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PubMed1994

Effects of a muscle exercise program on exercise capacity in subjects with osteoarthritis.

Maximal aerobic power and muscle function have been shown to decrease with age and to be even lower in patients with osteoarthritis (OA). This study was designed to determine if subjects with OA who underwent only a muscle exercise program had improved exercise capacity and cardiovascular fitness. A maximal graded exercise test was given before and after 3 months of exercise (isometric, isotonic, and isometric force generated as a function of time contractions, three times a week). Maximal strength and the tension-time index improved significantly. Peak aerobic power increased from 15.99 +/- 3.96 mL.kg-1.min-1 to 20.34 +/- 3.29 mL.kg-1.min-1. On average, maximal walking speed increased from 2.0 +/- 0.6 mph to 2.4 +/- 0.7mph. Exercise time increased 22%, from 9.2 +/- 2.3 minutes to 11.2 +/- 2.7 minutes. There were significant reductions in submaximal heart rate (15b.min-1) and systolic blood pressure (15mmHg) after training. It would appear that the reduction in aerobic fitness of subjects with OA is secondary to their reduced muscle function. By improving muscle function, increases in exercise capacity and aerobic fitness occurred.

Aged↗
PubMed1984

Factors affecting the equatorial X-ray diffraction pattern from contracting frog skeletal muscle.

Changes in the equatorial X-ray diffraction pattern from tetanized frog sartorius muscles (Rana catesbiana ) were studied by use of time-resolved data collection technique (time resolution, 0.5 sec) to give information about the dynamic properties of the cross-bridges. No significant changes in the intensity ratio of two equatorial reflections (I1,0/I1,1) were observed when isometrically contracting muscles were slowly stretched by 5-6%, in spite of marked force changes. The intensity ratio also showed no significant changes when the load on isometrically contracting muscles was suddenly increased from Po to 1.2-1.5 Po to produce isotonic muscle lengthening. Closer examination of the data indicated that a small decrease in the value of I1,1 was caused by both slow stretch and isotonic lengthening. Because of the scatter of experimental plots in I1,0, the effect of small change in I1,1 on the intensity ratio fell within the range of accuracy of measurement. It is suggested that no marked changes in myosin head orientation or in the number of the cross-bridges in the vicinity of the thin filaments take place in response to slow stretches or isotonic lengthening, and that the decreased regularity of the filament lattice may produce the change in I1,1.

Animals↗
PubMed1990

Changes in voluntary and electrically induced contractions during strength training and detraining.

To elucidate the changes in neuro-muscular function during strength training and detraining, five male subjects underwent progressive isotonic strength training of their calf muscles three times a week for 8 weeks with additional detraining for the same periods. Electrically evoked twitch contractions were induced in the triceps surae muscles of each subject every 4 weeks during the training and detraining periods. At the same time, maximal voluntary isometric contractions (MVC) and the maximal girth of the calf (MGC) were measured. During the training period, MVC increased significantly from 98.4 to 129.6 Nm (31.7%, P less than 0.01) for the first 4 weeks of training but MGC showed little increase. Neither of the changes correlated with each other. Twitch contraction parameters, i.e. maximal twitch torque (Pt), maximal rate of torque development (max dT/dt) and rate of relaxation (relax dT/dt) showed no statistical change. During detraining, on the contrary, a large and significant increase (22.5%, P less than 0.01) was observed in max dT/dt without any changes in Pt and relax dT/dt. The MVC/Pt showed both significant increases during training and decreases during detraining. Our data suggest that short term strength training as employed in the present study does not induce changes in the contractile properties of the muscle during training, but may significantly affect the rate of force development during the subsequent detraining period, indicating the possible existence of complex post-training muscle adaptation.

Adult↗
PubMedDate not supplied

The effects of activated complement on myocardial performance in vitro.

Activated complement has been implicated in the dysfunction of several organ systems, but can it directly affect the myocardium? This possibility was studied using human right atrial trabeculae contracting isometrically "in vitro" in four solutions: Tyrode's (T), autologous arterial blood (B), plasma (P) and denaturated plasma (DP). Complement was activated by the addition of Zymosan while vehicle alone was used as control. Complement activation occurred in the blood and plasma solutions, as assessed by a significant drop in CH50 (p less than 0.05), while there was no detectable complement activity in either T or DP. Myocardial functional integrity was assessed by the change in contractile parameters with time. Subsequent resting forces, relative developed forces (DF), and rates of decay of DF were similar between muscles contracting in the four solutions. We conclude that activated complement has no direct effect on myocardial performance.

Blood↗
PubMed1989

Effect of dextran on the stability of isolated, perfused rat heart.

Stability of cardiac function and myocardial intracellular ionic composition was examined in the Krebs-perfused isolated rat working heart. Hearts perfused by a conventional Krebs solution showed stable contraction for 2 h, but during this period, intracellular ionic environment (Na, K, Ca) substantially changed. Addition of dextran to the perfusate inhibited, though not completely, this time-dependent deterioration and made the heart less vulnerable to the hypoxia-reoxygenation.

