Transitions of muscle fiber phenotypic profiles

Pette, Dirk; Staron, Robert S.

doi:10.1007/s004180100268

Cited by 414 publications

(222 citation statements)

References 122 publications

(131 reference statements)

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“…The pathophysiology underlying the alteration in fibre type composition in different conditions is still unclear and both disease-related mechanisms and glucocorticoid treatment could be involved in myositis. A suggested shift from slow-twitch type I fibres to fast-twitch type II fibres is supported by the fibre type composition observed in the treated polymyositis or dermatomyositis patients in the present study and is in accordance with the most adapted path of muscle transition: type IMIICMIIA-MIIB (Pette & Staron, 2001). Additionally, similar changes from slow-twitch type I fibres to fast-twitch type II fibres have been reported in patients with other chronic inflammatory diseases such as rheumatoid arthritis, chronic obstructive pulmonary disease and chronic heart failure (Franssen et al, 2002), (Danneskiold-Samsoe & Grimby, 1986;Hildebrand et al, 1991).…”

Section: Groupsupporting

confidence: 89%

Higher proportion of fast-twitch (type II) muscle fibres in idiopathic inflammatory myopathies - evident in chronic but not in untreated newly diagnosed patients

Loell

Helmers

Dastmalchi

et al. 2010

Clinical Physiology and Functional Imaging

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Untreated polymyositis and dermatomyositis patients and healthy controls have a different fibre type composition than chronic polymyositis and dermatomyositis patients. Fibre CSA did not differ between healthy controls or any of the patient groups. A low proportion of oxidative muscle fibres can therefore be excluded as a contributing factor causing muscle fatigue at disease onset and the gender difference should be taken into consideration when evaluating fibre CSA in myositis.

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Section: Groupsupporting

confidence: 89%

Higher proportion of fast-twitch (type II) muscle fibres in idiopathic inflammatory myopathies - evident in chronic but not in untreated newly diagnosed patients

Loell

Helmers

Dastmalchi

et al. 2010

Clinical Physiology and Functional Imaging

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“…Treatment with ESA produced no changes in muscle fibre type distribution, while training alone produced an increase and corresponding decrease in the relative number of type IIa and IIx fibres, respectively. Furthermore, an overall training effect on type IIa and IIx fibres emerged when the two training groups were combined, supporting previous evidence that prolonged endurance-type training to some extent elicits a fibre transformation towards a more oxidative phenotype (Andersen & Henriksson, 1977;Jansson & Kaijser, 1977;Luden et al 2012) or simply increased physical activity (Pette & Staron, 2001).…”

Section: Comparative Effects Of Epo and Training On Skeletal Muscle Tsupporting

confidence: 82%

Erythropoietin administration alone or in combination with endurance training affects neither skeletal muscle morphology nor angiogenesis in healthy young men

Larsen

Vissing

Thams

et al. 2014

Experimental Physiology

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New Findings r What is the central question of this study?Is an erythropoiesis-stimulating agent (ESA), alone or in combination with endurance training, able to induce changes in human skeletal muscle fibre and vascular morphology? r What is the main finding and its importance?Human skeletal muscle morphology and angiogenetic effects did not exhibit sensitivity to ESA treatment alone. Endurance training stimulates angiogenesis and fibre type transition in the direction of a more oxidative fibre phenotype; however, addition of ESA had no further effect.The aim was to investigate the ability of an erythropoiesis-stimulating agent (ESA), alone or in combination with endurance training, to induce changes in human skeletal muscle fibre and vascular morphology. In a comparative study, 36 healthy untrained men were randomly dispersed into the following four groups: sedentary-placebo (SP, n = 9); sedentary-ESA (SE, n = 9); training-placebo (TP, n = 10); or training-ESA (TE, n = 8). The ESA or placebo was injected once weekly. Training consisted of progressive bicycling three times per week for 10 weeks. Before and after the intervention period, muscle biopsies and magnetic resonance images were collected from the thigh muscles, blood was collected, body composition measured and endurance exercise performance evaluated. The ESA treatment (SE and TE) led to elevated haematocrit, and both ESA treatment and training (SE, TP and TE) increased maximal O 2 uptake. With regard to skeletal muscle morphology, TP alone exhibited increases in whole-muscle cross-sectional area and fibre diameter of all fibre types. Also exclusively for TP was an increase in type IIa fibres and a corresponding decrease in type IIx fibres. Furthermore, an overall training effect (TP and TE) was statistically demonstrated in whole-muscle cross-sectional area, muscle fibre diameter and type IIa and type IIx fibre distribution. With regard to muscle vascular morphology, TP and TE both promoted a rise in capillary to muscle fibre ratio, with no differences between the two groups. There were no effects of ESA treatment on any of the muscle morphological parameters. Despite the haematopoietic effects of ESA, we provide novel evidence that endurance training rather than ESA treatment induces adaptational changes in angiogenesis and muscle morphology.

