Skeletal Muscle Tension Research Articles

Repolarization-induced reactivation of contracture tension in frog skeletal muscle.

In solutions containing perchlorate in place of chloride frog toe muscles or small bundles of semitendinosus fibers undergo maximum potassium (K) contractures of long duration at low [K]0 (5–10 mM). After relaxation at high [K]0, large protracted "reactivation" contractures (70–90% of maximum tension) again develop when repolarization is accomplished by a reduction of [K]0 to 2.5–10 mM. Somewhat smaller contractures also appear during repolarization at lower perchlorate concentrations (8–12 mM). The effects of perchlorate include disproportionate shifts in the relation between log [K]0 and K-contracture tension, and between log [K]0 and relaxation rate. Similar but smaller effects are observed in the presence of 1 mM caffeine or 1.5 mM chloroform. These observations implicate at least two potential-dependent processes in the regulation of contraction in frog twitch muscle.

Mean myoglobin oxygen tension in skeletal and cardiac muscle.

We have utilized the concept first developed by Millikan (1936, 1937) that myoglobin may be a useful indicator of intracellular oxygen tension. We have not made spectrophotometric measurements of oxymyoglobin % saturation, as did Millikan, since the presence of hemoglobin interferes with this measurement, but instead compute a mean myoglobin oxygen tension from measurements of carboxymyoglobin saturation (MBCO). This method has been described previously (Coburn and Mayers, 1971; Coburn et al, 1973). The basis of the method is illustrated in Fig. 1. Binding of O2 and CO to myoglobin is competitive, therefore, at a given partial pressure of CO, MBCO is a function of the oxygen tension in proximity to myoglobin molecules. This figure also illustrates that mean tissue Pco is equal to mean capillary Pco since CO is neither produced nor consumed at a significant rate.

Muscle tension in human operant heart rate conditioning.

The physiological mechanism involved in human operant heart rate conditioning is not known. If skeletal muscle tension is a mediator, it should be possible to generate significant heart rate increases by inconspicuous voluntary muscle tension. Eleven subjects were instructed to generate inconspicuous muscle tension for 90-second periods. No gross muscle movements were observed, but average heart rate during the trials was over 13 beats-per-minute greater than pre-trial base lines. Respiratory pattern changes and surface electromyogram changes did not reliably correlate with heart rate increases. Inconspicuous muscle tension could be a mediator in human operant heart rate conditioning, and cannot be ruled out by absence of change in respiratory pattern or electromyogram.

Effects of scorpion venom on squid axon membranes.

Effects of scorpion venom on squid axon membranes.

Action of diazepam on muscular contraction in man.

The action of diazepam has been examined in 18 healthy subjects by studying the correlation between electromyographically recorded mean voltage and isometric tension in skeletal muscle. A significantly increased slope of voltage tension curves was found after giving diazepam, i.e. the mean voltage at corresponding isometric tensions was about 20% higher. This finding is probably due to an action of the compound on contractile mechanisms.

Interaction of calcium and local anesthetics with skeletal muscle microsomes

AbstractThe influence of Ca++, several drugs, and pH on the binding of Ca++ by skeletal muscle microsomes was studied in vitro. A mass‐law graphic analysis revealed the presence of three distinct species of Ca++‐binding sites in the microsomes, and the binding at only one of these sites was antagonized by local anesthetics and quinidine. These drugs also decreased the maximum Ca++‐binding capacity of the microsomes. Caffeine and ouabain exerted no effect on the binding at any of the sites. Procaine was also bound by microsomes, and this binding was antagonized by Ca++, which also decreased the maximum procaine‐binding capacity of microsomes. The sites that bind procaine and Ca++ are not identical because the maximum‐binding capacities of the interacting sites are distinctly different. The influence of pH on the ability of drugs to antagonize Ca++ binding indicates that the displacing activity increases as the percentage of the drug in the nonionized form increases. All of the data obtained in the above studies are consistent with the interpretation that quinidine and local anesthetics of the procaine type noncompetitively antagonize the binding of Ca++ by microsomes. The pharmacological significance of a noncompetitive interaction may be related to the property of local anesthetics and quinidine to increase contractile tension in skeletal muscle rather than to their ability to stabilize the cell membrane.