Animals↗
PubMed1994

Evidence for differential roles of nitric oxide (NO) and hyperpolarization in endothelium-dependent relaxation of pig isolated coronary artery.

1. The possible roles of endothelial and smooth muscle cell hyperpolarization and nitric oxide (NO) in endothelium-dependent relaxation were examined in isolated rings of pig right coronary artery. 2. The effects of hyperpolarization were prevented with high K+ (30-125 mM), isotonic Krebs solutions. Functional antagonism due to high K(+)-induced smooth muscle contraction was prevented with 0.3 microM nifedipine (in all treatments, for consistency). All rings were contracted with the thromboxane-mimetic U46619, (1-100 nM) to bring them to an initial active force of within 30-50% of maximum contraction. 3. High K+ had no effects on the sensitivity (EC50) or time course of endothelium-dependent (substance P, SP; bradykinin, BK; calcimycin, A23187) and -independent (sodium nitroprusside, SNP) agents. Maximum relaxations (Rmax) to SP, BK and A23187 were reduced significantly by approximately 20% but only with 125 mM K+. 4. In normal K+ Krebs solution (5.9 mM), NG-nitro-L-arginine (L-NOARG; 100 microM) caused 40%, 20% and no reduction in Rmax for SP, BK and SNP respectively. EC50s for SP and BK were decreased significantly by approximately two fold whereas that for SNP was increased significantly by approximately ten fold. At all high K+ concentrations (30-125 mM), L-NOARG (100 microM) caused complete inhibition of relaxations to SP and BK but those to SNP were unaffected. 5. High K+ (30 mM) unmasked potent and concentration-dependent inhibition of relaxations of SP by L-NOARG. At 10 microM L-NOARG, all relaxation responses to SP were abolished and at the higher concentrations of SP (1-10 nM) small but significant contractions were observed. 6. N0-monomethyl-L-arginine (L-NMMA) had similar effects on relaxations to SP in the presence of 30 mM K+ except that maximum inhibition (40%) of Rmax was achieved at 10 MicroM L-NMMA and this was not increased with either 100 or 1000 MicroM L-NMMA. In normal K+, L-NMMA (1000 MicroM) only decreased the EC50 by approximately two fold, without affecting Rmax.7. High choline+ (25, 75 and 125 mM) isotonic Krebs also had no direct effect on the relaxations to SP,but like high K+, enabled L-NOARG (100 MicroM) to inhibit these responses completely. Neither charybdotoxin(30 nM) nor substitution of 25 mM NaCl with 50 mM sucrose had any direct effect on relaxations to SP or on the block of relaxations to SP by L-NOARG (100 MicroM).8. In conclusion, most if not all of the endothelium-dependent relaxation in the pig coronary artery in vitro is due to NO, but hyperpolarization can supplement 60% -80% of this response if NO synthesis is blocked. Multiple endothelium-derived factors could not only explain heterogeneity of the degree of block of endothelium-dependent relaxation responses by L-arginine analogues, but also constitute important 'back-up' mechanisms for control of arterial diameter.

Animals↗
PubMed2006

Acetylcholine-induced asynchronous calcium waves in intact human bronchial muscle bundle.

Calcium (Ca2+) is an important activator of the contractile machinery in airway smooth muscle (ASM). While agonist-induced Ca2+ signals are well characterized in animal ASM, little is known about what occurs in adult human ASM. In this study, we examined the Ca2+ signal elicited by acetylcholine (ACh) in smooth muscle cells of the intact human bronchial muscle strips obtained from fresh surgical specimens in relation to muscle contraction. We found that ACh induces repetitive Ca2+ waves that spread along the longitudinal axis of individual cells in the intact human bronchial smooth muscle strips. These Ca2+ waves display no apparent synchronization between neighboring cells, and their generation precedes force development. Comparison of the ACh concentration dependence of tissue contraction and selected parameters of the asynchronous Ca2+ waves (ACW) reveals that the graded force generation by ACh-stimulated human bronchial muscle strips is achieved by differential recruitment of cells to initiate Ca2+ waves and by enhancement of the frequency of ACW once the cells are recruited. Furthermore, pharmacologic characterization shows that the ACW are produced by repetitive cycles of SR Ca2+ release via ryanodine-sensitive channels followed by SR Ca2+ reuptake by sarco(endo)plasmic reticulum Ca2+ ATPase. Extracellular Ca2+ entry involving receptor-operated channels/store-operated channels, reverse-mode Na+/Ca2+ exchange, and to a lesser extent L-type voltage-gated Ca2+ channels is required to maintain the ACW. These findings for the first time demonstrate the occurrence and the role of ACW in excitation-contraction coupling in adult human ASM.

Acetylcholine↗
PubMedDate not supplied

Influence of sodium and potassium ions on the contraction induced by calcium ions in guinea-pig isolated vas deferens.

