scholarly journals Photobiomodulation Therapy in Skeletal Muscle: From Exercise Performance to Muscular Dystrophies

2015 ◽  
Vol 33 (2) ◽  
pp. 53-54 ◽  
Author(s):  
Ernesto Cesar Pinto Leal-Junior
2021 ◽  
Vol 22 (10) ◽  
pp. 5276
Author(s):  
Coralie Croissant ◽  
Romain Carmeille ◽  
Charlotte Brévart ◽  
Anthony Bouter

Muscular dystrophies constitute a group of genetic disorders that cause weakness and progressive loss of skeletal muscle mass. Among them, Miyoshi muscular dystrophy 1 (MMD1), limb girdle muscular dystrophy type R2 (LGMDR2/2B), and LGMDR12 (2L) are characterized by mutation in gene encoding key membrane-repair protein, which leads to severe dysfunctions in sarcolemma repair. Cell membrane disruption is a physiological event induced by mechanical stress, such as muscle contraction and stretching. Like many eukaryotic cells, muscle fibers possess a protein machinery ensuring fast resealing of damaged plasma membrane. Members of the annexins A (ANXA) family belong to this protein machinery. ANXA are small soluble proteins, twelve in number in humans, which share the property of binding to membranes exposing negatively-charged phospholipids in the presence of calcium (Ca2+). Many ANXA have been reported to participate in membrane repair of varied cell types and species, including human skeletal muscle cells in which they may play a collective role in protection and repair of the sarcolemma. Here, we discuss the participation of ANXA in membrane repair of healthy skeletal muscle cells and how dysregulation of ANXA expression may impact the clinical severity of muscular dystrophies.


2021 ◽  
Vol 12 ◽  
pp. 204173142098133
Author(s):  
Juan M. Fernández-Costa ◽  
Xiomara Fernández-Garibay ◽  
Ferran Velasco-Mallorquí ◽  
Javier Ramón-Azcón

Muscular dystrophies are a group of highly disabling disorders that share degenerative muscle weakness and wasting as common symptoms. To date, there is not an effective cure for these diseases. In the last years, bioengineered tissues have emerged as powerful tools for preclinical studies. In this review, we summarize the recent technological advances in skeletal muscle tissue engineering. We identify several ground-breaking techniques to fabricate in vitro bioartificial muscles. Accumulating evidence shows that scaffold-based tissue engineering provides topographical cues that enhance the viability and maturation of skeletal muscle. Functional bioartificial muscles have been developed using human myoblasts. These tissues accurately responded to electrical and biological stimulation. Moreover, advanced drug screening tools can be fabricated integrating these tissues in electrical stimulation platforms. However, more work introducing patient-derived cells and integrating these tissues in microdevices is needed to promote the clinical translation of bioengineered skeletal muscle as preclinical tools for muscular dystrophies.


2012 ◽  
Vol 5 (6) ◽  
pp. 812-818 ◽  
Author(s):  
Stewart H. Lecker ◽  
Alexandra Zavin ◽  
Peirang Cao ◽  
Ross Arena ◽  
Kelly Allsup ◽  
...  

2019 ◽  
Vol 126 (2) ◽  
pp. 341-353 ◽  
Author(s):  
Margaret B. Bell ◽  
Zachary Bush ◽  
Graham R. McGinnis ◽  
Glenn C. Rowe

Endurance exercise has been shown to be a positive regulator of skeletal muscle metabolic function. Changes in mitochondrial dynamics (fusion and fission) have been shown to influence mitochondrial oxidative capacity. We therefore tested whether genetic disruption of mitofusins (Mfns) affected exercise performance in adult skeletal muscle. We generated adult-inducible skeletal muscle-specific Mfn1 (iMS-Mfn1KO), Mfn2 (iMS-Mfn2KO), and Mfn1/2 (iMS-MfnDKO) knockout mice. We assessed exercise capacity by performing a treadmill time to exhaustion stress test before deletion and up to 8 wk after deletion. Analysis of either the iMS-Mfn1KO or the iMS-Mfn2KO did not reveal an effect on exercise capacity. However, analysis of iMS-MfnDKO animals revealed a progressive reduction in exercise performance. We measured individual electron transport chain (ETC) complex activity and observed a reduction in ETC activity in both the subsarcolemmal and intermyofibrillar mitochondrial fractions specifically for NADH dehydrogenase (complex I) and cytochrome- c oxidase (complex IV), which was associated with a decrease in ETC subunit expression for these complexes. We also tested whether voluntary exercise training would prevent the decrease in exercise capacity observed in iMS-MfnDKO animals ( n = 10/group). However, after 8 wk of training we did not observe any improvement in exercise capacity or ETC subunit parameters in iMS-MfnDKO animals. These data suggest that the decrease in exercise capacity observed in the iMS-MfnDKO animals is in part the result of impaired ETC subunit expression and ETC complex activity. Taken together, these results provide strong evidence that mitochondrial fusion in adult skeletal muscle is important for exercise performance. NEW & NOTEWORTHY This study is the first to utilize an adult-inducible skeletal muscle-specific knockout model for Mitofusin (Mfn)1 and Mfn2 to assess exercise capacity. Our findings reveal a progressive decrease in exercise performance with Mfn1 and Mfn2 deletion. The decrease in exercise capacity was accompanied by impaired oxidative phosphorylation specifically for complex I and complex IV. Furthermore, voluntary exercise training was unable to rescue the impairment, suggesting that normal fusion is essential for exercise-induced mitochondrial adaptations.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Benjamin Leon ◽  
Andrea Carnie ◽  
Shannon Jenkins ◽  
Kevin Smith ◽  
Gloria Zalos ◽  
...  

Introduction Obesity is associated with many negative health impacts, including hyperinsulinemia and reduced exercise performance, despite being associated with greater lean skeletal mass which works as the insulin-targeting and exercising organ. Purpose of Study We delineated the associations amongst cardiorespiratory capacity, fat mass, skeletal mass distributions, and fasting plasma insulin in overweight, non-diabetic women. Methods One hundred and seventy-two sedentary women, age 22 to 68 years (range), body mass index (BMI) (34.2 ± 6.3 [mean ± SD]; range 25.3 to 57.6 kg/m 2 ), underwent dual energy x-ray absorptiometry for body composition, fasting insulin, and graded treadmill exercise test using the Bruce protocol with measurement of oxygen consumption (peak VO 2 ). Results After adjustment for age, fasting insulin (9.8 ± 8.1; range 1.9 to 47.6 mcU/ml) was positively associated with BMI (r = 0.43, p<0.001), fat mass (r = 0.41, p< 0.001), load-bearing skeletal muscle mass (lower extremity lean mass; r = 0.29, p< 0.001), and non-load-bearing skeletal muscle mass (upper extremity lean mass; Figure, Panel A). By multiple regression analysis with age, fat mass and lower and upper extremity lean masses as covariates, fat mass, age and upper extremity lean mass (Figure, Panel B) were independent negative predictors of peak VO 2 (all p< 0.01). Lower extremity, however, trended to be positively predictive of peak VO 2 (p = 0.067). Conclusions In non-load-bearing muscle, increased lean mass associated with elevated plasma insulin is predictive of reduced oxygen consumption during exercise, suggesting additional load that may diminish cardiorespiratory exercise performance or intrinsic impairment in skeletal muscle function. In load-bearing muscle, compensatory hypertrophy due to increased fat and lean mass loads may preserve exercise performance.


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