Maximal Contraction Force Research Articles

2P1-A07 高強力PBO繊維を用いた高水圧駆動McKibben型人口筋の開発(サーチ&レスキューロボット・メカトロニクス)

Small and light-weighted actuators which generate high force and high energy are strongly required for realizing powerful robots. We have developed a new hydraulic artificial muscle generating very high force and high energy by applying an ultra high strength PBO fiber sleeve to McKibben type artificial muscle. While conventional McKibben muscles are driven by pneumatic pressure about 0.7[MPa] at a maximum, the newly developed muscles are driven by water hydraulic pressure of 2[MPa], resulting in very high force. This report shows materials and structure of the new artificial muscle with PBO fiber sleeve. Muscles are evaluated by two parameters in this paper, force density per volume (FDV) and energy density per volume (EDV) with the comparisons with other linear actuators. The prototype is 40[mm] in diameter and 700[mm] in length. It achieves the maximum contraction force of 12096[N], FDV of about 18000[N/mm^3], and EDV of 2484[J/mm^3], which are 5 to 20 times bigger than those of typical conventional actuators with the same volume.

Mechanical Muscle Function, Morphology, and Fiber Type in Lifelong Trained Elderly

Maximal muscle contraction force and muscle mass are both reduced during the natural aging process. Long-term training may be used to attenuate this age-related loss in muscle function and muscle size. Maximum isometric quadriceps strength (MVC), rate of force development (RFD), and muscle fiber composition and size (CSA) were studied in elderly individuals (68-78 yr) chronically exposed (> 50 yr) to either endurance (E) or strength (S) training, and in age-matched, untrained (U) elderly group. E and S showed greater MVC than did U. Contractile RFD was elevated in S compared with U, and S also demonstrated greater type II fiber CSA than did U and E. The proportion of type I fibers was greater in E compared with U and S. Muscle fiber size and mechanical muscle performance, particularly RFD, were consistently elevated in aged individuals exposed to chronic (i.e., lifelong) strength training. This relative preservation in muscle morphology and function may provide an important physical reserve capacity to retain muscle mass and function above the critical threshold for independent living at old age.

Comparison of Levator Ani Muscle Defects and Function in Women with and Without Pelvic Organ Prolapse

The levator ani muscles are critical for providing upward support to the pelvic organs and minimizing the load on the connective tissue that attaches these organs to the pelvis. When the muscles fail, pelvic organ prolapse may ensue, making surgery necessary. Vaginal birth substantially increases the risk of prolapse in occurring in parous women, but it is not clear whether levator ani defects lead to prolapse later in life. The possibility that this may be the case has lent support to cesarean delivery on request. This case-control study compared the structure and function of the levator ani muscle in 151 women with prolapse and 135 control subjects matched for age, race, and hysterectomy status. Case patients had prolapse of a vaginal wall, a hysterectomy scar, or the cervix extending at least 1 cm above the hymen during a Valsalva maneuver. MR imaging served to identify major defects with more than half the levator ani missing, and minor defects with less than half the muscle missing. An instrumented vaginal speculum was used to quantify vaginal closure force at rest and during maximum pelvic muscle contraction. The incidence of major levator ani defects was 55% in cases and 16% in controls, for an adjusted odds ratio (OR) of 7.3 (95% confidence interval [CI], 3.9-13.6). Women in the two groups were, however, about equally likely to have minor defects. Incidence rates of major defects were 53% for women reporting having had a forceps delivery and 28% for the others (adjusted OR, 3.4; 95% CI, 1.95-5.78). Women with prolapse had lower estimates of vaginal closure force during pelvic muscle contraction than did control subjects (2.0 versus 3.2 Newtons). Women with levator ani defects generated less force than those lacking defects (2.0 versus 3.1 Newtons). The genital hiatus was 50% longer in case women than in controls (4.7 versus 3.1 cm). In both the case and control groups, women without levator ani defects had higher maximal contraction force estimates than those with defects. This case-control study showed that women having pelvic organ prolapse more often have defective levator ani muscles than control women, and generate less vaginal closure force during maximal muscle contraction.

