Electromechanical delay in human skeletal muscle under concentric and eccentric contractions

1979 ◽  
Vol 42 (3) ◽  
pp. 159-163 ◽  
Author(s):  
P. R. Cavanagh ◽  
P. V. Komi
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Eccentric Contractions ◽  
Electromechanical Delay

Eccentric exercise markedly increases c-Jun NH2-terminal kinase activity in human skeletal muscle

1999 ◽  
Vol 87 (5) ◽  
pp. 1668-1673 ◽  
Author(s):  
Marni D. Boppart ◽  
Doron Aronson ◽  
Lindsay Gibson ◽  
Ronenn Roubenoff ◽  
Leslie W. Abad ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Eccentric Exercise ◽  
Intracellular Signaling ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Fold Increase ◽  
Mitogen Activated Protein Kinase ◽  
Eccentric Contractions ◽  
Vastus Lateralis Muscle

Eccentric contractions require the lengthening of skeletal muscle during force production and result in acute and prolonged muscle injury. Because a variety of stressors, including physical exercise and injury, can result in the activation of the c-Jun NH2-terminal kinase (JNK) intracellular signaling cascade in skeletal muscle, we investigated the effects of eccentric exercise on the activation of this stress-activated protein kinase in human skeletal muscle. Twelve healthy subjects (7 men, 5 women) completed maximal concentric or eccentric knee extensions on a KinCom isokinetic dynamometer (10 sets, 10 repetitions). Percutaneous needle biopsies were obtained from the vastus lateralis muscle 24 h before exercise (basal), immediately postexercise, and 6 h postexercise. Whereas both forms of exercise increased JNK activity immediately postexercise, eccentric contractions resulted in a much higher activation (15.4 ± 4.5 vs. 3.5 ± 1.4-fold increase above basal, eccentric vs. concentric). By 6 h after exercise, JNK activity decreased back to baseline values. In contrast to the greater activation of JNK with eccentric exercise, the mitogen-activated protein kinase kinase 4, the immediate upstream regulator of JNK, was similarly activated by concentric and eccentric exercise. Because the activation of JNK promotes the phosphorylation of a variety of transcription factors, including c-Jun, the results from this study suggest that JNK may be involved in the molecular and cellular adaptations that occur in response to injury-producing exercise in human skeletal muscle.

scholarly journals Connective tissue regeneration in skeletal muscle after eccentric contraction-induced injury

2017 ◽  
Vol 122 (3) ◽  
pp. 533-540 ◽  
Author(s):  
Abigail L. Mackey ◽  
Michael Kjaer
Keyword(s):  
Skeletal Muscle ◽  
Connective Tissue ◽  
Human Skeletal Muscle ◽  
Matrix Protein ◽  
Eccentric Contraction ◽  
Eccentric Contractions ◽  
Optimal Timing ◽  
Type I ◽  
Strong Response ◽  
Experimental Conditions

Human skeletal muscle has the potential to regenerate completely after injury induced under controlled experimental conditions. The events inside the myofibers as they undergo necrosis, followed closely by satellite cell-mediated myogenesis, have been mapped in detail. Much less is known about the adaptation throughout this process of both the connective tissue structures surrounding the myofibers and the fibroblasts, the cells responsible for synthesizing this connective tissue. However, the few studies investigating muscle connective tissue remodeling demonstrate a strong response that appears to be sustained for a long time after the major myofiber responses have subsided. While the use of electrical stimulation to induce eccentric contractions vs. voluntary eccentric contractions appears to lead to a greater extent of myofiber necrosis and regenerative response, this difference is not apparent when the muscle connective tissue responses are compared, although further work is required to confirm this. Pharmacological agents (growth hormone and angiotensin II type I receptor blockers) are considered in the context of accelerating the muscle connective tissue adaptation to loading. Cautioning against this, however, is the association between muscle matrix protein remodeling and protection against reinjury, which suggests that a (so far undefined) period of vulnerability to reinjury may exist during the remodeling phases. The role of individual muscle matrix components and their spatial interaction during adaptation to eccentric contractions is an unexplored field in human skeletal muscle and may provide insight into the optimal timing of rest vs. return to activity after muscle injury.

