Reinnervation of Vastus lateralis is increased significantly in seniors (70 years old) with a lifelong history of high-level exercise

It has long been recognized that histological changes observed in aging muscle suggest that denervation contributes to muscle deterioration and that disuse accelerates the process while running activity, sustained for decades, protects against age-related loss of motor units. here we show at the histological level that lifelong increased physical activity promotes reinnervation of muscle fibers. In muscle biopsies from 70-year old men with a lifelong history of high-level physical activity, we observed a considerable increase in fiber-type groupings (almost exclusively of the slow type) in comparison to sedentary seniors, revealing a large population of reinnervated muscle fibers in the sportsmen. Slow-type transformation by reinnervation in senior sportsmen seems to be a clinically relevant mechanism: the muscle biopsies fluctuate from those with scarce fiber-type transformation and groupings to almost fully transformed muscle, going through a process in which isolated fibers co-expressing fast and slow MHCs seems to fill the gaps. taken together, our results suggest that, beyond the direct effects of aging on the muscle fibers, changes occurring in skeletal tissue appear to be largely, although not solely, a result of sparse denervation. our data suggest that lifelong exercise allow the body to adapt to the consequences of the age-related denervation and to preserve muscle structure and function by saving otherwise lost muscle fibers through recruitment to different, mainly slow, motor units. These beneficial effects on motoneurons and, subsequently on muscle fibers, serve to maintain size structure and function of muscle fibers, delaying the functional decline and loss of independence that are commonly seen in the late aging

Dispersing agents prevent negative impact of oil on uptake of sinc by duckweed (Lemna minor)

Oil spills have had extremely negative effects upon the environment, affecting both animal and plant species living in and around the contaminated water. It is known that the oil can interfere with certain plant and animal functions, potentially causing death. Means developed to remove the oil from the water include physical methods such as skimmers and chemical approaches such as adsorbents and dispersants. In the cases of the chemical treatments, some people question whether the remedy may also cause problems. Here, we confirm that the aquatic duckweed plant (Lemna) can take up zinc from its environment and show that oil in the water will inhibit that uptake. Further, we demonstrate that the negative affect the oil has upon zinc uptake by duckweed can be ameliorated by treatment with a dispersant and that the dispersant itself does not inhibit zinc uptake by duckweed. We conclude that, treatment of oil contaminated water by dispersant may be a good method to clean up the water

Optimization of Ectopic Gene Expression in Skeletal Muscle Through DNA Transfer by Electroporation.

Background Electroporation (EP) is a widely used non-viral gene transfer method. We have attempted to develop an exact protocol to maximize DNA expression while minimizing tissue damage following EP of skeletal muscle in vivo. Specifically, we investigated the effects of varying injection techniques, electrode surface geometry, and plasmid mediums. Results We found that as the amount of damage increased in skeletal muscle in response to EP, the level of β-galactosidase (β-gal) expression drastically decreased and that there was no evidence of β-gal expression in damaged fibers. Two specific types of electrodes yielded the greatest amount of expression. We also discovered that DNA uptake in skeletal muscle following intra-arterial injection of DNA was significantly enhanced by EP. Finally, we found that DMSO and LipoFECTAMINE™, common enhancers of DNA electroporation in vitro, had no positive effect on DNA electroporationin vivo. Conclusions When injecting DNA intramuscularly, a flat plate electrode without any plasmid enhancers is the best method to achieve high levels of gene expression

Functional electrical stimulation of permanently denervated muscles, updated 2020

Spinal cord injury produces muscle wasting, which is especially severe after the complete and permanent damage of lower motor neurons that occurs in complete Cauda Equina Syndrome. Even in this worst-case scenario, we have shown that permanently denervated Quadriceps muscle can be rescued by surface Functional Electrical Stimulation and a purpose designed home-based rehabilitation regime. Here, our aim is to show that the effects are extended to both antagonist muscles and the skin of the thighs. Before and after 2 years of electrical stimulation, mass and structure of Quadriceps and Hamstrings muscles were quantitated by force measurements. Muscle gross cross section were evaluated using color computed tomography, muscle and skin biopsies by quantitative histology and immunohistochemistry. The treatment produced: a) an increase in cross-sectional area of stimulated muscles; b) an increase in muscle fiber mean diameter; c) improvements in ultrastructural organization; and d) increased force output during electrical stimulation. The recovery of Quadriceps muscle force was sufficient to allow 25% of the compliant subjects to perform stand-up and step-in place trainings. Improvements are extended to hamstring muscles and skin. Indeed, the cushioning effect provided by recovered tissues is a major clinical benefit. It is our hope that, with or without our advice, trials may start soon in Europe and Russia to provide persons-in-need the help they deserve

