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PubMed2006

[Creatine as a metabolic controller of skeletal muscles structure and function in strength exercises in humans].

The aim of study was to investigate the effect of oral creatine supplementation upon muscle performance and aerobic capacity of the organism. Knee extensor muscles of two groups with 9 subjects in each were subjected to strength training with and without creatine supplementation (Cre and Pla) for 10 weeks, three times a week with an effort of up to 85% of maximal voluntary contraction (MVC). The Cre group received 5 g of creatine monohydrate a day. After 10 weeks strength training, an increase of MVC by 29 and 40% in training (isotonic) regimen was recorded for the Pla and Cre groups respectively. The muscle isokinetic torque increments of 10-11% were obtained in the Pla group at angular velocities corresponding to training velocities, and in the Cre group increments of 11-17% were recorded at all angular velocities tested. No changes were found in the fatigue test by the Pla group, whereas Cre group showed a tendency for an increase. The aerobic and anaerobic capacities of the organism did not decrease in both groups. Thus the creatine supplementation during strength training potentates an increase of force-velocity characteristics of trained muscle group without impeding aerobic capacity of the organism.

Adult↗
PubMed1988

Inhibition of field stimulation-evoked relaxations in rat oesophageal smooth muscle by the calcium antagonist PN 200-110.

1. The inhibitory effects of the 1,4-dihydropyridine calcium channel antagonist, PN 200-110 (isradipine), on field stimulation-evoked tetrodotoxin (TTX)-sensitive and -insensitive relaxations were studied in rat oesophageal smooth muscle of the tunica muscularis mucosae. 2. The TTX-insensitive relaxation was inhibited by PN 200-110 in a stereoselective manner with the (+)-(S)-isomer displaying a 1000 fold greater inhibitory potency than the (--)-(R) isomer. A similar potency was noted for inhibition of high K+ -evoked contractions. 3. TTX-sensitive relaxations evoked by field stimulation and contractions elicited by the muscarinic cholinoceptor agonist, cis-2-methyl-4-dimethylamino-methyl-1,3-dioxolane methiodide (cisdioxolane) were considerably less sensitive to inhibition by PN 200-110, although, again, stereoselectivity for PN 200-110 was apparent. 4. Pretreatment with (+)-(S)-PN 200-110 resulted in a non-competitive displacement of the Ca2+ concentration-response curves obtained in the presence of either isotonic 50 mM KCl or cisdioxolane. The effect of K+ was 10 fold more sensitive than that of cis-dioxolane. 5. The potency rank orders for inhibition of TTX-insensitive field stimulation-evoked relaxations and K+ -mediated contractions in a series of calcium channel antagonists were closely correlated; (+)-(S)-PN 200-110 showing highest potency followed by nifedipine, verapamil, diltiazem, (--)-(R)-PN 200-110. 6. It is concluded that TTX-insensitive relaxations are dependent upon an influx of extracellular Ca2+ through potential-operated calcium channels.

Animals↗
PubMed1986

Plasma expansion does not precipitate the fall in plasma vasopressin in humans drinking isotonic fluids.

In a group of healthy humans, plasma vasopressin (AVP) levels fell on drinking either Tyrode or mannitol solutions isosmotic with plasma. Both the timing and magnitude of the fall were appropriate to account for the transient diuresis which followed the drinking. Although plasma expansion follows drinking Tyrode solution it occurred too late to account for the fall in plasma AVP. It was also too small to inhibit AVP secretion. Even though plasma volume tended to contract on drinking isosmotic mannitol solution a fall in plasma AVP and a diuresis occurred, similar to those found after drinking Tyrode solution. These findings appear to eliminate plasma volume expansion as the stimulus for the fall in plasma AVP and the associated diuresis on drinking isotonic fluids. In a further group of human subjects, bypassing the oropharynx by intragastric infusion resulted in a slower onset of diuresis after a water load. We suggest that receptors, as yet undefined, in the upper gastrointestinal tract contribute to the early stages of a water diuresis and account for the apparently inappropriate transient diuresis which follows the drinking of isotonic fluids.

Adult↗
PubMed1969

A lesion of the transverse tubules of skeletal muscle.

1. A method is described by which a selective lesion can be made in vitro in the transverse tubules of frog skeletal muscle.2. The method consists of exposing the muscle for 1 hr or more to a buffered salt solution made hypertonic by the inclusion of 400 mM glycerol and then returning the muscle to an isotonic salt solution. The lesion is induced during the washout of the glycerol.3. Electron micrographs reveal that the lesion consists of a rearrangement of the T-system membranes in such a way that the continuity of the tubules is lost. The membranes appear to coalesce into large vesicles scattered irregularly throughout the sarcoplasm.4. The glycerol treatment results in a depression of the resting potential of up to 30 mV. The treated fibres are depolarized by high concentrations of K as are normal muscle fibres.5. T-tubule lesioned fibres are unable to respond mechanically either to electrical stimulation or to elevated K but they do contract in the presence of caffeine and relax when the caffeine is removed.6. Problems concerning the variability of the procedure are presented and certain considerations concerning the mechanism of the effect are discussed.

