bluuebunny/crossref_metadata_2025 huggingface dataset:
EMG‐activity and muscular performance of lower leg during stretch‐shortening cycle after cooling
Authors: OKSA J. , RINTAMÄKI H. , MÄKINEN T. , MARTIKKALA V. , RUSKO H.
Published: October 2003

To test the effect of cooling on EMG‐activity of muscles working as an agonist and antagonist in the lower leg, 12 men dressed in shorts and jogging shoes performed a drop‐jump exercise after 60 min exposures to 27 °C and 10 °C. Cooling decreased mean skin temperature 5.6±0.4 °C (mean±SD, P<0.001), whereas rectal temperature was unaffected. The muscle temperature measured from m. gastrocnemius medialis decreased 4.1±0.3 °C (P<0.01) at the depth of 30 mm below skin surface. To find the optimal stretching velocity for potentiation of elastic energy, the drop‐jump exercise was performed from six different bench heights (10, 20, 30, 40, 50 and 60 cm). The optimal velocity was not altered on account of cooling. In cooled subjects during the stretch phase of the drop jumps the EMG‐activity of m. triceps surae complex (agonist) increased (P<0.05–0.001) while the activity of m. tibialis anterior (antagonist) remained unchanged. After cooling during the shortening phase of the jumps the EMG‐activity of m. triceps surae complex decreased (P<0.05–0.001), whereas the activity of m. tibialis anterior increased (P<0.05–0.001). In addition, after cooling the peak EMG‐activity appeared on the average 28 ms earlier, which shifted the peak activity from the shortening phase (at 27 °C) to the stretch phase (at 10 °C). Cooling increased the mean duration of stretch and shortening phases by 28±3 ms (P<0.001) and 23±2 ms (P<0.001), respectively. The average force production during the shortening phase was 26% less (P<0.05) after cooling, which resulted in a decreased rise of body centre of gravity (P<0.05–0.01). It is concluded that during a stretch‐shortening cycle cooling alters the EMG‐activity of agonist and antagonist muscles on a contradictory manner and results in an earlier peak EMG‐activity. Therefore, alterations in motor unit recruitment could be responsible for the prolonged muscle contraction and decreased force production on account of cooling.
Growth resistance‐sized arteries in response to bladder hypertrophy in the rat: time‐course, DNA‐synthesis and LDH‐isoform pattern
Authors: BOELS P. J. , ARNER A. , NILSSON B.‐O. , SVENSSON C. , UVELIUS B.
Published: October 2003

Bladder growth was induced by partial urethral obstruction. Bladder hypertrophy was evident at 53 h after obstruction and continued over a 6 weeks period. Small bladder arteries were taken from fixed anatomical locations of the bladder circulation, mounted in a small vessel myograph and the optimal diameter for maximal isometric force development was determined (Lmax, K+=125 mm stimulation). Bladder hypertrophy was associated with an enlarged Lmax from 53 h onward (compared with sham‐operated controls) and Lmax continued to increase until 10 days after urethral obstruction. Between 10 days and 6 weeks no further increase of the diameter was observed. Increased diameters in vitro were accompanied by a transiently increased [3H]Thymidine uptake in the small arteries which peaked at 53 h after obstruction but was still above background at 10 days. At this time point, small arterial growth was associated with a significant relative increase in the M isoform of LDH as determined with agarose electrophoresis on tissue homogenates. Thus organ growth induced small vessel growth in the rat is characterized by a rapid onset, increased but transient DNA‐turnover and LDH‐isoform changes. The latter mimic changes seen in other types of smooth muscle growth.
Vasoconstriction in active calf persists after discontinuation of combined exercise with high‐intensity elbow flexion
Authors: KAGAYA A. , OGITA F. , KOYAMA A.
Published: October 2003

The present study aimed to determine whether vasoconstriction in active calf occurring during combined exercise diminished or persisted when added low‐ and high‐intensity elbow flexion exercise ceased and single leg exercise continued. Six active women (mean age, 21.2 years) participated in this study. During 10‐min plantar flexion exercise at 10% of maximum voluntary contraction (MVC), elbow flexion exercise at 10% MVC was added over the 3rd and 4th min. Calf blood flow did not change significantly upon superimposition and cessation of this elbow flexion exercise. However, when elbow flexion exercise at 50% MVC was added during the 7th and 8th min, calf blood flow above the resting value (2.23±0.23 mL 100 mL‐1 min‐1) decreased significantly (P<0.05) from 6.72±0.87 (6th min) to 5.14±1.36 mL 100 mL‐1 min‐1 after 2 min of combined exercise and was accompanied by a similar change in the non‐exercising calf blood flow value. The vascular conductance of the exercising calf decreased significantly (P<0.01) from 6.48±1.08 (6th min) to 3.11±1.27 mL 100 mL‐1 min‐1 mmHg‐1 at the end of the 2nd min of combined plantar flexion exercise with elbow flexion exercise at 50% MVC. After elbow flexion exercise at 50% MVC was discontinued and plantar flexion exercise at 10% MVC alone was performed, the vascular conductance in the exercising calf remained significantly low for the next 2 min. These results indicate that the vasoconstriction induced by adding high‐intensity arm exercise is persistent, suggesting a major contribution of metabo‐receptor‐mediated vasoconstriction rather than central command‐ and mechano‐receptor‐mediated vasoconstriction.
Changes in muscle function in response to 10 days of lower limb unloading in humans
Authors: BERG H. E. , TESCH P. A.
Published: October 2003