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“…Ultimately, the intracellular calcium concentration ([Ca 2ϩ ]i) would be decreased. Diminished [Ca 2ϩ ]i precedes many of the functional changes resulting from hind-limb suspension (31), including the switch in predominant fiber type that occurs in slow twitch muscle undergoing atrophy; however, the mechanism(s) responsible for lowered [Ca 2ϩ ]i is not well understood (31,32). In summary, Merg1a channel function is an initiator of disuse-and cachexia-stimulated atrophy, acting upstream of UPP proteolysis.…”

Section: Discussionmentioning

confidence: 99%

Mergla K ⁺ channel induces skeletal muscle atrophy by activating the ubiquitin proteasome pathway

et al. 2006

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Skeletal muscle atrophy results from an imbalance in protein degradation and protein synthesis and occurs in response to injury, various disease states, disuse, and normal aging. Current treatments for this debilitating condition are inadequate. More information about mechanisms involved in the onset and progression of muscle atrophy is necessary for development of more effective therapies. Here we show that expression of the mouse ether-a-go-go related gene (Merg1a) K+ channel is up-regulated in skeletal muscle of mice experiencing atrophy as a result of both malignant tumor expression and disuse. Further, ectopic expression of Merg1a in vivo induces atrophy in healthy wt-bearing mice, while expression of a dysfunctional Merg1a mutant suppresses atrophy in hindlimb-suspended mice. Treatment of hindlimb-suspended mice with astemizole, a known Merg1a channel blocker, inhibits atrophy in these animals. Importantly, in vivo expression of Merg1a in mouse skeletal muscle activates the ubiquitin proteasome pathway that is responsible for the majority of protein degradation that causes muscle atrophy, yet expression of a dysfunctional Merg1a mutant decreases levels of ubiquitin-proteasome proteolysis. Thus, expression of Merg1a likely initiates atrophy by activating ubiquitin-proteasome proteolysis. This gene and its product are potential targets for prevention and treatment of muscle atrophy.

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Transitions of muscle fiber phenotypic profiles

Cited by 414 publications

References 122 publications

Higher proportion of fast-twitch (type II) muscle fibres in idiopathic inflammatory myopathies - evident in chronic but not in untreated newly diagnosed patients

Higher proportion of fast-twitch (type II) muscle fibres in idiopathic inflammatory myopathies - evident in chronic but not in untreated newly diagnosed patients

Erythropoietin administration alone or in combination with endurance training affects neither skeletal muscle morphology nor angiogenesis in healthy young men

Mergla K ⁺ channel induces skeletal muscle atrophy by activating the ubiquitin proteasome pathway

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Transitions of muscle fiber phenotypic profiles

Cited by 414 publications

References 122 publications

Higher proportion of fast-twitch (type II) muscle fibres in idiopathic inflammatory myopathies - evident in chronic but not in untreated newly diagnosed patients

Higher proportion of fast-twitch (type II) muscle fibres in idiopathic inflammatory myopathies - evident in chronic but not in untreated newly diagnosed patients

Erythropoietin administration alone or in combination with endurance training affects neither skeletal muscle morphology nor angiogenesis in healthy young men

Mergla K + channel induces skeletal muscle atrophy by activating the ubiquitin proteasome pathway

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Mergla K ⁺ channel induces skeletal muscle atrophy by activating the ubiquitin proteasome pathway