Work and chemical change in isotonic muscular contractions.
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Energy turnover in the isolated rat portal vein was investigated by measurement of oxygen consumption (JO2) and lactate production (JLA) under simultaneous recording of mechanical activity. In spontaneous activity under aerobic conditions and at optimal muscle length JO2 and JLA were 0.55 and 0.62 micromol/min X g, respectively, corresponding to an ATP-production of 4.3 micromol/min X G. When muscle length was changed, an approximately linear relation was found between energy turnover and mean isometric tension. The tension-indpendent part of ATP-production was 3.0 micromol/min X g. In Ca2+-free solution the metabolic rate was 20% lower still. JO2 was nearly equal in isometric contractions and in afterloaded isotonic contractions from the same initial muscle length. During a maximal tonic contracture in 5+-depolarized portal vein JO2 increased to about twice that in spontaneous activity. Changes in contracture force by variations in muscle length or in [Ca2+]0 were associated with identical linear relations between JO2 and active tension. This relation was less steep than the corresponding relation for spontaneous activity. The anaerobic lactate production of the portal vein was 2.7 times theaerobic leve. The accelerated glycolysis did not compensate for eliminated oxidative metabolism. Under substrate-free aerobic conditions no lactate was produced by the muscle and compared to the control situation JO2 declined more than could be accounted for by reduced mechanical activity alone. The metabolic turnover rate in relation to isometric tension is high in the rat portal vein compared to that of tonic vascular smooth muscle from larger vessels. This correlates with differences in dyanmic mechanical properties. At comaparable tension levels in the portal vein, the rate of cross-bridge turnover may be higher in spontaneous phasic activity than in sustained contracture.
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A system of differential equations describing myocardium contractions in isometric and isotonic regimes has been obtained. On the basis of these equations functioning of myocardium was modelled on an electronic computer. An effect has been revealed of the coefficients of rheological equations and activation function on isometric and isotonic contraction of the force/rate ratio. A good agreement between the results of modelling and the experimental data has been observed.
1. A technique is described whereby (i) quick stretches and releases of controlled velocity, amplitude and time of onset can be applied to muscle. (ii) Releases from isometric to isotonic contraction can be performed at controlled delays relative to the stimulus, and displayed on a delayed expanded oscilloscope sweep. An isotonic lever system with an equivalent mass of 12.8 mg is described.2. Quick stretch of rabbit or cat papillary muscle after excitation does not result in a level of tension equal to or greater than normal peak isometric tension appropriate to the stretched length. Stretches applied during the first half of the rising phase of tension development give responses nearly identical to the same stretches applied before the stimulus (indicating that Starling's Law of the heart holds until this time). Stretches applied in the later phase of tension development or during relaxation result in diminished peak isometric tensions or accelerated relaxation.3. The rate of tension development following quick releases of isometrically contracting muscle to zero tension is not maximal until the releases are made 150-200 msec after excitation.4. Shortening velocity with light afterloads is not initially maximal nor constant for an appreciable period of time. The shortening velocity with heavy afterloads reaches its maximum more rapidly when the load is not lifted within the first 200 msec of a contraction which, if maintained isometric, would have required 400-500 msec to reach peak tension. With these heavier loads, a period of 100-200 msec of constant shortening velocity may occur.5. Freeloaded isotonic contractions show an inflexion in their shortening curves occurring 150-200 msec after excitation.6. Maximum rate of isotonic shortening following releases from isometric to isotonic contraction with a given load is not maximal until the releases occur about 200 msec after the stimulus.7. It is concluded that contractility in cardiac muscle is relatively slow in its onset with maximum capacity to shorten occurring about midway through the rising phase of isometric tension development.
1. Within the range of the given conditions of measuring static and dynamic properties of the rabbit gastrocnemius muscle the following results were obtained: a) the dependence of the maxima of isotonic shortening upon the relative length of the muscle at constant load is linear; b) the parameters of the non-linear dependence of the passive elastic force of the muscle upon its relative length (measured in series) were identified using asymptotic regression; c) the time course of isotonic contractions (at an interval from 0 to 0.3 s after the beginning of stimulation) could be satisfactorily approximated by responses of a linear system to a step-function; d) the time course of isometric contractions (at an interval from 0 to 0.3 s after the beginning of stimulation) could be closely approximated by responses of a linear system to a step-function. 2. The time constants of isotonic and isometric contractions were determined as the parameters of the corresponding linear systems. 3. The maximum rates of the isometric and isotonic contractions were determined as maxima of the first derivatives of the responses of the corresponding models. 4. The experimental set-up made it possible to compare the values of the parameters concomitantly followed at various muscle lengths and at various loads.
