Temperature effect on the rates of isometric force development and relaxation in the fresh and fatigued human adductor pollicis muscle.
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The purpose of the present study was to investigate the effect of temperature on the rates of isometric force development and relaxation in electrically activated fresh and fatigued human adductor pollicis muscle. Following immersion of the lower arm for 20 min in water baths of four different temperatures, muscle temperatures were approximately 37, 31, 25 and 22 C. Maximal isometric force was reduced by 16.8 +/- 1.5 % at 22 C. The stimulation frequency-force and -rate of force development relationships were shifted to the left at lower temperatures. Q10 values for the maximal rates of force development and relaxation, and the times for 100 to 50 % and 50 to 25 % force relaxation, were about 2.0 between 37 and 25 C and about 3.8 between 25 and 22 C. However, the time for 50 to 25 % force relaxation had a relatively high Q10 value between 25 and 22 C (6.9) and this parameter also appeared to be more sensitive to fatigue compared to the other indices of relaxation. Nevertheless, the effect of fatigue on all parameters decreased with cooling over the entire (37-22 C) temperature range. (+info)
Differential effects of mibefradil, verapamil, and amlodipine on myocardial function and intracellular Ca(2+) handling in rats with chronic myocardial infarction.
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Mibefradil is a selective T-type Ca(2+) channel blocker that exerts a potent vasodilating but weak inotropic action. The present study compared mibefradil with traditional L-type Ca(2+) channel blockers in regard to the effects of chronic oral administration on hemodynamics, contractility, and intracellular Ca(2+) handling in failing myocardium from postinfarction rats. Male Wistar rats with ligation-induced myocardial infarction were assigned to placebo or treatment with mibefradil (10 mg/kg/day), verapamil (8 mg/kg/day), or amlodipine (4 mg/kg/day) by oral gavage starting 7 days before the induction of myocardial infarction. Six weeks after myocardial infarction, hemodynamic measurements were performed in conscious animals. In addition, isometric force and free [Ca(2+)](i) were determined in isolated left ventricular papillary muscles. Placebo-treated rats exhibited a decreased mean atrial pressure, an increased left ventricular end-diastolic pressure, and a reduced rate of pressure rise compared with sham-operated animals. Mibefradil treatment significantly improved all of these parameters, whereas both amlodipine and verapamil exerted only minor effects. beta-Adrenergic stimulation with isoproterenol (ISO) enhanced contractility and Ca(2+) availability in papillary muscles from sham-operated rats, whereas the ISO-induced inotropic effect in muscles from placebo-treated rats was severely blunted. Chronic mibefradil treatment significantly improved the inotropic response to ISO stimulation, although the Ca(2+)(i) availability appeared to be less than in muscles from placebo-treated animals. In contrast, both verapamil and amlodipine did not restore the inotropic and Ca(2+)(i) modulating effect of ISO in remodeled myocardium. Thus, T-type Ca(2+) current appears to be of pathophysiological relevance in postischemic reperfused myocardium. (+info)
Abnormal biopterin metabolism is a major cause of impaired endothelium-dependent relaxation through nitric oxide/O2- imbalance in insulin-resistant rat aorta.
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To investigate underlying mechanisms responsible for the impaired nitric oxide (NO)-dependent vascular relaxation in the insulin-resistant state, we examined production of both NO and superoxide anion radical (O2-) and those modulating factors in aortas obtained from normal (CTR), insulin-treated (INS), or high fructose-fed (FR) rats. FR rats showed insulin resistance with endogenous hyperinsulinemia, whereas INS rats showed normal insulin sensitivity. Only FR aortic strips with endothelium elicited impaired relaxation in response to either acetylcholine or calcium ionophore A23187. Endothelial NO synthase (eNOS) activity and its mRNA levels were increased only in vessels from INS rats (P < 0.001), whereas eNOS activity in FR rats was decreased by 58% (P < 0.05) when compared with CTR rats. NO production from aortic strips stimulated with A23187 was significantly lower in FR than CTR rats. In contrast, A23187-stimulated O2- production was higher (P < 0.01) in FR than CTR rats. These differences were abolished when aortic strips were preincubated in the media including (6R)-5,6,7,8-tetrahydrobiopterin (BH4), an active cofactor for eNOS. Furthermore, as compared with CTR rats, aortic BH4 contents in FR rats were decreased (P < 0.001), whereas the levels of 7,8-dihydrobiopterin, the oxidized form of BH4, were increased, with opposite results in INS rats. These results indicate that insulin resistance rather than hyperinsulinemia itself may be a pathogenic factor for decreased vascular relaxation through impaired eNOS activity and increased oxidative breakdown of NO due to enhanced formation of O2- (NO/O2- imbalance), which are caused by relative deficiency of BH4 in vascular endothelial cells. (+info)
Extensibility and symmetry of actin filaments in contracting muscles.
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When isometrically contracting muscles are subjected to a quick release followed by a shortening ramp of appropriate speed (V(o)), tension decays from its value at the isometric plateau (P(o)) to <0. 05 P(o) with the same time course as the quick part of the release; thereafter, tension remains at a negligible level for the duration of the shortening ramp. X-ray diffraction data obtained under these conditions provide evidence that 1) at V(o) very few heads form an actomyosin complex, while the number of heads doing so at P(o) is significant; 2) relative to rest the actin filament at V(o) is approximately 0.12% shorter and more twisted, while it is approximately 0.3% longer and less twisted at P(o); and 3) the myosin heads attaching to actin during force development do so against a thin filament compliance of at least 0.646 +/- 0.046% nm per P(o). (+info)
Eccentric and concentric isokinetic moment characteristics in the quadriceps and hamstrings of the chronic isolated posterior cruciate ligament injured knee.
