ascorbic-acid and Muscular-Atrophy

To assess whether a standardized dietary supplementation can help to decrease postoperative muscle atrophy and/or improve rehabilitation outcomes in patients who underwent anterior cruciate ligament reconstruction (ACLR).. A systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA). MEDLINE, Scopus, and Cochrane Library databases were searched, and articles that examined protein or amino acid, vitamin, or any other type of supplementation in ACLR were reviewed. Two independent reviewers conducted the search using pertinent Boolean operations.. A total of 1818 articles were found after our database search. Ten studies fulfilled our inclusion criteria and only assessed patients undergoing ACLR. Four studies assessed protein-based supplementation. One study assessed creatine as a supplement. Four studies assessed vitamin-based supplementation. One study assessed testosterone supplementation. Protein and amino acid supplementation showed potential benefits; multiple authors demonstrated a combination of improved achievement of rehabilitation benchmarks, graft maturation, muscular hypertrophic response, and peak dynamic muscle strength. When we examined creatine, vitamin, or hormone-based protocols, none demonstrated results, suggesting these factors may attenuate muscle atrophy after surgery. Vitamin C and E demonstrated potentially increased local inflammation in skeletal muscle, which runs contrary to the belief that antioxidant vitamin-based supplementation may decrease the inflammatory response that plays a role in the post injury/operative period.. Protein-based supplementation may play a role in mitigating muscle atrophy associated with ACLR, as multiple authors demonstrated a combination of improved achievement of rehabilitation benchmarks, thigh hypertrophic response, and peak dynamic muscle strength. However, based on current literature, it is not possible to recommend a specific protein-based supplementation protocol at this time for patients undergoing ACLR. Limited evidence suggests no benefit for creatine, vitamin, or hormone-based protocols.. II, a systematic review of level I-II studies.

Topics: Anterior Cruciate Ligament Injuries; Anterior Cruciate Ligament Reconstruction; Ascorbic Acid; Creatine; Dietary Supplements; Humans; Inflammation; Muscle Strength; Muscle, Skeletal; Muscular Atrophy; Vitamin E

Muscle atrophy and weakness are predominant impairments after anterior cruciate ligament (ACL) surgical repair. We tested the hypothesis that vitamin E and C supplementation will improve recovery from ACL injury. Men undergoing elective ACL surgery were randomly assigned to twice-daily supplements of either antioxidants (AO; vitamins E and C, n=10) or matching placebos (n=10) from 2 weeks before until 3 months after surgery. Each subject provided several fasting blood draws, two muscle biopsies from the thigh muscle of the injured limb, and strength and thigh circumference measurements of the lower limbs. Muscle atrophy was apparent in both groups before and several days after surgery. Compared with baseline measurements, peak isometric force of the injured limb increased significantly (P<0.05) by 3 months postsurgery in both treatment groups; however, AO supplementation did not augment these strength gains. By contrast, baseline plasma ascorbic acid concentrations correlated (r=0.59, P=0.006) with subsequent improvement in the strength of the injured limb. In summary, vitamin E and C supplementation was ineffective in potentiating the improvement in force production by the injured limb; however, baseline vitamin C status was associated with beneficial outcomes in strength, suggesting that long-term dietary habits are more effective than short-term supplements.

Topics: Anterior Cruciate Ligament; Ascorbic Acid; Biopsy; Body Size; Dietary Supplements; Humans; Lower Extremity; Male; Muscle Strength; Muscular Atrophy; Orthopedic Procedures; Postoperative Complications; Recovery of Function; Tocopherols