Lessons from Masters World Records: Lack of Gender Differences In Aging Muscle Decay Rates

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The mERG1a channel modulates skeletal muscle MuRF1, but not MAFbx, expression.

INTRODUCTION: We investigated the mechanism by which the MERG1a K+ channel increases ubiquitin proteasome proteolysis (UPP). METHODS: Hindlimb suspension and electro-transfer of Merg1a cDNA into mouse gastrocnemius muscles induced atrophy. RESULTS: Atrophic gastrocnemius muscles of hindlimb-suspended mice express Merg1a, Murf1, and Mafbx genes. Electrotransfer of Merg1a significantly decreases muscle fiber size (12.6%) and increases UPP E3 ligase Murf1 mRNA (2.1-fold) and protein (23.7%), but does not affect Mafbx E3 ligase expression. Neither Merg1a-induced decreased fiber size nor Merg1a-induced increased Murf1 expression is curtailed significantly by coexpression of inactive HR-Foxo3a, a gene encoding a transcription factor known to induce Mafbx expression. CONCLUSIONS: The MERG1a K+ channel significantly increases expression of Murf1, but not Mafbx. We explored this expression pattern by expressing inactive Foxo3a and showing that it is not involved in MERG1a-mediated expression of Murf1. These findings suggest that MERG1a may not modulate Murf1 expression through the AKT/FOXO pathway

Long-term high-level exercise promotes muscle reinnervation with age.

The histologic features of aging muscle suggest that denervation contributes to atrophy, that immobility accelerates the process, and that routine exercise may protect against loss of motor units and muscle tissue. Here, we compared muscle biopsies from sedentary and physically active seniors and found that seniors with a long history of high-level recreational activity up to the time of muscle biopsy had 1) lower loss of muscle strength versus young men (32% loss in physically active vs 51% loss in sedentary seniors); 2) fewer small angulated (denervated) myofibers; 3) a higher percentage of fiber-type groups (reinnervated muscle fibers) that were almost exclusive of the slow type; and 4) sparse normal-size muscle fibers coexpressing fast and slow myosin heavy chains, which is not compatible with exercise-driven muscle-type transformation. The biopsies from the old physically active seniors varied from sparse fiber-type groupings to almost fully transformed muscle, suggesting that coexpressing fibers appear to fill gaps. Altogether, the data show that long-term physical activity promotes reinnervation of muscle fibers and suggest that decades of high-level exercise allow the body to adapt to age-related denervation by saving otherwise lost muscle fibers through selective recruitment to slow motor units. These effects on size and structure of myofibers may delay functional decline in late aging

Peripheral endocannabinoids regulate skeletal muscle development and maintenance

As a principal tissue responsible for insulin-mediated glucose uptake, skeletal muscle is important for whole-body health. The role of peripheral endocannabinoids as regulators of skeletal muscle metabolism has recently gained a lot of interest, as endocannabinoid system disorders could cause peripheral insulin resistance. We investigated the role of the peripheral endocannabinoid system in skeletal muscle development and maintenance. Cultures of C2C12 cells, primary satellite cells and mouse skeletal muscle single fibers were used as model systems for our studies. We found an increase in cannabinoid receptor type 1 (CB1) mRNA and endocannabinoid synthetic enzyme mRNA skeletal muscle cells during differentiation. We also found that activation of CB1 inhibited myoblast differentiation, expanded the number of satellite cells, and stimulated the fast-muscle oxidative phenotype. Our findings contribute to understanding of the role of the endocannabinoid system in skeletal muscle metabolism and muscle oxygen consumption, and also help to explain the effects of the peripheral endocannabinoid system on whole-body energy balance