Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction

R M Crameri; P Aagaard; K Qvortrup; Henning Langberg; J Olesen; M Kjaer

doi:10.1113/jphysiol.2007.128827

Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction

R M Crameri, P Aagaard, K Qvortrup, Henning Langberg, J Olesen, M Kjaer

Institut for Folkesundhedsvidenskab

222 Citationer (Scopus)

Abstract

Disruption to proteins within the myofibre after a single bout of unaccustomed eccentric exercise is hypothesized to induce delayed onset of muscle soreness and to be associated with an activation of satellite cells. This has been shown in animal models using electrical stimulation but not in humans using voluntary exercise. Untrained males (n=8, range 22-27 years) performed 210 maximal eccentric contractions with each leg on an isokinetic dynamometer, voluntarily (VOL) with one leg and electrically induced (ES) with the other leg. Assessments from the skeletal muscle were obtained prior to exercise and at 5, 24, 96 and 192 h postexercise. Muscle tenderness rose in VOL and ES after 24 h, and did not differ between groups. Maximal isometric contraction strength, rate of force development and impulse declined in the VOL leg from 4 h after exercise, but not in ES (except at 24 h). In contrast, a significant disruption of cytoskeletal proteins (desmin) and a rise of myogenic growth factors (myogenin) occurred only in ES. Intracellular disruption and destroyed Z-lines were markedly more pronounced in ES (40%) compared with VOL (10%). Likewise, the increase in satellite cell markers [neural cell adhesion molecule (N-CAM) and paired-box transcription factor (Pax-7)] was more pronounced in ES versus VOL. Finally, staining of the intramuscular connective tissue (tenascin C) was increased equally in ES and VOL after exercise. The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extracellular matrix in the phenomenon of delayed onset of muscle soreness.

Originalsprog	Engelsk
Tidsskrift	Journal of Physiology
Vol/bind	583
Udgave nummer	Pt 1
Sider (fra-til)	365-80
Antal sider	16
ISSN	0022-3751
DOI	https://doi.org/10.1113/jphysiol.2007.128827
Status	Udgivet - 2007

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10.1113/jphysiol.2007.128827

Citationsformater

@article{a13c448e68ab44c7832423406396db4f,

title = "Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction",

abstract = "Disruption to proteins within the myofibre after a single bout of unaccustomed eccentric exercise is hypothesized to induce delayed onset of muscle soreness and to be associated with an activation of satellite cells. This has been shown in animal models using electrical stimulation but not in humans using voluntary exercise. Untrained males (n=8, range 22-27 years) performed 210 maximal eccentric contractions with each leg on an isokinetic dynamometer, voluntarily (VOL) with one leg and electrically induced (ES) with the other leg. Assessments from the skeletal muscle were obtained prior to exercise and at 5, 24, 96 and 192 h postexercise. Muscle tenderness rose in VOL and ES after 24 h, and did not differ between groups. Maximal isometric contraction strength, rate of force development and impulse declined in the VOL leg from 4 h after exercise, but not in ES (except at 24 h). In contrast, a significant disruption of cytoskeletal proteins (desmin) and a rise of myogenic growth factors (myogenin) occurred only in ES. Intracellular disruption and destroyed Z-lines were markedly more pronounced in ES (40%) compared with VOL (10%). Likewise, the increase in satellite cell markers [neural cell adhesion molecule (N-CAM) and paired-box transcription factor (Pax-7)] was more pronounced in ES versus VOL. Finally, staining of the intramuscular connective tissue (tenascin C) was increased equally in ES and VOL after exercise. The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extracellular matrix in the phenomenon of delayed onset of muscle soreness.",

keywords = "Adult, Biological Markers, Biopsy, Electric Stimulation, Exercise, Extracellular Matrix, Humans, Male, Muscle Contraction, Muscle, Skeletal, Myofibrils, Pain, Satellite Cells, Skeletal Muscle, Tenascin, Vimentin",

author = "Crameri, {R M} and P Aagaard and K Qvortrup and Henning Langberg and J Olesen and M Kjaer",

