Phosphorylation of the regulatory light chains of myosin affects Ca2+sensitivity of skeletal muscle contraction

2002 ◽  
Vol 92 (4) ◽  
pp. 1661-1670 ◽  
Author(s):  
Danuta Szczesna ◽  
Jiaju Zhao ◽  
Michelle Jones ◽  
Gang Zhi ◽  
James Stull ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Muscle Contraction ◽  
Muscle Fibers ◽  
Light Chains ◽  
Regulatory Light Chains ◽  
Force Development ◽  
Skeletal Muscle Contraction ◽  
State Force ◽  
Kinetics Of

The role of phosphorylation of the myosin regulatory light chains (RLC) is well established in smooth muscle contraction, but in striated (skeletal and cardiac) muscle its role is still controversial. We have studied the effects of RLC phosphorylation in reconstituted myosin and in skinned skeletal muscle fibers where Ca2+sensitivity and the kinetics of steady-state force development were measured. Skeletal muscle myosin reconstituted with phosphorylated RLC produced a much higher Ca2+sensitivity of thin filament-regulated ATPase activity than nonphosphorylated RLC (change in −log of the Ca2+concentration producing half-maximal activation = ∼0.25). The same was true for the Ca2+sensitivity of force in skinned skeletal muscle fibers, which increased on reconstitution of the fibers with the phosphorylated RLC. In addition, we have shown that the level of endogenous RLC phosphorylation is a crucial determinant of the Ca2+sensitivity of force development. Studies of the effects of RLC phosphorylation on the kinetics of force activation with the caged Ca2+, DM-nitrophen, showed a slight increase in the rates of force development with low statistical significance. However, an increase from 69 to 84% of the initial steady-state force was observed when nonphosphorylated RLC-reconstituted fibers were subsequently phosphorylated with exogenous myosin light chain kinase. In conclusion, our results suggest that, although Ca2+binding to the troponin-tropomyosin complex is the primary regulator of skeletal muscle contraction, RLC play an important modulatory role in this process.

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

2009 ◽  
Vol 297 (1) ◽  
pp. H433-H442 ◽  
Author(s):  
Ashok K. Dua ◽  
Nickesh Dua ◽  
Coral L. Murrant
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Muscle Fibers ◽  
Nitric Oxide Donor ◽  
Contraction Frequency ◽  
Skeletal Muscle Contraction ◽  
Train Duration ◽  
Arteriolar Vasodilation ◽  
40 Hz

To test the hypothesis that the vasodilator complement that produces arteriolar vasodilation during muscle contraction depends on both stimulus and contraction frequency, we stimulated four to five skeletal muscle fibers in the anesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibers. Diameter was measured before, during, and after 2 min of skeletal muscle contraction stimulated over a range of stimulus frequencies [4, 20, and 40 Hz; 15 contractions/min (cpm), 250 ms train duration] and a range of contraction frequencies (6, 15, and 60 cpm; 20 Hz stimulus frequency, 250 ms train duration). Muscle fibers were stimulated in the absence and presence of an inhibitor of adenosine receptors [10−6 M xanthine amine congener (XAC)], an ATP-dependent potassium (K+) channel inhibitor (10−5 M glibenclamide), an inhibitor of a source of K+ by inhibition of voltage-dependent K+ channels [3 × 10−4 M 3,4-diaminopyridine (DAP)], and an inhibitor of nitric oxide synthase [10−6 M NG-nitro-l-arginine methyl ester (l-NAME) + 10−7 S-nitroso- N-acetylpenicillamine (a nitric oxide donor)]. l-NAME inhibited the dilations at all stimulus frequencies and contraction frequencies except 60 cpm. XAC inhibited the dilations at all contraction frequencies and stimulus frequencies except 40 Hz. Glibenclamide inhibited all dilations at all stimulus and contraction frequencies, and DAP did not inhibit dilations at any stimulus frequencies while attenuating dilation at a contraction frequency of 60 cpm only. Our data show that the complement of dilators responsible for the vasodilations induced by skeletal muscle contraction differed depending on the stimulus and contraction frequency; therefore, both are important determinants of the dilators involved in the processes of arteriolar vasodilation associated with active hyperemia.