Force‐generating capacity and electromyographic (EMG) activity of the knee extensor muscles were studied before and after short‐term (10 d) unilateral lower limb unloading and during 4 days of recovery. Ten healthy males used crutches to prevent one of their lower limbs from weight‐bearing while maintaining joint mobility as well as daily ambulatory activities. Knee extensor torque and quadriceps rectified EMG during maximal voluntary isometric contraction (MVC) was measured repeatedly before and after the intervention. Also, EMG at a fixed submaximal level (100 Nm; 30–45% MVC) and maximal angular velocity (AVmax), during unresisted knee extension, were assessed. Maximum torque decreased (P<0.05) by 13±8% in response to unloading while maximum EMG activity did not change after unloading or during recovery (P=0.35). Submaximum EMG increased (P<0.05) by 25±16% after unloading. Maximum and submaximum torque/EMG ratios decreased (P<0.05) after unloading. AVmax decreased (P<0.05) by 9±8% after unloading. The post value, however, was not different from that of the weight‐bearing limb. Torque, EMG and AVmax were recovered (P>0.05) after 4 days of resumed weight‐bearing. The pronounced decrease and the rapid recovery in maximum torque appears not to be attributed to a change in muscle mass alone. Because the findings of unchanged maximum EMG and increased EMG at a submaximal force level suggest no change in neural drive, we propose that unspecific tissue factors in part impair muscle function in response to short‐term loss of weight‐bearing activity. Results also indicate that recovery in muscle function after short‐term unloading seems to be completed in a time span shorter than the period of preceding inactivity.
1α,25‐Dihydroxyvitamin D3 stimulated alkaline phosphatase activity in cultured pig kidney epithelial LLC‐PK1 cells
Authors: THANH X. DO , MASSICOT F. , DO B. , BREGET R. , NIVET V. , DURAND D. , WARNET J. M. , CLAUDE J. R. , CLOT J. P.
Published: October 2003

The effects of 1α,25‐dihydroxyvitamin D3 (1,25 (OH)2D3) and human growth hormone (hGH) on the activity of alkaline phosphatase (ALP) were evaluated in pig kidney LLC‐PK1 cultured cells. 1,25(OH)2D3 (10‐9–10‐6 mol L‐1) and hGH (10‐7 mol L‐1) increased ALP activity in these cells while no hormonal effect was detected on two other enzyme activities: γ‐glutamyl transferase and acid phosphatase. ALP activity was maximally increased after 4.5–6 h incubation with both hormones. The hormonal induction of ALP activity was prevented by a pretreatment of cells with actinomycin D. Thus, 1,25 (OH)2D3 and may be hGH could stimulate ALP activity via a transcription of some gene.
Human quadriceps cross‐sectional area, torque and neural activation during 6 months strength training
Authors: NARICI M. V. , HOPPELER H. , KAYSER B. , LANDONI L. , CLAASSEN H. , GAVARDI C. , CONTI M. , CERRETELLI P.
Published: October 2003

Quadriceps muscle and fibre cross‐sectional areas (CSA), torque and neural activation were studied in seven healthy males during 6 months of weight training on alternate days with six series of eight unilateral leg extensions at 80% of one repetition maximum. After training, the quadriceps cross‐sectional area increased by 18.8±7.2% (P<0.001) and 19.3±6.7% (P<0.001) in the distal and proximal regions respectively, and by 13.0±7.2% (P<0.001) in the central region of the muscle. Hypertrophy was significantly different between and within the four constituents of the quadriceps. Biopsies of the vastus lateralis at mid‐thigh did not show any increase in mean fibre cross‐sectional area. Maximum isometric voluntary torque increased by 29.6±7.9%–21.1±8.6% (P<0.01‐0.05) between 100° and 160° of knee extension, but no change in the optimum angle (110°‐120°) for torque generation was found. A 12.0±10.8% (P<0.02) increase in torque per unit area together with a right shift in the IEMG‐torque relation and no change in maximum IEMG were observed. Time to peak isometric torque decreased by 45.8% (P<0.03) but no change in time to maximum IEMG was observed. In conclusion, strength training of the quadriceps results in a variable hypertrophy of its components without affecting its angle‐torque relation. The increase in torque per unit area, in the absence of changes in IEMG, may indicate changes in muscle architecture. An increase in muscle‐tendon stiffness may account for the decrease in time to peak torque.
Studies on cutaneous blood flow in the mammary gland of lactating rats
Authors: ERIKSSON M. , LUNDEBERG T. , UVNÄS‐MOBERG K.
Published: October 2003

