction phase), and 5 weeks of remodeling period (consolidation phase). Macroscopic findings showed that lengthened TA muscles increased to approximately 42% longer and 10% heavier at the end of the process when compared to pre-surgery. During the distraction phase, VEGF and its receptors were induced in the vascular endothelial cells, myogenin-positive satellite cells and myocytes, and subsequently, capillary progression and myogenesis were increased. Real-time RT-PCR showed that Vegf, Vegfr-1, Vegfr-2, and myogenin genes expression was enhanced during the muscle lengthening. Vegf and Vegfr-1 were upregulated following the recession of angiogenesis at the consolidation phase. We conclude that upregulation of VEGF and its receptors by mechanical tension-stress could be involved in the process of angiogenesis and myogenesis in lengthened muscles. ß

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Effects of Distraction on Muscle Length: Mechanisms Involved in Sarcomerogenesis

Cited by 50 publications

References 29 publications

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

An MRI volumetric study for leg muscles in congenital clubfoot

Angiogenesis and myogenesis in mouse tibialis anterior muscles during distraction osteogenesis: VEGF, its receptors, and myogenin genes expression

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