In patients with chronic kidney disease, skeletal muscle dysfunction is associated with mortality. Uremic sarcopenia is caused by ageing, malnutrition, and chronic inflammation, but the molecular mechanism and potential therapeutics have not been fully elucidated yet. We hypothesize that accumulated uremic toxins might exert a direct deteriorative effect on skeletal muscle and explore the pharmacological treatment in experimental animal and culture cell models. The mice intraperitoneally injected with indoxyl sulfate (IS) after unilateral nephrectomy displayed an elevation of IS concentration in skeletal muscle and a reduction of instantaneous muscle strength, along with the predominant loss of fast-twitch myofibers and intramuscular reactive oxygen species (ROS) generation. The addition of IS in the culture media decreased the size of fully differentiated mouse C2C12 myotubes as well. ROS accumulation and mitochondrial dysfunction were also noted. Next, the effect of the β2-adrenergic receptor (β2-AR) agonist, clenbuterol, was evaluated as a potential treatment for uremic sarcopenia. In mice injected with IS, clenbuterol treatment increased the muscle mass and restored the tissue ROS level but failed to improve muscle weakness. In C2C12 myotubes stimulated with IS, although β2-AR activation also attenuated myotube size reduction and ROS accumulation as did other anti-oxidant reagents, it failed to augment the mitochondrial membrane potential. In conclusion, IS provokes muscular strength loss (uremic dynapenia), ROS generation, and mitochondrial impairment. Although the β2-AR agonist can increase the muscular mass with ROS reduction, development of therapeutic interventions for restoring skeletal muscle function is still awaited.

Topics: Adrenergic beta-2 Receptor Agonists; Animals; Ascorbic Acid; Cell Size; Clenbuterol; Female; Indican; Membrane Potential, Mitochondrial; Mice; Mice, Inbred C57BL; Mitochondria; Muscle Fibers, Skeletal; Muscle Proteins; Muscle Strength; Muscle, Skeletal; Muscular Atrophy; Oxidative Stress; Reactive Oxygen Species; Receptors, Adrenergic, beta-2; Sarcopenia; SKP Cullin F-Box Protein Ligases

L-Ascorbic acid (AsA) is a water-soluble antioxidant. We examined the effect of AsA deficiency on skeletal muscle using senescence marker protein-30 (SMP30)-knockout (KO) mice that are defective in AsA biosynthesis, which makes this mouse model similar to humans, to clarify the function of AsA in skeletal muscle. Eight-week-old female SMP30-KO mice were divided into the following two groups: an AsA-sufficient group [AsA(+)] that was administered 1.5 g/L AsA and an AsA-deficient group [AsA(-)] that was administered tap (AsA-free) water. At 4 weeks, the AsA content in the gastrocnemius muscle of AsA(-) mice was 0.7% compared to that in the gastrocnemius muscle of AsA(+) mice. Significantly lower weights of all muscles were observed in AsA(-) mice than those in AsA(+) mice at 12 and 16 weeks. The cross-sectional area of the soleus was significantly smaller in AsA(-) mice at 16 weeks than that in AsA(+) mice. The physical performance of AsA(-) mice was significantly less than that of AsA(+) mice at 12 weeks. Following AsA deficiency for 12 weeks, the expression of ubiquitin ligases, such as atrogin1/muscle atrophy F-box (MAFbx) and muscle RING-finger protein 1 (MuRF1), was upregulated. Furthermore, all detected effects of AsA deficiency on muscles of the AsA(-) group at 12 weeks were restored following AsA supplementation for 12 weeks. Thus, longer-term AsA deficiency is associated with muscle wasting, that this can be reversed by restoring AsA levels.

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Female; Mice; Mice, Knockout; Muscle Proteins; Muscle, Skeletal; Muscular Atrophy; Ubiquitin; Ubiquitin-Protein Ligases; Up-Regulation

Current nutrition and exercise focus during rehabilitation periods has been on reducing muscle atrophy associated with immobilisation. This case report outlines a best practice anterior cruciate ligament (ACL) rehabilitation programme undertaken by two professional rugby athletes, with the addition of an evidence-based supplementation (gelatine and vitamin C) and exercise protocol focused on collagenous tissue. Both players ruptured their left ACL and were repaired with a traditional hamstring graft. Players undertook a structured rehabilitation programme for 34 weeks before being clinically assessed ready to play. Players saw minimal changes in body composition in the early rehabilitation period (P1 - 0.8 kg; P2 - 0.4 kg). Leg lean mass reduced in both legs of Player 1 (Injured - 0.8 kg, Non-injured - 0.6 kg) at 17 weeks, with Player 2 only experiencing a loss of 0.3 kg of lean tissue in the injured leg. Both players returned to baseline body compositions after 24 weeks. Leg strength returned to a maximum at 24 and 15 weeks, respectively, with knee function returning to baseline by 30 weeks. This case report provides evidence that nutrition and rehabilitation programmes targeted at minimising the effects of disuse in both muscle and connective tissue may assist return to play after ACL injury.