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OBJECTIVE: Functional strength deficits associated with chronic isolated posterior cruciate ligament (PCL) insufficiency have received limited attention in the literature. The purpose of this study was to determine the eccentric and concentric isokinetic moment characteristics of the quadriceps and hamstrings in a sample of patients with isolated PCL injury. METHODS: Eccentric and concentric mean average and average peak moments were measured for 17 patients with a history of conservatively treated isolated PCL injury using an isokinetic dynamometer. Quadriceps and hamstring isokinetic moments were recorded from 10 degree to 90 degree of knee flexion. Strength ratios were calculated and compared with those reported in the literature for healthy subjects. RESULTS: The hamstrings of the involved side (eccentric/concentric (E/C) ratio = 1.06) were significantly weaker (p<0.05) eccentrically than those of the contralateral side (E/C ratio = 1.29). All hamstrings/quadriceps (H/Q) ratios were less than the universally accepted value of 0.60 and the eccentric H/Q ratio for the injured extremity was significantly lower than the non-injured (p<0.05). In a bilateral comparison, the injured/non-injured (I/N) ratio was less than 1.00 for concentric quadriceps, eccentric quadriceps, and hamstring isokinetic moments. Calculation of the E/C ratio showed that, for the quadriceps, it was 1.08 on the injured side and 1.07 on the non-injured extremity. CONCLUSIONS: Eccentric strengthening should be an integral part of functionally rehabilitating the quadriceps and hamstrings of athletes who suffer from the complications associated with chronic isolated PCL insufficiency. (+info)
Influence of muscle temperature on the contractile properties of the quadriceps muscle in humans with spinal cord injury.
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Low muscle temperature in paralysed muscles of individuals with spinal cord injury may affect the contractile properties of these muscles. The present study was therefore undertaken to assess the effects of increased muscle temperature on the isometric contractile properties of electrically stimulated paralysed quadriceps muscles. When muscle temperature at a depth of 3 cm was increased from approximately 32 degrees C to approximately 36 degrees C by ultra-short-wave application, the half-relaxation time shortened and low-frequency force responses became less fused, but the maximal rate of increase in force remained unchanged. Heating had no effect upon either force decline or slowing of relaxation during fatiguing contractions. The force-frequency relationship of the paralysed quadriceps muscle was shifted to the right after the muscle was heated. Despite this shift, however, the relationship still resembled that in muscles of non-paralysed individuals, probably due to the unexplained high twitch forces. These results indicate that reduced muscle temperature in spinal-cord-injured individuals may lead to an underestimation of the changes in contractile properties in terms of relaxation rate or the degree of fusion with low-frequency stimulation. In addition, the force-frequency relationship of paralysed muscles does not accurately reflect the magnitude of these changes, even when the muscle is heated, and should therefore be treated with caution. (+info)
Myosin molecular motor dysfunction in dystrophic mouse diaphragm.
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Cross-bridge properties and myosin heavy chain (MHC) composition were investigated in isolated diaphragm from 6-mo-old control (n = 12) and mdx (n = 12) mice. Compared with control, peak tetanic tension fell by 50% in mdx mice (P < 0.001). The total number of cross bridges per square millimeter (x10(9)), the elementary force per cross bridge, and the peak mechanical efficiency were lower in mdx than in control mice (each P < 0.001). The duration of the cycle and the rate constant for cross-bridge detachment were significantly lower in mdx than in control mice. In the overall population, there was a linear relationship between peak tetanic tension and either total number of cross bridges per square millimeter or elementary force per cross bridge (r = 0.996 and r = 0.667, respectively, each P < 0.001). The mdx mice presented a higher proportion of type IIA MHC (P < 0.001) than control mice and a reduction in type IIX MHC (P < 0.001) and slow myosin isoforms (P < 0.01) compared with control mice. We concluded that, in mdx mice, impaired diaphragm strength was associated with qualitative and quantitative changes in myosin molecular motors. It is proposed that reduced force generated per cross bridge contributed to diaphragm weakness in mdx mice. (+info)
Influence of elastic properties of tendon structures on jump performance in humans.
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The purpose of this study was to quantify the elastic properties of tendon structures in vivo and to investigate the influence of the tendon properties on jump performance with and without countermovement. Elongation of the tendon and aponeurosis of vastus lateralis muscle (dL) was directly measured by ultrasonography while subjects (n = 31) performed ramp isometric knee extension up to the voluntary maximum (MVC). The relationship between muscle force and dL was fitted to a linear regression above 50% MVC, the slope of which was defined as stiffness of the tendon structures. Statistical analysis revealed no significant difference between duplicated measurements of stiffness, with an interday reliability of r = 0.88 and a coefficient of variance of 6.1%. Although the stiffness was not significantly related to absolute jump height in either vertical jump, it was inversely correlated with the difference in jump height between the vertical jumps performed with and without countermovement. The results suggested that the stiffness of tendon structures has a favorable effect on stretch-shortening cycle exercise, possibly due to adequate storage and recoil of elastic energy. (+info)