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PubMed2004

Acetyl group availability influences phosphocreatine degradation even during intense muscle contraction.

We previously established that activation of the pyruvate dehydrogenase complex (PDC) using dichloroacetate (DCA) reduced the reliance on substrate-level phosphorylation (SLP) at the onset of exercise, with normal and reduced blood flow. PDC activation also reduced fatigue development during contraction with reduced blood flow. Since these observations, several studies have re-evaluated our observations. One study demonstrated a performance benefit without a reduction in SLP, raising a question mark over PDC's role in the regulation of ATP regeneration and our interpretation of fatigue mechanisms. Using a model of muscle contraction similar to the conflicting study (i.e. tetanic rather than twitch stimulation), we re-examined this question. Using canine skeletal muscle, one group was infused with saline while the other was pretreated with 300 mg (kg body mass)(-1) DCA. Muscle biopsies were taken at rest, peak tension (1 min) and after 6 min of tetanic electrical stimulation (75 ms on-925 ms off per second) and blood flow was limited to 25% of normal values observed during contraction. DCA reduced phosphocreatine (PCr) degradation by 40% during the first minute of contraction, but did not prevent the almost complete depletion of PCr stores at 6 min, while muscle fatigue did not differ between the two groups. During intermittent tetanic stimulation PCr degradation was 75% greater than with our previous 3 Hz twitch contraction protocol, despite a similar rate of oxygen consumption at 6 min. Thus, in the present study enhanced acetyl group availability altered the time course of PCr utilization but did not prevent the decline towards depletion. Consistent with our earlier conclusions, DCA pretreatment reduces muscle fatigue only when SLP is attenuated. The present study and our met-analysis indicates that enhanced acetyl group availability results in a readily measurable reduction in SLP when the initial rate of PCr utilization is approximately 1 mmol (kg dry mass)(-1) s(-1) or less (depending on intrinsic mitochondrial capacity). When measured early during an uninterrupted period of muscle contraction, acetyl group availability is likely to influence SLP under any condition where mitochondria are responsible for a significant proportion of ATP regeneration.

Adenosine Triphosphate↗
PubMed2006

Viscosity as an inseparable partner of muscle contraction.

A simple model is presented where, by an iterative procedure, the forces delivered by the power strokes are summed up to overcome the load. The system is moderated by the viscous hindrance. The model reproduces the features of muscle contraction as defined by the data of He et al. [1997. ATPase kinetics on activation of permeabilized isometric fibres from rabbit and frog muscle: a real time phosphate assay. J. Physiol. 501, 125-148] on rabbit psoas muscle fibres. According to the model power strokes are random. Energy summation take place if the subsequent power stroke occurs before the energy delivered by the previous power stroke is completely used. In order the sarcomere to be competent to contract initial driving force must reach a threshold whose value increases with the load. The step size of the power stroke decreases with the increase of the load. The viscous regime is simulated by the equation, where 1/k measures the viscous hindrance of the system. The relationship between water activity, viscosity and stiffness is discussed. It is concluded that the three parameters vary cyclically and that when water activity decreases (sarcomere shortening, cross-bridge attachment) viscosity and stiffness increase.

Animals↗
PubMed2001

Motor potentials evoked by transcranial magnetic stimulation during isometric and dynamic masseter muscle contraction in humans.

The facilitation of muscle motor potentials evoked by transcranial magnetic stimulation (TMS) has been demonstrated convincingly during both isometric and dynamic activity in the limbs but not in the jaw muscles. An experimental design involving TMS, surface electromyography and controlled muscle-activity was employed to investigate the motor response of the human masseter during voluntary isometric and dynamic voluntary conditions. During the isometric condition, an increase in muscle facilitation resulted in a progressive increase in motor-evoked potential (MEP) amplitude that was consistently greater on the side contralateral to that subjected to TMS (P < 0.05). No difference in MEP amplitude or laterality of response was revealed for the two dynamic conditions. The sample size may have been too small to reveal any differences. The modulation of MEPs during isometric activity was probably due to cortical and brainstem mechanisms. Putative variation in masseter MEPs during dynamic conditions cannot be discounted.

Adult↗
PubMed1986

A model for the Ca2+-induced conformational transition of troponin C. A trigger for muscle contraction.

