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Reliability of surface EMG during sustained contractions of the quadriceps.

The purpose of this study was to determine test-retest reliability for median frequency (MDF) and amplitude of surface EMG during sustained fatiguing contractions of the quadriceps. Twenty-two healthy subjects (11 males and 11 females) were tested on two days held one week apart. Surface EMG was recorded from rectus femoris (RF), vastus lateralis (VL) and vastus medialis (VM) during sustained isometric contractions at 80% and 20% of maximal voluntary contraction (MVC) held to exhaustion. Quadriceps fatigue was described using four measures for both MDF and amplitude of EMG: initial, final, normalized final and slope. For both MDF and amplitude, the initial, final and normalized EMG showed moderate to high reliability for all three muscle groups at both contraction levels (ICC=0.59-0.88 for MDF; ICC=0.58-0.99 for amplitude). Slope of MDF and amplitude was associated with a large degree of variability and low ICCs for the 80% but not the 20% MVC. MDF and amplitude of EMG during sustained contractions of the quadriceps are reproducible; normalized final values of MDF and amplitude show better reliability than slope.

Adult↗

The effect of 5'-N-ethylcarboxamideadenosine on the isolated hemidiaphragm of the rat during direct and indirect electrical stimulation.

Similar to adenosine and some of its derivatives, 5'-N-ethylcarboxamideadenosine (NECA) produced a biphasic effect on the isolated hemidiaphragm of the rat: a potentiation of the isometric contraction during direct electrical stimulation (in the presence of dipyridamole), and a depression during indirect electrical stimulation, and particularly so in a partially curarized preparation. The potentiating effect is presumed to be due to activation of the cAMP system, probably through A2 receptor sites, although a differentiation of the receptor subtype could not be made with aminophylline and XAC. Inhibition is most probably due to a depressant action of NECA on the acetylcholine release from the motor nerve terminals. These results accord with our previous findings, suggesting that adenosine may be part of a buffer system which participates in balancing the excitatory and inhibitory influences on skeletal muscle contraction.

Adenosine↗

Conditions for dipyridamole potentiation of skeletal muscle active hyperemia.

The effects of dipyridamole on active hyperemia were evaluated in dog gracilis muscles undergoing sustained isometric contractions. Muscles were stimulated to contract for 5, 15, 25, and 50 s at 20% maximal tension (20% Tmax) or for 10 s at 100% Tmax during intra-arterial infusion of either saline or dipyridamole (1 microM). In two separate groups of dogs, muscles were stimulated to contract under free-flow or restricted-flow (ischemic) conditions. In the later group, blood flow was reduced to 50% of precontraction level during the period of contraction. Dipyridamole increased resting vascular conductance by about 45%; however, it did not affect the change in vascular conductance resulting from muscle contraction. The recovery time for active hyperemia following free-flow contractions at 20% Tmax was not altered by dipyridamole. However, dipyridamole increased the recovery time following 50 s of restricted-flow contraction (20% Tmax) and 10 s of 100% Tmax contractions by 46 and 169%, respectively. These results suggest that adenosine contributes to active hyperemia following sustained ischemic contractions at 20% Tmax and contractions at 100% Tmax but not from contractions at 20% Tmax where blood flow is allowed to increase freely.

Animals↗

Influence of forskolin on the force-frequency behavior in nonfailing and end-stage failing human myocardium.

