Individualized isometric neuromuscular electrical stimulation training promotes myonuclear accretion in mouse skeletal muscle

2021 ◽  
Author(s):  
Aliki Zavoriti ◽  
Aurélie Fessard ◽  
Masoud Rahmati ◽  
Peggy Del Carmine ◽  
Bénédicte Chazaud ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Damage ◽  
Neuromuscular Electrical Stimulation ◽  
Training Session ◽  
Force Production ◽  
Main Function ◽  
Muscle Stem Cells ◽  
Exercise Induced ◽  
Electrical Stimuli

Skeletal muscle is a plastic tissue that adapts to exercise through fusion of muscle stem cells (MuSCs) with myofibers, a physiological process referred to as myonuclear accretion. However, it is still unclear whether myonuclear accretion is driven by increased mechanical loading per se , or occurs, at least in part, in response to exercise-induced muscle injury. Here, we developed a carefully monitored and individualized neuromuscular electrical stimulation (NMES) training protocol of the mouse plantar flexor muscles. Each NMES training session consisted of 80 isometric contractions at a submaximal mechanical intensity corresponding to ≈15% of maximal tetanic force to avoid muscle damage. NMES trained mice were stimulated for 2 × 3 consecutive days separated by one day of rest, for a total of 6 sessions. Experiments were conducted on C57BL/6J and BALB/c males at 10-12 weeks of age. NMES led to a robust myonuclear accretion and higher MuSC content in gastrocnemius muscle of both mouse lines, without overt signs of muscle damage/regeneration or muscle hypertrophy or force improvement. This new mouse model of myonuclear accretion relying on the main function of skeletal muscles, i.e., force production in response to electrical stimuli, will be of utmost interest to further understand the role of MuSCs in skeletal muscle adaptations.

scholarly journals Neuromuscular Electrical Stimulation as a Method to Maximize the Beneficial Effects of Muscle Stem Cells Transplanted into Dystrophic Skeletal Muscle

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e54922 ◽  
Author(s):  
Giovanna Distefano ◽  
Ricardo Jose Ferrari ◽  
Christopher Weiss ◽  
Bridget M. Deasy ◽  
Michael L. Boninger ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Electrical Stimulation ◽  
Neuromuscular Electrical Stimulation ◽  
Muscle Stem Cells ◽  
Beneficial Effects

scholarly journals Hormone therapy attenuates exercise-induced skeletal muscle damage in postmenopausal women

2009 ◽  
Vol 107 (3) ◽  
pp. 853-858 ◽  
Author(s):  
Christina M. Dieli-Conwright ◽  
Tanya M. Spektor ◽  
Judd C. Rice ◽  
E. Todd Schroeder
Keyword(s):  
Skeletal Muscle ◽  
Hormone Therapy ◽  
Mrna Expression ◽  
Postmenopausal Women ◽  
Muscle Damage ◽  
Exercise Bout ◽  
Control Group ◽  
Skeletal Muscle Damage ◽  
Tnf Α ◽  
Exercise Induced

Hormone therapy (HT) is a potential treatment to relieve symptoms of menopause and prevent the onset of disease such as osteoporosis in postmenopausal women. We evaluated changes in markers of exercise-induced skeletal muscle damage and inflammation [serum creatine kinase (CK), serum lactate dehydrogenase (LDH), and skeletal muscle mRNA expression of IL-6, IL-8, IL-15, and TNF-α] in postmenopausal women after a high-intensity resistance exercise bout. Fourteen postmenopausal women were divided into two groups: women not using HT (control; n = 6, 59 ± 4 yr, 63 ± 17 kg) and women using traditional HT (HT; n = 8, 59 ± 4 yr, 89 ± 24 kg). Both groups performed 10 sets of 10 maximal eccentric repetitions of single-leg extension on the Cybex dynamometer at 60°/s with 20-s rest periods between sets. Muscle biopsies of the vastus lateralis were obtained from the exercised leg at baseline and 4 h after the exercise bout. Gene expression was determined by RT-PCR for IL-6, IL-8, IL-15, and TNF-α. Blood draws were performed at baseline and 3 days after exercise to measure CK and LDH. Independent t-tests were performed to test group differences (control vs. HT). A probability level of P ≤ 0.05 was used to determine statistical significance. We observed significantly greater changes in mRNA expression of IL-6, IL-8, IL-15, and TNF-α ( P ≤ 0.01) in the control group compared with the HT group after the exercise bout. CK and LDH levels were significantly greater after exercise ( P ≤ 0.01) in the control group. Postmenopausal women not using HT experienced greater muscle damage after maximal eccentric exercise, indicating a possible protective effect of HT against exercise-induced skeletal muscle damage.

EXERCISE-INDUCED MUSCLE DAMAGE AND COLLAGEN METABOLISM IN RAT SKELETAL MUSCLE

1995 ◽  
Vol 27 (Supplement) ◽  
pp. S37 ◽  
Author(s):  
J. Komulainen ◽  
X. Han ◽  
W. Wang ◽  
S. Koskinen ◽  
V. Kovanen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Collagen Metabolism ◽  
Rat Skeletal Muscle ◽  
Exercise Induced

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.