The initial contractile event in muscle is the binding of Ca2+ ions to troponin C of the troponin complex, leading to a series of conformational changes in the members of the thin and thick filaments. Knowledge of the crystal structure of turkey skeletal muscle troponin C has provided a structural basis for the modeling of the first stage of this process in atomic detail. This crystal structure probably represents the molecule in the relaxed state of muscle, with two of the maximum of 4 Ca2+ ions bound. The basis for the model presented here is that upon binding of the additional two Ca2+ ions, the regulatory domain of the molecule undergoes a conformational transition to become closely similar in structure to the domain which always binds Ca2+ or Mg2+ under physiological conditions. The root mean square discrepancy in atomic coordinates between the apo and the modeled Ca2+-bound states of the regulatory domain is 4.8 A, with some shifts as large as 10-15 A in the region near the linker between the two Ca2+ binding sites. It is demonstrated that this Ca2+-bound conformation of the regulatory domain conforms to accepted protein structure rules and that the change in conformation can be accomplished without encountering any barriers too high to be surmounted on the physiological time scale.

Amino Acid Sequence↗
PubMed1990

Different responses in skin and muscle sympathetic nerve activity to static muscle contraction.

We microneurographically recorded the traffic of sympathetic nerves leading to foot volar skin activity (SSA) and leg skeletal muscle activity (MSA) during isometric handgrip and simultaneously determined sweat rate by the ventilated capsule method and skin blood flow by laser-Doppler flowmetry in the innervating area of SSA. SSA increased abruptly and was almost constant during handgrip, accompanied by an increase in sweat rate, whereas skin blood flow showed no significant change during the handgrip. MSA showed a time-dependent increase during the course of handgrip. During arterial occlusion of the working forearm after handgrip, SSA decayed to the precontraction control level, whereas MSA remained at a higher level than during control. During involuntary biceps muscle contraction induced by electrical stimulation, both SSA and MSA increased. The results suggest that the SSA response during voluntary handgrip, which was demonstrated to contain mainly sudomotor activity, might be influenced by central command and input from peripheral mechanoreceptors but be influenced little by input from muscle chemoreceptors.

Adult↗
PubMedDate not supplied

[Statistics on actin globule chains, stretched by hydrogen bonds, and the Hill law in quantum mechanics theory of muscle contraction].

The process of sarcomere membranes approaching under the action of actin and myosin filament stretching is studied theoretically. In elaboration of previous studies it is supposed that this stretching is due to the formation of hydrogen bonds excited by the energy of ATP splitting. A possibility for the hydrogen bond breakage at different stages of contraction is considered to be the greater the more are the polymers stretched, and the larger statistical scatter in the moments of H-bonds formation at different filaments if it is supposed that sarcomere contraction occurs much slower than stretching of each separate filament. As a result, one obtains a relationship between the rate of contraction and the external force which is close to the Hill's law, and the external force efficiency of a muscle contraction and heat extraction value are related to parameters of polymers and their properties.

Actins↗
PubMed1996

Mechanisms of smooth muscle contraction elicited by cationic proteins in guinea pig trachealis.

Cationic proteins elicit contraction of airway smooth muscle, but the mechanisms by which this occurs are not completely understood. We studied potential mechanisms by which eosinophil major basic protein (MBP) and the synthetic cationic proteins poly-L-lysine (PL) and poly-L-arginine (PA) cause contraction of isolated guinea pig tracheal smooth muscle (TSM) in vivo. Topical application of 10(-8) mol/cm2 of each protein to an isolated tracheal segment elicited TSM contraction with potency PL > MBP > PA. Pretreatment with atropine blocked the subsequent response to MBP but did not block the response to either PL or PA. Pretreatment with indomethacin blocked the subsequent response to both MBP and PL but did not block the response to PA. We demonstrate that MBP causes contraction of guinea pig TSM both through stimulation of the parasympathetic nervous system and secretion of a cyclooxygenase mediator. Neither PL nor PA, while of similar molecular weight and charge as MBP, cause TSM contraction via the parasympathetic nervous system, though some cationic proteins may act via a prostanoid mediator. Thus the cationic charge of MBP is not solely responsible for its effects on TSM in the guinea pig.

Acetylcholine↗
PubMed2001

Invited Review: pathophysiology of cardiac muscle contraction and relaxation as a result of alterations in thin filament regulation.