The mechanisms that regulate mammary blood flow during lactation are not fully understood. In the present study laser Doppler flowmetry (LDF) was used to measure blood flow in the cutaneous microvessels of the mammary gland of lactating rats. The effects of suckling on blood flow were examined, as were those of local injection of oxytocin (0.5–5 mU) and the vasoactive peptides calcitonin gene‐related peptide (CGRP; 0.1–10 pmol), vasoactive intestinal polypeptide (VIP; 0.4–20 pmol) and neuropeptide Y (NPY; 1–40 pmol). Blood flow responses to suckling varied depending on how much time had lapsed since the previous suckling. In rats with milk in the gland, suckling caused an initial increase in blood flow. In connection with milk let‐down, the blood flow decreased, but was followed by a second increase. In recently suckled rats with no milk in the gland the increase in blood flow corresponded to the number of pups suckling. Oxytocin injections also had varying effects on mammary blood flow depending on how recently suckling had taken place. In non‐suckled rats with milk in the gland, oxytocin injections caused a rise in blood flow that was interrupted by a fall during milk ejection. In recently suckled rats, all doses of oxytocin caused an increase in blood flow of similar magnitude. However, the effect of the higher doses had a longer duration. CGRP and VIP injections caused a dose‐dependent increase in mammary blood flow regardless of when suckling last occurred. NPY injections caused a dose‐dependent decrease in blood flow.
Energy requirement of sodium reabsorption in the thick ascending limb of Henle's loop in the dog kidney: effects of bumetanide and ouabain
Authors: ØSTENSEN J. , STOKKE E. S.
Published: October 2003

To examine whether sodium reabsorption in the thick ascending limb of Henle's loop (TALH) in the dog kidney has a passive component, the ratios between reductions in sodium reabsorption and oxygen consumption (ΔNa/ΔQo2 ratio) were measured by inhibiting tubular transport with bumetanide (30 μg kg‐1) and ouabain (120 ng kg‐1 intrarenally). Clearance studies were performed in volume expanded dogs treated with acetazolamide (100 mg kg‐1) or maleate (400 mg kg‐1). In five acetazolamide‐treated dogs, bumetanide gave a ΔNa/ΔQo2 ratio of 29.9±2.5, whereas the combination of bumetanide and ouabain gave 19.0±0.6. When ouabain was given before bumetanide, ouabain gave a ΔNa/ΔQo2 ratio of 19.2±1.1 and the combination gave 19.9±1.2. In the maleate‐treated dogs, bumetanide gave a ΔNa/Qo2 ratio 30.3±1.7, and the combination of bumetanide and ouabain gave 27.1±1.5. To localize the metabolic effect of bumetanide and ouabain, local heat production was measured at 18 places in four kidneys with copper‐constantan thermocouples. Bumetanide reduced metabolic rate in the outer medulla by 51±4%, and in the cortex by 16±6%. Subsequent infusion of ouabain reduced metabolic rate in the outer medulla by only 9±3%, whereas cortical metabolism was reduced by 33±4%. The results show that bumetanide mainly acts in the outer medullar where TALH is located, whereas the additional effect of ouabain is mainly located in cortical segment of the nephron including the proximal tubules. Bumetanide inhibits the reabsorption of 30 mol sodium for each mole oxygen consumed, which show that for each 18 mol sodium that are transported through the cells in the TALH in dog kidneys, 12 mol (40%) are transported along the paracellular route without additional requirement of energy.
Maximal muscle activation is not limited by pulmonary ventilation in chronic hypoxia
Authors: SAVARD G. K. , ARESKOG N.‐H. , SALTIN B.
Published: October 2003

This study was conducted to test the hypothesis that inhibitory reflexes from respiratory centres in the brain or respiratory muscles limit the central motor drive to limb muscles during exhaustive exercise in chronic hypoxia. Experiments were performed on five members of an expedition to the Himalayas, following 56–81 days at altitudes of 5200–7500 m. During the last minute of exhaustive maximal two‐legged cycling with and without 4% CO2 inhalation performed on different days, repeated maximal voluntary handgrip contractions (MVC) over 60 s (5 s contraction, 5 s rest; ×6) were performed at rest and exhaustive exercise. MVC or rate of decay of MVC was unaffected by simultaneous engagement of a major fraction of the muscle mass (leg muscles) and a very high pulmonary ventilation. With 4% CO2, peak pulmonary ventilation during the exhaustive exercise increased further by 41 L min‐1 (140–181 L min‐1; P<0.05) without affecting the handgrip strength. These findings suggest that during exhaustive exercise of large muscle groups in chronic hypoxia, both maximal voluntary contraction force and dynamic muscle contractile force are not limited by extreme activation of respiratory centres or muscles.
Equal changes in L‐type calcium channel density after 60 min of ischaemia in normal and ischaemically preconditioned porcine myocardium
Authors: STOKKE M. , KIRKEBØEN K. A. , NÆSS P. A. , HAGELIN E. M. , ILEBEKK A. , BRØRS O.
Published: October 2003

