Maximal Contractile Force Research Articles

電気刺激による筋力増強と筋損傷の評価

The purpose of this study was to investigate muscle damage and reinforcement by electrical muscle stimulation (EMS).The first experiment involved two groups of athletes (Group 1 and Group 2) and one group of healthy volunteers who did not engage in daily exercises (Group 3 served as the control). The subjects’ triceps brachii muscles were stimulated electrically (EMS, subject&RSQUO;s variable tolerance: Group 1) and mechanically (concentric- and eccentric-resistance training of 60% MVC, RT: Group 2). For one of the subjects with EMS, the serum CPK levels of 3 and 4 days after the stimulation were approximately six times as high as that before the stimulation. The serum CPK levels of other subjects with EMS increased to twice or less of those before the stimulation. The serum CPK levels of subjects with RT did not change. The levels showed significant difference between subjects with EMS and RT, 2 and 5 days after the stimulation (Mann-Whitney test, p&LT;0.05).In the second experiment, the quadriceps femoris muscles were stimulated. EMS generating a force of 60% MVC was applied to each subject in Group 4 for 30 minutes every other day for a week. RT of 60% MVC was applied to each subject in Group 5. The subject did 30 trials, with 60 s resting time between every 10 trials, every other day for a week. The serum CPK levels of the subjects with EMS increased, but the increase rate varied with subjects. One of the subjects had more than six times as high serum CPK levels as that before the stimulation. Another subject had only one and half times as high serum CPK levels as that before the stimulation. There were significant changes with time after the stimulation (Friedman test, p<0.05). However, there were no significant differences between subjects with EMS and the control. For subjects with RT, the serum CPK levels increased slightly but there were no significant changes with time after the stimulation (p>0.05).In the third experiment, EMS was applied to the triceps brachii muscles of Group 1 and Group 3 for eight weeks. The non-athletes with EMS showed 30% increase of the maximum voluntary contractile force and they showed 38-54% improvement of endurance. The maximum voluntary contractile force of athletes with EMS did not change but the endurance showed 59% improvement. However the maximum voluntary contractile force of athletes without EMS decreased and the endurance did not change.In conclusion, we suggest that EMS could cause more severe muscle damage than concentric-, eccentric-resistance training. EMS reinforced the muscles of both athletes and non-athletes. Moreover, EMS showed stronger effects on non-athletes compared with the athletes.

Contractile response of femoral arteries in pigs with acute liver failure

Background: Acute liver failure (ALF) is characterized haemodynamically by a progressive hyperdynamic circulation. The pathophysiological mechanism is unknown, but impaired contractility of vascular smooth muscle may play an important role. The aim of this study was to evaluate the vascular response to stimulation with norepinephrine and angiotensin II in endothelium‐denuded femoral artery rings. Methods: Norwegian Landrace pigs weighing 27.1 ± 0.5 kg (mean ± sx(standard error of the mean)) were used. ALF was induced by performing a portacaval shunt followed by ligation of the hepatic arteries (n = 6). Sham‐operated animals served as controls (n = 5). Cumulative isometric concentration contraction curves were obtained after in vitro stimulation of the femoral artery rings with either angiotensin II (10−13–10−5mol/L) or norepinephrine (10−13–10−3mol/L). Results: Pigs suffering from ALF developed a hyperdynamic circulation with an increased cardiac index (P = 0.017) and decreased systemic vascular resistance index (P = 0.015). Studies of the hind leg revealed a decreased vascular resistance index and increased blood flow compared to sham‐operated controls (P = 0.003 and P = 0.01, respectively). Angiotensin II caused a concentration‐dependent contraction of the arterial segments, with no significant differences in vascular responses between the two groups. Maximum force generated did not differ (55 ± 7 versus 56 ± 7 mN, P = 0.95). Furthermore, there were no differences for norepinephrine in the cumulative concentration–response curves and the maximum contractile force was not significantly different (87 ± 8 versus 93 ± 16 mN, P = 0.55). Conclusions: This study documents for the first time that there are no signs of endothelium‐independent peripheral vascular hyporesponsiveness to angiotensin II and norepinephrine in pigs with ALF.

Between-days reliability of electromyographic measures of paraspinal muscle fatigue at 40, 50 and 60% levels of maximal voluntary contractile force.

