Mechanical response of skeletal muscle following oral administration of pesticides

1971 ◽  
Vol 20 (1) ◽  
pp. 66-72 ◽  
Author(s):  
J.A. Santolucito ◽  
E. Whitcomb
Keyword(s):  
Skeletal Muscle ◽  
Oral Administration ◽  
Mechanical Response

Nitrendipine blocks high potassium contractures but not twitches in rat skeletal muscle

1988 ◽  
Vol 66 (9) ◽  
pp. 1210-1213 ◽  
Author(s):  
G. B. Frank ◽  
L. Konya ◽  
T. Subrahmanyam Sudha
Keyword(s):  
Skeletal Muscle ◽  
Calcium Ions ◽  
Calcium Uptake ◽  
Channel Blocker ◽  
Mechanical Response ◽  
Extracellular Calcium ◽  
The Other ◽  
Rat Skeletal Muscle ◽  
Potassium Depolarization ◽  
High Potassium

The effects of the organic calcium channel blocker nitrendipine was tested on electrically evoked twitches and on potassium depolarization-induced contractures of rat lumbricalis muscles. Nitrendipine (10−7 to 5 × 10−5 M) blocked only the potassium contractures. It was concluded that blocking calcium uptake through the slow voltage-senstitive calcium channels during potassium depolarization blocks the mechanical response of the muscle. Thus extracellular calcium ions are required for the excitation–contraction (E–C) coupling during depolarization contractures. On the other hand, electrically evoked twitches were not affected by nitrendipine; therefore, extracellular calcium ions entering via the slow voltage-sensitive channels are not required for E–C coupling during the twitch.

The Refractory Period and the Duration of the Plateau of the Active State in Frog Skeletal Muscle

1973 ◽  
Vol 51 (12) ◽  
pp. 966-975
Author(s):  
N. F. Clinch ◽  
V. Tennant
Keyword(s):  
Skeletal Muscle ◽  
Electrical Properties ◽  
Refractory Period ◽  
Mechanical Response ◽  
State Theory ◽  
Active State ◽  
Isometric Contractions ◽  
Frog Skeletal Muscle ◽  
Plateau Region ◽  
Measurement Artifact

Isometric contractions of frog sartorii in response to paired stimuli (I ms apart) were compared with isometric twitches following single shocks in order to find the time of the first detectable mechanical response to the second shock (ts). For I > 25 ms at 0°, ts = 0.99 I + 13.3 ms; while for I < 25 ms, ts was found to be independent of I. Electrical recording from the muscle surface showed that for I < 25 ms, the second action potential fell within the relative refractory period of the first. The plateau region of the ts–I plot is consistent with the active state theory, but can also be interpreted as (a) a measurement artifact, or (b) revealing electrical properties of the membrane rather than a property of the contractile mechanism itself.

Evidence for an essential role for calcium in excitation-contraction coupling in skeletal muscle

1964 ◽  
Vol 160 (981) ◽  
pp. 504-512 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibre ◽  
Calcium Ions ◽  
Essential Role ◽  
Mechanical Response ◽  
Frog Heart ◽  
Muscle Fibres ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Spontaneous Action

The events and processes that link the electrical events which occur at the surface of a muscle fibre with the contractile process that takes place within the fibre, have been a continuing source of interest. Recently attention has been concentrated on the role played by calcium ions in linking these two events. As often happens in physiological investigations, the idea that calcium ions play an essential role in excitation-contraction coupling is not new. As long ago as 1883 Ringer demonstrated that the frog heart fails to contract and remains relaxed when calcium ions are absent from its perfusion fluid. Later it was shown that under this condition the rhythmic spontaneous action potentials of this preparation are still present in an only slightly modified form (Mines 1913). It was known at that time that the depolarization of the muscle fibre membrane is the electrical event responsible for initiating the mechanical response (Biedermann 1896) and although this point has been disputed from time to time, the evidence presently available makes it obvious that this is the case. One explanation of these observations is that the action potential or depolarization permits or promotes the movement of calcium ions from the surface to the interior of the muscle fibre and that these ions then initiate the mechanical response. A working hypothesis of this type was proposed by Sandow (1952). However, until fairly recently the only direct evidence supporting such an hypothesis was the demonstration by Heilbrunn & Wiercinski (1947) that calcium was the only physiologically occurring cation which would cause shortening when injected into bits of skeletal muscle fibres in low concentrations. This effect was later confirmed under more physiological conditions by Niedergerke (1955). Although there is considerable evidence of recent origin showing that calcium ions play an essential role in coupling in smooth and cardiac muscles, for the sake of brevity attention will be concentrated on skeletal muscle in the present discussion.

