scholarly journals Does Phototherapy Enhance Skeletal Muscle Contractile Function and Postexercise Recovery? A Systematic Review

2013 ◽  
Vol 48 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Paul A. Borsa ◽  
Kelly A. Larkin ◽  
Jerry M. True
Keyword(s):  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Contractile Function ◽  
Placebo Control ◽  
Original Research ◽  
Data Sets ◽  
Electromyographic Activity ◽  
Postexercise Recovery ◽  
Exercise Induced ◽  
Muscle Contractile

Context Recently, researchers have shown that phototherapy administered to skeletal muscle immediately before resistance exercise can enhance contractile function, prevent exercise-induced cell damage, and improve postexercise recovery of strength and function. Objective To critically evaluate original research addressing the ability of phototherapeutic devices, such as lasers and light-emitting diodes (LEDs), to enhance skeletal muscle contractile function, reduce exercise-induced muscle fatigue, and facilitate postexercise recovery. Data Sources We searched the electronic databases PubMed, SPORTDiscus, Web of Science, Scopus, and Rehabilitation & Physical Medicine without date limitations for the following key words: laser therapy, phototherapy, fatigue, exercise, circulation, microcirculation, and photobiomodulation. Study Selection Eligible studies had to be original research published in English as full papers, involve human participants, and receive a minimum score of 7 out of 10 on the Physiotherapy Evidence Database (PEDro) scale. Data Extraction Data of interest included elapsed time to fatigue, total number of repetitions to fatigue, total work performed, maximal voluntary isometric contraction (strength), electromyographic activity, and postexercise biomarker levels. We recorded the PEDro scores, beam characteristics, and treatment variables and calculated the therapeutic outcomes and effect sizes for the data sets. Data Synthesis In total, 12 randomized controlled trials met the inclusion criteria. However, we excluded data from 2 studies, leaving 32 data sets from 10 studies. Twenty-four of the 32 data sets contained differences between active phototherapy and sham (placebo-control) treatment conditions for the various outcome measures. Exposing skeletal muscle to single-diode and multidiode laser or multidiode LED therapy was shown to positively affect physical performance by delaying the onset of fatigue, reducing the fatigue response, improving postexercise recovery, and protecting cells from exercise-induced damage. Conclusions Phototherapy administered before resistance exercise consistently has been found to provide ergogenic and prophylactic benefits to skeletal muscle.

scholarly journals Dysfunction of muscle contraction with impaired intracellular Ca2+ handling in skeletal muscle and the effect of exercise training in male db/db mice

2019 ◽  
Vol 126 (1) ◽  
pp. 170-182 ◽  
Author(s):  
Hiroaki Eshima ◽  
Yoshifumi Tamura ◽  
Saori Kakehi ◽  
Kyoko Nakamura ◽  
Nagomi Kurebayashi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Contraction ◽  
Contractile Function ◽  
Contractile Force ◽  
Contractile Dysfunction ◽  
Muscle Contractile ◽  
Type 2 Diabetic

Type 2 diabetes is characterized by reduced contractile force production and increased fatigability of skeletal muscle. While the maintenance of Ca2+ homeostasis during muscle contraction is a requisite for optimal contractile function, the mechanisms underlying muscle contractile dysfunction in type 2 diabetes are unclear. Here, we investigated skeletal muscle contractile force and Ca2+ flux during contraction and pharmacological stimulation in type 2 diabetic model mice ( db/db mice). Furthermore, we investigated the effect of treadmill exercise training on muscle contractile function. In male db/db mice, muscle contractile force and peak Ca2+ levels were both lower during tetanic stimulation of the fast-twitch muscles, while Ca2+ accumulation was higher after stimulation compared with control mice. While 6 wk of exercise training did not improve glucose tolerance, exercise did improve muscle contractile dysfunction, peak Ca2+ levels, and Ca2+ accumulation following stimulation in male db/db mice. These data suggest that dysfunctional Ca2+ flux may contribute to skeletal muscle contractile dysfunction in type 2 diabetes and that exercise training may be a promising therapeutic approach for dysfunctional skeletal muscle contraction. NEW & NOTEWORTHY The purpose of this study was to examine muscle contractile function and Ca2+ regulation as well as the effect of exercise training in skeletal muscle in obese diabetic mice ( db/db). We observed impairment of muscle contractile force and Ca2+ regulation in a male type 2 diabetic animal model. These dysfunctions in muscle were improved by 6 wk of exercise training.

scholarly journals Stimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise

2019 ◽  
Vol 126 (1) ◽  
pp. 30-43 ◽  
Author(s):  
Henning Wackerhage ◽  
Brad J. Schoenfeld ◽  
D. Lee Hamilton ◽  
Maarit Lehti ◽  
Juha J. Hulmi
Keyword(s):  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Muscle Damage ◽  
Muscle Hypertrophy ◽  
Muscle Protein ◽  
Large Body ◽  
Focal Adhesions ◽  
Indirect Evidence ◽  
Skeletal Muscle Hypertrophy ◽  
Exercise Induced