To ascertain which percentage of maximal voluntary contractile force of the paraspinal muscles, when tested in a functional position, is most reliable for assessing electromyographic (EMG) fatigue changes. Ten healthy volunteers with no history of low back pain (six males). The surface EMG signal during 60-second isometric contractions of the paraspinal muscles at 40, 50 and 60% levels of maximal voluntary contractile force was captured and analysed. Each contraction level was assessed on two occasions, at least three days apart. The initial median frequency, the decline in median frequency slope and the increase in root mean square values were assessed for between-days reliability, using intraclass correlation coefficients (ICCs) and standard errors of measurements (SEM). Normalized median frequency and root mean square values were also assessed. At 40% of maximal voluntary contraction, little or no EMG fatigue changes occurred in any of the observed parameters. At 50% maximal voluntary contraction the initial mean frequency and root mean square changes proved highly reliable, with ICCs ranging from 0.74 to 0.86 and 0.75 to 1.00 respectively. Normalizing the root mean square data reduced the reliability, but this was still acceptable with ICCs 0.70-0.83. The median frequency decline slope proved less reliable with ICCs 0.24-0.74 for raw and 0.26-0.77 for normalized data. At 60% maximal voluntary contraction the initial mean frequency proved as reliable as initial median frequency at 50% with ICCs 0.70-0.89. The raw and normalized root mean squares (ICCs 0.43-0.89 and 0.30-0.87 respectively) and raw and normalized median frequency (ICCs 0.27-0.51 and 0.24-0.53 respectively) changes were less reliable than at 50% MVC. Overall, the reliability is better at the L4/5 than at the L2/3 level. Outcome measures taken at 50% maximal voluntary contraction are the most reliable in functional testing the paraspinal muscles of healthy volunteers. With initial median frequency and root mean square values being more reliable parameters than median frequency decline. At the L4/5 level, however, all parameters were acceptably reliable at 50% of maximum effort. However the between-subject variability of the median frequency decline and root mean square incline slopes suggest that these parameters are not yet fully suitable for monitoring fatigue changes during prolonged isometric contraction.

Effect of vitamin A deficiency on cardiovascular function in the rat

Selected parameters of cardiovascular function were evaluated in vitamin A-deficient rats at 70 days of age. Resting heart rate was increased by an average of 100 bpm (21.4+/-2.7%), whereas resting systolic blood pressure was normal in vitamin A-deficient animals. The maximal contractile force developed per milligram weight of tissue by aortic rings excised from vitamin A-deficient animals was reduced in response to high potassium (-25.0+/-8.7%) and phorbol 12,13-dibutyrate (-36.8+/-8.4%) but was only slightly reduced in response to norepinephrine (-17.8+/-11.1%). Intimal rubbing to remove the endothelium had no effect on the loss in contractile responsiveness, and the relaxant response to acetylcholine was similar between control and vitamin A-deficient tissue groups. This suggests that the decrease in contractility of vascular smooth muscle from the vitamin A-deficient rats did not involve altered release of endothelium-derived vasoactive factors. Western blot analysis suggested a reduction in the protein levels of several differentiation markers including alpha-actin (-22%), calponin (-37%), desmin (-37%), and vinculin (-40%), whereas the level of PKCalpha was unchanged from control values. Our findings indicate a significant decrease in contractile responsiveness of aortic smooth muscle of the vitamin A-deficient rat that may be associated with a down regulation in the expression of contractile-related proteins.

Spring balance evaluation of the ischiocavernosus muscle.

We studied the voluntary contractile activity of the ischiocavernosus muscle (ICM) in 21 sexually potent and 97 erectile dysfunction (ED) subjects using a spring balance. A strap was placed around the coronal grove of the glans penis and tensioned with the spring balance. Subjects were asked and encouraged to contract the ICM against the spring balance. We evaluated the length of stroke, duration of contraction, and maximum contractile force. The length of stroke, duration of contraction, and maximum contractile force showed statistically significant differences between potent and ED subjects. Diagnosed psychogenic ED and arteriogenic ED showed higher contractile activity than cavernous ED and neurogenic ED. Our results corresponded to those of previous studies that have urged consideration of the role of the ICM during the process of erection in animal experiments and in human electrophysiological studies. The spring balance evaluation is a useful, inexpensive method for evaluating the ICM.

A mechanism for increased contractile strength of human pennate muscle in response to strength training: changes in muscle architecture.