Several investigators have found experimentally that the force-time integral varies non-linearly with energy expenditure over the course of a cardiac contraction. Also, recent research findings have indicated that the crossbridge cycle to ATP hydrolysis ratio in muscle fiber systems may not be coupled with a one-to-one ratio. In order to investigate these findings, Huxley's sliding filament crossbridge muscle model coupled with parallel and series elastic components was simulated to examine the behavior of the crossbridge energy utilization and force-time integral vs time. Crossbridge (CB) energy utilization was determined by considering the ATP hydrolysis for the crossbridge cycling, and this CB energy was compared with the force-length energy in a contraction. This CB energy was calculated in both isometric and isotonic contractions as a function of contraction time and compared to the force-time integral. Simulation results demonstrated that the ratio of the force-time integral to CB energy varies strongly throughout the cardiac cycle for both isometric and isotonic cases, as has been observed experimentally. Simulations also showed that using the force-length energy component of energy vs the CB energy gave a better correlation between the total energetic predictions and the force-time integral, agreeing with recent finding that the crossbridge cycle to ATP hydrolysis ratio may not be coupled one-to-one, especially at lower force levels.
Two animal models with contrasting responses to pressure overloading were used to determine whether cardiac dysfunction is a general property of pressure hypertrophied myocardium or a specific property of a particular model. Chronic progressive cardiac pressure overload was compared in (a) the left ventricle of the adult and aged spontaneously hypertensive rat, in which pressure overloading begins in the pup, and (b) the right ventricle of the adult cat, in which pressure overloading was initiated surgically in the kitten. Nine hypertensive and nine control rats were studied at 1 year of age, when hypertension is stable in this model; five hypertensive and five control rats were then studied at 2 years of age, when both groups of rats are beginning to show appreciable senile mortality. Systolic blood pressure was similarly increased in both hypertensive groups; compared with the normotensive control groups, the ratio of left ventricular to body weight was 36% and 76% higher in the 1 and 2 year old hypertensive groups respectively. During isotonic contractions of left ventricular papillary muscles the extent and velocity of shortening in muscles from the control and hypertensive rats in each group were the same, but shortening and relaxation times were prolonged in muscles from the hypertensive rats in both age groups. During isometric contractions developed tension and the rate of tension rise were the same throughout, but the time integral of active tension was increased in muscles from the hypertensive rats in both age groups. The ratio of oxygen consumption to either external work or developed tension was decreased in muscles from the hypertensive rats. In contrast to these data, previous data from the hypertrophied cat model showed reductions in both the velocity and the extent of isotonic shortening as well as in the rate and amount of isometric tension development, and prolongation of contraction was not observed. A similar but smaller decrease in the oxygen requirements of contraction was found in hypertrophied cat myocardium. These contrasting data suggest not only that pressure induced hypertrophy is more fully compensatory in the rodent model but, more importantly, that general conclusions derived from any particular animal model of hypertrophy may be inappropriate.
The relaxation effects of forskolin and methylxanthines on noradrenaline (NA)-induced contractions were investigated by measuring isotonic contraction and intracellular calcium concentration ([Ca2+]i) in the epididymal side of guinea-pig vas deferens. NA (100 microM) and high K+ (55 mM) induced a biphasic contraction; fast, transient (phasic) and slow, sustained (tonic) phases. Both phases in either NA or high K+ stimulation were abolished in Ca2+-free solution. Pretreatment with 10 microM nifedipine, an L-type Ca2+ channel blocker, reduced both phasic and tonic contractions induced by high K+. In the case of NA-induced contraction, however, nifedipine reduced the phasic contraction but not the tonic contraction. The nifedipine-insensitive tonic contraction was relaxed by the application of polyvalent cations (Mn2+, Co2+, Cd2+ and La3+). These findings indicate that NA-induced biphasic contraction is mainly due to nifedipine-insensitive Ca2+ influx, especially in the tonic phase. Cyclic AMP-increasing agents such as forskolin (0.5-10 microM), IBMX (5-500 microM) and caffeine (1-20 mM) relaxed the NA-induced contraction extensively in a concentration-dependent manner. However, these agents only partially relaxed the high K+-induced contraction. Forskolin (10 microM) and IBMX (100 microM) reduced the [Ca2+]i response to NA, but had no effect on the [Ca2+]i response to high K+. These results suggest that an increase in intracellular cAMP may relax the NA-induced contraction by attenuating a nifedipine-insensitive Ca2+ influx and by a mechanism independent of a reduction in [Ca2+]i.
Huxley's sliding filament crossbridge muscle model coupled with parallel and series elastic components was simulated to examine the effect of various solution techniques in cardiac contractions. Solutions of both isometric and isotonic contraction cases showed that the force versus time curves were not significantly altered by solving the three-element Hill model with Huxley's Equation written as either an ordinary or partial differential equation (ODE or PDE), but this makes a difference in the solution time required. Various theoretical studies have used either the ODE or PDE representation. The crossbridge cycles at the end of a contraction showed approximately 25% and 15% difference in the isometric and isotonic cases when Huxley's Equation was written as either an ODE or PDE. Examination of the crossbridge distribution (distribution among states of reach) showed that assuming that the crossbridge distribution is a Gaussian function is a poor approximation since the shape changes considerably between the cardiac contracting and expanding phases, and using a technique such as a distribution moment approximation is questionable. Recent experimental studies have demonstrated that solving Huxley-type relations as ordinary differential equations gives good agreement with cardiac data, implying that as a first approximation, this can be successfully used.