One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mammalian target of rapamycin complex 1 (mTORC1)-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as “hypertrophy stimulus,” and the sensor of such a signal as “hypertrophy sensor.” In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers, as potential hypertrophy stimuli. Mechanical signals are the prime hypertrophy stimuli candidates, and a filamin-C-BAG3-dependent regulation of mTORC1, Hippo, and autophagy signaling is a plausible albeit still incompletely characterized hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signaling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells. While exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli, but this is based on indirect evidence and metabolite candidates are poorly characterized.

scholarly journals Effects of fasting on isolated murine skeletal muscle contractile function during acute hypoxia

PLoS ONE ◽  
2020 ◽  
Vol 15 (4) ◽  
pp. e0225922
Author(s):  
Cameron A. Schmidt ◽  
Emma J. Goldberg ◽  
Tom D. Green ◽  
Reema R. Karnekar ◽  
Jeffrey J. Brault ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Contractile Function ◽  
Acute Hypoxia ◽  
Murine Skeletal Muscle ◽  
Muscle Contractile

scholarly journals Effect of green tea extract supplementation on glycogen replenishment in exercised human skeletal muscle

2017 ◽  
Vol 117 (10) ◽  
pp. 1343-1350 ◽  
Author(s):  
Tsen-Wei Tsai ◽  
Chia-Chen Chang ◽  
Su-Fen Liao ◽  
Yi-Hung Liao ◽  
Chien-Wen Hou ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Green Tea ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Recovery Period ◽  
Glycogen Resynthesis ◽  
Postexercise Recovery ◽  
Exercise Induced ◽  
Tea Extract

AbstractThe purpose of this study was to investigate the effects of 8-week green tea extract (GTE) supplementation on promoting postexercise muscle glycogen resynthesis and systemic energy substrate utilisation in young college students. A total of eight healthy male participants (age: 22·0 (se 1·0) years, BMI: 24·2 (se 0·7) kg/m2, VO2max: 43·2 (se 2·4) ml/kg per min) participated in this study. GTE (500 mg/d for 8 weeks) was compared with placebo in participants in a double-blind/placebo-controlled and crossover study design with an 8-week washout period. Thereafter, all participants performed a 60-min cycling exercise (75 % VO2max) and consumed a carbohydrate-enriched meal immediately after exercise. Vastus lateralis muscle samples were collected immediately (0 h) and 3 h after exercise, and blood and gaseous samples were collected during the 3-h postexercise recovery period. An 8-week oral GTE supplementation had no effects on further promoting muscle glycogen resynthesis in exercised human skeletal muscle, but the exercise-induced muscle GLUT type 4 (GLUT4) protein content was greater in the GTE supplementation trial (P<0·05). We observed that, during the postexercise recovery period, GTE supplementation elicited an increase in energy reliance on fat oxidation compared with the placebo trial (P<0·05), although there were no differences in blood glucose and insulin responses between the two trials. In summary, 8-week oral GTE supplementation increases postexercise systemic fat oxidation and exercise-induced muscle GLUT4 protein content in response to an acute bout of endurance exercise. However, GTE supplementation has no further benefit on promoting muscle glycogen resynthesis during the postexercise period.

LIF is a contraction-induced myokine stimulating human myocyte proliferation

2011 ◽  
Vol 111 (1) ◽  
pp. 251-259 ◽  
Author(s):  
Christa Broholm ◽  
Matthew J. Laye ◽  
Claus Brandt ◽  
Radhika Vadalasetty ◽  
Henriette Pilegaard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Resistance Exercise ◽  
Satellite Cell ◽  
Quadriceps Muscle ◽  
Human Myotubes ◽  
Myoblast Proliferation ◽  
Satellite Cell Proliferation ◽  
Exercise Induced ◽  
Sirna Knockdown

The cytokine leukemia inhibitory factor (LIF) is expressed by skeletal muscle and induces proliferation of myoblasts. We hypothesized that LIF is a contraction-induced myokine functioning in an autocrine fashion to activate gene regulation of human muscle satellite cell proliferation. Skeletal muscle LIF expression, regulation, and action were examined in two models: 1) young men performing a bout of heavy resistance exercise of the quadriceps muscle and 2) cultured primary human satellite cells. Resistance exercise induced a ninefold increase in LIF mRNA content in skeletal muscle, but LIF was not detectable in plasma of the subjects. However, electrically stimulated cultured human myotubes produced and secreted LIF, suggesting that LIF is a myokine with local effects. The well established exercise-induced signaling molecules PI3K, Akt, and mTor contributed to the regulation of LIF in cultured human myotubes as chemical inhibition of PI3K and mTor and siRNA knockdown of Akt1 were independently sufficient to downregulate LIF. Human myoblast proliferation was increased by recombinant exogenous LIF and decreased by siRNA knockdown of the endogenous LIF receptor. Finally, the transcription factors JunB and c-Myc, which promote myoblast proliferation, were induced by LIF in cultured human myotubes. Indeed, both JunB and c-Myc were also increased in skeletal muscle following resistance exercise. Our data suggest that LIF is a contraction-induced myokine, potentially acting in an autocrine or paracrine fashion to promote satellite cell proliferation.