The extensor tibiae muscle of the stick insect: biomechanical properties of an insect walking leg muscle

We investigated the properties of the extensor tibiae muscle of the stick insect (Carausius morosus) middle leg. Muscle geometry of the middle leg was compared to that of the front and hind legs and to the flexor tibiae, respectively. The mean length of the extensor tibiae fibres is 1.41+/-0.23 mm and flexor fibres are 2.11+/-0.30 mm long. The change of fibre length with joint angle was measured and closely follows a cosine function. Its amplitude gives effective moment arm lengths of 0.28+/-0.02 mm for the extensor and 0.56+/-0.04 mm for the flexor. Resting extensor tibiae muscle passive tonic force increased from 2 to 5 mN in the maximum femur-tibia (FT)-joint working range when stretched by ramps. Active muscle properties were measured with simultaneous activation (up to 200 pulses s(-1)) of all three motoneurons innervating the extensor tibiae, because this reflects most closely physiological muscle activation during leg swing. The force-length relationship corresponds closely to the typical characteristic according to the sliding filament hypothesis: it has a plateau at medium fibre lengths, declines nearly linearly in force at both longer and shorter fibre lengths, and the muscle's working range lies in the short to medium fibre length range. Maximum contraction velocity showed a similar relationship. The force-velocity relationship was the traditional Hill curve hyperbola, but deviated from the hyperbolic shape in the region of maximum contraction force close to the isometric contraction. Step-like changes in muscle length induced by loaded release experiments characterised the non-linear series elasticity as a quadratic spring.

In vivo myograph measurement of muscle contraction at optimal length

BackgroundCurrent devices for measuring muscle contraction in vivo have limited accuracy in establishing and re-establishing the optimum muscle length. They are variable in the reproducibility to determine the muscle contraction at this length, and often do not maintain precise conditions during the examination. Consequently, for clinical testing only semi-quantitative methods have been used.MethodsWe present a newly developed myograph, an accurate measuring device for muscle contraction, consisting of three elements. Firstly, an element for adjusting the axle of the device and the physiological axis of muscle contraction; secondly, an element to accurately position and reposition the extremity of the muscle; and thirdly, an element for the progressive pre-stretching and isometric locking of the target muscle.Thus it is possible to examine individual in vivo muscles in every pre-stretched, specified position, to maintain constant muscle-length conditions, and to accurately re-establish the conditions of the measurement process at later sessions.ResultsIn a sequence of experiments the force of contraction of the muscle at differing stretching lengths were recorded and the forces determined. The optimum muscle length for maximal force of contraction was established. In a following sequence of experiments with smaller graduations around this optimal stretching length an increasingly accurate optimum muscle length for maximal force of contraction was determined. This optimum length was also accurately re-established at later sessions.ConclusionWe have introduced a new technical solution for valid, reproducible in vivo force measurements on every possible point of the stretching curve. Thus it should be possible to study the muscle contraction in vivo to the same level of accuracy as is achieved in tests with in vitro organ preparations.

Different effects of ATP on the contractile activity of mice diaphragmatic and skeletal muscles

Apart from acetyl-choline (Ach), adenosine-5′-trisphosphate (ATP) is thought to play a role in neuromuscular function, however little information is available on its cellular physiology. As such, effects of ATP and adenosine on contractility of mice diaphragmatic and skeletal muscles (m. extensor digitorum longa—MEDL) have been investigated in in vitro experiments. Application of carbacholine (CCh) in vitro in different concentrations led to pronounced muscle contractions, varying from 9.15 ± 4.76 to 513.13 ± 15.4 mg and from 44.65 ± 5.01 to 101.46 ± 9.11 mg for diaphragm and MEDL, respectively. Two hundred micromolars of CCh in both muscles caused the contraction with the 65% (diaphragm) to 75% (MEDL) of maximal contraction force—this concentration was thus used in further experiments. It was found that application of ATP (100 μM) increased the force of diaphragmatic contraction caused by CCh (200 μM) from 335.2 ± 51.4 mg ( n = 21) in controls to 426.5 ± 47.8 mg ( n = 10; P < 0.05), but decreased the contractions of MEDL of CCh from 76.6 ± 6.5 mg ( n = 26) in control to 40.2 ± 9.0 mg ( n = 8; P < 0.05). Application of adenosine (100 μM) had no effect on CCh-induced contractions of these muscles. Resting membrane potential (MP) measurements using sharp electrodes were done at 10, 20 and 30 min after the application of ATP and adenosine. Diaphragm showed depolarization from 75 ± 0.6 down to 63.2 ± 1.05, 57.2 ± 0.96 and 53.6 ± 1.1 mV after 10, 20 and 30 min of exposition, respectively (20 fibers from 4 muscles each, P < 0.05 in all three cases). Adenosine showed no effect on diaphragmatic MP. Both agents were ineffective in case of MEDL. The effects of ATP in both tissues were abolished by suramin (100 μM), a P2-receptor antagonist, and chelerythrin (50 μM), a specific protein-kinase C (PKC) inhibitor, but were not affected by 1 H-[1,2,4]-oxadiazolo-[4,3-α]-quinoxalin-1-one (ODQ, 1 μM), a guanylyl-cyclase inhibitor, or by adenosine-3,5-monophosphothioate (Rp-cAMP, 1 μM), a protein-kinase A (PKA) inhibitor. Besides the action on contractile activity, ATP (100 μM) led to a significant ( P < 0.001) depolarization of diaphragm muscle fibers from 74.5 ± 2.3 down to 64 ± 2.1, 58.2 ± 2.2 and 54.3 ± 2.4 mV after 10, 20 and 30 min of incubation, respectively. Incubation of MEDL with the same ATP concentration showed no significant change of MP. Denervation of the muscles for 28 days led to a decrease of CCh-induced contractions of diaphragm down to 171.1 ± 34.5 mg ( n = 11, P < 0.05), but increased the contractile force of MEDL up to 723.9 ± 82.3 mg ( n = 9, P < 0.01). Application of ATP elevated the contractility of denervated diaphragm caused by CCh up to normal values (311.1 ± 79.7 mg, n = 6, P > 0.05 versus control), but did not significantly affect of contractility of MEDL, which became 848.1 ± 62.7 mg ( n = 6). These results show that the effects of ATP on both diaphragmatic and skeletal muscles are mediated through P2Y receptors coupled to chelerytrin-sensitive protein-kinase C.