Dynamics and Consequences of Potassium Shifts in Skeletal Muscle and Heart During Exercise

2000 ◽  
Vol 80 (4) ◽  
pp. 1411-1481 ◽  
Author(s):  
Ole M. Sejersted ◽  
Gisela Sjøgaard
Keyword(s):  
Skeletal Muscle ◽  
Force Production ◽  
Membrane Conductance ◽  
Cell Swelling ◽  
Modifying Factors ◽  
Fast Twitch Muscle ◽  
T Tubules ◽  
Exercise Induced ◽  
Fast Twitch ◽  
Muscle Excitability

Since it became clear that K+shifts with exercise are extensive and can cause more than a doubling of the extracellular [K+] ([K+]s) as reviewed here, it has been suggested that these shifts may cause fatigue through the effect on muscle excitability and action potentials (AP). The cause of the K+shifts is a transient or long-lasting mismatch between outward repolarizing K+currents and K+influx carried by the Na+-K+pump. Several factors modify the effect of raised [K+]sduring exercise on membrane potential ( Em) and force production. 1) Membrane conductance to K+is variable and controlled by various K+channels. Low relative K+conductance will reduce the contribution of [K+]sto the Em. In addition, high Cl−conductance may stabilize the Emduring brief periods of large K+shifts. 2) The Na+-K+pump contributes with a hyperpolarizing current. 3) Cell swelling accompanies muscle contractions especially in fast-twitch muscle, although little in the heart. This will contribute considerably to the lowering of intracellular [K+] ([K+]c) and will attenuate the exercise-induced rise of intracellular [Na+] ([Na+]c). 4) The rise of [Na+]cis sufficient to activate the Na+-K+pump to completely compensate increased K+release in the heart, yet not in skeletal muscle. In skeletal muscle there is strong evidence for control of pump activity not only through hormones, but through a hitherto unidentified mechanism. 5) Ionic shifts within the skeletal muscle t tubules and in the heart in extracellular clefts may markedly affect excitation-contraction coupling. 6) Age and state of training together with nutritional state modify muscle K+content and the abundance of Na+-K+pumps. We conclude that despite modifying factors coming into play during muscle activity, the K+shifts with high-intensity exercise may contribute substantially to fatigue in skeletal muscle, whereas in the heart, except during ischemia, the K+balance is controlled much more effectively.

scholarly journals Comparison of Pro-Regenerative Effects of Carbohydrates and Protein Administrated by Shake and Non-Macro-Nutrient Matched Food Items on the Skeletal Muscle after Acute Endurance Exercise

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 744 ◽  
Author(s):  
Eduard Isenmann ◽  
Franziska Blume ◽  
Daniel Bizjak ◽  
Vera Hundsdörfer ◽  
Sarah Pagano ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Damage ◽  
Serum Insulin ◽  
Serum Markers ◽  
Serum Creatine Kinase ◽  
Skeletal Muscle Regeneration ◽  
Skeletal Muscle Damage ◽  
Leg Strength ◽  
Exercise Induced

Physical performance and regeneration after exercise is enhanced by the ingestion of proteins and carbohydrates. These nutrients are generally consumed by athletes via whey protein and glucose-based shakes. In this study, effects of protein and carbohydrate on skeletal muscle regeneration, given either by shake or by a meal, were compared. 35 subjects performed a 10 km run. After exercise, they ingested nothing (control), a protein/glucose shake (shake) or a combination of white bread and sour milk cheese (food) in a randomized cross over design. Serum glucose (n = 35), serum insulin (n = 35), serum creatine kinase (n = 15) and myoglobin (n = 15), hematologic parameters, cortisol (n = 35), inflammation markers (n = 27) and leg strength (n = 15) as a functional marker were measured. Insulin secretion was significantly stimulated by shake and food. In contrast, only shake resulted in an increase of blood glucose. Food resulted in a decrease of pro, and stimulation of anti-inflammatory serum markers. The exercise induced skeletal muscle damage, indicated by serum creatine kinase and myoglobin, and exercise induced loss of leg strength was decreased by shake and food. Our data indicate that uptake of protein and carbohydrate by shake or food reduces exercise induced skeletal muscle damage and has pro-regenerative effects.

α7β1-Integrin regulates mechanotransduction and prevents skeletal muscle injury

2006 ◽  
Vol 290 (6) ◽  
pp. C1660-C1665 ◽  
Author(s):  
Marni D. Boppart ◽  
Dean J. Burkin ◽  
Stephen J. Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Intracellular Signaling ◽  
Ex Vivo ◽  
Negative Regulator ◽  
Blue Dye ◽  
The Matrix ◽  
Mitogen Activated Protein ◽  
Exercise Induced

α7β1-Integrin links laminin in the extracellular matrix with the cell cytoskeleton and therein mediates transduction of mechanical forces into chemical signals. Muscle contraction and stretching ex vivo result in activation of intracellular signaling molecules that are integral to postexercise injury responses. Because α7β1-integrin stabilizes muscle and provides communication between the matrix and cytoskeleton, the role of this integrin in exercise-induced cell signaling and skeletal muscle damage was assessed in wild-type and transgenic mice overexpressing the α7BX2 chain. We report here that increasing α7β1-integrin inhibits phosphorylation of molecules associated with muscle damage, including the mitogen-activated protein kinases (JNK, p38, and ERK), following downhill running. Likewise, activation of molecules associated with hypertrophy (AKT, mTOR, and p70S6k) was diminished in mice overexpressing integrin. While exercise resulted in Evans blue dye-positive fibers, an index of muscle damage, increased integrin protected mice from injury. Moreover, exercise leads to an increase in α7β1 protein. These experiments provide the first evidence that α7β1-integrin is a negative regulator of mechanotransduction in vivo and provides resistance to exercise-induced muscle damage.

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