chondroitin-sulfates and Muscular-Diseases

Delayed onset of muscle soreness (DOMS) often results from unaccustomed exercise or exercise that involves heavy eccentric loading of skeletal muscle. Chondroitin sulfate (CS) has been reported to possess anti-inflammatory and analgesic properties and has been used widely in the treatment of osteoarthritis. Based on these findings, the investigators sought to determine whether CS supplementation might reduce DOMS symptoms associated with eccentric arm exercise.. Sixteen non-resistance-trained males participated in a double-blind protocol. Subjects consumed 3,600 mg x day-1 of encapsulated CS or placebo for 14 days preceding the exercise protocol and during 48 hours of follow-up measurements. Subjects performed a maximum of 50 eccentric contractions of the elbow flexors against a resistance that was 120% of the concentric one-repetition maximum.. Significant time effects were present for soreness, relaxed elbow extension (joint angle), and creatine kinase; all measures were significantly altered 48 hours after the exercise session. No effects were present for complement system fragment C3a and prostaglandin E2. No significant treatment or interaction effects were detected for any of the variables.. CS supplementation was not found to be effective in the prevention of DOMS, nor did it influence biochemical indices of inflammation and muscle damage following heavy eccentric loading of the arm flexors.

Topics: Adult; Arm; Chondroitin Sulfates; Creatine Kinase; Dietary Supplements; Double-Blind Method; Exercise; Humans; Inflammation; Male; Muscle Contraction; Muscle Fatigue; Muscle, Skeletal; Muscular Diseases; Premedication; Range of Motion, Articular; Time Factors; Treatment Outcome

Topics: Adult; Anti-Inflammatory Agents; Atrophy; Biopsy; Chondroitin Sulfates; Diagnosis, Differential; Female; Glucocorticoids; Humans; Immunohistochemistry; Japan; Muscular Diseases; Ocular Motility Disorders; Oculomotor Muscles; Pharyngeal Muscles; Prednisone; Respiration Disorders; Treatment Outcome

A 71-year-old man developed severe limb, bulbar, and respiratory weakness over 18 months. A muscle biopsy showed only a moderate degree of type 2 atrophy, but immunocytochemistry showed absence of chondroitin sulfate C glycosaminoglycan in the endomysium. Prednisone produced a marked increase in strength. Diffuse loss of endomysial chondroitin sulfate C was a feature of this treatable myopathy with severe weakness, but few pathologic changes.

Topics: Aged; Amyotrophic Lateral Sclerosis; Atrophy; Biopsy; Chondroitin Sulfates; Diagnosis, Differential; Hand Strength; Humans; Immunohistochemistry; Male; Muscle Fibers, Skeletal; Muscle, Skeletal; Muscular Diseases; Prednisone; Reference Values; Regeneration

The effects of heparin and other polyanions on the myotoxicity of Bothrops jararacussu venom and purified bothropstoxin (BthTX) were investigated. The release rate of creatine kinase (CK) from isolated extensor digitorum longus muscle and the plasma CK activity of mice were used to quantify the results. The myotoxic effects of B. jararacussu venom or BthTX were inhibited by preincubation of these agents with one of the following: a heterogeneous heparin preparation (designated 'heparin'), low mol. wt heparin (H-4500) or dextran sulfates (DS-8000 and DS-500,000). Non-sulfated dextran (D-40,000) and two chondroitin sulfates were ineffective. The antimyotoxic effects of the polyanions are ascribed to their forming inactive acid-base complexes with the basic myotoxins of Bothrops venoms. Gel-filtration experiments in Sephadex provided direct evidence for complex formation between heparin and BthTX. Intravenous (i.v.) administration of H-4500 or DS-8000 opposed the increase in plasma CK activity induced by a subsequent i.m. injection of venom or BthTX. In contrast, pretreatment with i.v. heparin or DS-500,000 enhanced the venom-induced increase in plasma CK activity. This effect was not observed (1) when the animals were treated with a polyvalent antivenom, which inhibits the coagulation and local stasis induced by Bothrops venoms, and (2) when BthTX, which has no thrombotic or hemorrhagic properties, was the myotoxic agent. The potentiation of the venom-induced increase in plasma CK activity by heparin and DS-500,000 is ascribed to improved washout of the CK released from damaged fibers, because of the anticoagulant properties of the drugs.

Topics: Animals; Chondroitin Sulfates; Chromatography, Gel; Creatine Kinase; Crotalid Venoms; Dextran Sulfate; Heparin; History, 20th Century; Mice; Molecular Weight; Muscles; Muscular Diseases