1. In human pennate muscle, changes in anatomical cross-sectional area (CSA) or volume caused by training or inactivity may not necessarily reflect the change in physiological CSA, and thereby in maximal contractile force, since a simultaneous change in muscle fibre pennation angle could also occur. 2. Eleven male subjects undertook 14 weeks of heavy-resistance strength training of the lower limb muscles. Before and after training anatomical CSA and volume of the human quadriceps femoris muscle were assessed by use of magnetic resonance imaging (MRI), muscle fibre pennation angle (theta(p)) was measured in the vastus lateralis (VL) by use of ultrasonography, and muscle fibre CSA (CSA(fibre)) was obtained by needle biopsy sampling in VL. 3. Anatomical muscle CSA and volume increased with training from 77.5 +/- 3.0 to 85.0 +/- 2.7 cm(2) and 1676 +/- 63 to 1841 +/- 57 cm(3), respectively (+/- S.E.M.). Furthermore, VL pennation angle increased from 8.0 +/- 0.4 to 10.7 +/- 0.6 deg and CSA(fibre) increased from 3754 +/- 271 to 4238 +/- 202 microm (2). Isometric quadriceps strength increased from 282.6 +/- 11.7 to 327.0 +/- 12.4 N m. 4. A positive relationship was observed between theta(p) and quadriceps volume prior to training (r = 0.622). Multifactor regression analysis revealed a stronger relationship when theta(p) and CSA(fibre) were combined (R = 0.728). Post-training increases in CSA(fibre) were related to the increase in quadriceps volume (r = 0.749). 5. Myosin heavy chain (MHC) isoform distribution (type I and II) remained unaltered with training. 6. VL muscle fibre pennation angle was observed to increase in response to resistance training. This allowed single muscle fibre CSA and maximal contractile strength to increase more (+16 %) than anatomical muscle CSA and volume (+10 %). 7. Collectively, the present data suggest that the morphology, architecture and contractile capacity of human pennate muscle are interrelated, in vivo. This interaction seems to include the specific adaptation responses evoked by intensive resistance training.

Force recovery after eccentric exercise in males and females.

In this study we investigated force loss and recovery after eccentric exercise, and further characterized profound losses in muscle function (n = 192 subjects--98 males, 94 females; population A). Maximal voluntary contractile force (MVC) was assessed before, immediately after, and at 36 and 132 h after eccentric exercise. Two groups were then established (A1 and A2). Group A1 demonstrated a > 70% reduction in MVC immediately after exercise, but were recovering at 132 h after exercise. These subjects performed a follow-up MVC 26 days later (n = 32). Group A2 demonstrated a > 70% reduction in MVC immediately post-exercise, but still exhibited a > 65% reduction in force at 132 h post-exercise; these subjects also performed a follow-up MVC every 7 days until full recovery was established (n = 9). In population A, there was a 57% reduction in MVC immediately post-exercise and a 67% recovery by 132 h post-exercise (P < 0.01), with no significant gender differences (P > 0.05). In group A1, although more females (two-thirds) showed large force losses after exercise, these females demonstrated greater %MVC recovery at 132 h post-exercise (59% vs 44%) and at 26 days post-exercise (93% vs 81%) compared to the males. In group A2, MVC recovery occurred between 33 and 47 days post-exercise. In conclusion, 21% of all subjects showed a delayed recovery in MVC after high-force eccentric exercise. Although there were no significant gender differences in force loss, a disproportionately larger number of females demonstrated force reductions of > 70%. However, their recovery of force was more rapid than that observed for the males who also demonstrated a > 70% force loss.

Glycine preserves function and decreases necrosis in skeletal muscle undergoing ischemia and reperfusion injury

