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Mammalian Skeletal Muscle (mammalian + skeletal_muscle)
Selected AbstractsDifferent adaptations of alpha-actinin isoforms to exercise training in rat skeletal musclesACTA PHYSIOLOGICA, Issue 3 2009Y. Ogura Abstract Aim:, Alpha (,)-actinins are located in the skeletal muscle Z-line and form actin,actin cross-links. Mammalian skeletal muscle has two isoforms: ,-actinin-2 and ,-actinin-3. However, the response of ,-actinin to exercise training is little understood. Therefore, the current study examined the effects of exercise training on the expression level of two ,-actinin isoforms in skeletal muscles. Methods:, Twelve male Wistar rats were assigned randomly to a control (C; n = 6) or exercise training (T; n = 6) group. After T animals were trained on an animal treadmill for 9 weeks, ,-actinin-2 and ,-actinin-3 levels in the plantaris, white and red gastrocnemius muscles were analysed. In addition, changes in the myosin heavy chain (MyHC) composition were assessed, and muscle bioenergetic enzyme activities were measured. Results:, Results show that exercise training increased ,-actinin-2 expression levels in all muscles (P < 0.05). However, no significant difference was found in ,-actinin-3 expression levels between C and T animals. Subsequent MyHC analyses of all muscle showed an MyHC shift with direction from IIb to IIa. Furthermore, enzymatic analysis revealed that exercise training improved enzyme activities related to aerobic metabolism. Conclusion:, The results of this study demonstrate that exercise training alters the expression level of ,-actinin at the isoform level. Moreover, the increase in expression levels of ,-actinin-2 is apparently related to alteration of skeletal muscle: its aerobic capacity is improved. [source] Neurovascular Alignment in Adult Mouse Skeletal MusclesMICROCIRCULATION, Issue 2 2005SHAWN E. BEARDEN ABSTRACT Objective: Muscle blood flow increases with motor unit recruitment. The physical relationships between somatic motor nerves, which control muscle fiber contraction, and arterioles, which control microvascular perfusion, are unexplored. The authors tested the hypothesis that motor axons align with arterioles in adult skeletal muscle. Methods: Transgenic mice (C57BL/6 background, n = 5; 10 months of age) expressing yellow fluorescent protein in all motor nerves underwent vascular casting (Microfil). Excised epitrochlearis, gracilis, gluteus maximus, and spinotrapezius muscles were imaged at 380× and 760× and a computer-integrated tracing system (Neurolucida) was used to acquire 3-dimensional digital renderings of entire arteriolar and neural networks within each muscle. Results: Arteriolar networks were typically ,3-fold longer than neural networks. Nerves coursed with arterioles until terminating at motor endplates. Across muscles, proximity analyses revealed that , 75% of total nerve length (9.8,48.8 mm) lay within 200 ,m of the nearest arteriole (diameters of 15,60 , m). Conclusions: Somatic motor nerves and arterioles align closely within adult mammalian skeletal muscle. Understanding the signals governing neurovascular alignment may hold important clues for the advancement of tissue engineering and regeneration. [source] Extracellular ATP inhibits chloride channels in mature mammalian skeletal muscle by activating P2Y1 receptorsTHE JOURNAL OF PHYSIOLOGY, Issue 23 2009Andrew A. VossArticle first published online: 30 NOV 200 ATP is released from skeletal muscle during exercise, a discovery dating back to 1969. Surprisingly, few studies have examined the effects of extracellular ATP on mature mammalian skeletal muscle. This electrophysiological study examined the effects of extracellular ATP on fully innervated rat levator auris longus using two intracellular microelectrodes. The effects of ATP were determined by measuring the relative changes of miniature endplate potentials (mEPPs) and voltage responses to step current pulses in individual muscle fibres. Exposure to ATP (20 ,m) prolonged the mEPP falling phase by 31 ± 7.5% (values ±s.d., n= 3 fibres). Concurrently, the input resistance increased by 31 ± 2.0% and the time course of the voltage responses increased by 59 ± 3.0%. Analogous effects were observed using 2 and 5 ,mATP, and on regions distal from the neuromuscular junction, indicating that physiologically relevant levels of ATP enhanced electrical signalling over the entire muscle fibre. The effects of extracellular ATP were blocked by 200 ,manthracene-9-carboxylic acid, a chloride channel inhibitor, and reduced concentrations of extracellular chloride, indicating that ATP inhibited chloride channels. A high affinity agonist for P2Y receptors, 2-methylthioadenosine-5,- O -diphosphate (2MeSADP), induced similar effects to ATP with an EC50 of 160 ± 30 nm. The effects of 250 nm2MeSADP were blocked by 500 nmMRS2179, a specific P2Y1 receptor inhibitor, suggesting that ATP acts on P2Y1 receptors to inhibit chloride channels. The inhibition of chloride channels by extracellular ATP has implications for muscle excitability and fatigue, and the pathophysiology of myotonias. [source] Rapid Ca2+ flux through the transverse tubular membrane, activated by individual action potentials in mammalian skeletal muscleTHE JOURNAL OF PHYSIOLOGY, Issue 10 2009Bradley S. Launikonis Periods of low frequency stimulation are known to increase the net Ca2+ uptake in skeletal muscle but the mechanism responsible for this Ca2+ entry is not known. In this study a novel high-resolution fluorescence microscopy approach allowed the detection of an action potential-induced Ca2+ flux across the tubular (t-) system of rat extensor digitorum longus muscle fibres that appears to be responsible for the net uptake of Ca2+ in working muscle. Action potentials were triggered in the t-system of mechanically skinned fibres from rat by brief field stimulation and t-system [Ca2+] ([Ca2+]t-sys) and cytoplasmic [Ca2+] ([Ca2+]cyto) were simultaneously resolved on a confocal microscope. When initial [Ca2+]t-sys was , 0.2 mm a Ca2+ flux from t-system to the cytoplasm was observed following a single action potential. The action potential-induced Ca2+ flux and associated t-system Ca2+ permeability decayed exponentially and displayed inactivation characteristics such that further Ca2+ entry across the t-system could not be observed after 2,3 action potentials at 10 Hz stimulation rate. When [Ca2+]t-sys was closer to 0.1 mm, a transient rise in [Ca2+]t-sys was observed almost concurrently with the increase in [Ca2+]cyto following the action potential. The change in direction of Ca2+ flux was consistent with changes in the direction of the driving force for Ca2+. This is the first demonstration of a rapid t-system Ca2+ flux associated with a single action potential in mammalian skeletal muscle. The properties of this channel are inconsistent with a flux through the L-type Ca2+ channel suggesting that an as yet unidentified t-system protein is conducting this current. This action potential-activated Ca2+ flux provides an explanation for the previously described Ca2+ entry and accumulation observed with prolonged, intermittent muscle activity. [source] Reversible changes in Ca2+ -activation properties of rat skeletal muscle exposed to elevated physiological temperaturesTHE JOURNAL OF PHYSIOLOGY, Issue 3 2002Chris van der Poel Exposure of relaxed rat extensor digitorum longus (EDL; predominantly fast-twitch) muscle to temperatures in the upper physiological range for mammalian skeletal muscle (43-46 °C) led to reversible alterations of the contractile activation properties. These properties were studied using the mechanically skinned fibre preparation activated in Ca2+ -buffered solutions. The maximum Ca2+ -activated force (maximum force per cross-sectional area) and the steepness of force-pCa (-log10[Ca2+]) curves as measured by the Hill coefficient (nH) reversibly decreased by factors of 8 and 2.5, respectively, when the EDL muscle was treated at 43 °C for 30 min and 5 and 2.8, respectively, with treatment at 46 °C for 5 min. Treatment at 47 °C for 5 min produced an even more marked depression in maximum specific force, which fully recovered after treatment, and in the Hill coefficient, which did not recover after treatment. After all temperature treatments there was no change in the level of [Ca2+] at which 50 % maximum force was generated. The temperature-induced depression in force production and steepness of the force-pCa curves were shown to be associated with superoxide (O2,) production in muscle (apparent rate of O2, production at room temperature, 0.055 ± 0.008 nmol min,1 (g wet weight),1; and following treatment to 46 °C for 5 min, 1.8 ± 0.2 nmol min,1 (g wet weight),1) because 20 mm Tiron, a membrane-permeant O2, scavenger, was able to markedly suppress the net rate of O2, production and prevent any temperature-induced depression of contractile parameters. The temperature-induced depression in force production of the contractile apparatus could be reversed either by allowing the intact muscle to recover for 3-4 h at room temperature or by treatment of the skinned fibre preparation with dithiothreitol (a potent reducing agent) in the relaxing solution. These results demonstrate that mammalian skeletal muscle has the ability to uncouple force production reversibly from the activator Ca2+ as the temperature increases in the upper physiological range through an increase in O2, production. [source] | ||||||||||