UNLABELLED: End-stage failing human myocardium is characterized by a negative force-frequency relationship (FFR), possibly as a result of reduced SR Ca2+ uptake capacity. We investigated the effects of the direct adenylate cyclase stimulator, forskolin, on force of contraction and FFR in isolated human myocardium from 7 nonfailing hearts (NF) and end-stage failing hearts (NYHA IV) due to either ischemic (ICM; n = 13) or dilated cardiomyopathy (DCM; n = 16). METHODS: Isolated left ventricular muscle strips, isometric contraction, electrical stimulation at a basal stimulation rate of 1 Hz (37 degrees C). Inotropic responses: Cumulative concentration-response curves for forskolin (0.01-10 microM) and for Ca2+ (2.5-15 mM). Force-frequency experiments: stepwise increase in stimulation rate from 0.5 to 3.0 Hz without and in the presence of 0.3, 1.0 or 3.0 microM forskolin. RESULTS: Forskolin concentration-dependently increased force of contraction to 386 +/- 28% (n = 5) in NF, to 256 +/- 48% (n = 7) in ICM, and to 212 +/- 13% (n = 14) in DCM. The effectiveness of forskolin was significantly reduced in failing myocardium. Ca2+ increased force of contraction to maximally 438 +/- 108% in NF, to 267 +/- 15% in ICM, and to 292 +/- 20% in DCM. Again, the effectiveness of Ca2+ was significantly reduced in failing myocardium. Forskolin activated contractile reserve to similar extents in all types of myocardium (90%, 95%, and 82%, respectively). Force of contraction continuously increased with increasing stimulation rates in nonfailing myocardium (positive FFR), but was blunted or inversed in ICM and DCM. Prestimulation with forskolin (0.3 microM) further enhanced frequency-potentiation in nonfailing, and normalized the slope and optimum stimulation frequency in ICM and DCM. However, at higher concentrations of forskolin, FFR was blunted or inversed in non-failing myocardium, and further impaired in failing myocardium. CONCLUSION: Low concentrations of forskolin with only marginal inotropic effects may partially normalize the inverse force-frequency relation in end-stage failing human myocardium. Reduced cAMP levels in conjunction with reduced expression of SR Ca2+ ATPase may be the underlying cause for altered excitation-contraction coupling in diseased human hearts.

Biomechanical Phenomena↗

Loss of power during fatigue of human leg muscles.

1. We have investigated the loss of power seen during high-intensity exercise of human leg muscles such as might occur during sprinting. Subjects exercised the quadriceps and hamstring muscle groups using a Cybex dynamometer at an angular velocity of 90 deg s-1 once a second for 6 min. At 1 min intervals the quadriceps were electrically stimulated via the femoral nerve to produce an isometric contraction which was then released into an isokinetic shortening contraction at 90 deg s-1. 2. The extent of central fatigue was assessed by comparing the force of a voluntary isokinetic contraction with that elicited by electrical stimulation during isokinetic releases. Two subjects were repeatedly tested. In the first series of experiments, exercising the quadriceps of one leg, the instantaneous power fell to about 50% over the course of 2 min and remained constant for the rest of the exercise. For one subject the voluntary and electrically stimulated forces declined in parallel while for the second subject the voluntary force was 10% less than the stimulated force at the end of the exercise. These results show that central fatigue represented a minor factor contributing no more than one-fifth of the total loss of power in these circumstances. 3. In a second series of experiments the subjects alternately contracted the quadriceps and the hamstrings of both legs in an exercise which had a high rating of perceived exertion and entailed considerable respiratory and cardiovascular effort. The time course and proportionate loss of power were very similar to those seen with the one-leg exercise and neither subject showed evidence of significant central fatigue. The pattern of force loss was very similar for the hamstrings. We conclude that, for determined subjects, afferent feedback from muscles, tendons and joints or from the respiratory and cardiovascular systems does not have a major role in inhibiting voluntary activation of the quadriceps during heavy exercise. 4. In both series of experiments the power output during electrically stimulated isokinetic contractions was reduced to 50% of the initial value after 2 min of exercise while the isometric force, measured immediately before the release, fell to only 75%. This suggests that fatigue affects isometric and shortening contractions to different extents and the loss of power may be due to a combination of factors, only one of which is evident in the loss of isometric force.

Adult↗

Influences of repetitive muscle contractions with different modes on tendon elasticity in vivo.