year = "2007",

doi = "10.1113/jphysiol.2007.128827",

language = "English",

volume = "583",

pages = "365--80",

journal = "The Journal of Physiology",

issn = "0022-3751",

publisher = "Wiley-Blackwell",

number = "Pt 1",

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TY - JOUR

T1 - Myofibre damage in human skeletal muscle

T2 - effects of electrical stimulation versus voluntary contraction

AU - Crameri, R M

AU - Aagaard, P

AU - Qvortrup, K

AU - Langberg, Henning

AU - Olesen, J

AU - Kjaer, M

PY - 2007

Y1 - 2007

N2 - Disruption to proteins within the myofibre after a single bout of unaccustomed eccentric exercise is hypothesized to induce delayed onset of muscle soreness and to be associated with an activation of satellite cells. This has been shown in animal models using electrical stimulation but not in humans using voluntary exercise. Untrained males (n=8, range 22-27 years) performed 210 maximal eccentric contractions with each leg on an isokinetic dynamometer, voluntarily (VOL) with one leg and electrically induced (ES) with the other leg. Assessments from the skeletal muscle were obtained prior to exercise and at 5, 24, 96 and 192 h postexercise. Muscle tenderness rose in VOL and ES after 24 h, and did not differ between groups. Maximal isometric contraction strength, rate of force development and impulse declined in the VOL leg from 4 h after exercise, but not in ES (except at 24 h). In contrast, a significant disruption of cytoskeletal proteins (desmin) and a rise of myogenic growth factors (myogenin) occurred only in ES. Intracellular disruption and destroyed Z-lines were markedly more pronounced in ES (40%) compared with VOL (10%). Likewise, the increase in satellite cell markers [neural cell adhesion molecule (N-CAM) and paired-box transcription factor (Pax-7)] was more pronounced in ES versus VOL. Finally, staining of the intramuscular connective tissue (tenascin C) was increased equally in ES and VOL after exercise. The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extracellular matrix in the phenomenon of delayed onset of muscle soreness.

AB - Disruption to proteins within the myofibre after a single bout of unaccustomed eccentric exercise is hypothesized to induce delayed onset of muscle soreness and to be associated with an activation of satellite cells. This has been shown in animal models using electrical stimulation but not in humans using voluntary exercise. Untrained males (n=8, range 22-27 years) performed 210 maximal eccentric contractions with each leg on an isokinetic dynamometer, voluntarily (VOL) with one leg and electrically induced (ES) with the other leg. Assessments from the skeletal muscle were obtained prior to exercise and at 5, 24, 96 and 192 h postexercise. Muscle tenderness rose in VOL and ES after 24 h, and did not differ between groups. Maximal isometric contraction strength, rate of force development and impulse declined in the VOL leg from 4 h after exercise, but not in ES (except at 24 h). In contrast, a significant disruption of cytoskeletal proteins (desmin) and a rise of myogenic growth factors (myogenin) occurred only in ES. Intracellular disruption and destroyed Z-lines were markedly more pronounced in ES (40%) compared with VOL (10%). Likewise, the increase in satellite cell markers [neural cell adhesion molecule (N-CAM) and paired-box transcription factor (Pax-7)] was more pronounced in ES versus VOL. Finally, staining of the intramuscular connective tissue (tenascin C) was increased equally in ES and VOL after exercise. The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extracellular matrix in the phenomenon of delayed onset of muscle soreness.

KW - Adult

KW - Biological Markers

KW - Biopsy

KW - Electric Stimulation

KW - Exercise

KW - Extracellular Matrix

KW - Humans

KW - Male

KW - Muscle Contraction

KW - Muscle, Skeletal

KW - Myofibrils

KW - Pain

KW - Satellite Cells, Skeletal Muscle

KW - Tenascin

KW - Vimentin

U2 - 10.1113/jphysiol.2007.128827

DO - 10.1113/jphysiol.2007.128827

M3 - Journal article

C2 - 17584833

SN - 0022-3751

VL - 583

SP - 365

EP - 380

JO - The Journal of Physiology

JF - The Journal of Physiology

IS - Pt 1

ER -

Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction

Abstract

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