Lactate production upon short-term non–ischemic forearm exercise in mitochondrial disorders and other myopathies

The nonischemic forearm exercise test (NIFET) has been shown to be as effective as the classic ischemic forearm exercise test (IFET) in the diagnosis of patients with McArdle disease. Recently, the lactate increase normalized to the mechanical energy production in NIFET was suggested to have a intermediate sensitivity and satisfactory specifity for the screening of mitochondrial disorders. NIFET at 80% maximal contraction force (MCF) was performed in normal controls (n = 41), patients with mitochondrial disorders (n = 15) and other myopathies (diseased controls, n = 20). 26 healthy volunteers also underwent IFET at 80% MCF. The ratio of lactate increase and workload was defined as specific lactate production (mmol x s/N x l). In normal controls there was no significant different lactate increase during NIFET and IFET. The workload performed showed only a weak significant positive correlation with the lactate increase in the NIFET in normal controls (r(2) = 0.20) but not in IFET and NIFET with patients. A moderate negative correlation of specific lactate production and the absolute workload was found in all groups and in both protocols (r(2) = 0.22-0.34). The specific lactate production was highest in patients with other myopathies, intermediate in patients with mitochondrial disorders and lowest in normal controls. NIFET showed a sensitivity of only 20 % and a specifity of 95% for normal controls, but only 75 % for diseased controls. The specific lactate production during NIFET is neither sufficiently specific nor sensitive for the diagnosis of mitochondrial disorders. Increased specific lactate production during rest-to-work transition period might be caused by increased acetyl group deficits.

Lactate increase and oxygen desaturation in mitochondrial disorders – Evaluation of two diagnostic screening protocols

Mitochondrial disorders are characterized by an accumulation of lactate and an insufficient oxygen extraction from blood during exercise. Therefore, both parameters (lactate and oxygen saturation) can be used as screening tests in mitochondrial disorders. However, conflicting results regarding sensitivities and specifities of both tests have been reported. We examined 27 patients with genetically defined mitochondrial disorders (single deletions n = 15, multiple deletions n = 5, A3243G mutation n = 7), patients with other neuromuscular disorders, and healthy controls. In the first test subjects performed intermittent isometric handgrip exercise (0.5 Hz) at 80% (3 minutes) and 30% (3 and 15 minutes) of maximal contraction force (MCF). Oxygen saturation and partial pressure in cubital venous blood from the exercising arm were measured. In the second test subjects underwent cycle ergometry at 30 W for 15 minutes. Venous lactate at rest, during and 15 minutes postexercise was determined. Both tests showed specificities of 92-96%. Sensitivities for changes of venous oxygen partial pressure and oxygen saturation ranged from 21-26% at 80% MCF for 3 minutes to 47-58% at 30% MCF for 15 minutes. Sensitivities for venous resting, peak, and post-exercise lactate was 33%, 58%, and 67%, respectively. The degree of deoxygenation, however,was independent of the intensity and duration of the applied forces. Oxygen desaturation and lactate increase in patients with mitochondrial disorders were not different in patients with and without clinical symptoms of myopathy. There were significant correlations between the heteroplasmy and both the degree of oxygen desaturation and lactate increase in patients with single deletions. In patients who performed both protocols (n = 16) a combination of both tests increased sensitivity up to 87%. Oxygen desaturation in forearm exercise tests and lactate increase in cycle ergometry tests show a high specifity but only moderate sensitivity. Combination of the two screening test clearly increases the sensitivity.