Long‐lasting myocardial ischaemia reduces the density of sarcolemmal L‐type calcium channels (LCC). Ischaemic preconditioning protects the myocardium against development of infarction. The aim of this study was to investigate if ischaemia‐induced loss in LCC is affected by ischaemic preconditioning. Specific (+)‐[3H]isradipine binding to LCC was compared in membranes and homogenates from control and ischaemic regions of non‐preconditioned and ischaemically preconditioned hearts [two 10 min left anterior descending coronary artery (LAD) occlusions, each followed by 30 min reperfusion]. Biopsies were sampled after 60 min mid LAD occlusion from ischaemic and control (supplied by circumflex artery) regions. Sixty min ischaemia reduced binding density of specific (+)‐[3H]isradipine in membranes by 23±11% (n=7, P<0.05) in the non‐preconditioned group and by 20±8% (n=6, P<0.05) in the preconditioned group. Binding density in homogenates was reduced by 36±5% (n=5, P<0.05) in the non‐preconditioned group and by 21±5% (n=5, P<0.05) in the preconditioned group. The reductions in the two groups and reductions in membranes and homogenates were not statistically different. The dissociation constant of binding was similar in the groups. In conclusion, 60 min of ischaemia reduced the binding density of (+)‐[3H]isradipine in membranes and homogenates by 20–36%. The reduction in density of binding sites was not caused by redistribution of sarcolemmal LCC to an intracellular compartment. Ischaemic preconditioning did not affect the decline in binding density as hypothesized.
Peroxisomal fatty acid oxidation capacity is more resistant to ischaemic and reperfusion injury than mitochondrial fatty acid oxidation capacity in feline hearts
Authors: BRUNVAND H. , FRØYLAND L. , WESTBY J. , HEXEBERG E. , BERGE R. K. , GRONG K.
Published: October 2003

We investigated ischaemic and postischaemic mitochondrial and peroxisomal fatty acid oxidation capacity, ATP levels and regional function in 40 anaesthetized open chest cats subjected to 10 or 40 min of regional myocardial ischaemia with or without 3 h of reperfusion (n=10 in each situation). Following 10 min of ischaemia, the mitochondrial fatty acid oxidation capacity measured in tissue extracts from ischaemic tissue (nmol min‐1 mg protein‐1) was reduced in both subepi‐ and subendocardium, but was normalized in reperfused tissue extracts from both wall layers (0.29±0.03 and 0.30±0.04 vs. 0.57±0.05 and 0.59±0.05, P<0.05). Peroxisomal fatty acid oxidation capacity in tissue extracts was unaffected by ischaemia and reperfusion. ATP levels and regional function measured in the LAD region was partly restored transmurally. After 40 min of LAD occlusion, mitochondrial fatty acid oxidation capacity was reduced, with higher activity in subepi‐ than in subendocardium (0.27±0.05 vs. 0.19±0.04, P<0.05). Reperfusion did not restore mitochondrial fatty acid oxidation capacity. Peroxisomal fatty acid oxidation capacity was increased in the ischaemic subendocardium compared with levels in non‐ischaemic subendocardium (0.53±0.02 vs. 0.45±0.03, P<0.05), with normalization at the end of reperfusion. ATP levels were non‐uniformly reduced during ischaemia and not repleted during reperfusion. Regional function recovered in circumferential segments but not in longitudinal segments following 40 min of ischaemia. In conclusion fatty acid oxidation enzymes seem to be more resistant to ischaemia in peroxisomes than in mitochondria. Mitochondrial fatty acid oxidation is fully reversible following shortlasting ischaemia, but remains depressed following prolonged ischaemia and reperfusion.
Vasoactivity mediated by endothelin ETA and ETB receptors in isolated porcine ophthalmic artery
Authors: WHITE L. R. , BAKKEN I. J. , SJAAVAAG I. , ELSÅS T. , VINCENT M. B. , EDVINSSON L.
Published: October 2003