Chemical Physiology of Muscle Contraction

2017 ◽  
Vol 68 (5) ◽  
pp. 1095-1097
Author(s):  
Liliana Lacramioara Pavel ◽  
Carmen Tiutiuca ◽  
Sorin Ioan Berbece ◽  
Alina Plesea Condratovici ◽  
Nicoleta Ioanid
Keyword(s):  
Skeletal Muscle ◽  
Lactic Acid ◽  
Mechanical Response ◽  
Recovery Phase ◽  
Nitrogen Atmosphere ◽  
Lactic Acid Concentration ◽  
Skeletal Muscle Fatigue ◽  
Additional Amount ◽  
Oxidative Processes ◽  
Contraction And Relaxation

The mechanical response of an isolated muscle to an excitant is not accompanied by any oxygen consumption increase; the additional amount of oxygen is not consumed as long as contraction and relaxation have not occurred. Thus, there are two contraction phases, an anaerobic (anoxidative) phase and an aerobic (oxidative) or recovery phase, during which the muscle resumes its previous stage. When the muscle is repeatedly excited in a nitrogen atmosphere, it strongly contracts at the beginning, but it gets quickly exhausted, since between contractions it cannot get the necessary oxygen for its recovery. Lactic acid gathers in the muscle, which becomes stiff. If it gets oxygen at the beginning of its fatigue, the lactic acid disappears and the muscle recovers its initial contraction strength. The lactic acid concentration at which complete skeletal muscle fatigue sets in (i.e. the lactic acid peak) ranges between 0.3 and 06%. In order to release the energy it needs for its contraction, the muscle does not depend on immediate oxidative processes. It continues to contract for a certain amount of time even when it is completely deprived of oxygen.

SUN-PP074: Skeletal Muscle Atrophy is Induced at Early Phase in Endotoxemic Rats and Oral Administration of Tributyrin Attenuates the Atrophy

2015 ◽  
Vol 34 ◽  
pp. S50-S51
Author(s):  
Y. Nishiyama ◽  
M. Miyoshi ◽  
M. Kai ◽  
M. Aoyama-Ishikawa ◽  
N. Maeshige ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oral Administration ◽  
Muscle Atrophy ◽  
Early Phase ◽  
Skeletal Muscle Atrophy

scholarly journals Lactate Stimulates a Potential for Hypertrophy and Regeneration of Mouse Skeletal Muscle

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 869 ◽  
Author(s):  
Ohno ◽  
Ando ◽  
Ito ◽  
Suda ◽  
Matsui ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oral Administration ◽  
Muscle Mass ◽  
Recovery Process ◽  
C2c12 Cells ◽  
Muscle Weight ◽  
Cross Sectional ◽  
Mouse Skeletal Muscle ◽  
C2c12 Myotube ◽  
Mouse Myoblast

The effects of lactate on muscle mass and regeneration were investigated using mouse skeletal muscle tissue and cultured C2C12 cells. Male C57BL/6J mice were randomly divided into (1) control, (2) lactate (1 mol/L in distilled water, 8.9 mL/g body weight)-administered, (3) cardio toxin (CTX)-injected (CX), and (4) lactate-administered after CTX-injection (LX) groups. CTX was injected into right tibialis anterior (TA) muscle before the oral administration of sodium lactate (five days/week for two weeks) to the mice. Oral lactate administration increased the muscle weight and fiber cross-sectional area, and the population of Pax7-positive nuclei in mouse TA skeletal muscle. Oral administration of lactate also facilitated the recovery process of CTX-associated injured mouse TA muscle mass accompanied with a transient increase in the population of Pax7-positive nuclei. Mouse myoblast-derived C2C12 cells were differentiated for five days to form myotubes with or without lactate administration. C2C12 myotube formation with an increase in protein content, fiber diameter, length, and myo-nuclei was stimulated by lactate. These observations suggest that lactate may be a potential molecule to stimulate muscle hypertrophy and regeneration of mouse skeletal muscle via the activation of muscle satellite cells.

Absorption and distribution of sodium [2-14C]barbital in tissues of normal and dystrophic mice

1978 ◽  
Vol 56 (1) ◽  
pp. 76-82
Author(s):  
Heather R. Stephens ◽  
Denis Nadeau ◽  
Edmund B. Sandborn
Keyword(s):  
Skeletal Muscle ◽  
Gastrointestinal Tract ◽  
Gastric Emptying ◽  
Oral Administration ◽  
Distribution Volume ◽  
Tissue Concentrations ◽  
Dystrophic Mouse ◽  
Rapid Absorption ◽  
Dystrophic Mice ◽  
Mutant Homozygote

The absorption and distribution of [2-14C]barbital after oral administration was studied in various tissues, including skeletal muscle, of normal and dystrophic mice. There appeared to be a more rapid gastric emptying in the mutant homozygote as reflected in lower levels of the drug recuperated from the gastrointestinal tract. This resulted in initially higher plasma and tissue concentrations of barbital in the dystrophic mice. Two hours after oral administration, this kinetic profile was reversed so that less barbital remained in the tissues of the dystrophic mouse. The tissue:plasma concentration ratios were consistently, but not significantly, higher in all tissues of the dystrophic animals. Analysis of the half-life of the drug in both groups suggests that there is an increase in the distribution volume of barbital in the dystrophic mice. The phenomenon of more rapid absorption of the barbiturate seems to be more consistent as the symptoms of the disease progress. The altered absorption and disposition of barbital in various tissues of the dystrophic mouse support the concept that a generalized multisystemic disorder may be crucial to the pathogenesis of murine muscular dystrophy, in contradistinction to a purely myogenic origin.

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