The present study aimed to investigate the effects of repetitive muscle contractions on the elasticity of human tendon structures in vivo. Before and after each endurance test, the elongation of the tendon and aponeurosis of vastus lateralis muscle (L) was directly measured by ultrasonography while the subjects performed ramp isometric knee extension up to maximal voluntary isometric contraction (MVC). Six male subjects performed muscle endurance tests that consisted of knee extension tasks with four different contraction modes: 1) 50 repetitions of maximal voluntary eccentric action for 3 s with 3 s of relaxation (ET1), 2) three sets of 50 repetitions of MVC for 1 s with 3 s of relaxation (ET2), 3) 50 repetitions of MVC for 3 s with 3 s of relaxation (ET3), and 4) 50 repetitions of 50% MVC for 6 s with 6 s of relaxation (ET4). In ET1 and ET2, there were no significant differences in L values at any force production levels between before and after endurance tests. In the cases of ET3 and ET4, however, the extent of elongation after the completion of the tests tended to be greater. The L values above 330 N in ET3 and 440 N in ET4, respectively, were significantly greater after endurance tests than before. These results suggested that the repeated longer duration contractions would make the tendon structures more compliant and that the changes in the elasticity might be not be affected by either muscle action mode or force production level but by the duration of action.

Adult↗

Energy expenditure of longitudinal smooth muscle of rabbit urinary bladder.

Heat production, oxygen consumption, and lactate production of longitudinal smooth muscle from rabbit urinary bladder has been measured at 27 degrees C. In isometric contractions (initiated by 1-Hz electrical stimulation) ranging in duration from 2 to 300 s, total energy expenditure correlated linearly with the force-time integral. For any given force-time integral oxygen consumption could account for only approximately 60% of the total energy measured as heat production. A substantial contribution of aerobic lactate production to the total energy flux was observed. This lactate production was also linearly correlated with force-time integral and was of sufficient magnitude to account for the discrepancy between total energy expenditure determined as heat production and oxygen consumption. The suprabasal rate of energy expenditure during the maintenance of force was approximately 2.6 mW/g and remained constant throughout contractions of up to 5-min duration, suggesting that in this muscle there is no change in the energetic cost of force maintenance with increasing duration of contraction. The rate of energy expenditure during the initial period of force development was, however, about twofold greater than that during subsequent force maintenance, indicating that there is an extra energy cost associated with the activation of contraction and development of force above that required for force maintenance.

Animals↗

[Spontaneous rhythmic contractions of human placental vessels: is it an evidence for a physiological pacemaker in blood vessels?].

BACKGROUND: Placental vessels are not innervated. Therefore the vasomotor activity and vascular tone is not regulated by the nervous system. AIM: To assess the existence of pacemaker mechanisms related to rhythmic motor activity of blood vessels. MATERIAL AND METHODS: Isometric contractions of rings from umbilical and chorionic vessels of term human placentas were monitored. RESULTS: Recordings of the circular layer of chorionic and umbilical vessels revealed rhythmic spontaneous contractions with a frequency of 1.4 +/- 0.05 cycles/min, the duration of each cycle was 42.8 +/- 0.24 s (n = 12). The amplitude of contractions was larger in veins than in arteries, predominating in umbilical vein biopsies, proximal to the fetus. Both the frequency and the amplitude of contractions were relatively constant during the first 30 min. However, after an hour, the frequency declined while the amplitude increased. The absence of the endothelium neither modified the frequency nor the amplitude of the rhythmic activity. Blockage of voltage dependent sodium channels or calcium channels did not alter the frequency of spontaneous contractions, although their magnitude was reduced. Glibenclamide, an ATP-dependent K+ channel blocker or the blockade of gap junctions ablated the frequency and amplitude of spontaneous contractions. CONCLUSIONS: We propose that rhythmic contractions are triggered by pacemaker cells located in the circular layer of the smooth muscle of blood vessels and spread via gap junctions; they likely contribute to the control of blood flow.

Biological Clocks↗

Muscle fatigue simulator.