Cardiac muscle contraction depends on the tightly regulated interactions of thin and thick filament proteins of the contractile apparatus. Mutations of thin filament proteins (actin, tropomyosin, and troponin), causing familial hypertrophic cardiomyopathy (FHC), occur predominantly in evolutionarily conserved regions and induce various functional defects that impair the normal contractile mechanism. Dysfunctional properties observed with the FHC mutants include altered Ca(2+) sensitivity, changes in ATPase activity, changes in the force and velocity of contraction, and destabilization of the contractile complex. One apparent tendency observed in these thin filament mutations is an increase in the Ca(2+) sensitivity of force development. This trend in Ca(2+) sensitivity is probably induced by altering the cross-bridge kinetics and the Ca(2+) affinity of troponin C. These in vitro defects lead to a wide variety of in vivo cardiac abnormalities and phenotypes, some more severe than others and some resulting in sudden cardiac death.

Actin Cytoskeleton↗
PubMed1993

Endothelin ETA and ETB receptors mediate vascular smooth-muscle contraction.

Endothelin (ET) ETA receptors on vascular smooth muscle are believed to mediate the vasoconstrictor effects of ET isopeptides, and ETB receptors on the endothelium are thought to mediate the vasodilator effects. This study has investigated the receptors mediating endothelin-induced contraction of isolated ring preparations of rat thoracic aorta (RTA) and rabbit carotid artery (RCA), pulmonary artery (RPA), and jugular vein (RJV). In RTA and RCA, ET-1 (EC50 4.5 and 5.2 nM, respectively) was 82- and 108-fold, respectively, more potent than ET-3, whereas the ETB receptor-selective agonists sarafotoxin S6c (S6c) and Ala1,3,11,15-ET-1 (4-Ala-ET-1) were without effect up to > or = 1 microM. In contrast, in RPA and RJV, ET-1 (EC50 3.1 and 0.7 nM, respectively) and ET-3 (EC50 4.4 and 0.9 nM, respectively) were equipotent, and 4-Ala-ET-1 (EC50 10.7 and 2.1, respectively) and S6c (EC50 0.4 and 0.1 nM, respectively) were potent contractile agonists. The ETA receptor antagonist BQ123 (D-Val-Leu-D-Trp-D-Asp-Pro) competitively antagonized the effects of ET-1 in RTA and RCA (pA2 values 6.9 +/- 0.1 and 6.8 +/- 0.2, respectively) but did not antagonize (at 10 microM) contractions to ET-1, ET-3, or 4-Ala-ET-1 in RPA and RJV. In conclusion, contraction of vascular smooth muscle by endothelins can be mediated by both ETA and ETB receptors.

Animals↗
PubMed1997

Static muscle contraction elicits a baroreflex-dependent increase in glutamate concentration in the ventrolateral medulla.

In anesthetized cats, static contraction of the hindlimb reflexly increases mean arterial pressure (MAP). This cardiovascular adjustment is reduced by the arterial baroreflex. Both of these reflex responses are mediated through activation of ventrolateral medullary (VLM) regions. We tested the hypothesis that the concentration of glutamate (Glu) increases in the caudal ventrolateral medulla (cVLM) during static hindlimb contractions in anesthetized cats, and that barodenervation reduces this elevation in Glu levels. Static contractions of the triceps surae muscle of one hindlimb were evoked by electrical stimulation of the peripheral ends of cut L7 and S1 ventral roots. After the insertion of the microdialysis probes and a 3-h recovery period, a 2-min static contraction increased MAP by 47 +/- 7 mmHg. The concentration of Glu increased from 606 +/- 189 to 1042 +/- 228 nM. These results were repeatable in that Glu, as well as MAP, rose by a similar amount in two subsequent contractions. By contrast, in a subset of cats paralyzed prior to the third contraction, neither MAP nor Glu were significantly increased over baseline levels during the third stimulation period. In a third group of cats, hindlimb contraction increased MAP and Glu levels. However, the Glu release was attenuated in subsequent contractions after these cats were barodenervated. During the same periods of stimulation, the denervation accentuated the rise in MAP. These data demonstrate that static contraction of the hindlimb increases the extracellular concentration of Glu in the cVLM. Further, our study implicates this neurotransmitter in the baroreflex mediated reduction of the pressor reflex response to static muscle contraction.

