Publications by authors named "Valero-Breton M"

Article Synopsis
  • A low metabolic flexibility to lipid (MetF-lip) in skeletal muscle may lead to fat accumulation and metabolic issues, prompting a study on its effects in non-obese individuals.
  • The study involved 17 participants (average age 55.4) and analyzed how MetF-lip related to various metabolic health measures and inflammatory signals during exercise.
  • Findings revealed that while MetF-lip did not link to metabolic health outcomes, it was inversely related to inflammatory markers in the muscles, suggesting it might reflect some inflammation activation rather than directly causing metabolic disruptions.
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Skeletal muscle possesses regenerative potential via satellite cells, compromised in muscular dystrophies leading to fibrosis and fat infiltration. Angiotensin II (Ang-II) is commonly associated with pathological states. In contrast, Angiotensin (1-7) [Ang-(1-7)] counters Ang-II, acting via the Mas receptor.

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With extended life expectancy, the quality of life of elders is a priority. Loss of mobility, increased morbidity and risks of falls have dramatic individual and societal impacts. Here we consider the age-related modifications of gait, from a biomechanical and neurophysiological perspective.

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Background: Skeletal muscle is sensitive to bile acids (BA) because it expresses the TGR5 receptor for BA. Cholic (CA) and deoxycholic (DCA) acids induce a sarcopenia-like phenotype through TGR5-dependent mechanisms. Besides, a mouse model of cholestasis-induced sarcopenia was characterised by increased levels of serum BA and muscle weakness, alterations that are dependent on TGR5 expression.

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Background: Skeletal muscle generates force and movements and maintains posture. Under pathological conditions, muscle fibers suffer an imbalance in protein synthesis/degradation. This event causes muscle mass loss and decreased strength and muscle function, a syndrome known as sarcopenia.

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Fibrosis is a condition characterized by an increase in the components of the extracellular matrix (ECM). In skeletal muscle, the cells that participate in the synthesis of ECM are fibroblasts, myoblasts, and myotubes. These cells respond to soluble factors that increase ECM.

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Muscle atrophy decreases muscle mass with the subsequent loss of muscle function. Among the mechanisms that trigger sarcopenia is mitochondrial dysfunction. Mitochondria, whose primary function is to produce ATP, are dynamic organelles that present the process of formation (mitogenesis) and elimination (mitophagy).

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Chronic obstructive pulmonary disease (COPD) patients manifest muscle dysfunction and impaired muscle oxidative capacity, which result in reduced exercise capacity and poor health status. This study examined the effects of 12-week eccentric (ECC) and concentric (CONC) cycling training on plasma markers of cardiometabolic health, oxidative stress, and inflammation in COPD patients. A randomized trial in which moderate COPD was allocated to ECC ( = 10; 68.

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Muscle mass and strength are subjected to several regulations. We found endocrine signals such as growth hormone, insulin-like growth factor 1, testosterone, thyroid hormones, and glucocorticoids among them. Neural inputs also influence muscle development, modulating mass and strength.

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Cholestatic chronic liver disease is characterized by developing sarcopenia and elevated serum levels of bile acids. Sarcopenia is a skeletal muscle disorder with the hallmarks of muscle weakness, muscle mass loss, and muscle strength decline. Our previous report demonstrated that deoxycholic acid (DCA) and cholic acid (CA), through the membrane receptor TGR5, induce a sarcopenia-like phenotype in myotubes and muscle fibers.

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An interaction between mitochondrial dynamics, physical activity levels, and COVID-19 severity has been previously hypothesized. However, this has not been tested. We aimed to compare mitochondrial morphology and cristae density of PBMCs between subjects with non-severe COVID-19, subjects with severe COVID-19, and healthy controls.

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Sarcopenia is a highly prevalent complication of non-alcoholic fatty liver disease (NAFLD). We aimed to conduct a systematic review and meta-analyses to elucidate the exercise training (ET)'s efficacy on NAFLD adult patients' sarcopenia criteria. We identified relevant randomized controlled trials (RCT) in electronic databases PubMed, CINAHL, and Scopus.

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Electrical pulse stimulation (EPS) has been suggested to be a useful method to investigate the mechanisms underlying the adaptations of human skeletal muscle to both endurance and resistance exercise. Although different myotube stimulation protocols mimicking acute and chronic endurance exercise have been developed, no convincing protocol mimicking resistance exercise exists. Adaptations to resistance exercise mainly ensue via the Akt/mTOR pathway.

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