1. When guinea-pig isolated vas deferens was pretreated with 0.01% tetrasodium edetate in an isotonic sucrose medium and then transferred to an edetate-free sucrose medium, the addition of CaCl2 (0.28-8.80 mmol/l) induced a contraction. 2. When the edetate-free sucrose medium was replaced by saline containing NaHCO3 and glucose, the contraction induced by CaCl2 was only slightly smaller than that obtained in the sucrose medium. 3. When the saline medium was replaced by Ca-free Locke's solution, the contraction induced by CaCl2 was almost the same as that obtained in the saline medium. 4. When the Ca-free Locke's solution was replaced by Ca-free K-Locke's solution (in which NaCl and CaCl2 were replaced by KCl), the contraction induced by CaCl2 was almost the same as that obtained in the sucrose medium.

Animals↗
PubMed1978

The effect of hypertonic solutions on the rate of relaxation of contracture tension in Mytilus smooth muscle.

1. The effect of the bathing solution tonicity on the mechanical properties of the anterior byssal retractor muscle (ABRM) of Mytilus edulis was examined. 2. The rate of relaxation of contracture tension produced by acetylcholine (ACh) was greatly reduced when the bathing solution tonicity was increased by adding NaCl, KCl or LiCl after the removal of ACh, whereas a decreased tonicity increased the rate of relaxation. 3. The contracted ABRM in hypertonic solutions showed no active shortening after an isotonic release and barely redeveloped active tension after a quick release. 4. The resistance to stretch increased with increasing tonicity of the bathing solution. 5. The wet weight of the ABRM decreased much more markedly in sucrose-hypertonic solution than in Na-, K- or Li-hypertonic solutions, but the decrease in the rate of relaxation was less marked in the former, indicating that there may be little relation between the rate of relaxation and the degree of osmotic deformation of the ABRM fibres. 6. It is suggested that the elevated ionic strength in the myoplasm may be related to a reduction in the rate of detachment of the cross-linkages between the thick and thin filaments.

Animals↗
PubMed2000

[The effects of hypertonic saline solution perfusion on the isolated hearts of burned rats].

OBJECTIVE: To observe the effect of hypertonic saline solution perfusion on the function of isolated hearts of burned rats. METHODS: The isolated rat heart was taken as the model. The hearts from normal control and burned rats were perfused by improved isotonic (Na(+) 118 mmol/L) and hypertonic Krebs-Henseleit (Na(+) 215 mmol/L) solutions, respectively. The dynamic changes of the cardiac function were monitored during heart perfusion. RESULTS: The cardiac contractive and diastolic function were transiently inhibited and followed by quick recovery during the perfusion with hypertonic solution in both control and burned rat hearts. But when the hypertonic solution was replaced by isotonic, there appeared significant enhancement of the cardiac contractive and diastolic function. These findings indicated that hypertonic solution exerted more powerful influence on the contractive and diastolic function of burned rat heart. CONCLUSION: Hypertonic saline solution could influence the cardiac contractile and diastolic function significantly. And the magnitude of the effects was correlated with the basic cardiac condition.

Animals↗
PubMed1984

Functional cardiac depression caused by defibrillator shocks. Quantitation of the safety factor for electrical defibrillation.

The overdose shock strengths required to depress ventricular contraction were determined for damped sinusoidal current in 7 metabolically supported, isolated contracting canine hearts. Each heart was suspended in an isoresistive and isotonic solution-through which the defibrillating shocks were delivered. Defibrillation thresholds were determined with standard damped sine wave shocks of 4.4-5.5 msec duration. Then overdose shocks were delivered and the depressant effect on systolic left ventricular pressure was measured for shocks of 3-12 times threshold current. The minimum (threshold) current and energy densities required to defibrillate were 59.5 +/- 4.6 mA/cm2 (average) and 3.12 +/- 0.2 mJ/cm3. Increasing the shock strength above threshold produced a concomitant reduction of postshock left ventricular systolic pressure. The current and energy densities required to produce 50% depression (TD50) of left ventricular systolic pressure were 5.0 and 24.1 times the threshold current and energy densities respectively, indicating a wide safety margin using this criterion.

Animals↗
PubMed1979

Swelling and contraction of potato mitochondria.

Mitochondria isolated from potato tubers fail to undergo passive osmotic swelling when suspended in isotonic Na(+) acetate or phosphate, in NaCl following addition of tripropyltin, or in Na(+) nitrate following addition of an uncoupler. Swelling under each of these conditions in mitochondria from other sources has been attributed to the inward movement of Na(+) on an endogenous Na(+)/H(+) exchanger. Such a monovalent cation/H(+) exchanger has also been implicated in respiration-dependent cation extrusion and contraction of swollen mitochondria. Potato mitochondria swollen in chloride and nitrate salts extrude ions and contract when respiration is initiated. The contraction reaction is slower and less efficient than that in beef heart mitochondria, but like the latter, is sensitive to uncouplers and stimulated by nigericin, butacaine, and Mg(2+). These comparative studies suggest that a cation(+)/H(+) exchanger is present in potato tuber mitochondria, but that it functions exclusively as a cation-extruding mechanism. They further suggest that cation(+)/H(+) exchange activity is not identical in mitochondria from different sources and that these exchange components may have a directionality and regulatory features which differ with the metabolic needs of the source tissue.

Journal Article↗