Endothelin isopeptides and sarafotoxin S6b induced strong contractions in isolated porcine ophthalmic artery at basal tension, which were antagonized in a concentration‐dependent manner by the specific ETA antagonist FR 139317. The maximum contraction and potency of endothelin‐1 and sarafotoxin S6b were similar, whereas endothelin‐3 was significantly less potent and induced weaker contractions. Schild plot analysis was only obtained for endothelin‐1 and sarafotoxin S6b, but indicated competitive binding at the same ETA receptor site for these peptides. However, the slope obtained for endothelin‐1 was significantly less than unity, suggesting more than one receptor. FR 139317 was a more potent antagonist of contractions induced by endothelin‐3 than the other peptides. In arteries pre‐contracted by prostaglandin F2α, high endothelin‐3 concentrations induced additional contraction, except in the presence of FR 139317 when a marked relaxation was observed, an ability which was otherwise masked by the strong contractile activity. The relaxation was significantly reduced in endothelin‐denuded segments. Both contraction and relaxation were abolished by the ETA/B antagonist bosentan. The results suggest the presence of ETB as well as ETA receptors in this artery type, though ETB receptor activity is only demonstrated at an unusually high concentration of endothelin in this preparation in vitro.
Muscle glycogen repletion from endogenous carbon sources during recovery from high intensity exercise in the fasted rat
Authors: NIKOLOVSKI S. , FAULKNER D. L. , PALMER T. N. , FOURNIER P. A.
Published: October 2003

During recovery from high intensity exercise, substantial and rapid muscle glycogen repletion from endogenous carbon sources is reported in a variety of vertebrate species, the rat being the only reported exception. The major aim of this study was to re‐examine the process of glycogen repletion during recovery from high intensity exercise in the rat. In response to 3 min of vigorous swimming, muscle glycogen concentrations decrease markedly from initial levels of 20.2±1.5 and 21.2±0.9 μmol g‐1 to 6.4±1.1 and 7.9±1.4 μmol g‐1 in the tibialis anterior and plantaris muscles respectively. The equivalent of 58% of the glycogen carbons mobilized during exercise by the plantaris and 73% of that mobilized by the tibialis anterior muscle is repleted within 1 h following exercise. Using the hepatectomized rat as experimental model, a secondary aim of the study was to evaluate whether the liver is essential for the repletion of muscle glycogen. Although the absence of significant differences in the magnitude of post‐exercise muscle glycogen repletion between sham‐operated and hepatectomized rats suggests that the resynthesis of muscle glycogen can take place in the absence of hepatic gluconeogenesis, the present study identifies several limitations in the use of acute hepatectomy. Overall, the present study indicates that, in contrast to published views, the rat resembles other vertebrates in that it can support extensive muscle glycogen repletion from endogenous carbon sources during the recovery phase following high intensity exercise.
Nasal vasoconstriction and decongestant effects of nitric oxide synthase inhibition in the pig
Authors: RINDER J. , LUNDBERG J. M.
Published: October 2003

The effects of systemic administration of the nitric oxide synthase‐inhibitor Nω‐nitro‐l‐arginine on the vasculature of the pig nasal mucosa were compared with the effects of α‐adrenoceptor agonists and of sympathetic nerve stimulation. A novel in vivo pig model was used in which standard measurements of nasal mucosal blood flow were complemented with measurements of nasal cavity volume using an acoustic rhinometer. The vasodilatory effects of capsaicin, substance P, acetylcholine, vasoactive intestinal polypeptide and nitroprusside, before and after nitric oxide synthase inhibition, were also investigated. Nω‐nitro‐l‐arginine evoked a marked, slowly developing, long‐lasting reduction in nasal vascular conductance with a parallel increase in nasal cavity volume (by ∼30%) comparable in magnitude with the response upon α‐adrenoceptor stimulation. l‐Arginine partly reversed the Nω‐nitro‐l‐arginine‐evoked vasoconstriction, although nasal cavity volume was unaffected. Nasal vasodilation and decrease in nasal cavity volume resulting from capsaicin‐evoked activation of sensory nerves were unaltered after administration of Nω‐nitro‐l‐arginine. Nitric oxide synthase inhibition did not attenuate the vasodilator responses evoked by either substance P, acetylcholine, vasoactive intestinal polypeptide or nitroprusside. The present data suggest that nitric oxide synthase activity is of importance both for basal nasal vascular conductance and nasal cavity volume in the pig in vivo. In contrast, nitric oxide synthase inhibition does not reduce the vascular effects of a variety of vasodilating agents, including capsaicin, acetylcholine and substance P.
Endothelin‐1 causes a prolonged protein kinase C activation and acts as a co‐mitogen in vascular smooth muscle cells
Authors: ASSENDER J. W. , IRENIUS E. , FREDHOLM B. B.
Published: October 2003