The above description of the structure and operation of the Muscle Fatigue Simulator was necessarily presented in an abridged fashion (a more complete description to be found in the report (3). The main goal of the construction of the model was creation of a system simulating the changes occurring in the EMG signal under the impact of local muscle fatigue. The performed verification of the model in the aspect of time, frequency and dynamic changes of simulated parameters confirmed simulating faithfulness of the model and thereby the initial assumptions and the general idea of the model may be considered correct. The muscle fatigue simulator has the capability to display some changes occurring in myoelectric signals during fatiguing contractions, and it is believed to have a great merit in demonstration of the signal processes within the muscle. For that reason, the Muscle Fatigue Simulator can be of use in teaching and in demonstration of particulars of the myoelectric signal during isometric contraction. It may also be used in instrument calibrating and in checking the operation of the EMG-signal measuring and analysing equipment applied in ergonomic studies.

Action Potentials↗

Arm tremor and precision of hand force control in a short and long term flight on the MIR-Space-Station.

To determine whether long and short time exposure of man in 0g alters normal physiological tremor patterns we recorded arm tremor using an accelerometer as well as hand forces and tremor during constant isometric contraction using a load cell. Arm tremor was decreased during both flights in amplitude and frequency. Shortly after the long term flight arm tremor amplitude was increased, indicating adaptive changes in the tonic reflex loop. Isometric hand tremor remained unchanged during the long and short time flight demonstrating that the contractile properties of hand muscles remained constant. Precision of hand force was decreased until the half duration of the long term flight.

Arm↗

Quantitative analysis of sarcomere non-uniformities in active muscle following a stretch.

Electron microscopy of toad (Bufo marinus) muscle fixed without relaxing after a single eccentric contraction at muscle lengths greater than optimum showed over-stretched half-sarcomeres in sufficient numbers to account for more than half of the imposed stretch. Such sarcomeres were absent in another muscle fixed without relaxing after an isometric contraction at the same length and largely absent in a third muscle that underwent eccentric contraction at muscle lengths less than optimum. This provides direct evidence in support of the hypothesis that lengthening of muscles at long length involves lengthening of a few half sarcomeres to beyond filament overlap, while most half sarcomeres are extended much less than in proportion to muscle extension.

Animals↗

Physiological significance of myosin phosphorylation in skeletal muscle.

Each S-1 or head portion of the myosin molecule in skeletal muscle contains a subunit known as the regulatory or phosphorylatable light chain (P-LC). Phosphorylation of the P-LC is mediated by the second messenger Ca2+ and takes place when the muscle fibre is activated. In smooth muscle, phosphorylation of the P-LC is the principal mechanism that initiates contraction, but in skeletal muscle myosin P-LC phosphorylation is not required for contraction and a definitive role has not been established. It has been proposed that P-LC phosphorylation modulates the intrinsic nature of actin-myosin interactions, leading to force potentiation under suboptimal activation conditions. An example of this is posttetanic potentiation. This paper describes a P-LC phosphorylation induced mechanism for force enhancement during isometric contraction. In addition, it summarizes recent data revealing that P-LC phosphorylation is associated with enhanced work output of fast-twitch muscle during shortening and lengthening contractions.

Actins↗

Relaxation from a voluntary contraction is preceded by increased excitability of motor cortical inhibitory circuits.

Termination of a muscle contraction is as important a part of movement as muscle activation yet the mechanisms responsible are less well understood. In the present experiments we examined the possible role of intracortical inhibitory circuits in terminating a 20% maximum isometric contraction of the first dorsal interosseous muscle (FDI) in eight healthy subjects. Subjects performed the task simultaneously with both hands and received single or pairs (at an interstimulus interval of 3 ms to evaluate short interval intracortical inhibition, SICI) of transcranial magnetic stimuli (TMS) via a focal coil over the motor hand area of the left hemisphere at different times before and after the onset of relaxation. The amplitude of the motor-evoked potential (MEP) following a single or a pair of TMS pulses was measured in the right FDI and plotted relative to the onset of relaxation as estimated from the surface electromyogram (EMG) of the left FDI. MEPs were larger during contraction than after relaxation whereas SICI was absent during contraction and reappeared after relaxation. We found that in all subjects, the time course of MEP changes during relaxation was closely fitted by a Boltzmann sigmoidal curve which allowed us to estimate the mean MEP amplitudes as well as the ratio of the amplitudes after single or pairs of TMS pulses (i.e.%SICI) at any time in the task. The data showed that the amplitude of MEPs to single pulse TMS had started to decline at about the same time as the onset of EMG silence. Furthermore, the size of the MEPs evoked by paired pulses decreased up to 30 ms beforehand. The latter suggests that an increase in SICI occurs prior to the onset of MEP changes, and hence that increased cortical inhibition may play a role in suppressing corticospinal excitability during relaxation. A subsidiary experiment showed that the time relations of changes in SICI and MEP were unchanged by a period of 10 min training on the task.