Topics: Adult; Anterior Cruciate Ligament Injuries; Anterior Cruciate Ligament Reconstruction; Ascorbic Acid; Body Composition; Diet; Dietary Supplements; Exercise Therapy; Football; Gelatin; Hamstring Muscles; Humans; Male; Muscle Strength; Muscular Atrophy; Return to Sport; Vitamins

A rat model of multifidus muscles injury and atrophy after posterior lumbar spine surgery.. We determined the effect of ascorbic acid (AA) on the postoperative multifidus muscles in rat model.. Previous studies show oxidative stress and inflammation are two main molecular mechanisms in multifidus muscle injury and atrophy after posterior lumbar surgery. AA may have a protective effect in postoperative multifidus muscles.. Rats were divided into sham surgery, control surgery, and surgery plus AA groups. Multifidus muscles of the control and AA groups were excised from the osseous structures. The muscles were retracted continuously for 2 hours. In the sham and AA groups, AA was administered via oral gavage daily in the first week. In each group, the oxidative stress was evaluated by measuring malondialdehyde (MDA) and Total superoxide dismutase (T-SOD). The inflammation, fat degeneration, or fibrosis of multifidus muscle were evaluated by quantitative real-time polymerase chain reaction (q-PCR), histology, or immunohistochemical analysis.. T-SOD activity was significantly lower in the control group than that in the AA group in the first week. MDA levels were significantly higher in the AA group. Interleukin-6 and tumor necrosis factor-α in multifidus muscles also showed significant differences when treated with AA. The inflammation score on histology was significantly lower in the AA group postoperatively in the first week. In the long run, marker genes for fibrosis and fat degeneration, and fibrosis and fat degeneration scores, were significantly lower in the AA than the control group on days 14 and 28 postoperatively.. In conclusion, AA attenuated the oxidative stress and inflammation response in the postoperative multifidus muscles, and remarkable differences were observed from the histological assessment and related marker genes expression. Our results provided important insight into the anti-inflammatory and anti-oxidative effects of AA in the postoperative multifidus muscles.. N/A.

Topics: Adipose Tissue; Animals; Antioxidants; Ascorbic Acid; Fibrosis; Inflammation; Interleukin-6; Lumbar Vertebrae; Male; Malondialdehyde; Muscular Atrophy; Neurosurgical Procedures; Orthopedic Procedures; Oxidative Stress; Paraspinal Muscles; Rats; Superoxide Dismutase; Tumor Necrosis Factor-alpha

The proteolytic autophagy pathway is enhanced in the lower limb muscles of patients with chronic obstructive pulmonary disease (COPD). Reactive oxygen species (ROS) have been shown to regulate autophagy in the skeletal muscles, but the role of oxidative stress in the muscle autophagy of patients with COPD is unknown. We used cultured myoblasts and myotubes from the quadriceps of eight healthy subjects and twelve patients with COPD (FEV1% predicted: 102.0% and 32.0%, respectively; p < 0.0001). We compared the autophagosome formation, the expression of autophagy markers, and the autophagic flux in healthy subjects and the patients with COPD, and we evaluated the effects of the 3-methyladenine (3-MA) autophagy inhibitor on the atrophy of COPD myotubes. Autophagy was also assessed in COPD myotubes treated with an antioxidant molecule, ascorbic acid. Autophagosome formation was increased in COPD myoblasts and myotubes (p = 0.011; p < 0.001), and the LC3 2/LC3 1 ratio (p = 0.002), SQSTM1 mRNA and protein expression (p = 0.023; p = 0.007), BNIP3 expression (p = 0.031), and autophagic flux (p = 0.002) were higher in COPD myoblasts. Inhibition of autophagy with 3-MA increased the COPD myotube diameter (p < 0.001) to a level similar to the diameter of healthy subject myotubes. Treatment of COPD myotubes with ascorbic acid decreased ROS concentration (p < 0.001), ROS-induced protein carbonylation (p = 0.019), the LC3 2/LC3 1 ratio (p = 0.037), the expression of SQSTM1 (p < 0.001) and BNIP3 (p < 0.001), and increased the COPD myotube diameter (p < 0.001). Thus, autophagy signaling is enhanced in cultured COPD muscle cells. Furthermore, the oxidative stress level contributes to the regulation of autophagy, which is involved in the atrophy of COPD myotubes in vitro.