Animals↗
PubMed2006

Cardiac autonomic modulation following high-intensity static muscle contractions.

BACKGROUND: The purpose of this investigation was to examine cardiac autonomic modulation, as measured by wavelet analysis of heart rate variability, following a series of high-intensity static muscle contractions. METHODS: After 10 minutes of rest, electrocardiograms (ECGs) were collected in 17 participants (age, 24.5 +/- 1 yr) 2.5 minutes before (REST) and 10 minutes after a series of static contractions of the knee extensors. Participants performed contractions with the nondominant leg (knee fixed at 90 degrees) at either 70% or 85% (randomized order) of their maximal voluntary contraction (MVC) on two separate visits. The postexercise ECGs were further divided into four consecutive 2.5-minute segments (POST 1-POST 4) to evaluate the time course of any possible autonomic changes after exercise. Each 2.5-minute segment was evaluated for the standard deviation of normal RR intervals (SDNN) and the percentage of successive RR intervals that differed by more than 50 ms (pNN50). Frequency-domain indices were obtained via wavelet transformation giving coefficients that reflected high- and low-frequency fluctuations in heart period (HFw and LFw). RESULTS: SDNN was elevated during POST-1 and pNN50 was reduced during POST-3 and POST-4 (P < 0.05) compared to REST for both intensities. Furthermore, HFw and LFw were increased during POST-1 and reduced during POST-3 and POST-4 compared to REST for both intensities (P < 0.05). CONCLUSION: These data suggest that complex alterations cardiac autonomic modulation exist for at least 10 minutes following a series of high-intensity static contractions performed at either 70% or 85% of MVC.

Adult↗
PubMed1996

Uncoupling in the wall of the cartilaginous bronchus of the pig produced by smooth muscle contraction.

Studies in small non-cartilaginous airways suggest that the cross sectional area of the airway wall (comprising the smooth muscle and mucosa) is unaltered during the contraction-relaxation cycle produced by bronchial provocation. In the present study we examined whether the wall area of large cartilaginous bronchi remained constant during bronchoconstriction produced by acetylcholine (ACh, 10(-4)-10(-2)M), and if not the effect of this on the narrowing of the bronchial lumen. Narrowing of the lumen and adventitia of bronchial segments, 3.6 mm id from pigs, was simultaneously recorded using endoscopy and video imaging of the airway lumen. Concurrently, the shortening of the smooth muscle was estimated morphometrically from the same bronchi fixed during muscle contraction. In individual bronchi, ACh produced from 5 to 60% shortening of the smooth muscle, which caused up to 64% narrowing of the bronchial lumen, but only approximately 10% narrowing of the adventitia. Lumen narrowing was greater than predicted. Morphological assessment showed a doubling of the area between the smooth muscle and the cartilage, in response to maximum smooth muscle contraction by ACh. In contrast the area of the smooth muscle and mucosa did not change. Similar changes in bronchial morphology were produced in whole lung slices, incubated in ACh or histamine. We conclude that the inner airway wall uncouples from the outer wall during muscle contraction and that this increases the narrowing of the airway lumen relative to the adventitia.

Acetylcholine↗
PubMed2001

Influence of ribose on adenine salvage after intense muscle contractions.

The influence of ribose supplementation on skeletal muscle adenine salvage rates during recovery from intense contractions and subsequent muscle performance was evaluated using an adult rat perfused hindquarter preparation. Three minutes of tetanic contractions (60 tetani/min) decreased ATP content in the calf muscles by approximately 50% and produced an equimolar increase in IMP. Effective recovery of muscle ATP 1 h after contractions was due to reamination of IMP via the purine nucleotide cycle and was complete in the red gastrocnemius but incomplete in the white gastrocnemius muscle section. Adenine salvage rates in recovering muscle averaged 45 +/- 4, 49 +/- 5, and 30 +/- 3 nmol. h(-1). g(-1) for plantaris, red gastrocnemius, and white gastrocnemius muscle, respectively, which were not different from values in corresponding nonstimulated muscle sections. Adenine salvage rates increased five- to sevenfold by perfusion with approximately 4 mM ribose (212 +/- 17, 192 +/- 9, and 215 +/- 14 nmol. h(-1). g(-1) in resting muscle sections, respectively). These high rates were sustained in recovering muscle, except for a small (approximately 20%) but significant (P < 0.001) decrease in the white gastrocnemius muscle. Ribose supplementation did not affect subsequent muscle force production after 60 min of recovery. These data indicate that adenine salvage rates were essentially unaltered during recovery from intense contractions.