Adult↗

Intracellular pH regulation in resting and contracting segments of rat mesenteric resistance vessels.

1. The pH-sensitive dye 2',7'-bis-(2-carboxyethyl)-5 (and -6)-carboxyfluorescein (BCECF) was used to measure intracellular pH (pHi) in segments of rat resistance vessels (internal diameter about 200 microns) with the vessels mounted in a myograph for simultaneous measurements of isometric contraction. 2. BCECF loaded slowly into the vessels over 1 h and did not affect the maximal contractility of the vessels. There was a loss of dye with time which, however, was very slow when the segments were only excited for 2 s/min, suggesting that the loss was mainly due to dye bleaching with only a very slow leak. 3. The ratio of the emissions (at 540 nm) with excitation at 495 and 450 nm was calibrated in terms of pH using the K+-H+ ionophore nigericin. This calibration gave a pHi value of 7.15 +/- 0.02 (n = 20), suggesting that hydrogen ions are not in electrochemical equilibrium in these vascular smooth muscles which have a membrane potential of about -60 mV. 4. Addition of 10 mM-NH4Cl caused a transient alkalinization and wash-out of 10 mM-NH4Cl a transient acidification. Increasing CO2 with maintained bicarbonate caused a rapid acidification followed by an incomplete recovery. Removal of CO2 and bicarbonate (HEPES-buffered solution) with constant extracellular pH caused a transient alkalinization but steady-state pHi was not significantly altered. 5. In bicarbonate-free buffer the Na+-H+ exchange blocker 5-(N-ethyl-N-isopropyl) amiloride (EIPA) and sodium-free conditions caused a slow acidification. In bicarbonate buffer (PSS) EIPA had no detectable effect after 10 min but the anion exchange blocker diisothio-cyanatostilbenedisulphonic acid (DIDS) caused a small acidification over that time course. 6. The rate of recovery after an acid load was about 50% lower in HEPES buffer compared to PSS and it was inhibited by EIPA. In PSS amiloride and EIPA each had a small inhibitory effect on the pH recovery after an acid load. DIDS also inhibited the recovery from an acid load in PSS and this effect was additive to that of EIPA. DIDS and EIPA also had additive inhibitory effects on the 22Na+ influx stimulated by the acid loading, while in HEPES buffer DIDS had no effect on either pH recovery or 22Na+ influx. These results suggest that a Na+-H+ exchange and an influx of bicarbonate coupled to sodium influx are of importance for pHi control in these vessels.(ABSTRACT TRUNCATED AT 400 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Force deficits after repeated stretches of activated skeletal muscles in female and male rats.

Force deficits after stretches of activated plantar flexor muscles were measured in six male Sprague-Dawley rats (285 +/- 10 g, age 62 +/- 4 days, mean +/- SE) and compared with six age-matched (193 +/- 6 g, age 67 +/- 3 days) and six weight-matched female rats (273 +/- 7 g, age 141 +/- 9 days). Twenty stretches, imposed on isometric contractions at 90 degrees (0.2 ms pulse duration, 80 Hz, 5.4 +/- 0.3 V, duty cycle 0.006), were produced by ankle rotation from 90 to 40 degrees. Before the stretch protocol, weight-matched groups had similar isometric forces at an ankle position of 90 degrees at 5, 10, 20, 40, 60 and 80 Hz but forces were lower for age-matched females. For all groups, normalized force-frequency relationships were similar. During the stretch protocol, deficits for isometric force at 90 degrees and peak stretch force at 40 degrees with stretch number were similar for all groups. One hour after the stretches, isometric force deficits at 90 degrees at 40, 60 and 80 Hz were larger for females in weight-matched groups (e.g. 80 Hz, female: 47.8 +/- 1.7%; male: 41.1 +/- 1.7%; P < 0.05), perhaps because of a difference in age (P < 0.05). For age-matched groups, isometric force deficits at 90 degrees were similar at all frequencies. The susceptibility for force deficits by stretches of activated skeletal muscles was not gender-dependent for 2-month-old rats.