Animals↗
PubMed1975

Inotropic and electrophysiological actions of verapamil and D 600 in mammalian myocardium. I. Pattern of inotropic effects of the racemic compounds.

A pattern analysis of inotropic actions was carried out on isotonically chortening cat papillary muscles exposed to (+/-)-verapamil and (+/-)-D 600 and compared to other Ca-antagonistic interventions. 1. (+/-)-Verapamil (1--5mug/ml) leaves contraction amplitudes nearly unchanged at 6/min, whereas at 60/min more than 90% depression (5 mug/ml) occurs. (+/-)-D 600 is about twice as effective as (+/-)-berapamil. 2. An increase of [Ca2+]O in the presence of (+/-)-verapamil or (+/-)-D 600 does not restitute the normal amplitude-frequency relationship. There is only a shift toward higher contraction amplitudes. 3. (+/-)-Verapamil and (+/-)-D 600 lead to typical biphasic inotropic transients after step changes of the friving rhythm. First a fast and (at higher frequencies) very pronounced negative staircase occurs, followed by a rather slowly developing positive staircase. 4. These drug effects contrast to the effects of lowering [Ca2+]O or of adding Ni2+ or La3+, which all produce a rather uniform depression of contraction amplitudes at all frequencies and do not elicit staircase phenomena such as seen under the influence of (+/-)-verapamil or (+/-)-D 600. 5. In contrast to the action of Ni2+, La3+ or low [Ca2+]O, (+/-)-verapamil slows down the restitution kinetics of Ca-reavailability from internal stores as determined by the amplitude of test contractions elicited after various periods of rest. 6. Drug-induced changes in the time course of the transmembrane action potential as depending on frequency may partially but not fully explain the contractile phenomena. 7. Possible interpretations as to the sites where (+/-)-verapamil or (+/-)-D 600 interferes with cardiac excitation-contraction coupling are given by the aid of a multicompartment model. This model describes excitation-contraction coupling in terms of transmembrane and intracellular Ca-movements.

Action Potentials↗
PubMed1983

Metabolic alkalosis in the rat. Evidence that reduced glomerular filtration rather than enhanced tubular bicarbonate reabsorption is responsible for maintaining the alkalotic state.

Maintenance of chronic metabolic alkalosis might occur by a reduction in glomerular filtration rate (GFR) without increased bicarbonate reabsorption or, alternatively, by augmentation of bicarbonate reabsorption with a normal GFR. To differentiate these possibilities, free-flow micropuncture was performed in alkalotic Munich-Wistar rats with a glomerular ultrafiltrate total CO2 concentration of 46.5 +/- 0.9 mM (vs. 27.7 +/- 0.9 mM in controls). Alkalotic animals had a markedly reduced single nephron GFR compared with controls (27.4 +/- 1.5 vs. 51.6 +/- 1.6 nl/min) and consequently unchanged filtered load of bicarbonate. Absolute proximal bicarbonate reabsorption in alkalotic animals was similar to controls (981 +/- 49 vs. 1,081 +/- 57 pmol/min), despite a higher luminal bicarbonate concentration, contracted extracellular volume, and potassium depletion. When single nephron GFR during alkalosis was increased toward normal by isohydric volume expansion or in another group by isotonic bicarbonate loading, absolute proximal bicarbonate reabsorption was not substantially augmented and bicarbonaturia developed. To confirm that a fall in GFR occurs during metabolic alkalosis, additional clearance studies were performed. Awake rats were studied before and after induction of metabolic alkalosis associated with varying amounts of potassium and chloride depletion. In all cases, the rise in blood bicarbonate concentration was inversely proportional to a reduction in GFR; filtered bicarbonate load remained normal. In conclusion, a reduction in GFR is proposed as being critical for maintaining chronic metabolic alkalosis in the rat. Constancy of the filtered bicarbonate load allows normal rates of renal bicarbonate reabsorption to maintain the alkalotic state.

Absorption↗
PubMed1982

Role of glycolysis in the tension development under anoxia in guinea pig taenia coli.