Endothelin‐1 (ET‐1) is known to act via G‐protein coupled receptors. It has therefore been suggested that any mitogenic activity it may possess, is due to activation of phospholipase C and protein kinase C (PKC). We have therefore examined both the ability of ET‐1 to act as a mitogen and its ability to activate PKC. We found that ET‐1 significantly increased thymidine incorporation and enhanced platelet‐derived growth factor‐induced DNA synthesis, as well as causing a prolonged translocation of PKC to the cell membrane. ET‐1 significantly increased PKC dependent phosphorylation of two specific substrates. The phosphorylation of MBP4–14 (from myelin basic protein) was partially dependent on extracellular Ca2+, implicating activation of PKC‐α, whereas phosphorylation of the so called ε‐peptide was Ca2+‐independent and prolonged. This could be due either to the δ or ζ isoform of PKC, known to be present in these cells. However, ET‐1 induced little proliferation or PKC activity in a transformed smooth muscle cell line, DDT1 MF‐2, which lacks expression of the PKC‐αisoform, but expresses the ζ‐isoform. Thus, it would appear that ET‐1‐induced mitogenicity in smooth muscle cells may be related to the sustained, Ca2+‐independent activation of PKC‐δ.
Effects of angiotensin‐converting enzyme inhibition on arterial, venous and capillary functions in cat skeletal muscle in vivo
Authors: EKELUND U.
Published: October 2003

The aim of the present study was to analyse quantitatively, on a cat gastrocnemius muscle preparation in vivo, the effects of local angiotensin‐converting enzyme (ACE) inhibition by enalaprilat on total regional vascular resistance (tone) and its distribution to the large‐bore arterial resistance vessels (>25 μm), the small arterioles (<25 μm) and the veins. Associated effects on capillary pressure and fluid exchange were also studied. Close‐arterial infusion of enalaprilat (0.05–0.20 mg kg muscle tissue min‐1) elicited a moderate dilator response in all three consecutive sections of the muscle vascular bed, an increase in capillary pressure and transcapillary fluid filtration. This dilation could be abolished by the selective bradykinin B2‐receptor antagonist Hoe 140 (2 mg kg‐1 min‐1, i.a.), indicating that the dilator mechanism of ACE inhibition was an increased local concentration of bradykinin, and hardly at all a decreased concentration of angiotensin (AT) II. The generalized dilator response to ACE inhibition along the vascular bed suggested a relatively uniform distribution of ACE from artery to vein and this was further supported by the finding that a close‐arterial infusion of AT I (0.04–0.32 μg kg‐1 min‐1), which was vasoactive only after conversion to AT II by local ACE, elicited a generalized constrictor response in all three vascular sections. In contrast, infused AT II (0.01–0.16 μg kg‐1 min‐1) constricted almost selectively the large‐bore arterial vessels. The specific angiotensin AT1‐receptor antagonist losartan (2 mg kg‐1 min‐1, i.a.) abolished the constrictor response to AT II but did not affect vascular tone under control conditions, indicating that AT II is not involved in the initiation of basal vascular tone in muscle. These results, taken together, indicate that under basal conditions vascular ACE contributes to the local control of vascular tone in skeletal muscle by degrading the endogenous dilator bradykinin, and not by converting AT I into vasoconstrictor AT II.
Perchlorate is hypoglycaemic by amplifying glucose‐stimulated insulin secretion in mice
Authors: LARSSON‐NYRÉN G.
Published: October 2003

The chaotropic anion perchlorate (CIO4‐) is a potent amplifier of stimulated insulin secretion in vitro. Acute effects of perchlorate on serum glucose and insulin levels were investigated in normal mice. Intraperitoneal injection of single doses of NaClO4 at 10–300 mg kg‐1 body wt showed only a slight, reducing effect on the basal serum glucose level, reaching statistical significance only at 300 mg kg‐1 body wt. However, a single dose of NaClO4 (300 mg kg‐1 body wt) given together with a glucose load (0.9 g kg‐1 body wt) significantly counteracted the increase in serum glucose and reduced the serum glucose/insulin ratio 20 min after administration. The perchlorate effect was transient and at 60 and 90 min after administration the serum insulin and glucose levels were comparable with those of the glucose‐treated control animals. The results suggest that perchlorate enhances glucose‐stimulated insulin secretion in mice in vivo and thereby reduces the serum glucose level after a glucose load but does not much affect the basal serum glucose level.
Carbohydrate ingestion augments creatine retention during creatine feeding in humans
Authors: GREEN A. L. , SIMPSON E. J. , LITTLEWOOD J. J. , MACDONALD I. A. , GREENHAFF P. L.
Published: October 2003

Blood and urine samples were obtained from four groups of healthy male subjects (A–D, total n=22) before, during and after ingesting the following: group A, 5 g of creatine in solution; groups B and C, 5 g of creatine and 93 g of simple carbohydrate in solution; group D, a creatine‐ and carbohydrate‐free solution. Subjects ingested the above preparations every 4 h for the remainder of the day and throughout the next day (total daily creatine dose=20 g), and reported back to the laboratory on day 3 to undergo the same procedures as on day 1. Throughout this time, subjects weighed and recorded all dietary intake, and those in groups B and C ingested a prescribed isoenergetic high carbohydrate diet. Subjects in group C also performed 1 h of cycling exercise at 70% of their maximal oxygen consumption on the morning of each day. On both days 1 and 3, peak plasma creatine concentration, the area under the plasma creatine concentration/time curve and urinary creatine concentration were lower in groups B and C than in group A. Conversely, serum insulin concentration was higher in groups B and C than in A. No differences were evident when comparing groups B and C. These data suggest carbohydrate ingestion augmented creatine retention during creatine feeding and that creatine retention was not further increased when exercise was performed prior to ingestion.
The immunosuppressant FK506 ameliorates ischaemic damage in the rat brain
Authors: DRAKE M. , FRIBERG H. , BORIS‐MÖLLER F. , SAKATA K. , WIELOCH T.
Published: October 2003