Animals↗

Effect of ankle joint position and electrode placement on the estimation of the antagonistic moment during maximal plantarflexion.

During maximal efforts, antagonistic activity can significantly influence the joint moment. During maximal voluntary "isometric" contractions, certain joint rotation can not be avoided. This can influence the estimation of the antagonistic moment from the EMG activity. Our study aimed to quantify the influence on the calculated agonistic moment produced during maximal voluntary isometric plantarflexions (a) when estimating antagonistic moments at different ankle angles and (b) when placing the EMG electrodes at different portions over the m. tibialis anterior. Ten subjects performed maximal voluntary isometric plantarflexions at 90 degrees ankle angle. In order to estimate the antagonistic moment, submaximal isometric dorsiflexions were performed at various ankle angles. Moment and EMG signals from mm. triceps surae and tibialis anterior were measured. The RMS differences between plantarflexors moment calculated considering the antagonistic cocontraction estimated at the same ankle angle at which the maximal plantarflexion moment was achieved and at different ankle angles ranged from 0.10 to 2.94 Nm. The location of the electrodes led to greater RMS differences (2.35-5.18 Nm). In conclusion, an angle 10 degrees greater than the initial plantarflexion angle is enough to minimize the effect of the change in length of the m. tibialis anterior during the plantarflexion on the estimation of the plantarflexors moment. The localisation of the electrodes over the m. tibialis anterior can influence the estimation of its cocontraction during maximal plantarflexion efforts.

Adult↗

GABAergic mechanisms involved in the vagally mediated heart rate response to muscle contraction as revealed by studies with benzodiazepines.

The aim of this study was to determine if central GABA mechanisms are involved in the cardiac vagal withdrawal at the beginning of exercise in man. We tested whether GABA-enhancing effects of a benzodiazepine could be observed in the HR change (R-R interval) immediately following the onset of a brief (10s) isometric contraction (60 % maximum) of the biceps muscle. The difference between the change in R-R interval occurring during the same phase of respiration was compared for placebo (Pla) and 10 mg oral diazepam (Dz) treatment in a double blind, crossover trial. ECG, blood pressure, respiration and biceps muscle tension were recorded. The subjects breathed to a metronome and R-R interval measurements were plotted for early and late inspiration and early and late expiration. The mean values of the first late expiration R-R interval immediately following the start of contraction in early expiration were compared to the same measurements without contraction. Contractions initiated following diazepam treatment resulted in a significantly greater reduction in R-R interval (P < 0.05) implying that GABAergic suppression of cardiac vagal outflow may be responsible for contraction-induced tachycardia in man.

Adolescent↗

Basic aspects of action tremors in the human M. brachioradialis.

Since the first measurements of tremors it was obvious that the tremor signal originates from very complicated and continuously changing nervous and mechanical factors. However, the tremors originate in the beginning from the action tremors of the skeletal muscles. In this study the basic structure of the action tremors, regular 13-Hz oscillations, was revealed (measured by an accelerometer fixed on the distal end of the muscle belly of the m. brachioradialis). The mechanical oscillations measured with this technique had a linear relationship to the electrical oscillations of the EMG. Further, harmonic interference of isometric contraction with faradic contraction was observed. During simultaneous contraction of neighbouring muscles, completely synchronous but exactly out-of-phase oscillations were observed.

Adult↗