Highlights Low levels of physical activity are a risk factor associated with Alzheimer's disease. Older adults who exercise are more likely to maintain cognition. Exercise modulates amyloid β turnover, inflammation, synthesis, and release of neurotrophins, and cerebral blood flow.
Muscle repair without stem cells Skeletal muscle is a mechanical organ that endures cellular damage after contraction. Lesions caused by external injury can be repaired by muscle stem cells, which fuse with injured cells or create entirely new myofibers. Roman et al . describe a cell-autonomous repair process that is independent of muscle stem cells (see the Perspective by McNally and Demonbreun). After localized damage, myonuclei migrate to injury sites and locally deliver messenger RNA for cellular reconstruction. This myofiber self-repair represents a model for understanding the restoration of muscle architecture in health and disease. —BAP
Research in redox biology of exercise has made considerable advances in the last 70 years. Since the seminal study of George Pake's group calculating the content of free radicals in skeletal muscle in resting conditions in 1954, many discoveries have been made in the field. The first section of this review is devoted to highlight the main research findings and fundamental changes in the exercise redox biology discipline. It includes: i) the first steps in free radical research, ii) the relation between exercise and oxidative damage, iii) the redox regulation of muscle fatigue, iv) the sources of free radicals during muscle contractions, and v) the role of reactive oxygen species as regulators of gene transcription and adaptations in skeletal muscle. In the second section of the manuscript, we review the available biomarkers for assessing health, performance, recovery during exercise training and overtraining in the sport population. Among the set of biomarkers that could be determined in exercise studies we deepen on the four categories of redox biomarkers: i) oxidants, ii) antioxidants, iii) oxidation products (markers of oxidative damage), and iv) measurements of the redox balance (markers of oxidative stress). The main drawbacks, strengths, weaknesses, and methodological considerations of every biomarker are also discussed.
Hypomorphic Glucose 6-P dehydrogenase (G6PD) alleles, which cause G6PD deficiency, affect around one in twenty people worldwide. The high incidence of G6PD deficiency may reflect an evolutionary adaptation to the widespread prevalence of malaria, as G6PD-deficient red blood cells (RBCs) are hostile to the malaria parasites that infect humans. Although medical interest in this enzyme deficiency has been mainly focused on RBCs, more recent evidence suggests that there are broader implications for G6PD deficiency in health, including in skeletal muscle diseases. G6PD catalyzes the rate-limiting step in the pentose phosphate pathway (PPP), which provides the precursors of nucleotide synthesis for DNA replication as well as reduced nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is involved in the detoxification of cellular reactive oxygen species (ROS) and de novo lipid synthesis. An association between increased PPP activity and the stimulation of cell growth has been reported in different tissues including the skeletal muscle, liver, and kidney. PPP activity is increased in skeletal muscle during embryogenesis, denervation, ischemia, mechanical overload, the injection of myonecrotic agents, and physical exercise. In fact, the highest relative increase in the activity of skeletal muscle enzymes after one bout of exhaustive exercise is that of G6PD, suggesting that the activation of the PPP occurs in skeletal muscle to provide substrates for muscle repair. The age-associated loss in muscle mass and strength leads to a decrease in G6PD activity and protein content in skeletal muscle. G6PD overexpression in Drosophila Melanogaster and mice protects against metabolic stress, oxidative damage, and age-associated functional decline, and results in an extended median lifespan. This review discusses whether the well-known positive effects of exercise training in skeletal muscle are mediated through an increase in G6PD.
Background Frailty is a major age‐associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6‐P dehydrogenase (G6PD). The G6PD‐overexpressing mouse (G6PD‐Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty. Methods Old wild‐type (WT) and G6PD‐Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigated. Results The percentage of frail mice was significantly lower in the G6PD‐Tg than in the WT genotype, especially in 26‐month‐old mice where 50% of the WT were frail vs. only 13% of the Tg ones (P < 0.001). Skeletal muscle transcriptomic analysis showed an up‐regulation of respiratory chain and oxidative phosphorylation (P = 0.009) as well as glutathione metabolism (P = 0.035) pathways in the G6PD‐Tg mice. Accordingly, the Tg animals exhibited an increase in reduced glutathione (34.5%, P < 0.01) and a decrease on its oxidized form (−69%, P < 0.05) and in lipid peroxidation (4‐HNE: −20.5%, P < 0.05). The G6PD‐Tg mice also showed reduced apoptosis (BAX/Bcl2: −25.5%, P < 0.05; and Bcl‐xL: −20.5%, P < 0.05), lower levels of the intramuscular adipocyte marker FABP4 (−54.7%, P < 0.05), and increased markers of mitochondrial content (COX IV: 89.7%, P < 0.05; Grp75: 37.8%, P < 0.05) and mitochondrial OXPHOS complexes (CII: 81.25%, P < 0.01; CIII: 52.5%, P < 0.01; and CV: 37.2%, P < 0.05). Energy expenditure (−4.29%, P < 0.001) and the respiratory exchange ratio were lower (−13.4%, P < 0.0001) while the locomotor activity was higher (43.4%, P < 0.0001) in the 20‐month‐old Tg, indicating a major energetic advantage in these mice. Short‐term exercise training in young C57BL76J mice induced a robust activation of G6PD in skeletal muscle (203.4%, P < 0.05), similar to that achieved in the G6PD‐Tg mice (142.3%, P < 0.01). Conclusions Glucose 6‐P dehydrogenase deficiency can be an underestimated risk factor for several human pathologies and even frailty. By overexpressing G6PD, we provide the first molecular model of robustness. Because G6PD is regulated by pharmacological and physiological interventions like exercise, our results provide molecular bases for interventions that by increasing G6PD will delay the onset of frailty.