Ibuprofen treatment blunts early translational signaling responses in human skeletal muscle following resistance exercise

2014 ◽  
Vol 117 (1) ◽  
pp. 20-28 ◽  
Author(s):  
James F. Markworth ◽  
Luke D. Vella ◽  
Vandre C. Figueiredo ◽  
David Cameron-Smith
Keyword(s):  
Resistance Exercise ◽  
Ribosomal Protein ◽  
Placebo Control ◽  
S6 Kinase ◽  
Ribosomal Protein S6 ◽  
Cyclooxygenase 1 ◽  
Postexercise Recovery ◽  
Muscle Biopsies ◽  
Muscle Responses

Cyclooxygenase-1 and -2 pathway-derived prostaglandins (PGs) have been implicated in adaptive muscle responses to exercise, but the role of PGs in contraction-induced muscle signaling has not been determined. We investigated the effect of inhibition of cyclooxygenase-1 and -2 activities with the nonsteroidal anti-inflammatory drug ibuprofen on human muscle signaling responses to resistance exercise. Subjects orally ingested 1,200 mg ibuprofen (or placebo control) in three 400-mg doses administered ∼30 min before and ∼6 h and ∼12 h following a bout of unaccustomed resistance exercise (80% one repetition maximum). Muscle biopsies were obtained at rest (preexercise), immediately postexercise (0 h), 3 h postexercise, and at 24 h of recovery. In the placebo (PLA) group, phosphorylation of ERK1/2 (Thr202/Tyr204), ribosomal protein S6 kinase (RSK, Ser380), mitogen-activated kinase 1 (Mnk1, Thr197/202), and p70S6 kinase (p70S6K, Thr421/Ser424) increased at both 0 and 3 h postexercise, with delayed elevation of phospho (p)-p70S6K (Thr389) and p-rpS6 (Ser235/S36 and Ser240/244) at 3 h postexercise. Only p-ERK1/2 (Thr202/Tyr204) remained significantly elevated in the 24-h postexercise biopsy. Ibuprofen treatment prevented sustained elevation of MEK-ERK signaling at 3 h (p-ERK1/2, p-RSK, p-Mnk1, p-p70S6K Thr421/Ser424) and 24 h (p-ERK1/2) postexercise, and this was associated with suppressed phosphorylation of ribosomal protein S6 (Ser235/236 and Ser240/244). Early contraction-induced p-Akt (Ser473) and p-p70S6K (Thr389) were not influenced by ibuprofen, but p-p70S6K (Thr389) remained elevated 24 h postexercise only in those receiving ibuprofen treatment. Early muscle signaling responses to resistance exercise are, in part, ibuprofen sensitive, suggesting that PGs are important signaling molecules during early postexercise recovery.

Role of myokines in exercise and metabolism

2007 ◽  
Vol 103 (3) ◽  
pp. 1093-1098 ◽  
Author(s):  
Bente Klarlund Pedersen ◽  
Thorbjörn C. A. Åkerström ◽  
Anders R. Nielsen ◽  
Christian P. Fischer
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Contractile Activity ◽  
Endocrine Effects ◽  
Skeletal Muscle Function ◽  
The Past ◽  
Exercise Induced ◽  
Immune Changes ◽  
Muscle Contractile

During the past 20 yr, it has been well documented that exercise has a profound effect on the immune system. With the discovery that exercise provokes an increase in a number of cytokines, a possible link between skeletal muscle contractile activity and immune changes was established. For most of the last century, researchers sought a link between muscle contraction and humoral changes in the form of an “exercise factor,” which could mediate some of the exercise-induced metabolic changes in other organs such as the liver and the adipose tissue. We suggest that cytokines and other peptides that are produced, expressed, and released by muscle fibers and exert either paracrine or endocrine effects should be classified as “myokines.” Since the discovery of interleukin (IL)-6 release from contracting skeletal muscle, evidence has accumulated that supports an effect of IL-6 on metabolism. We suggested that muscle-derived IL-6 fulfils the criteria of an exercise factor and that such classes of cytokines should be named “myokines.” Interestingly, recent research demonstrates that skeletal muscles can produce and express cytokines belonging to distinctly different families. Thus skeletal muscle has the capacity to express several myokines. To date the list includes IL-6, IL-8, and IL-15, and contractile activity plays a role in regulating the expression of these cytokines in skeletal muscle. The present review focuses on muscle-derived cytokines, their regulation by exercise, and their possible roles in metabolism and skeletal muscle function and it discusses which cytokines should be classified as true myokines.

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