Fall in intracellular Po 2 at the onset of contractions in Xenopus single skeletal muscle fibers

2001 ◽  
Vol 90 (5) ◽  
pp. 1871-1876 ◽  
Author(s):  
Michael C. Hogan
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Ringer Solution ◽  
Work Period ◽  
Force Development ◽  
Delayed Onset ◽  
Maximal Force ◽  
Skeletal Muscle Fibers ◽  
Lumbrical Muscle ◽  
Kinetics Of

It remains uncertain whether the delayed onset of mitochondrial respiration on initiation of muscle contractions is related to O2 availability. The purpose of this research was to measure the kinetics of the fall in intracellular Po 2 at the onset of a contractile work period in rested and previously worked single skeletal muscle fibers. Intact single skeletal muscle fibers ( n = 11) from Xenopus laevis were dissected from the lumbrical muscle, injected with an O2-sensitive probe, mounted in a glass chamber, and perfused with Ringer solution (Po 2 = 32 ± 4 Torr and pH = 7.0) at 20°C. Intracellular Po 2 was measured in each fiber during a protocol consisting sequentially of 1-min rest; 3 min of tetanic contractions (1 contraction/2 s); 5-min rest; and, finally, a second 3-min contractile period identical to the first. Maximal force development and the fall in force (to 83 ± 2 vs. 86 ± 3% of maximal force development) in contractile periods 1 and 2, respectively, were not significantly different. The time delay (time before intracellular Po 2 began to decrease after the onset of contractions) was significantly greater ( P < 0.01) in the first contractile period (13 ± 3 s) compared with the second (5 ± 2 s), as was the time to reach 50% of the contractile steady-state intracellular Po 2(28 ± 5 vs. 18 ± 4 s, respectively). In Xenopus single skeletal muscle fibers, 1) the lengthy response time for the fall in intracellular Po 2 at the onset of contractions suggests that intracellular factors other than O2 availability determine the on-kinetics of oxidative phosphorylation and 2) a prior contractile period results in more rapid on-kinetics.

Diaphragmatic lymphatic vessel behavior during local skeletal muscle contraction

2015 ◽  
Vol 308 (3) ◽  
pp. H193-H205 ◽  
Author(s):  
Andrea Moriondo ◽  
Eleonora Solari ◽  
Cristiana Marcozzi ◽  
Daniela Negrini
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Lymphatic Vessel ◽  
Muscle Fibers ◽  
Video Recording ◽  
Three Dimensional ◽  
Longitudinal Axis ◽  
Vessel Diameter ◽  
Skeletal Muscle Contraction ◽  
Lymphatic Network

The mechanism through which the stresses developed in the diaphragmatic tissue during skeletal muscle contraction sustain local lymphatic function was studied in 10 deeply anesthetized, tracheotomized adult Wistar rats whose diaphragm was exposed after thoracotomy. To evaluate the direct effect of skeletal muscle contraction on the hydraulic intraluminal lymphatic pressures (Plymph) and lymphatic vessel geometry, the maximal contraction of diaphragmatic fibers adjacent to a lymphatic vessel was elicited by injection of 9.2 nl of 1 M KCl solution among diaphragmatic fibers while Plymph was recorded through micropuncture and vessel geometry via stereomicroscopy video recording. In lymphatics oriented perpendicularly to the longitudinal axis of muscle fibers and located at <300 μm from KCl injection, vessel diameter at maximal skeletal muscle contraction ( Dmc) decreased to 61.3 ± 1.4% of the precontraction value [resting diameter ( Drest)]; however, if injection was at >900 μm from the vessel, Dmc enlarged to 131.1 ± 2.3% of Drest. In vessels parallel to muscle fibers, Dmc increased to 122.8 ± 2.9% of Drest. During contraction, Plymph decreased as much as 22.5 ± 2.6 cmH2O in all submesothelial superficial vessels, whereas it increased by 10.7 ± 5.1 cmH2O in deeper vessels running perpendicular to contracting muscle fibers. Hence, the three-dimensional arrangement of the diaphragmatic lymphatic network seems to be finalized to efficiently exploit the stresses exerted by muscle fibers during the contracting inspiratory phase to promote lymph formation in superficial submesothelial lymphatics and its further propulsion in deeper intramuscular vessels.

Metabolic responses from rest to steady state determine contractile function in ischemic skeletal muscle

1997 ◽  
Vol 273 (2) ◽  
pp. E233-E238 ◽  
Author(s):  
J. A. Timmons ◽  
S. M. Poucher ◽  
D. Constantin-Teodosiu ◽  
I. A. Macdonald ◽  
P. L. Greenhaff
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Muscle Contraction ◽  
Metabolic Response ◽  
Contractile Function ◽  
Pyruvate Dehydrogenase Complex ◽  
Force Production ◽  
Critical Factor ◽  
Control Group ◽  
State Force