Effects of exhaustive stretch‐shortening cycle exercise on muscle blood flow during exercise

The influence of exhaustive stretch-shortening cycle exercise (SSC) on skeletal muscle blood flow (BF) during exercise is currently unknown. Quadriceps femoris (QF) BF was measured in eight healthy men using positron emission tomography before and 3 days after exhaustive SSC exercise. The SSC protocol consisted of maximal and submaximal drop jumps with one leg. Needle biopsies of the vastus lateralis muscles were taken immediately and 2 days after SSC for muscle endothelial nitric oxide synthase (eNOS) and interleukin-1-beta (IL-1beta) mRNA level determinations. All subjects reported subjective muscle soreness after SSC (P < 0.001), which was well in line with a decrease in maximal isometric contraction force (MVC) and increase in serum creatine kinase activity (CK) (P = 0.018). After SSC muscle BF was 25% higher in entire QF (P = 0.043) and in its deep and superficial muscle regions, whereas oxygen uptake remained unchanged (P = 0.893). Muscle biopsies revealed increased IL-1beta (30 min: 152 +/- 75%, P = 0.012 and 2 days: 108 +/- 203%, P = 0.036) but decreased or unchanged eNOS (30 min; -21 +/- 57%, P = 0.050 and 2 days: +101 +/- 204%, P = 0.779) mRNA levels after SSC. It was concluded that fatiguing SSC exercise induces increased muscle BF during exercise, which is likely to be associated with pro-inflammatory processes in the exercised muscle.

Increased K+ release during exercise in myotonic dystrophy type 1 (DM1) but not type 2 (DM2)

Background: Previously excessive K+ increase upon exercise has been described in myotonic dystrophy, but not in non-dystrophic myotonias or other muscular dystrophies. However, at that time the differentiation into myotonic dystrophy type 1 (DM1) or type 2 (DM2) was not yet possible. Objective: Resting venous and interstitial (intramuscular) lactate and K+ levels were measured in patients with genetically defined DM1 (n=6) and DM2 (n=6). Control groups included mitochondrial disorders (n=9) and healthy volunteers (n=9). In all individuals venous and interstitial lactate and K+ were analysed upon standardized forearm exercise using both an ischemic and nonischemic protocol. Results: There was no difference in resting venous and interstitial lactate and K+ levels between DM1, DM2, and both control groups. Maximal contraction force (MCF), workload, venous and interstitial lactate increase were significantly lower in DM1 than in the other groups. Patients with DM2 and mitochondrial disorders exhibited intermediate values. Venous and interstitial K+ increases were not different between DM1, DM2, and both control groups. Venous K+ increase related to workload (specific K+ production) was significantly higher in both protocols in patients with DM1, but not in those with DM2 compared to both control groups. In contrast venous lactate increase related to workload (specific lactate production) was not different in all four groups. Due to the used temporal resolution the interstitial increases were less pronounced than in venous blood. Conclusion: An abnormally high increase of venous K+ upon exercise seems to be specific for DM1 but could not be observed in DM2. Even if a higher K+ production upon exercise might be related to myotonia in DM1, other mechanisms seems to be responsible in DM2. For example, altered splicing has been shown for the small conductance Ca 2+-activiated K+-channel (apamin receptor) mRNA and might contribute to increased K+ release and subsequently to myotonic phenomenon in DM1.

Vascular Abnormalities and Pulmonary Hypertension in the Berkeley Sickle Mouse.