Adenine↗
PubMed1993

Use of the endothelin antagonists BQ-123 and PD 142893 to reveal three endothelin receptors mediating smooth muscle contraction and the release of EDRF.

1. We have compared the receptors mediating the contractions of rings of rat thoracic aorta or rabbit pulmonary artery and rat stomach strips in response to the endothelin/sarafotoxin (ET/SX) family of peptides and to those mediating endothelium-dependent vasodilations within the isolated perfused mesentery of the rat. To discriminate ETA receptors from ETB receptors we have used the criteria that ET-1 is more active than SX6c on ETA receptors, and that the ET/SX peptides are equiactive on ETB receptors. We have also assessed the effects of the ETA receptor-selective antagonist BQ-123, and the non-selective ET receptor antagonist PD 142893 on the responses of each preparation to the ET/SX peptides. 2. ET-1-induced constrictions of the rat thoracic aorta (EC50 3 x 10(-10) M), a prototypic ETA receptor-mediated response, or isolated perfused mesentery of the rat were antagonized by BQ-123 (10(-5) M) or PD 142893 (10(-5) M). SX6c did not constrict either the rat isolated perfused mesentery or the rat thoracic aorta. Thus, ETA receptors mediate these constrictions. 3. ET-1 and SX6c were approximately equipotent in constricting rabbit pulmonary artery rings (EC50S 3-6 x 10(-10) M). Neither BQ-123 (10(-5) M) nor PD 142893 antagonized the contractions induced by ET-1. These effects suggest mediation by ETB receptors but PD 142893 (10(-5) M) did give a 3 fold antagonism of constrictions induced by SX6c. 4. SX6c was more potent than ET-1 in contracting the rat stomach strip (threshold concentrations 10(-10) and 3 x 10(-10) M). Contractions to ET-1 or SX6c were unaffected by BQ-123 (10-5 M), again indicative of ETB receptor-mediated events. PD 142893 (10-5 M) was ineffective against ET-1 but produced a 3 fold antagonism of SX6c.5. In the rat isolated perfused mesentery ET-1 or SX6c (0.3-300pmol) were equipotent in producing dose-related vasodilatations that were unaffected by BQ-123 (10-6 M), indicative of an ETB receptor mediated response. In contrast to the other ETB-mediated responses, PD 142893 (10-6 M) strongly antagonized these vasodilatations.6. Thus, ETA receptors mediate constrictions of the rat thoracic aorta and rat isolated perfused mesentery whereas ETB receptors mediate constrictions of the rabbit pulmonary artery and rat stomach strip and endothelium-dependent dilatations within the mesentery. However, within the group of ETB receptor-mediated responses, endothelium-dependent vasodilatations are sensitive to PD 142893, whereas contractions of the isolated smooth muscle preparations are not. Thus, the receptor present on the endothelium responsible for the release of nitric oxide in response to the ET/SX peptides is most probably different from that present on smooth muscle that mediates BQ-123-insensitive contractions.

Amino Acid Sequence↗
PubMed1990

Maturation of acetylcholinesterase expression in tracheal smooth muscle contraction.