Sodium-induced tension in slow skeletal muscle deprived of external calcium.

Sodium-induced tension in slow skeletal muscle deprived of external calcium.

Caffeine-induced activation of contraction in stick insect skeletal muscle

1. 1. In low concentrations (1–2 mM/1), caffeine causes significant potentiation of twitch and tetanus tension in stick insect skeletal muscle. 2. 2. Caffeine increases the duration of the active state of the muscle, evident by the protracted time course of twitches elicited in caffeine salines. 3. 3. The early increase in the rate of twitch tension development in caffeine salines suggests that this alkaloid potentiates by lowering the mechanical threshold of the muscle fibres. 4. 4. In moderate concentrations (3–6 mM/1), caffeine induces phasic contractures, while in high concentrations (8–10 mM/1) the contractures are of long persistence, and in addition caffeine is able to induce contractures in depolarized muscle. 5. 5. It is suggested that simple caffeine potentiation is mediated via the normal excitation-contraction coupling channels, but the contracture-induction effect of caffeine appears to be independent of the normal triggering stages of the excitation-contraction mechanism. 6. 6. It is suggested that caffeine may induce contractures by accelerating calcium release and inhibiting reactivation of the calcium pump by a direct effect on the muscle cell sarcoplasmic reticulum.

Anion-induced potentiation of contraction in insect skeletal muscle

1. 1. Iodide, bromide and nitrate ions all caused potentiation of twitch tension in insect skeletal muscle without altering tetanus tension, while thiocyanate ions depressed both twitch and tetanus tension. 2. 2. All of these anions greatly prolonged the twitch time course while thiocyanate ions induced contractures. 3. 3. It is suggested that these anions prolong the active state of the muscle probably dy depolarizing the muscle fibres and inhibiting the reticular calcium pump.

Effect of catecholamines on temperature, oxygen tension, and blood flow in skeletal muscles

Effect of catecholamines on temperature, oxygen tension, and blood flow in skeletal muscles

Oxygen tension in skeletal muscle of unanesthetized rats during hypothermia

Oxygen tension in skeletal muscle of unanesthetized rats during hypothermia

Isometric twitch tension of frog skeletal muscle as a function of temperature.

Isometric twitch tension of frog skeletal muscle as a function of temperature.

Sympathetic control of the circulation in the hind leg of the dog.

Experiments were undertaken to test the effects of ablation or stimulation of the lumbar sympathetic nerves upon the circulation of the skin and skeletal muscle in the hind leg of the dog. Insulation of the skin was abolished by wetting the fur. Insulation of the muscles was abolished by incising and reflecting the skin which covered the part to be studied. As indices of circulation, the temperatures of skin and muscle were recorded by means of thermocouples, and the tensions of oxygen in skin and muscle were recorded as measured by the polarograph. Most of the experiments were conducted in a room in which temperature and humidity were controlled. After chronic sympathetic denervation, the temperature and oxygen tension of skeletal muscle were lower than in the contralateral control. Those of the skin were higher than in the control side. Electric stimulation of the lumbar sympathetic trunk consistently caused a rise in the tension of oxygen in muscle and a fall in skin. This was not attributable to hematometakinesia but to active vasodilation in muscle. Changes in temperature were always in the same direction as changes in oxygen tension.

Mechanisms of skeletal muscle pain and fatigue.

Lewis1postulated that pain in ischemic, active muscles was brought about by the accumulation in the tissue spaces of a metabolite which he designated as P. He also indicated that Factor P was the stimulus responsible for the pain of intermittent claudication and coronary occlusion. In these syndromes the pathologic process leading to obstruction of vessels supplying blood to the active muscles was the key to the production of pain. Recent investigations of headache and backache syndromes* demonstrate that sustained skeletal muscle tension can evoke pain in the absence of pathologic involvement of either the blood vessels or the muscles. In light of evidence † indicating that tetanic contractions cause reduction in muscle blood flow, it seemed desirable to explore the hypothesis that the pain mechanisms in these syndromes were essentially those involved in the genesis of ischemic muscle pain. The following experiments concerning the relationship of skeletal