Clinically, pulmonary hypertension is a major risk factor for mortality in adults with sickle cell disease. Contributing factors probably include red cell hemolysis and vaso-occlusive injury with their associated oxidative and inflammatory stimuli. Previously, we have described RBC hemolysis and endothelial oxidative stress in the Berkeley sickle mouse model and extend those studies in this work to investigate cardiovascular and endothelial dysfunction. Eight to ten month old homozygous and hemizygous Berkeley sickle mice and C57BL/6 control mice were used for all aspects of these experiments. In vivo measurements of mean arterial pressure and right ventricular pressures were conducted in fully anesthetized mice using a pressure transducer inserted in the carotid and right ventricle respectively. Following in vivo readings hearts were excised for measurement of ventricular mass. The ascending aorta was removed and cut into 5 mm rings for in vitro studies of agonist- induced contractility and relaxation. The mean arterial pressure of the hemizygous sickle mice (70.6 ± 3.4) was significantly lower than the control mice (86.0 ± 3.1) and the mean arterial pressure of homozygous sickle mice (59.0 ± 2.2 mmHg) was significantly lower than the hemizygous and control mice (p≤0.05 and p≤0.001, respectively). The right ventricular pressure showed a trend that approached significance (p= 0.08) such that pressures in homozygous mice were ≥ than those in hemizygous which were ≥ than those in control mice. Increased basal cardiac output was suggested by significant left ventricular hypertrophy. In vitro examination of potassium chloride activation of voltage gated calcium channels showed no significant difference in sensitivity or maximal contraction. Similarly, there was no difference in sensitivity to the α1 agonist, phenylephrine. However, both hemi- and homozygous mice showed a significant reduction in maximal force of contraction (normalized to cross sectional area when compared to controls. Maximal acetylcholine induced relaxation of aortic rings was significantly reduced (p≤0.05) in homozygous sickle mice compared to controls. The same effect was not seen with sodium nitroprusside induced relaxation indicating that the acetylcholine effect was not due to effects on the smooth muscle but was endothelium-dependent. The Berkeley mouse model shows cardiac hypertrophy consistent with the increased cardiac output associated with chronic anemia and a reduced basal mean arterial blood pressure similar to that seen in humans. 8–10 month old mice have increased right ventricular pressure and RV mass indicative of pulmonary hypertension. Further endothelial dysfunction is characterized by a reduction in the maximal relaxation elicited by acetylcholine. Therefore, the Berkeley mouse is a good model for investigating sickle related endothelial dysfunction.

Comparing brain activation across groups with different motor abilities

Sirs: A recent article by Schoenfeld et al. in your journal misquoted our work on ALS by stating that we “directly compared ALS patients with controls who executed the same motor task” [1]. This is not correct, as a major focus of our study was to adjust individually the motor task to patients’ impaired motor abilities [2]. The work of Schoenfeld et al. touches the important question of how groups with different motor abilities can be compared using functional imaging techniques. This question gains clinical relevance as many studies consider brain activation as a biological correlative for reorganization. However, increased brain activation might be misleading if patients with impaired motor abilities are challenged with the same motor task as healthy controls. For example the use of a simple joy stick paradigm [3] is more difficult for patients with paresis than for healthy controls, resulting in greater brain activation. To date there have been only a few studies taking into account different motor abilities between groups, using different methodological approaches: In their first experiment, Schoenfeld et al. use a 2 x 2 factorial design distinguishing between group (ALS or control) and task difficulty (easy or hard sequence of button presses). In this study, task difficulty was defined as the complexity of a sequence of button presses. From Fig. 3 it becomes evident that ALS patients show higher brain activation in premotor and cerebellar areas independent of task complexity [1]. This corresponds well with the results of our study [2]. In a second experiment, task frequency was only increased in one group (controls), but not the other (ALS patients), preventing statistic separation of this factor. Therefore the conclusions of the second experiment remain descriptive. In contrast to other approaches, subjective effort and forces exerted during motor performance were not assessed in this experimental design. We have previously addressed the problem of comparing groups with different motor abilities by adjusting task difficulty on an individual basis [2]: The individual maximum hand grip force of each ALS patient and control subject was determined before scanning. During functional imaging, a hand grip force transducer was adapted to 10 % of each individual’s maximum voluntary contraction force, such that ALS patients and controls experienced equal subjective effort and task difficulty during the experiment. Movement amplitude and frequency were controlled and similar between groups. This design was extended by Ward et al. who examined stroke survivors at 10, 20, 40, and 60 % of voluntary maximum contraction force at 40 % of their maximum movement rate, assessing subjective effort on a visual analogue scale [4]. This design is well suited to adjust the relevant parameters between groups. Compared with the design of Schoenfeld et al. we believe that it is advantageous to normalize effort, force, and frequency (if different) on an individual basis rather than to adjust mean error rates between groups. In sum it is most relevant that different motor abilities are taken into account by adjusting task difficulty in future imaging studies, even if the methodological details are open to debate. The physiological basis of increased motor area activation in patients with ALS is not yet proven. Current studies [1, 2] suggest that the human brain can exploit neural reserves when motor neurons degenerate, a strategy that might also be applied when motor demands increase [1]. Unmasking of intracortical connections as suggested by Jacobs and Donogue might be the physiological correlative [5]. It will be challenging for future research to investigate if therapeutic strategies might take advantage of these compensatory mechanisms.