The effect of shortening on contractile activity was studied in experiments in which shortening during the rising phase of an isotonic contraction was suddenly stopped. At the same muscle length and the same time after stimulation the rise in tension was much faster, if preceded by shortening, than during an isometric contraction, demonstrating an increase in contractile activity. In this experiment the rate of tension rise determined in various phases of contraction was proportional to the rate of isotonic shortening at the same time after stimulation. Therefore, the time course of the isotonic rising phase could be derived from the tension rise after shortening. The rate of isotonic shortening was found to be unrelated to the tension generated at various lengths and to correspond closely to the activation process induced by shortening. The length response explains differences between isotonic and isometric contractions with regard to energy release (Fenn effect) and time relations. These results extend previous work which showed that shortening during later phases of a twitch prolongs, while lengthening abbreviates contraction. Thus the length responses, which have been called shortening activation and lengthening deactivation, control activity throughout an isotonic twitch.
Changes in discharge rate of fusimotor neurones to pretibial flexor muscles were recorded during and after long-lasting fatiguing isometric and/or isotonic contractions of triceps surae in decerebrate cats. The contractions were elicited by electrical stimulation of the nerves to triceps. Fusimotor spikes were recorded from nerve filaments dissected free from the peroneal nerve. Responses of the fusimotor neurones were diverse. In isometric regime, 22 out of 40 units recorded exhibited an initial increase at the onset of muscle contraction, different in amplitude and duration among the units. In seven of these units an additional brisk burst of spike discharges, of different duration, occurred at the end of the contraction. In 15 fusimotor neurones (14 units with the initial response and an additional unit without it) a slow increase in discharge rate developed, starting during the contraction and outlasting it. In another eleven units the initial response was a decrease in discharge rate, lasting in six of them throughout the contraction. Another six units exhibited a sustained increase in discharge rate throughout the contraction, as well as, at a lower level, but still above the spontaneous one, thereafter. Similar patterns of changes in discharge rate, recorded in 31 of the units, were encountered during isotonic triceps contractions. It should be mentioned that many (about 20) additional silent neurones, responding to manipulating the skin and paw and/or stroking the fur, but not to triceps contractions were encountered. The majority of changes in discharge rate of fusimotor neurones to pretibial flexors differed markedly from those found previously in fusimotor neurones to triceps and hamstring muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
Even though it is well known that electromyography (EMG) characteristics are influenced by electrode placement it is common to use a single pair of sensors per muscle for EMG. This study was designed to determine if the ability to distinguish between contraction conditions was influenced by sensor location. Subjects (n = 10; 27+/-5.3 years; 82+/-13.4 kg; 178+/-7.1 cm) completed six elbow flexor conditions: three isometric contraction intensities (100% maximum effort, 80%, 50%) and three isotonic contraction intensities (heavy weight, 80% and 50% of the weight). Three pairs of electrodes were placed centrally, medially and laterally on the biceps brachii belly in line with the muscle fibers. Isometric contractions were held for 5s, with the middle 3 s analyzed. Isotonic exercises included five repetitions of elbow flexion-extension, with the middle three repetitions analyzed. Average EMG (EMG(AVG)), root mean square EMG (EMG(RMS)) and mean power frequency (MPF) were calculated for each extracted data set. Dependent variables were analyzed using 2 (contraction type) x 3 (intensity) repeated measures ANOVAs per sensor. EMG(AVG) was influenced by the interaction between contraction type and intensity for all sensors (p < 0.05). EMG(RMS) as well as MPF were influenced by the interaction between contraction type and intensity for the lateral and central leads (p < 0.05) but not the medial leads (p > 0.05). Different conclusions could have been reached from the same experiment due to different sensor locations. These differences were primarily related to comparing contraction types (i.e., isotonic vs. isometric).
This paper compares the effects of 6 wk of sub-maximal training by electrostimulation (100 Hz) and voluntary contractions on the contractile properties of the adductor pollicis muscle in intact man. The daily training program consisted of ten series of twenty 1-s isotonic contractions (60 to 65% of maximum) separated by 1-s intervals. The observed increase in muscle force, tested in maximal voluntary and electrically evoked contractions, appears to be significantly smaller during electrostimulation than during a training session performed by voluntary contractions. The increase in force recorded during electrostimulation is not associated with changes in the tetanus rates of tension development and tension relaxation (dP0/dt). Conversely, the tetanus time course is found to be significantly accelerated in muscles trained by voluntary contractions. No change of the surface action potential total area was observed during both training procedures. Furthermore, electrostimulation does not improve muscle resistance to fatigue, which is observed to be significantly increased after training by voluntary contractions. This study indicates that electrostimulation augments the muscle force of contraction by changing peripheral processes associated with intra-cellular events, without modifying the nervous command of the contraction. The comparison of the peripheral changes recorded during sub-maximal training by electrostimulation and voluntary contractions suggests that electrostimulation is less efficient, but complementary to voluntary training because the number and the type of trained motor units are different in the two procedures.