Background. Glycine (GLY) is a neutral amino acid that has been shown to be cytoprotective in the kidneys of dogs and rabbits undergoing ischemia-reperfusion injury. To investigate whether GLY exhibits a protective effect on skeletal muscle subjected to ischemia and reperfusion injury, we used a well-described gracilis muscle model in canines. Methods. Twelve adult mongrel dogs were subjected to 6 hours of ischemia in 1 randomly selected side. The dogs were randomized into 2 groups: group 1 (6 animals) underwent 15 minutes of perfusion with 2.2% GLY, and group 2 (6 animals) underwent 15 minutes of perfusion with normal saline solution (NS) only. Both groups had normothermic reperfusion for 1 hour along with the corresponding perfusate. Muscle biopsy specimens were taken, frozen in liquid nitrogen, and stored at −70°C. Muscle injury was evaluated at 48 hours by measuring weight gain (edema), maximal contractile force, and percent of muscle necrosis. Adenosine triphosphate (ATP) and phosphocreatine (Pcr) (an energy store for ATP synthesis) levels were determined by using high performance liquid chromatography. Results. In group 1, the average weight gain was 57% ± 11.27% while in group 2 it was 100% ± 12.48%. Maximal muscle contractile force was 712.5 ± 68 g for group 1 and 511 ± 27.91 g for group 2. The amount of muscle necrosis was 30 ± 3.7% in group 1, as opposed to 63 ± 10% in group 2. The ATP content was 0.07 ± 0.03 nmol/mg wet tissue weight (post-ischemia with NS) and 0.21 ± 0.08 nmol/mg wet tissue weight (post-ischemia with GLY). Pcr content was 0.19 ± 0.04 mmol/mg wet tissue weight (post-ischemia with NS) and 0.27 ± 0.04 μmol/mg wet tissue (post-ischemia and infused with GLY) (P < .05). Conclusions. These data show that GLY preserves muscle function, decreases edema and the amount of muscle necrosis and preserves energy stores in this canine model. Because GLY can be safely given systemically in human beings in higher concentrations than that given in our model, as it is given in parenteral nutrition, its mechanism of action should be further investigated for its potential use in the clinical setting of ischemia and reperfusion injury. (Surgery 2001;129:231-5.)

Effects of castration on contraction and alpha(1)-adrenoceptor expression in rat prostate.

1. The prostate function is regulated by androgens and alpha-adrenergic activity. Clinically, antiandrogens and/or alpha(1)-adrenergic antagonists are commonly used to treat symptomatic prostatic hypertrophy. To elucidate the effects of androgen deprivation on prostate contractility via alpha(1)-adrenoceptor, the characteristics and expression of alpha(1)-adrenoceptors were examined in castrated rats. 2. Isolated prostate strips from intact and castrated rats were subjected to a phenylephrine stimulated contraction. Prazosin (10 nM), [(3)H]-prazosin and phenoxybenzamine (3 - 300 nM) were used for inhibition assay, receptor characterization and partial alkylation of alpha-adrenoceptor, respectively. The mRNA content of three subtypes of alpha-adrenoceptors was determined by reverse transcription combined with polymerase chain reaction (RT - PCR). 3. Contractile response to phenylephrine increased in castrated rats, which could be explained by a relative increase of the stromal component. A lowered contraction potency was also noted in castrated rats. Receptor binding assay indicated minimal changes in the affinity or density of alpha(1)-adrenoceptor. Escalating alkylation of the alpha(1)-adrenoceptor population resulted in a rightward shift in the contraction-response curves before depressing maximal contractile force, and the suppression was detected at lower doses in castrated rats. RT - PCR study confirmed the expression of three types of alpha(1)-adrenoceptor, alpha(1a), alpha(1b) and alpha(1d)-adrenoceptors, in intact rat prostate, and revealed that alpha(1a)-adrenoceptor, but not alpha(1b) or alpha(1d)-adrenoceptors, was down-regulated in castrates. 4. The results show that androgen deprivation suppressed alpha(1)-adrenergic contractility of rat prostate strips, and the suppression was associated with down-regulation of receptor reserve for the alpha(1a)-adreneroceptor population expressed in intact rat prostate.

Effects of treatment with FK409, a nitric oxide donor, on collar-induced intimal thickening and vascular reactivity

Intimal thickening in arteries is considered a site of predilection for atherosclerosis. In a rabbit model of early atherosclerosis, a silastic collar was placed around the carotid artery, which resulted in the formation of intimal thickening. We investigated whether the oral application of FK409 ((±)-( E)-4-ethyl-2-[( E)-hydroxyimino]-5-nitro-3-hexenamide, 10 mg kg −1 day −1, p.o.), a nitric oxide donor, inhibited the collar-induced intimal thickening as well as accompanying reactivity changes in rabbit carotid artery. The intimal thickening was significantly inhibited by FK409. The collar treatment increased the pD 2 value of 5-hydroxytryptamine (5-HT) whereas it decreased those of phenylephrine and acetylcholine and did not significantly alter that of nitroglycerine. Maximal contractile force development in response to potassium chloride (KCl), 5-HT and phenylephrine was decreased in collared arteries. The collar did not alter the maximal relaxant effects of acetylcholine and nitroglycerine. Despite the significant reduction of intimal thickening, FK409 treatment did not affect these collar-induced modifications in vascular reactivity.