The effect of the immunosuppressant FK506 on ischaemic neuronal damage was studied in a rat model of transient cerebral ischemia induced by occlusion of both common carotid arteries in combination with hypotension for 10 min. Neuronal damage was assessed morphologically after 4 days of recovery. Treatment with FK506, given at a dose of 2 mg kg‐1 by intraperitoneal injections 30 min prior to ischemia and once daily during recovery, decreased neuronal damage by 52% in the hippocampal CA1 region and by 48% in the temporal cortex. The protection was not due to diminished body temperature or a marked reduction of ischaemia‐induced synaptic overflow of glutamate. We propose that FK506 decreases neuronal damage either by inhibiting calcineurin‐mediated events or by preserving mitochondrial function.
Permeation from the synovial fluid as nutritional pathway for the anterior cruciate ligament in rabbits
Authors: MURAKAMI Y. , OCHI M. , IKUTA Y. , HIGASHI Y.
Published: October 2003

The anterior cruciate ligament of the knee receives its nutrition from a direct vascular supply and by permeation of nutrients from synovial fluid. In order to quantitate the relative importance of these two routes and to compare the anterior cruciate ligament with the medial collateral ligament, we injected [3H]methyl‐glucose as a tracer intravenously or directly into the knee in rabbits. Tracer concentrations in plasma, synovial fluid, the anterior cruciate ligament and the medial collateral ligament were analysed by a pharmacokinetic compartment model developed for this study. The contribution of [3H]methyl‐glucose permeation from the synovial fluid was calculated at 59.7% in the anterior cruciate ligament and at 18.1% in the medial collateral ligament. We concluded from these results that the nutrition for the medial collateral ligament, which is an extraarticular structure, is provided mainly by its vascular supply. In contrast, synovial fluid permeation is an important transport route for small molecules for the normal anterior cruciate ligament.
Multiple actions of iontophoretically applied serotonin on motorneurones in the turtle spinal cord in vitro
Authors: SKYDSGAARD M. , HOUNSGAARD J.
Published: October 2003

The effects of focal activation of serotonergic receptors in motorneurones were investigated in a slice preparation of the turtle spinal cord. The test response to glutamate evoked from a dendrite by iontophoresis was attenuated by serotonin or 8‐hydroxy‐dipropyl‐aminotetralin (8‐OH‐DPAT) applied from an independent pipette within 100 μm of the glutamate pipette. This effect was not associated with a conductance change and did not affect glutamate responses evoked more than 100 μm from the serotonin pipette. The effect of serotonin was not reproduced by H+ ions. Plateau potentials were rarely facilitated by serotonin when applied in the dendritic field. Plateau potentials were readily facilitated by serotonin applied near the soma. This effect was preceded by attenuation of the slow after‐hyperpolarization following an action potential. Applied near the soma, serotonin inhibited the response to a depolarizing current pulse of moderate strength and enhanced the response to a current pulse of high amplitude. These effects were associated with a conductance increase. We conclude that serotonin has spatially diverse effects on motorneurones.
An evaluation of the role of skin temperature during heat adaptation
Authors: REGAN J. M. , MACFARLANE D. J. , TAYLOR N. A. S.
Published: October 2003

This project sought to evaluate the importance of skin temperature during heat acclimation, using an isothermal‐strain model. Two groups of seven matched males, participated (1 h per day, 10 days) in one of two conditions: (i) temperate physical training (TEMP: 22.4±0.7 °C, relative humidity (r.h.) 41.0±0.9%); or (ii) combined physical training and heat acclimation (HEAT: 38.2±0.7 °C, r.h. 39.7±1.3%). Isothermal strain was induced in both groups by rapidly elevating rectal temperature by 1 °C (cycling), then holding it constant by manipulating external work. Subjects completed two three‐phase heat stress tests (39.8±0.1 °C, r.h. 38.6±1.2), consisting of 20 min rest, then 20 min cycling at each of 30% and 45% of peak power, before and after each regimen. While there was a difference of 4.2 °C in mean skin temperature between treatments, both regimens elicited a similar peripheral sudomotor increase, indicating a core temperature dependent adaptation. However, based on significant pre‐ vs. post‐acclimation decreases in average auditory canal temperature (0.4±0.1 °C), average forehead skin blood flow (26%), average perceived exertion (11%), and a 5% increase in average forehead sweat rate (0.1±0.04 mg cm−2 min−1), the HEAT regimen elicited a more complete acclimation. While elevation in core temperature is critical to acclimation, it also appears necessary to expose subjects to an external thermal stress. This observation has not been previously demonstrated under conditions of isothermal strain, and verifies the importance of skin temperature elevation in the acclimation process.
Reduced arterial O2 saturation during supine exercise in highly trained cyclists
Authors: PEDERSEN P. K. , MANDØE H. , JENSEN K. , ANDERSEN C. , MADSEN K.
Published: October 2003

