Force-velocity Relation and Isomyosins in Soleus Muscles From I Strains of Mice (c57 and Nmri)

We compared soleus muscles, from two strains of mice, NMRI and C57. Soleus muscles from NMRI mice produced slower twitches and lower maximum tetanic force (F(o)) but higher maximum tetanic stress (S(o)), (owing to their smaller weight). Their Hill's velocity constant (b) was lower, but their force constant (a/S(o)), their maximum velocity of unloaded shortening (V(u)) and their maximal mechanical power (P(max)) were similar. All soleus muscles contained two isomyosins (SM2 and IM) and the two myosin heavy chains (MHC1 and MHC2A) corresponding to type I fibres and type IIA fibres; however, soleus muscles from NMRI strain had higher proportions of isomyosin SM2 and of myosin heavy chain 2A. Regression equations were, computed between the mechanical variables and the myosin heavy chain content. Using a simple hypothesis, the results were used to estimate the mechanical properties of type I and type IIA fibres. We conclude that type IIA fibres from soleus muscle are mechanically more similar to slow-twitch type I fibres than to fast-twitch type II fibres. The results also suggest a hypothesis to account for the diversity of isomyosins, by a matching diversity of mechanical properties based on a separate physiological control of the three factors that control P(max)

Effect of nitric oxide on the maximal velocity of shortening of a mouse skeletal muscle.

Maximum velocity of shortening, Vo, was measured by the method of Edman [J Physiol (Lond) 291:143-159, 1979] on extensor digitorum longus muscles of a mouse in vitro at 20 degreesC. Blockers of nitric oxide synthase, 10 mM nitro-l-arginine or 1 mM 7-nitroindazole, reduced Vo by 18% and 22%, respectively. On removal of the inhibitor, Vo returned to the control value. It was found that 10 mM nitro-d-arginine, an enantiomer of nitro-l-arginine inactive against nitric oxide synthase, did not affect Vo. A donor of nitric oxide, 0.1 mM nitroprusside, increased Vo by 15%. It removed the inhibition caused by nitro-l-arginine. Another donor of nitric oxide, 1 microM (+/-)-S-nitroso-N-acetylpenicillamine (SNAP), increased Vo by 8%. An inhibitor of cGMP synthase, 0.01 mM Ly-83583, decreased Vo by 18%. An analogue of cGMP, 0.1 mM 8-bromo-cGMP, increased Vo by 17%. A general inhibitor of phosphodiesterases, 0.02 mM 3-isobutyl-1-methylxanthine (IBMX), increased Vo by 17%. An inhibitor specific of cGMP phosphodiesterase, 0.01 mM dipyridamole, increased Vo by 8%. The maximal isometric force (F0) was not modified by the drugs, except by 7-nitroindazole and Ly-83583, which depressed F0 by 12%. The cGMP level in tetanized muscles decreased by 12-27% in the presence of blockers of nitric oxide synthase. We conclude that the level of intracellular nitric oxide modulates Vo through the cGMP pathway

Parvalbumin contents, myosin heavy chain distribution and contractile properties of mouse skeletal muscles.

Parvalbumin contents, myosin heavy chain distribution and contractile properties of mouse skeletal muscles

Mechanical power and myosin composition of soleus and extensor digitorum longus muscles of ky mice

Muscles of ky/ky homozygote mice exhibit neonatal muscle fiber necrosis and regeneration with subsequent motor nerve sprouting and development of a prominent kyphoscoliosis from approximately 100 days onward. Soleus and extensor digitorum longus (EDL) muscles from ky mice weighted < 50% of control muscles from age-matched NMRI mice. Maximal tetanic force was more reduced in soleus than in EDL. In EDL, the velocity constant of the force-velocity relation, maximal velocity, twitch time-to-peak, and isomyosin content were normal at all ages. The early mechanical changes seen in ky soleus muscles (47 day) were not accompanied by significant alterations in isomyosin or myosin heavy- and light-chain composition, since ky and NMRI expressed slow-twitch native myosin 2 (SM2, type I fibers) and intermediate-twitch native myosin (IM, type IIa fibers). Adult ky soleus (172 day) showed wholesale loss of IM and sole expression of SM2. This is sufficient to account for the markedly slowing of the force-velocity relation and the twitches observed in adult ky soleus. We propose that since shifts in muscle type only occurred in soleus, this reflects the persistent requirement to withstand the force of gravity

Critical illness myopathy unrelated to corticosteroids or neuromuscular blocking agents.

Acute myopathy occurs in critically ill patients, receiving neuromuscular blocking agents or corticosteroids during intensive care hospitalisation. We report three patients with acute quadriplegic myopathy, two of whom were not exposed to corticosteroids or neuromuscular blocking agents. The first of these latter two patients had a history of generalised anoxia with coma related to surgery, complicated by multiple organ failure and sepsis. The second patient, suffering from acute leukaemia, developed sepsis and acute respiratory distress syndrome with the need for mechanical ventilation in the intensive care unit. Electrophysiological studies and muscle biopsy findings were consistent with the diagnosis of critical illness myopathy with loss of myosin filaments. Selective loss of myosin was confirmed by biochemical analysis of muscle. These findings demonstrate that acute myopathy with loss of myosin filaments may occur in patients with severe systemic illness without exposure to corticosteroids or neuromuscular blocking agents