Wild Blueberry-Rich Diets Affect the Contractile Machinery of the Vascular Smooth Muscle in the Sprague–Dawley Rat

Weanling male Sprague-Dawley rats were randomly fed a control diet (AIN-93) (C) or a blueberry diet (B) for 13 weeks, or a reverse diet (R) (C diet for 13 weeks, switched to the B diet for 8 weeks). Aortas were excised, and two intact and two endothelium-denuded rings were immersed in tissue baths containing physiological salt solution at 37 degrees C and aerated with 95% O(2) and 5% CO(2) (pH 7.4). Following equilibration and preconditioning under 1.5-g preload, cumulative dose-response curves were generated with six doses of the alpha1-adrenergic receptor-selective agonist L-phenylephrine (L-Phe, 10(8)-3 x 10(-6) M) and relaxed with one dose of acetylcholine (3 x 10(-6) M) to assess intact endothelium. The maximum force of contraction (Fmax) and vessel sensitivity (pD(2)) were determined in intact and endothelium-denuded rings. A two-way analysis of variance test revealed that blueberry-fed animals (B and R diets) developed a significantly lower F (max) (0.873 +/- 0.0463 and 0.9266 +/- 0.0463 g, respectively) when contracted with L-Phe, compared with the animals on the C diet (1.109 +/- 0.0463 g) (P < .05). The pD(2) of the intact rings was not significantly different among diet groups. Additionally, diet did not significantly affect the mean F (max) or pD(2) of endothelium-denuded rings. Our results indicate for the first time that wild blueberries incorporated into the diet affect the vascular smooth muscle contractile machinery by suppressing the alpha1-adrenergic receptor agonist-mediated contraction while having no effect on membrane sensitivity of the endothelial or vascular smooth muscle cell layer. Furthermore, their mechanism of action seems to be accomplished through an endothelium-dependent pathway.

Dietary manganese suppresses α 1 adrenergic receptor-mediated vascular contraction

We examined the effect of dietary manganese (Mn) on the vascular contractile machinery in rat thoracic aortas. Weanling male Sprague–Dawley rats were fed either an Mn-deficient (MnD), Mn-adequate (MnA) or Mn-supplemented (MnS) diet (<1, 10–15 and 45–50 ppm Mn, respectively). After 15 weeks on the diets the rats were sacrificed and 3-mm aortic rings were contracted in six cumulative doses of the α 1 adrenergic receptor agonist l-phenylephrine ( l-Phe, 10 −8 to 3×10 −6 M) under 1.5-g preload and relaxed with one dose of acetylcholine (3×10 −6 M) to assess intact endothelium. The maximal force ( F max) of contraction and relaxation, as well as the vessel sensitivity (pD 2) were determined. Manganese deficiency, assessed by hepatic Mn content, significantly lowered the rate of animal growth. A two-way analysis of variance revealed that MnS animals developed lower F max when contracted with l-Phe compared with the MnD and MnA animals ( P≤.001). Thus, dietary Mn at levels of 45–50 ppm affects the contractile machinery by reducing maximal vessel contraction to an α 1 adrenergic agonist. The observed pD 2 was significantly greater in the MnD group compared with the MnA and MnS animals ( P≤.001). Thus, restriction of dietary Mn affects vascular sensitivity to the α 1 adrenergic receptor. Our results demonstrate for the first time that dietary Mn influences the receptor signaling pathways and contractile machinery of vascular smooth muscle cells in response to an α 1 adrenergic receptor.

骨格筋ひずみ傷害による組織損傷と力学特性の変化に関する実験的検討(S02-2 生体組織のマルチスコープメカニクス(2).微細構造とメカニクス,S02 生体組織のマルチスコープメカニクス)

The relationship between tissue damage and changes of mechanical properties of. skeletal muscle with strain injury was discussed. Tibialis anterior muscle was extended 20, 25 or 30 % at 200 mm/sec to induce tissue damage. From pathological view points, severity of tissue damage could be classified into three grades and we could find a threshold of strain injury based on the relation between applied energy during injury-inducing process and the injury severity. We also evaluated the effects of strain injury on isometric contraction force. The results of biomechanical tests showed that the maximum contraction forces of 25%- and 30%-stretched muscles decreased. It indicates the injury severity could be related with biomechanical function of skeletal muscle.

Videomimicography: the standards of normal revised.