We examined postganglionic development of acetylcholinesterase (AChase) activity and tracheal smooth muscle (TSM) contraction elicited by cholinomimetic activation and electrical field depolarization in vitro. Epithelium-intact tracheal strips excised from 21 2-wk-old swine (2ws) and 19 10-wk-old swine (10ws) were tethered isometrically at optimal resting length, and responses were expressed as percent of the maximum to 63 mM potassium-chloride (%KCl). Cumulative concentration-response curves to KCl were equivalent for TSM from 2 and 10ws. However, maximal contraction to ACh in 2ws (168 +/- 8.4 %KCl) was greater than for 10ws (142 +/- 2.3 %KCl; P less than 0.02). Stimulus-response curves (field electrodes; AC source) demonstrated greater sensitivity for TSM in 10ws (stimulus causing 50% of the maximal response = 3.32 +/- 0.13 V in 2ws vs. 2.25 +/- 0.12 V in 10ws; P less than 0.001), indicating that the greater cholinomimetic responsiveness of 2ws did not result from augmented presynaptic nerve conduction. The AChase inhibitor, physostigmine, caused 1) greater sensitivity of responses elicited by electrical field stimulation in 2ws (P less than 0.05) but not in 10ws (P = NS), 2) augmentation of maximal responses to exogenous ACh in 10ws (27% increase; P less than 0.01) but not 2ws (2% increase; P = NS), and 3) a greater increase in sensitivity to cholinomimetic activation in 2ws compared with 10ws (P less than 0.02). These data demonstrate increased cholinergic contraction of TSM in 2 vs. 10ws that results at least in part from reduced AChase activity in the trachea of immature animals.

Acetylcholine↗
PubMed2005

Hydrogen sulfide is synthesized in the gills of the clam Mercenaria mercenaria and acts seasonally to modulate branchial muscle contraction.

Previously we showed that when the gill muscles of the venerid clam Mercenaria mercenaria are stimulated to contract by 5-hydroxytryptamine (5HT), the contraction is about doubled when another identical dose of 5HT is applied after washout. Furthermore, this "endogenous potentiation" is mimicked by nitric oxide (NO), which is synthesized in the gill. We now report that the isolated gills also synthesize H2S; the basal rate of synthesis was 0.70 micromol.g(-1).h(-1) (se = 0.14; n = 24), but in the presence of 5HT (10(-2) M), the rate increased markedly to 35.82 micromol.g(-1).h(-1) (se = 4.93; n = 4). In addition, dithiothreitol (DTT; 2.2 mM) increased the rate of synthesis significantly to 4.9 micromol.g(-1).h(-1) (se = 0.8; n = 8). Stimulation of H2S synthesis by 5HT (5 x 10(-3) M) was seasonal; that is, the rates measured monthly from December through June are significantly lower than those measured from July through November. We also found that if isolated gills were pretreated with the H2S donor, sodium hydrosulfide (NaHS), their contractions in response to 5HT were potentiated. The threshold of the potentiation was 10(-8) M NaHS, and the largest effect was at 10(-6) M. During August, however, when endogenous and NO-induced potentiations are both absent, 10(-6) M NaHS was also ineffective. Like the effect of NO, that of NaHS (10(-6) M) was blocked by oxadiasoloquinoxalin (ODQ; 5 x 10(-5) M), an inhibitor of soluble guanylate cyclase (sGC). Moreover, Rp-8-CPT-cGMPS (10(-5) M), which inhibits protein kinase-G, also blocked the effect of NaHS (10(-6) M). When isolated gills were treated with 2.2 mM DTT, the endogenous potentiation of a second 5HT-induced contraction more than doubled in comparison to untreated controls. In conclusion, H2S is synthesized in the gill and, along with NO, is a seasonal, endogenous modulator of branchial muscle contraction; its action may be mediated through a sGC/cGMP signaling cascade.

Animals↗
PubMed1980

Autogenetic effects of muscle contraction on extensor gamma motoneurones in the cat.

The effect of isometric twitch contractions of hind limb muscles on the discharge of gamma motoneurones has been studied in decerebrated cats with thoracic spinal cord section. Contractions of flexor digitorum longus (FDL) or gastrocnemiussoleus (GS) strongly inhibited the background discharge of their homonymous gamma motoneurones. In contrast, contraction of FDL generally caused less inhibition, or did not affect the discharge, of the synergist GS gamma motoneurones. Both the autogenetic and synergist inhibition were considerably weaker in decerebrated cats with intact spinal cords. The inhibition lasted 20 to 50 ms and occurred principally during the rising phase of contraction. It could be followed or terminated by a weaker period of facilitation during relaxation of the muscle. Shortening the muscle so that no active tension developed during contraction either abolished or substantially curtailed the inhibition. We discuss the probability that the inhibition is a spinal segmental reflex brought about by impulses generated in Ib afferents of tendon organs. The inhibition is under tonic inhibitory control in the decerebrated cat when the spinal cord is intact. Unlike the Ib inhibition of alpha motoneurones that of gamma motoneurones has a particularly strong autogenetic component.

Animals↗