The role of glycolysis in the tension development under anoxic conditions in a high-K medium was studied in the intestinal smooth muscle of guinea pig taenia coli. After exposure to the high-K medium (isotonic, 60 mM) under normal oxygen for 30 min, the muscles were exposed to a high-K medium bubbled with N2 gas. The tonic contraction decreased gradually to about 10% of the original level. Glucose was then cumulatively added to the high-K medium under anoxia. The maximum tension was observed following the addition of the higher concentrations of glucose. The muscle tension which developed in the high-K medium with a high concentration of glucose under anoxia was dependent on the external Ca2+ and was inhibited by iodoacetic acid (IAA). The addition of glucose to a high-K medium under anoxia also increased lactate release from the muscle. Pretreatment with 1 mM IAA decreased the lactate release from the muscle. In a Ca2+-free medium under anoxia, the addition of glucose did not increase the muscle tension although there was a significant increase in the lactate release. In summary, it is considered that the smooth muscle of taenia coli develops tension utilizing energy produced by the glycolytic pathway under anoxia in a high-K medium.

Animals↗
PubMed2002

Effects of chronic cadmium exposure on contractility of the rat detrusor.

The chronic effects of Cd2+ on the myogenic contractions induced by acetylcholine (ACh), and the neurogenic contractions induced by electrical field stimulation (EFS) of the rat detrusor were investigated. Wistar Kyoto rats weighing 150-250 g were randomly divided into four groups each containing ten animals. Three groups received intraperitoneal Cd2+ (0.25, 0.5 and 1 mg/kg, respectively) dissolved in saline twice a week for 3 months. The control group received only saline (0.3 ml). At the end of 3 months, the urinary bladders were surgically removed and a strip of detrusor was prepared from each bladder. An atomic absorption device and the standard addition method were used to determine blood levels of Cd2+ and the Cd2+ levels of the remaining parts of each bladder. The responses of the detrusor strips were studied in organ chambers. The tissues were first treated with ACh and then with EFS. The responses were recorded by isotonic transducers. The tissue Cd2+ levels were significantly increased in the Cd2+ treated rats in a dose-dependent manner except in the 0.25 mg/kg Cd2+ treated group. ACh-induced contractions were significantly attenuated only in the 1 mg/ kg Cd2+ treated rats. The contractions induced by EFS were significantly decreased in all of the Cd2+-treated groups. but there were no significant differences between the groups. This study showed that Cd2+ exposure for 3 months impairs neurogenic and myogenic contractile activity in the rat detrusor muscle. This action seems to be at least partly due to an inhibition of the cholinergic muscarinic system. This may have clinical implications for people who are exposed to Cd2+.

Animals↗
PubMed2004

Influence of viscosity on myocardium mechanical activity: a mathematical model.

We have previously proposed and validated a mathematical model of myocardium contraction-relaxation cycle based on current knowledge of regulatory role of Ca2+ and cross-bridge kinetics in cardiac cell. That model did not include viscous elements. Here we propose a modification of the model, in which two viscous elements are added, one in parallel to the contractile element, and one more in parallel to the series elastic element. The modified model allowed us to simulate and explain some subtle experimental data on relaxation velocity in isotonic twitches and on a mismatch between the time course of sarcomere shortening/lengthening and the time course of active force generation in isometric twitches. Model results were compared with experimental data obtained from 28 rat LV papillary muscles contracting and relaxing against various loads. Additional model analysis suggested contribution of viscosity to main inotropic and lusitropic characteristics of myocardium performance.

Animals↗
PubMedDate not supplied

[Effect of carnosine and anserine on excitation and contraction of fatigued skeletal muscle].

The effect of dipeptides (carnosine and anserine) on a neuromuscular preparation under fatigue or diplacine blocking is shown to result in a significant restoration of the muscle contraction. The analysis of this phenomenon evidences that synaptic processes are not responsible for the restoration, at least under the given experimental conditions. At the same time, the absence of any effect of the compounds studied on the maximal rate of isotonic shortening and on the tension of glycerinized fibres and ATPPase of native and desenitized actomyosine indicates that the contractile mechanism is not involved in the effect described. On the other hand, the dipeptides restore the value of the transmembrane potential depolarized by exhaustion, increase the amplitude of isometric twitch and the value of maximal load under isotonic conditions. Moreover, the time of the contractile cycle in the presence of the dipeptides is considcted to the processes of electromechanical coupling in skeletal muscles.

Actomyosin↗
PubMed1996

Phase switching of oscillatory contraction in relation to the regulation of amoeboid behavior by the plasmodium of Physarum polycephalum.

The plasmodium of the true slime mould Physarum polycephalum is a large aggregate of protoplasm and behaves like an amoeboid cell, exhibiting rhythmic contraction everywhere within the organism. Phase dynamics of these oscillations were studied in relation to the global organization of amoeboid behavior, by analysing the thickness oscillation, isotonic tension and the motive force of the streaming. Usually the plasmodium showed synchrony, the phase of the oscillation being the same everywhere excepting the peripheral part. We found several situations where this in-phase relationship switched to anti-phase. This occurred either at the early stages of the plasmodial coalescence, or when a single plasmodium was nearly separated by partition, or when the streaming of the protoplasm was hindered by applying the hydrostatic pressure. Furthermore, the motive force of the protoplasmic streaming increased once the anti-phase relationship was established. In this way, the weak interactions among plasmodial parts induce the switching of phase relationship from in-phase to anti-phase, and this transition in turn acts to increase the interaction by promoting a rapid mixing of the protoplasm. This global feedback mechanism by phase switching should help maintain a large single plasmodium without separating into parts. The possible mechanism of phase switching is discussed in terms of coupled nonlinear oscillators.