Studies aiming to objectively evaluate facial movements have focused on the technique of measurement, whereas the most pertinent measurements of basic facial movements have not been well characterized. To determine the best normal measures of 5 basic facial movements in healthy patients. In 5 healthy subjects, 11 facial landmarks were placed on the face, and 5 movements (forehead lift, eye closure, nose wrinkling, lip puckering, and smiling) with maximal contraction force were requested. Each subject repeated each movement 3 times, and the entire session was repeated on 4 different days. No specific immobilization of the head was performed. The session was filmed with a digital camera, and the frames with maximal movement were selected. Measurements were performed with Osiris public domain image analysis software. For each measure, the change from rest was computed. Intersubject and intrasubject variability were determined by a multivariate analysis of variance. In all movements, surface changes (mean +/- SD) were higher than distance changes. For forehead lifting and eye closure, the best measure was the eye surface changes of 13% +/- 5% and -32% +/- 9%, respectively. For nasal wrinkling, lip puckering, and smiling, the best measures were the paranasal area (change, -28% +/- 9%), upper lip area (change, -23% +/- 8%), and mouth area (change, 63% +/- 21%), respectively. Most distance changes were below 10%. Same-day repeatability variation was below 15%, and day-to-day repeatability variation was below 7%. In healthy subjects, more than 80% of the total variation was accounted for by the intersubject variability. Videomimicography is a simple and objective linear measurement system based on facial surface changes. The measures exhibit good reliability.

Sepsis alters vessel contraction by adrenoceptor-induced nitric oxide and prostanoid

Background.Alpha-adrenergic agents contract vascular smooth muscle (VSM) and stimulate endothelial release of secondary factors which modulate VSM contraction. Our study examined constrictor prostanoid (cPN) and nitric oxide (NO) as secondary factors which could alter alpha-1 adrenoceptor-mediated contraction during sepsis. Methods.Sepsis was induced in rats by inoculation of an implanted sponge with Escherichia coli and Bacteroides fragilis. Aortic rings at 24 h from septic (n = 21) and control (n = 21) rats were suspended in physiological salt solution (PSS) with or without blockers to NO (NG-monomethylarginine), cPN (mefenamic acid, MFA), or thromboxane A2 (SQ29548). Contraction dose-response curves were generated to determine maximal contraction force (Fmax) and pD2 (sensitivity) to phenylephrine in each experimental group. Results.Sepsis increased Fmax to phenylephrine (PHE) (1.18 vs 0.90 g, SEM 0.0703). COX inhibition reduced the Fmax in control (0.63 vs 0.90 g, SEM 0.0675) but not in septic animals (1.19 vs 1.18 g, SEM 0.0433). TXA2 receptor inhibition did not alter Fmax in control (1.017 vs 0.973 g, SEM 0.0959) or septic animals (1.28 vs 1.12 g, SEM 0.0823). NOS inhibition enhanced the Fmax in both nonseptic (2.03 vs 0.83 g, SEM 0.0523) and septic rats (1.96 vs 1.15 g, SEM 0.0526), but did less so in the septic animals. Conclusions.PHE-induced Fmax is determined by a balance between PHE-stimulated VSM alpha-adrenoceptor activity, and PHE-stimulated endothelial release of cPN and NO. Sepsis enhances total PHE-induced Fmax by increasing VSM alpha-adrenoceptor activity and reducing PHE-stimulated endothelial release of dilator NO. Sepsis abolishes the PHE-stimulated endothelial release of cPN. PHE-stimulated cPN is not thromboxane A2, but could be a nonprostanoid dilator in the lipoxygenase (HETE) or cytochrome P450 (EET) pathways.

Improvement of voluntary quadriceps muscle activation after total knee arthroplasty

Berth A, Urbach D, Awiszus F. Improvement of voluntary quadriceps muscle activation after total knee arthroplasty. Arch Phys Med Rehabil 2002;83:1432-6. Objective: To evaluate the maximal voluntary contraction (MVC) force and the voluntary activation of the quadriceps femoris muscle in patients with knee osteoarthritis (OA) before and after total knee arthroplasty (TKA). Design: A prospective intervention study. Setting: University hospital clinic in Germany. Patients: Fifty patients (32 women, 18 men; mean age ± standard deviation, 65.8±5.6y) with knee OA and 23 healthy age- and gender-matched control subjects. Intervention: Unilateral TKA without patella resurfacing. Main Outcome Measures: Voluntary activation, MVC, and true maximal contraction forces of the bilateral quadriceps femoris muscles, using the twitch interpolation technique before and 33±8 months after TKA. Assessment of postoperative knee pain by the Lewis score. Results: Voluntary activation increased bilaterally after surgery (P<.01 operated side, P=.02 nonoperated side) but remained lower than the voluntary activation of the controls. MVC (P<.001) and true maximal contraction forces (P=.01) increased significantly on the operated side. MVC remained unchanged (P=.45), and true maximal contraction forces decreased significantly (P=.04) on the nonoperated side. Conclusion: Patients with knee OA have significant bilateral voluntary activation deficits that are, at least in part, reversible within 3 years after TKA. Rehabilitation programs immediately after TKA should focus on reduction of voluntary activation deficits. After voluntary activation improves, physical therapy should target the augmentation of quadriceps femoris muscle strength. © 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