Subacute Sepsis Impairs Vascular Smooth Muscle Contractile Machinery and Alters Vasoconstrictor and Dilator Mechanisms

Introduction.Sepsis results in hyporesponsiveness to α-adrenergic stimulation. This is thought to be mediated by the release of vasoactive compounds from the septic endothelium or by the direct effect of sepsis on vascular smooth muscle (VSM) contractile mechanics and machinery. Previous studies have used lethal models of sepsis or endotoxemia to examine this phenomenon. The present study utilizes a clinically relevant, nonlethal model of soft tissue infection to determine the effects of sepsis on α-adrenergic mechanisms. We hypothesize that subacute sepsis causes impaired α-adrenergic vascular responsiveness by a combination of effects on adrenergic constrictor mechanisms, endogenous dilator tone, and VSM contractile function.Methods.Male Sprague-Dawley rats underwent implantation of a 2 × 2-cm2gauze sponge into a subcutaneous pocket created at the base of the tail. Five days after implantation, sepsis (S) was induced by inoculation of the sponge with 109CFUEscherichia coliandBacteroides fragilis.Controls (C) were inoculated with saline. Thoracic aortic harvest was performed 24 and 48 h after sponge inoculation for organ bath ring studies. Receptor-mediated (phenylephrine) and nonreceptor-mediated (KCl) maximum force of contraction (Fmax) was measured. Vessel sensitivity (pD2) to phenylephrine, acetylcholine, and KCl was calculated from dose-response curves.Results.At 24 h, sepsis resulted in a lowerFmaxto phenylephrine (1.15 for C vs 0.5 for S,P< 0.05 by ANOVA), despite an increase in vessel sensitivity (pD2) to α-adrenergic stimulation (6.70 for C vs 6.88 for S,P< 0.05 by ANOVA).Fmaxto KCl was lower in septic animals at 24 h (3.50 for C vs 2.77 for S,P< 0.05 by ANOVA) and sensitivity to acetylcholine (pD2) was markedly increased (6.56 for C vs 7.23 for S,P< 0.05 by ANOVA). At 48 h, the impairment inFmaxto α-adrenergic stimulation (2.29 for C vs 1.72 for S,P< 0.05 by ANOVA) and KCl (3.5 for C vs 3.08 for S.P< 0.05 vs 24 h C by ANOVA) persisted without any change in sensitivity to phenylephrine or acetylcholine.Conclusions.Subacute sepsis results in an early suppression of maximum contractile force despite an increase in adrenergic receptor sensitivity (pD2). This may be secondary to an elevation in dilator sensitivity combined with a direct effect of sepsis on VSM contractile mechanisms. Later in the septic process, however, α-adrenergic hyporesponsiveness (↓Fmax) is primarily due to changes in VSM contractile machinery.

Age dependent response to exogenous estrogen on micturition, contractility and cholinergic receptors of the rat bladder

The age related effects of 17β-estradiol (E) supplementation on micturition and contractility of ovariectomized rats (OVX) were evaluated. Studies were carried out in young, 2 month, and mature, 10 month old rats which were distributed into three groups: Sham-operated (SHAM), (OVX), and (OVX+E). Following treatment, urodynamic studies were performed followed by an in vitro bladder tissue evaluation. Urodynamic studies show age and time related changes in bladder function. The in vitro results show that the hormone deprived tissues of 2 months old rats had a decreased responsiveness to cholinergic stimulation; maximum contractile force occurred at 78% and 187% for the SHAM. The response from the OVX+E tissues was evident at 113%. E supplementation of the mature rats increased bladder contractile force to the same levels as SHAM (156% and 176%). The response of the mature OVX rats remained significantly below that of SHAM or OVX+E rats. Findings suggest that the impact of E on bladder function depends on age at which it is given. Differential response between young and mature to exogenous E indicates that endogenous estrogen plays a major role in the neuromuscular development of normal bladder function and micturition reflexes. Contractility data show that OVX in young rats irreversibly decreases the response of the bladder to cholinergic stimulation, suggesting that exogenous E partially restores function while in mature rats, exogenous E was able to reverse the effects of OVX.

Electrical stimulation of human tibialis anterior: (A) contractile properties are stable over a range of submaximal voltages; (B) high- and low-frequency fatigue are inducible and reliably assessable at submaximal voltages.