Changes in the electromechanical delay components during a fatiguing stimulation in human skeletal muscle: an EMG, MMG and force combined approach

2016 ◽  
Vol 117 (1) ◽  
pp. 95-107 ◽  
Author(s):  
Emiliano Cè ◽  
Susanna Rampichini ◽  
Elena Monti ◽  
Massimo Venturelli ◽  
Eloisa Limonta ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Combined Approach ◽  
Electromechanical Delay

Static stretch increases c-Jun NH2-terminal kinase activity and p38 phosphorylation in rat skeletal muscle

2001 ◽  
Vol 280 (2) ◽  
pp. C352-C358 ◽  
Author(s):  
Marni D. Boppart ◽  
Michael F. Hirshman ◽  
Kei Sakamoto ◽  
Roger A. Fielding ◽  
Laurie J. Goodyear
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Protein Kinases ◽  
Human Skeletal Muscle ◽  
Fiber Type ◽  
Eccentric Contractions ◽  
Sprague Dawley ◽  
Static Stretch

Physical exercise and contraction increase c-Jun NH2-terminal kinase (JNK) activity in rat and human skeletal muscle, and eccentric contractions activate JNK to a greater extent than concentric contractions in human skeletal muscle. Because eccentric contractions include a lengthening or stretch component, we compared the effects of isometric contraction and static stretch on JNK and p38, the stress-activated protein kinases. Soleus and extensor digitorum longus (EDL) muscles dissected from 50- to 90-g male Sprague-Dawley rats were subjected to 10 min of electrical stimulation that produced contractions and/or to 10 min of stretch (0.24 N tension, 20–25% increase in length) in vitro. In the soleus muscle, contraction resulted in a small, but significant, increase in JNK activity (1.8-fold above basal) and p38 phosphorylation (4-fold). Static stretch had a much more profound effect on the stress-activated protein kinases, increasing JNK activity 19-fold and p38 phosphorylation 21-fold. Increases in JNK activation and p38 phosphorylation in response to static stretch were fiber-type dependent, with greater increases occurring in the soleus than in the EDL. Immunohistochemistry performed with a phosphospecific antibody revealed that activation of JNK occurred within the muscle fibers. These studies suggest that the stretch component of a muscle contraction may be a major contributor to the increases in JNK activity and p38 phosphorylation observed after exercise in vivo.

scholarly journals Enhanced Glycogen Storage of a Subcellular Hot Spot in Human Skeletal Muscle during Early Recovery from Eccentric Contractions

PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0127808 ◽  
Author(s):  
Joachim Nielsen ◽  
Jean Farup ◽  
Stine Klejs Rahbek ◽  
Frank Vincenzo de Paoli ◽  
Kristian Vissing
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Hot Spot ◽  
Glycogen Storage ◽  
Eccentric Contractions ◽  
Early Recovery

ELECTROMECHANICAL DELAY IN HUMAN SKELETAL .MUSCLE

1977 ◽  
Vol 9 (1) ◽  
pp. 49 ◽  
Author(s):  
P. V. Komi ◽  
P. R. Cavanagh ◽  
Paavo V. Komi
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Electromechanical Delay

scholarly journals A systems-based investigation into vitamin D and skeletal muscle repair, regeneration, and hypertrophy

2015 ◽  
Vol 309 (12) ◽  
pp. E1019-E1031 ◽  
Author(s):  
Daniel J. Owens ◽  
Adam P. Sharples ◽  
Ioanna Polydorou ◽  
Nura Alwan ◽  
Timothy Donovan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Human Skeletal Muscle ◽  
Peak Torque ◽  
Skeletal Muscle Regeneration ◽  
Eccentric Contractions ◽  
Knee Extensors ◽  
Muscle Repair ◽  
Supplemental Vitamin

Skeletal muscle is a direct target for vitamin D. Observational studies suggest that low 25[OH]D correlates with functional recovery of skeletal muscle following eccentric contractions in humans and crush injury in rats. However, a definitive association is yet to be established. To address this gap in knowledge in relation to damage repair, a randomised, placebo-controlled trial was performed in 20 males with insufficient concentrations of serum 25(OH)D (45 ± 25 nmol/l). Prior to and following 6 wk of supplemental vitamin D3 (4,000 IU/day) or placebo (50 mg of cellulose), participants performed 20 × 10 damaging eccentric contractions of the knee extensors, with peak torque measured over the following 7 days of recovery. Parallel experimentation using isolated human skeletal muscle-derived myoblast cells from biopsies of 14 males with low serum 25(OH)D (37 ± 11 nmol/l) were subjected to mechanical wound injury, which enabled corresponding in vitro studies of muscle repair, regeneration, and hypertrophy in the presence and absence of 10 or 100 nmol 1α,25(OH)2D3. Supplemental vitamin D3 increased serum 25(OH)D and improved recovery of peak torque at 48 h and 7 days postexercise. In vitro, 10 nmol 1α,25(OH)2D3 improved muscle cell migration dynamics and resulted in improved myotube fusion/differentiation at the biochemical, morphological, and molecular level together with increased myotube hypertrophy at 7 and 10 days postdamage. Together, these preliminary data are the first to characterize a role for vitamin D in human skeletal muscle regeneration and suggest that maintaining serum 25(OH)D may be beneficial for enhancing reparative processes and potentially for facilitating subsequent hypertrophy.

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