VARIATION OF BLOOD PRESSURE WITH SKELETAL MUSCLE TENSION AND RELAXATION. II. THE HEART BEAT

Article1 March 1940VARIATION OF BLOOD PRESSURE WITH SKELETAL MUSCLE TENSION AND RELAXATION. II. THE HEART BEATEDMUND JACOBSON, Ph.D., M.D., F.A.C.P.EDMUND JACOBSON, Ph.D., M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-13-9-1619 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn previous studies1, 2systolic and diastolic pressure were measured in man, lying at rest, at intervals beginning about 15 minutes after reclining, while potentials were recorded (in microvolts within the frequency rate, 30-4000) from electrodes in one or more of the following groups: the flexor muscle in the right upper arm, the left quadriceps femoris muscles, the abdominal muscles, muscles in the region of the right eye. Apart from fall of pressure following soon after and attributable to change to the recumbent position, there were indications that the blood pressure variable is a function of skeletal muscular tension. Prolonged...Bibliography1. JACOBSON E: The influence of skeletal muscle tension and relaxation on blood pressure, Am. Jr. Physiol., 1936, cxvi, 86. Google Scholar2. JACOBSON E: Variation of blood pressure with skeletal muscle tension and relaxation, ANN. INT. MED., 1939, xii, 1194. Google Scholar3. EINTHOVENHUGENHOLTZ WFW: L'électrocardiogramme tracé dans le cas ou il n'y a pas de contraction visible due coeur, Arch. Neérland. de Physiol., 1918, v, 11. Google Scholar4. FULTON JF: On the summation of contractions in skeletal muscle, Am. Jr. Physiol., 1925, lxxv, 211. CrossrefGoogle Scholar5. JACOBSON E: Electrical measurements of neuromuscular states during mental activities. IV. Evidence of contraction of specific muscles during imagination, Am. Jr. Physiol., 1930, xcv, 703. CrossrefGoogle Scholar6. DAVISDAVIS HPA: Fatigue in skeletal muscle in relation to the frequency of stimulation, Am. Jr. Physiol., 1932, ci, 339. CrossrefGoogle Scholar7. HOFFGREEN ECHD: Cardiovascular reactions induced by electrical stimulation of the cerebral cortex, Am. Jr. Physiol., 1936, cxvii, 411. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, Illinois*Received for publication December 19, 1938. (Partially reported before the American Physiological Society, March 31, 1938.)From the Physiological Laboratory of the University of Chicago and the Laboratory for Clinical Physiology, Chicago.Aided by a grant from the National Research Council.Mr. William M. Lees assisted during the experiments. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTraumatologyAt least 9 h of supervised relaxation training may reduce state anxiety and improve heart rate variability, prognosis and return to work for people with ischaemic heart diseaseRelaxation training inhibits fear and arousal during in vivo exposure to phobia-cue stimuliHypertension and BiofeedbackStress, Psychosomatics, and Stress Coping from a Clinical-Psychological Point of ViewBehavioral Interventions as Adjunctive Treatments for Chronic AsthmaSome Antecedents of BiofeedbackTheoretical Aspects of BiofeedbackDysponesis: A Neurophysiologic Factor in Functional DisordersBiofeedback and Progressive Relaxation: Effects on Systolic and Diastolic Blood Pressure and Heart RateGroup Desensitization of Test Anxiety in Elementary SchoolDysponesis: A neurophysiology factor in functional disordersThe Conditioning and Deconditioning of Neurotic AnxietyZentralnervöse Beeinflussung des ElektromyogrammsThe Systematic Desensitization Treatment of NeurosesA Neurophysiologic View of Functional Disorders: (A Contribution to Our Understanding and Management of Functional Illness) 1 March 1940Volume 13, Issue 9Page: 1619-1625KeywordsBlood pressureClinical laboratoriesDeceptionElectrode recordingFallsHeartMusclesResearch laboratoriesSkeletal musclesSystolic pressure ePublished: 1 December 2008 Issue Published: 1 March 1940 PDF downloadLoading ...