To investigate the validity and reliability of submaximal voltage stimulation for assessing the 'fresh' contractile properties of human tibialis anterior muscle (TA) and the efficacy of such stimulation in inducing and assessing high- and low-frequency fatigue. (A) Contractile properties of fresh TA were assessed in six normal volunteers using multifrequency stimulation trains (comprising 2 seconds at each of 10, 20 and 50 Hz, arranged contiguously) over a range of submaximal voltages. (B) On three separate occasions, fatigue was induced in the TA of 10 normal volunteers by means of a 3-minute unbroken sequence of the described multifrequency stimulation trains, delivered at a 'standardized' submaximal voltage. This fatiguing protocol was preceded by discrete multifrequency stimulation trains, at the same standardized voltage, but followed by discrete multifrequency trains delivered over a range of submaximal voltages (which included the standardized voltage). In experiment A the 10:50 Hz and 20:50 Hz force ratios were analysed for between-voltages variability using coefficients of variation (CVs), and for trends using Friedman tests and post-hoc Wilcoxon tests. In experiment B low-frequency fatigue was detected using 10:50 Hz and 20:50 Hz force ratios derived from the discrete multifrequency trains. High-frequency fatigue was calculated from the decline in high-frequency force which occurred during the fatiguing protocol itself. Each parameter was assessed for between-days repeatability using CVs. In experiment A the 'fresh' 10:50 Hz force ratio was clearly unreliable at voltages which generated <10% of maximal voluntary contractile force (MVC) (CV< or =29.7%), but was reasonably reliable at voltages which generated 20-30% of MVC (CV < or = 11.5%; p = 0.847). The 'fresh' 20:50 Hz force ratio was,in contrast, extremely reliable throughout the tested voltage range (CV< or =5.8%; p = 0.636) in fresh muscle. In experiment B paired t-tests indicated that the fatiguing protocol induced significant high-frequency fatigue (p <0.0037) and low-frequency fatigue (p <0.0008 for 'fresh' versus 'fatigued' 10:50 Hz force ratio; p <0.0001 for 'fresh' versus 'fatigued' 20:50 Hz force ratio). In muscle thus fatigued, the 20:50 Hz force ratio was extremely reliable in the 20-33% of MVC range (CV < or =7.3%; p = 0.847). Between-days repeatability was poor for the 10:50 Hz force ratio in both fresh and fatigued muscle (CV < or =23.8 and 44.4% respectively), but was highly acceptable for both voluntary and stimulated fatigue indices and for the 20:50 Hz force ratio, the latter in both fresh and fatigued muscle. These results confirm the validity and reliability of submaximal voltages in assessing contractile properties (including low-frequency fatiguability) and inducing fatigue of human TA.

Frequency dependence of muscarinic facilitation of transmitter release in urinary bladder strips from neurally intact or chronic spinal cord transected rats.

1. Electrical stimulation evoked release of 3H-noradrenaline (NA) and 14C-acetylcholine (ACh), as well as neurally evoked contractions were measured at various (1-40 Hz, 100 shocks) stimulation frequencies in bladder strips from neurally intact (NI) and spinal cord transected (SCT) rats. 2. The frequency response curves for ACh and NA release were shifted to the left in SCT bladder strips as compared to NI bladder strips. 3. Atropine (1 microM) depressed ACh release in NI bladder strips at high frequency stimulation (10 and 40 Hz) but not at low frequency stimulation (2-5 Hz). However, in SCT bladders, atropine depressed ACh release both at low and high frequencies of stimulation, indicating that muscarinic facilitation occurs at lower frequencies. 4. Atropine depressed the release of NA in NI bladders at only 40 Hz stimulation, but depressed release at all frequencies in SCT bladders. 5. The amplitude of neurally evoked contractions of bladder strips from NI rats was enhanced as the frequency of stimulation was increased from 1 to 40 Hz (80 shocks). The frequency response curve was shifted to the left in SCT bladders. Atropine blocked the neurally evoked contractions in SCT bladder strips to a greater extent than the contractions in NI strips indicating a cholinergic dominance in the SCT bladders. 6. Maximal contractile force of SCT bladder strips evoked by neural stimulation at 20 Hz 10 shocks and 80 shocks was significantly lower than that of NI bladder strips, whereas the release of ACh was significantly higher in SCT than NI bladders indicating a postjunctional defect in the SCT preparations. 7. It is suggested that presynaptic muscarinic facilitatory mechanisms are upregulated in the cholinergic and adrenergic nerve terminals in SCT bladders leading to a larger relative contractile response at lower frequencies of stimulation (2-5 Hz). Thus the hyperreflexic bladder occurring after spinal cord injury may be due in part to an enhancement of transmitter release at bladder postganglionic nerve terminals.