Oxidative stress refers to an imbalance between oxidant and antioxidant molecules, which is usually associated with oxidative damage to biomolecules and mitochondrial malfunction. Redox state-related parameters include (1) the direct measurement of ROS, (2) the assessment of the antioxidant defense status, and (3) the analysis of the resulting oxidative damage to molecules. Directly measuring ROS appears to be the preferred method among scientists, but most ROS are extremely unstable and difficult to measure. The processes of determining both the oxidative damage to biomolecules and the antioxidant system status, although both are indirect approaches, provide a reliable method to measure oxidative stress on a given sample. Recently, the Seahorse XF and the Oroboros O2k systems have provided new insights into the redox state from a more dynamic point of view. These techniques assess mitochondrial oxidative phosphorylation function and bioenergetics on isolated mitochondria, cultured cells, or specific tissues such as permeabilized fibers. This review describes a range of methodologies to measure redox state-related parameters, their strengths, and their limitations. In conclusion, all these techniques are valid and none of them can be replaced by another. Indeed, they have the potential to complement each other for a complete evaluation of the redox state of a given sample.
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Actualmente, están disponibles en el mercado nuevos modelos de calzado deportivo, como el calzado inestable. Sin embargo, todavía existe una falta de evidencia respecto a los cambios que este tipo de calzado puede producir en la biomecánica de la marcha. Así pues, el objetivo de esta investigación fue analizar los efectos agudos del calzado inestable sobre los impactos de aceleración, así como también sobre la variación de temperatura superficial plantar. Seis deportistas (estudiantes físicamente activos, edad 28±8 años, altura 1.73±0.05 m, masa corporal 68.7±6.7 kg, talla de pie 41±1.6 cm) participaron voluntariamente en el estudio. Las características de la pisada se obtuvieron mediante el test Foot Posture Index. La prueba de marcha se llevó a cabo sobre tapiz rodante (10 minutos a 1.44 m/s) bajo dos condiciones de calzado: zapatillas estables y zapatillas inestables. Se analizaron los impactos de aceleración (en tibia y cabeza), y la temperatura superficial plantar (en antepié, mediopié y retropié) en diferentes momentos de la prueba. Los resultados no mostraron diferencias significativas entre ambos tipos de zapatillas en las variables de acelerometría analizadas en ninguno de los momentos de registro. Sin embargo, sí se encontraron diferencias significativas entre ambos calzados (estable=1.40ºC, inestable=3.10ºC, p=0.004) en la variación de temperatura plantar del mediopié en ΔTPost5 (diferencia entre antes del inicio de la prueba y 5 minutos después de finalizarla). En conclusión, las zapatillas inestables parecen no producir ningún beneficio adicional al calzado tradicional para el deportista durante la marcha. Palabras clave: zapatillas, marcha, biomecánica, acelerometría, termografía. Abstract. Nowadays, new models of sports footwear are available on the market, such as unstable shoes. However, there is still a lack of evidence regarding the changes that this type of footwear can produce on gait biomechanics. Therefore, the aim of this research was to analyze the acute effects of unstable shoes on acceleration impacts, as well as on plantar surface temperature variation. Six athletes (physically active college students, age 28±8 years, height 1.73±0.05 m, body mass 68.7±6.7 kg, shoe size 41±1.6 cm) voluntarily participated in the study. Gait characteristics were obtained by means of the Foot Posture Index test. The walking test was performed on a treadmill (10 minutes at 1.44 m/s) under two footwear conditions: stable shoes and unstable shoes. Acceleration impacts (tibia and head), and plantar surface temperature (forefoot, midfoot and rearfoot) were analysed at different moments during the test. The results showed no significant differences between the two types of shoes in the accelerometry variables analyzed at any of the recording times. However, significant differences were found between both shoes (stable=1.40ºC, unstable=3.10ºC, p=0.004) in the variation of midfoot plantar temperature at ΔTPost5 (difference between before the start of the test and 5 minutes after the end of the test). In conclusion, unstable shoes do not seem to produce any additional benefit to traditional shoes for the athlete during walking. Keywords: sport shoes, gait, biomechanics, accelerometry, thermography.
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