Topics: Adenine; Aged; Ascorbic Acid; Autophagy; Biomarkers; Cells, Cultured; Female; Humans; Male; Microtubule-Associated Proteins; Middle Aged; Muscle Cells; Muscle Fibers, Skeletal; Muscular Atrophy; Myoblasts; Oxidative Stress; Phagosomes; Pulmonary Disease, Chronic Obstructive

Oxidative stress is thought to be one of the most important mechanisms implicated in the muscle wasting of chronic obstructive pulmonary disease (COPD) patients, but its role has never been demonstrated. We therefore assessed the effects of both pro-oxidant and antioxidant treatments on the oxidative stress levels and atrophic signaling pathway of cultured COPD myotubes. Treatment of cultured COPD myotubes with the pro-oxidant molecule H2O2 resulted in increased ROS production (P = 0.002) and protein carbonylation (P = 0.050), in association with a more pronounced atrophy of the myotubes, as reflected by a reduced diameter (P = 0.003), and the activated expression of atrophic markers MuRF1 and FoxO1 (P = 0.022 and P = 0.030, respectively). Conversely, the antioxidant molecule ascorbic acid induced a reduction in ROS production (P<0.001) and protein carbonylation (P = 0.019), and an increase in the myotube diameter (P<0.001) to a level similar to the diameter of healthy subject myotubes, in association with decreased expression levels of MuRF1, atrogin-1 and FoxO1 (P<0.001, P = 0.002 and P = 0.042, respectively). A significant negative correlation was observed between the variations in myotube diameter and the variations in the expression of MuRF1 after antioxidant treatment (P = 0.047). Moreover, ascorbic acid was able to prevent the H2O2-induced atrophy of COPD myotubes. Last, the proteasome inhibitor MG132 restored the basal atrophy level of the COPD myotubes and also suppressed the H2O2-induced myotube atrophy. These findings demonstrate for the first time the involvement of oxidative stress in the atrophy of COPD peripheral muscle cells in vitro, via the FoxO1/MuRF1/atrogin-1 signaling pathway of the ubiquitin/proteasome system.

Topics: Aged; Antioxidants; Ascorbic Acid; Female; Forkhead Box Protein O1; Humans; Hydrogen Peroxide; Leupeptins; Male; Middle Aged; Muscle Fibers, Skeletal; Muscle Proteins; Muscular Atrophy; Oxidative Stress; Pulmonary Disease, Chronic Obstructive; Signal Transduction; SKP Cullin F-Box Protein Ligases; Tripartite Motif Proteins; Ubiquitin-Protein Ligases