Variations of arterial responses in vitro in different sections of rat main superior mesenteric artery.

We examined the control of vascular tone in rat main superior mesenteric artery. Three standard rings (3 mm in length) of the mesenteric artery were cut, beginning 5 mm, 13 mm and 21 mm distally from the mesenteric arteryaorta junction. In noradrenaline-precontracted rings, relaxations to acetylcholine in the absence and presence of the cyclooxygenase inhibitor diclofenac, did not differ in the studied sections. However, the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, attenuated the diclofenac-resistant responses to acetylcholine more effectively in the proximal than the distal section. Glibenclamide, an inhibitor of ATP-sensitive K+ channels, diminished relaxations evoked by acetylcholine only in the distal section, whereas the inhibitor of Ca2+ activated K+ channels, apamin, attenuated the responses in all sections. Furthermore, relaxation sensitivity to nitroprusside and isoprenaline was lower in the proximal than distal section. Arterial contractile sensitivity to noradrenaline and potassium chloride was higher, while the maximal contractile force generation was lower in the proximal than the distal part. In conclusion, in different sections of rat main superior mesenteric artery considerable variability was observed in vasoconstrictor and vasodilator responses, as well as in the contribution of endothelial nitric oxide and endothelium-mediated hyperpolarization to vasodilation. Therefore, the present results emphasize the fact that only corresponding vessel segments should be used when investigating the control of arterial tone.

Organization and mechanical behaviour of myocyte-ligament composites in a sea-urchin lantern: the compass depressors of Stylocidaris affinis (Echinodermata, Echinoida)

Certain components of the jaw apparatus, or lantern, of regular sea-urchins form a ’compass system’ the function of which has still to be established. This system includes ten compass depressors (CDs) which connect the compass ossicles to the inner edge of the test. Previous studies focused on the CDs of euechinoid sea-urchins. This paper provides the first detailed account of the organization and mechanical behaviour of the CDs of a cidaroid sea-urchin, Stylocidaris affinis. The outermost layer of its CDs is a coelothelium comprising apical peritoneocytes, sparse subapical myocytes and two types of granule-containing cells. The central core of the CD is dominated by longitudinally orientated collagen fibrils arranged in bundles surrounded by networks of beaded microfibrils. Myocytes are scattered throughout the core and are always surrounded by a basal lamina which usually encloses the same two types of granule-containing cells observed in the coelothelium. Each CD is attached to the outer coelomic septum by a mesentery, both the connective tissue and coelothelia of which lack myocytes and granule-containing cells. From data on the relationship between the vertical position of the lantern and the passive and active forces developed by intact CD sets, it appears that the CDs resist elevation of the lantern above its ’resting position’ and that they develop a maximal contractile force when their length corresponds to that at the resting position. The connective tissue of the CDs has the capacity to undergo nervously mediated changes in stretch resistance, although this is expressed more weakly than in the euechinoid CDs. These results are related to current views on the physiological role of the compass system.

Comparison of eccentric knee extensor muscle actions at two muscle lengths on indices of damage and anglespecific force production in humans

In this study, we investigated the effects of knee extensor length during eccentric exercise on indices of muscle damage and adaptation. Subjects (n=7) performed two bouts of 75 maximal voluntary eccentric muscle actions at a knee joint angular velocity of 1.57 rad s-1. One bout was performed at a short muscle length (bout S) with a knee joint range of motion of 2.79 to 1.40 radians (160" to 80°), and a second with the contralateral knee extensors at a long muscle length (bout L) with a range of motion of 2.01 to 0.7 radians (120" to 40"). The maximum voluntary contractile force (MVC) was measured before and 5 min after exercise, and again on days 3, 5,7,10 and 12, at knee angles of 1 60°, 120" and 80". Muscle soreness was measured before exercise and on each day after exercise. Serum creatine kinase activity was measured before exercise and on days 3, 5, 7, 10 and 12 post-exercise. The MVC declined after each bout (P<0.01), with a greater decline after bout L (P<0.05). Muscle soreness was higher relative to bout S on days 1,2,3, 5 and 6 (P<0.05). Although serum creatine kinase activity was elevated after both exercise bouts (P<0.01), there was no difference between bouts. Functional muscle damage markers and muscle soreness suggest greater damage after bout L. Post-exercise angle-specific force decrements suggest a transient increase in muscle length after bout L but not bout S.