Reliability of pelvic floor muscle strength measurement in elderly incontinent women.

Pelvic floor muscles (PFM) play an important role in maintaining urinary continence with increasing age. Therefore, their contractile properties need to be evaluated. The aim of the study was to examine the reliability and correlation of simple techniques to measure PFM strength in elderly women with urinary incontinence. An interview was used to evaluate the ability to stop the urinary stream during micturition and to calculate the incontinence index. A pad test was applied to objectively evaluate the severity of the disease. Functional testing included a digital examination to measure the force and duration of one contraction, a perineometer measurement (Peritron) to assess maximal contraction force and contraction force of 5 s, and a cone-retention test (Femcon) while walking for 1 min and during Valsalva's manoeuvre. This procedure was performed on three separate occasions within one week. The 37 participating women with a mean age of 62+/-8 (mean+/-SD) years had a severity index of 4.4+/-2.6 and a urine loss of 9.5+/-13.6 mg during the pad test. Sixteen women were able to completely stop the urinary stream during micturition. The digital examination showed no intratester variability. The perineometer measurement showed that the absolute difference in maximal contraction force and mean contraction force within 5 s was less than 5.3 mm Hg and 4.5 mm Hg, respectively, with a probability of 0.95. While walking and during Valsalva's manoeuvre, 19 and 20 women, respectively, held the same cone in place on all three occasions. The maximal contraction force and mean force during the 5-s contraction correlated well with the ability to stop the urinary stream and the digital examination but only weakly with the cone-retention tests. The reliability of PFM strength measurement is highest in the digital examination, followed by perineometer measurements, and then by vaginal cone tests. As PFM function is easy to assess, it should be routinely done in the assessment of urinary incontinence in elderly women.

The exercise metaboreflex is maintained in the absence of muscle acidosis: insights from muscle microdialysis in humans with McArdle's disease.

1. In McArdle's disease, muscle glycogenolysis is blocked, which results in absent lactate and enhanced ammonia production in working muscle. Using McArdle patients as an experimental model, we studied whether lactate and ammonia could be mediators of the exercise pressor reflex. 2. Changes in muscle interstitial ammonia and lactate were compared with changes in blood pressure and muscle sympathetic nerve activity (MSNA) during static arm flexor exercise at 30% of maximal contraction force. Muscle interstitial changes in lactate and ammonia were assessed by microdialysis of the biceps muscle, and MSNA by peroneal nerve microneurography, in six McArdle patients and 11 healthy, matched controls. One McArdle patient also had myoadenylate deaminase deficiency, a condition associated with abolished ammonia production in exercise. 3. Exercise-induced increases were higher in McArdle patients vs. controls for MSNA (change of 164 +/- 71 vs. 59 +/- 19%) and blood pressure (change of 47 +/- 7 vs. 38 +/- 4 mmHg). Interstitial lactate increased in controls (peak change 1.3 +/- 0.2 mmol x l(-1)) and decreased in McArdle patients (peak change -0.5 +/- 0.1 mmol x l(-1)) during and after exercise. Interstitial ammonia did not change during exercise in either group, but was higher post-exercise in McArdle patients, except in the patient with myoadenylate deaminase deficiency who had a flat ammonia response. This patient had an increase in MSNA and blood pressure comparable to other patients. MSNA and blood pressure responses were maintained during post-exercise ischaemia in both groups, indicating that sympathetic activation was caused, at least partly, by a metaboreflex. 4. In conclusion, changes in muscle interstitial lactate and ammonia concentrations during and after exercise are temporally dissociated from changes in MSNA and blood pressure in both patients with McArdle's disease and healthy control subjects. This suggests that muscle acidification and changes in interstitial ammonia concentration are not mediators of sympathetic activation during exercise.