Skeletal muscle contraction during ischemia, such as that experienced by peripheral vascular disease patients, is characterized by rapid fatigue. Using a canine gracilis model, we tested the hypothesis that a critical factor determining force production during ischemia is the metabolic response during the transition from rest to steady state. Dichloroacetate (DCA) administration before gracilis muscle contraction increased pyruvate dehydrogenase complex activation and resulted in acetylation of 80% of the free carnitine pool to acetylcarnitine. After 1 min of contraction, phosphocreatine (PCr) degradation in the DCA group was approximately 50% lower than in the control group (P < 0.05) during conditions of identical force production. After 6 min of contraction, steady-state force production was approximately 30% higher in the DCA group (P < 0.05), and muscle ATP, PCr, and glycogen degradation and lactate accumulation were lower (P < 0.05 in all cases). It appears, therefore, that an important determinant of contractile function during ischemia is the mechanisms by which ATP regeneration occurs during the period of rest to steady-state transition.

scholarly journals Lymph flow pattern in pleural diaphragmatic lymphatics during intrinsic and extrinsic isotonic contraction

2016 ◽  
Vol 310 (1) ◽  
pp. H60-H70 ◽  
Author(s):  
Andrea Moriondo ◽  
Eleonora Solari ◽  
Cristiana Marcozzi ◽  
Daniela Negrini
Keyword(s):  
Skeletal Muscle ◽  
Shear Stress ◽  
Muscle Contraction ◽  
Ex Vivo ◽  
Muscle Fibers ◽  
Lymphatic Vessels ◽  
Smooth Muscle Contraction ◽  
Skeletal Muscle Fibers ◽  
Skeletal Muscle Contraction

Peripheral rat diaphragmatic lymphatic vessels, endowed with intrinsic spontaneous contractility, were in vivo filled with fluorescent dextrans and microspheres and subsequently studied ex vivo in excised diaphragmatic samples. Changes in diameter and lymph velocity were detected, in a vessel segment, during spontaneous lymphatic smooth muscle contraction and upon activation, through electrical whole-field stimulation, of diaphragmatic skeletal muscle fibers. During intrinsic contraction lymph flowed both forward and backward, with a net forward propulsion of 14.1 ± 2.9 μm at an average net forward speed of 18.0 ± 3.6 μm/s. Each skeletal muscle contraction sustained a net forward-lymph displacement of 441.9 ± 159.2 μm at an average velocity of 339.9 ± 122.7 μm/s, values significantly higher than those documented during spontaneous contraction. The flow velocity profile was parabolic during both spontaneous and skeletal muscle contraction, and the shear stress calculated at the vessel wall at the highest instantaneous velocity never exceeded 0.25 dyne/cm2. Therefore, we propose that the synchronous contraction of diaphragmatic skeletal muscle fibers recruited at every inspiratory act dramatically enhances diaphragmatic lymph propulsion, whereas the spontaneous lymphatic contractility might, at least in the diaphragm, be essential in organizing the pattern of flow redistribution within the diaphragmatic lymphatic circuit. Moreover, the very low shear stress values observed in diaphragmatic lymphatics suggest that, in contrast with other contractile lymphatic networks, a likely interplay between intrinsic and extrinsic mechanisms be based on a mechanical and/or electrical connection rather than on nitric oxide release.

Local and remote arteriolar dilations initiated by skeletal muscle contraction

2000 ◽  
Vol 279 (5) ◽  
pp. H2285-H2294 ◽  
Author(s):  
Coral L. Murrant ◽  
Ingrid H. Sarelius
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Muscle Fibers ◽  
Muscle Metabolism ◽  
Cremaster Muscle ◽  
Remote Site ◽  
Upstream Site ◽  
Skeletal Muscle Contraction ◽  
Perivascular Nerves ◽  
The Relationship

To investigate the relationship between skeletal muscle metabolism and arteriolar dilations in the region local to contracting muscle fibers as well as dilations at remote arteriolar regions upstream, we used a microelectrode on cremaster muscle of anesthetized hamsters to stimulate four to five muscle fibers lying approximately perpendicular to and overlapping a transverse arteriole. Before, during, and after muscle contraction, we measured the diameter of the arteriole at the site of muscle fiber overlap (local) and at a remote site ∼1,000 μm upstream. Two minutes of 2-, 4-, or 8-Hz stimulation (5–10 V, 0.4-ms duration) produced a significant dilation locally (8.2 ± 2.0-, 22.5 ± 2.4-, and 30.9 ± 2.1-μm increase, respectively) and at the remote site (4.2 ± 0.8, 11.0 ± 1.1, and 18.9 ± 2.7 μm, respectively). Muscle contraction at 4 Hz initiated a remote dilation that was unaffected by 15-min micropipette application of either 2 μM tetrodotoxin, 0.07% halothane, or 40 μM 18-β-glycyrrhetinic acid between the local and upstream site. Therefore, at the arteriolar level, muscle contraction initiates a robust remote dilation that does not appear to be transmitted via perivascular nerves or gap junctions.

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