Effect of hyperoxia on substance P expression and airway reactivity in the developing lung.

This study was undertaken to characterize changes in the tachykinin system induced by hyperoxic exposure and the potential effects on airway contractile responses. We exposed 7-day-old rat pups to either room air or hyperoxia (> 95% O2) for 7 days to assess pulmonary beta-preprotachykinin (beta-PPT) gene expression, substance P (SP) levels, and airway contractile responses to cholinergic stimulation before and after neurokinin-1 (NK1) receptor blockade. Lung beta-PPT mRNA expression, lung and tracheal SP levels, and contractile responses to exogenous acetylcholine and electrical field stimulation were measured in vitro in normoxia- and hyperoxia-exposed tracheal cylinders. Hyperoxia caused a 1.1- to 2.6-fold increase in steady-state lung beta-PPT mRNA and a 50 and 32% increase in SP levels of lung and trachea, respectively. In response to cholinergic stimulation, maximal contractile force (Emax) of hyperoxia exposed tracheal muscle was significantly higher than for normoxic controls. Addition of the SP (NK1) receptor blocker CP-99994 (10 microM) decreased sensitivity to electrical field stimulation in both hyperoxic and normoxic trachea without a significant decline in Emax. These data provide evidence for both increased SP production and enhanced maximal contractile responses of hyperoxia-exposed neonatal trachea to cholinergic stimulation. The tachykinin peptide SP does not, however, appear to play a major role in the enhanced airway reactivity associated with hyperoxic lung injury during early postnatal life.

Preconditioning with Ischemia or Adenosine Protects Skeletal Muscle from Ischemic Tissue Reperfusion Injury

Prolonged tissue ischemia and subsequent reperfusion results in significant tissue injury due to the ischemic-reperfusion (IR) syndrome. Ischemic preconditioning (IPC) or adenosine (ADO) pretreatment are known to protect IR injury in cardiac muscle. Our aim was to determine whether IPC or ADO pretreatment attenuates and protects against ischemic tissue reperfusion injury in skeletal muscle. Rats were anesthetized and global hindlimb ischemia was induced by 60 min of suprarenal aortic clamping followed by 30 min of reperfusion period. The degree of skeletal muscle dysfunction was determined by decreases in maximum contractile force, and adenosine triphosphate (ATP) and creatine phosphate (CP) levels of extensor digitorum longus (EDL) muscle. The distal tendon of the EDL was attached to a force transducer for maximum isometric force measurement. Samples were taken from the EDL for measurement of ATP and CP levels. The following were protective protocols prior to the IR challenge: (1) four consecutive 5-min periods of ischemia separated by 5-min reperfusion periods (PC/I) or (2) i.v. adenosine infusion (350 μg/kg/min × 10 min, PC/A). Our data suggest that pretreatment with brief periods of ischemia or systemic ADO infusion attenuates ischemic tissue reperfusion injury in skeletal muscle [Table]

Endogenous inotropic factor-induced endothelium-dependent relaxation of vascular smooth muscle.

1. Possible contractile or relaxation effects of an endogenous inotropic factor (EIF) isolated and purified from porcine heart left ventricle were examined in rat isolated aortic ring preparations. 2. EIF induced a dose-dependent relaxation of the rat isolated aortic ring preparation pre-contracted with 0.4 microM phenylephrine (PE); 200 microliters (in 5 ml bath) of EIF caused relaxation of aortic rings by as much as 67.4 +/- 4.5%. In another set of experiments, in the presence of 100 microliters EIF, the PE concentration-response contractile curve shifted to the right, the maximal contractile force was reduced by as much as 32.8% and the EC50 of PE increased from 0.2 to 0.3 microM. 3. The relaxation effect of EIF was demonstrated to be endothelium-dependent. Additional experiments demonstrated that EIF-induced relaxation in an isolated aortic ring could be inhibited by 2 microM NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, suggesting the involvement of nitric oxide in EIF-induced relaxation of the muscle. 4. Atropine (0.2 microM) or indomethacin (10 microM) had no significant effect on EIF-induced relaxation. 5. These data suggest that EIF, a novel endogenous inotrope from porcine myocardium, also acts as an endothelium-dependent vasodilator substance mediating relaxation in the rat isolated aorta mainly by release of nitric oxide. The possibility of EIF acting through muscarinic receptor and the involvement of prostacyclin were excluded.