Animals↗
PubMed1990

Aging increases calcium influx at motor nerve terminal.

To determine whether increased transmitter release from soleus nerve terminals of old C57BL/6J mice is caused by an altered Ca2+ regulation, the time course of post-tetanic potentiation of miniature endplate potential (MEPP) frequency was used as an indicator of the kinetics of Ca2+ metabolism in young (10 months) and old (24 months) mice. Post-tetanic potentiation properties were studied in either (1) 0.2 mM Ca2+, 5.0 mM Mg2+ Krebs; or (2) Ca2(+)-free/EGTA Krebs to eliminate Ca2+ influx, and thereby isolated Ca2+ buffering. In the 0.2 mM Ca2+ Krebs, the time constants of decay of augmentation (TA) and potentiation (TP) were longer in old (TA = 10.3 +/- 1.0 sec, TP = 195.3 +/- 5.4 sec) than in young (TA = 7.0 +/- 0.7 sec, TP = 78.8 +/- 6.6 sec) nerve terminals. Evoked transmitter release was measured in 0.4 mM Ca2+, 2.75 mM Mg2+ Krebs. Quantal content of the endplate potential was positively correlated with TA (r = 0.95) and with TP (r = 0.98). In the Ca2(+)-free/EGTA Krebs, there was no difference in post-tetanic potentiation properties between young and old terminals. These results suggest that Ca2+ influx into the soleus nerve terminal increases with aging. This may explain, at least in part, the increased quantal content observed at old terminals.

Aging↗
PubMed1966

The ionic dependence of cardiac excitability and contractility.

In contrast to the large volume of data supporting the dependence of cardiac excitability and phasic contractility on external Na, Van der Kloot and Rubin (1962) and Singh (1962) have reported the persistence of both electrical and phasic mechanical activity in frog atrial and ventricular preparations soaked in isotonic sucrose solutions. The acute ionic dependence of excitability and contractility in small frog atrial trabeculae has been investigated with the conclusion that excitability and phasic contractions may continue for extended periods of time in sucrose media if the extracellular ionic concentrations remain above 2% of normal. This behavior is attributed to the slow exchange properties of the cell surfaces of the frog cardiac trabeculae and the antagonistic effects of Na, K, and Ca ions on both membrane excitability and fiber contractility.

Animals↗
PubMed1984

Mechanisms of action of noradrenaline and carbachol on smooth muscle of guinea-pig anterior mesenteric artery.

Membrane potential was recorded by micro-electrode in segments of small (200-500 microns o.d.) mesenteric arteries of guinea-pig. Isotonic shortening was recorded in helical strips cut from these arteries. Raising the external potassium concentration, [K+]o, caused shortening and substantial depolarization. The threshold for contraction was about 30 mM which corresponded to a membrane potential of about -45 mV. Since high-potassium contractions were abolished in calcium-free solution it was suggested that they occur due to potential-sensitive calcium channels opening positive to about -45 mV. Noradrenaline weakly depolarized the muscle and produced contractions resistant to calcium-free conditions. It was suggested that noradrenaline contractions are mainly caused by mechanisms other than the opening of potential-sensitive calcium channels, namely entry of calcium via other channels and release of stored calcium. Carbachol had no effect on basal tension but inhibited shortening by noradrenaline or by raising [K+]o. The inhibitory effect of carbachol on tension under various conditions was associated with hyperpolarization or depolarization in a range negative to -45 mV, or no effect on potential, so that modulation of the number of open potential-sensitive calcium channels could not be evoked to explain its relaxant action. Removal or destruction of the endothelium by rubbing or by distilled water perfusion left tension responses to noradrenaline or raised [K+]o essentially unchanged. However, the inhibitory effect of carbachol on tension was attenuated and hyperpolarization of the resting artery was converted to a depolarization. It was concluded that carbachol has both a strong inhibitory and a weak excitatory effect on these vascular smooth muscle cells. Membrane potential changes are not essential to its inhibitory action but may, by closing potential-sensitive calcium channels, sometimes reinforce it. Hyperpolarization by carbachol may be caused by a factor released by the action of carbachol on endothelial cells: in its absence carbachol may weakly depolarize but this alone is normally insufficient to generate tension.

Action Potentials↗