Proximal spinal muscular atrophy (SMA), a neurodegenerative disorder that causes infant mortality, has no effective treatment. Sodium vanadate has shown potential for the treatment of SMA; however, vanadate-induced toxicity in vivo remains an obstacle for its clinical application. We evaluated the therapeutic potential of sodium vanadate combined with a vanadium detoxification agent, L-ascorbic acid, in a SMA mouse model.. Sodium vanadate (200 μM), L-ascorbic acid (400 μM), or sodium vanadate combined with L-ascorbic acid (combined treatment) were applied to motor neuron-like NSC34 cells and fibroblasts derived from a healthy donor and a type II SMA patient to evaluate the cellular viability and the efficacy of each treatment in vitro. For the in vivo studies, sodium vanadate (20 mg/kg once daily) and L-ascorbic acid (40 mg/kg once daily) alone or in combination were orally administered daily on postnatal days 1 to 30. Motor performance, pathological studies, and the effects of each treatment (vehicle, L-ascorbic acid, sodium vanadate, and combined treatment) were assessed and compared on postnatal days (PNDs) 30 and 90. The Kaplan-Meier method was used to evaluate the survival rate, with P < 0.05 indicating significance. For other studies, one-way analysis of variance (ANOVA) and Student's t test for paired variables were used to measure significant differences (P < 0.05) between values.. Combined treatment protected cells against vanadate-induced cell death with decreasing B cell lymphoma 2-associated X protein (Bax) levels. A month of combined treatment in mice with late-onset SMA beginning on postnatal day 1 delayed disease progression, improved motor performance in adulthood, enhanced survival motor neuron (SMN) levels and motor neuron numbers, reduced muscle atrophy, and decreased Bax levels in the spinal cord. Most importantly, combined treatment preserved hepatic and renal function and substantially decreased vanadium accumulation in these organs.. Combined treatment beginning at birth and continuing for 1 month conferred protection against neuromuscular damage in mice with milder types of SMA. Further, these mice exhibited enhanced motor performance in adulthood. Therefore, combined treatment could present a feasible treatment option for patients with late-onset SMA.

Topics: Adult; Animals; Ascorbic Acid; Cells, Cultured; Disease Progression; Drug Therapy, Combination; Feasibility Studies; Female; Humans; Mice; Mice, Knockout; Mice, Transgenic; Motor Skills; Muscle Weakness; Muscular Atrophy; Muscular Atrophy, Spinal; Vanadates

We determined the respiration, respiratory control, and Pi:O ratios with different substrates in mitochondria isolated from five cases of human neuromuscular disorders (two cases of central core disease, two cases of neuropathy of Dejerine-Sottas, and one case of Kugelberg-Welander's disease) and compared them with normal human muscle. In all the myopathies studied, a severe derangement of the respiratory control with variable derangement of oxidative phosphorylation was found. This supports the idea that a group of neuromyopathies shares the same biochemical lesion as the so-called mitochondrial myopathies, forming with them a group of myopathies which may be related through a similar biochemical lesion of varying degree. Alternatively, disturbance of mitochondrial functions in a number of myopathies could be considered as a non-specific finding.

Topics: Adenosine Diphosphate; Adolescent; Adult; Ascorbic Acid; Child; Female; Glutamates; Humans; Hypertrophy; Infant; Malates; Male; Middle Aged; Mitochondria, Muscle; Motor Neurons; Muscular Atrophy; Muscular Diseases; Myotonic Dystrophy; Neuromuscular Diseases; Oxidative Phosphorylation; Oxidative Phosphorylation Coupling Factors; Oxygen Consumption; Phosphates; Spinal Cord Diseases; Succinates

Topics: Adenine Nucleotides; Adenosine Triphosphatases; Aniline Compounds; Animals; Ascorbic Acid; Biological Transport; Body Weight; Calcium; Endoplasmic Reticulum; Female; Malates; Mitochondria, Muscle; Muscles; Muscular Atrophy; Oligomycins; Organ Size; Oxidative Phosphorylation; Oxygen Consumption; Polarography; Pyruvates; Rats; Rotenone; Succinates; Time Factors; Triamcinolone; Triamcinolone Acetonide; Uncoupling Agents

Topics: Adrenal Glands; Animals; Anura; Ascorbic Acid; Hindlimb; Keto Acids; Kidney; Muscle Denervation; Muscles; Muscular Atrophy

Topics: Animals; Ascorbic Acid; Biological Transport, Active; Glycogen; In Vitro Techniques; Muscle Denervation; Muscles; Muscular Atrophy; Rats; Subcellular Fractions