Performance of intense dynamic exercise in highly trained athletes is associated with a reduced arterial haemoglobin saturation for O2 (SaO2) and lower arterial PO2 (PaO2). We hypothesized that compared with upright exercise, supine exercise would be accompanied by a smaller reduction in SaO2 because of a lower maximal O2 uptake (VPO2max) and/or a more even ventilation–perfusion distribution. Eight elite bicyclists completed progressive cycle ergometry to exhaustion in both positions with concomitant determinations of ventilatory data, arterial blood gases and pH. During upright cycling VPO2max averaged 75±1.6 mL O2 min‐1 kg‐1 (±SEM) and it was 10.6±1.7% lower during supine cycling (P<0.001). Also the maximal pulmonary and alveolar ventilation were lower during supine cycling (by 15±2% and 21±3%, respectively; P< 0.001) which related to a 0.8±0.1 L lower tidal volume (P<0.001). In all subjects and independent of work posture PaO2 and SaO2 decreased from rest to exhaustion (from 99±3 to 82±2 Torr and 98.1±0.2 to 95.2±0.4%, respectively; P<0.001); alveolar–arterial PO2 difference increased from 6±2 to 37±3 Torr in both body positions. At exhaustion arterial PCO2 was lower in upright than in supine (33.4±0.6 vs. 35.9±0.9 Torr; P<0.01), suggesting a greater relative hyperventilation in upright. Arterial pH was similar in upright and supine at rest (both 7.41±0.01) and at exhaustion (7.31±0.01 vs. 7.32±0.01, respectively). We conclude that despite a lower VPO2max and supposedly an improved ventilation–perfusion distribution, altering body position from upright to supine does not influence arterial O2 desaturation during intense exercise.
Local actions of acetylcholine on vasomotor regulation in rat incisor pulp
Authors: OLGART L. , KOSTOUROS G. D. , EDWALL L.
Published: October 2003

Local actions of acetylcholine on vasomotor regulation in rat incisor pulp were investigated in anaesthetized animals. Pulpal blood flow was measured with laser Doppler flowmetry. Iontophoresis (40 or 60 μA for 20 s) with acetylcholine or carbachol on an exposed dentin surface caused a biphasic response: an initial vasoconstriction was followed by an atropine‐sensitive vasodilation. The vasoconstrictor response was enhanced by 171% in the presence of atropine, whereas in control experiments, using isotonic saline as a medium for the direct current, similar vasoconstriction was unaffected by atropine. Carbachol‐induced vasodilation was significantly reduced by 30% after intravenous injection of the nitric oxide synthesis blocker Nωw‐nitro‐L‐arginine methyl ester (10 mg kg‐1), and the remaining vasodilation was abolished by atropine. The present results support the concept of a cholinergic modulation of sympathetic vasoconstrictor function and of a partial contribution of nitric oxide in carbachol‐induced vasodilation in rat incisor pulp.
The significance of active Na+,K+ transport in the maintenance of contractility in rat skeletal muscle
Authors: NIELSEN O. B. , CLAUSEN T.
Published: October 2003

The effects of reduced Na+,K+ pump capacity on contractile endurance and excitation‐induced changes in intracellular Na+ content were investigated in isolated rat soleus and extensor digitorum longus muscles. Pre‐incubation with 10‐5m ouabain increased the rate of force decline measured over the first 5–20 s of tetanic contraction from 0.32 to 0.94% s‐1 and 1.4 to 4.6% s‐1 in soleus and extensor digitorum longus muscles, respectively. Soleus muscles from K+‐deficient rats exhibited 54% reduction in the concentration of Na+,K+ pumps and the force decline during 30 s of 60 Hz stimulation was increased from 0.53 to 1.15% s‐1. A similar change was induced in control muscles when a comparable reduction in the concentration of functional Na+,K+ pumps was elicited by pre‐incubation with ouabain (10‐6‐2×10‐6m). In soleus, the force decline during 60 s of 60 Hz stimulation showed linear correlation to the increase in intracellular Na+ content. In extensor digitorum longus, force decline and increase in Na+ content during 60 Hz stimulation were both four times faster than in soleus as measured over 15 s of excitation. These results indicate that during maximal contractions the Na+,K+ pump capacity is one of the determinants for the contractile endurance in skeletal muscle. Furthermore, the maintenance of contractile force seems to be a function of the rate of Na+‐influx and this relationship may account for the difference in endurance between slow‐twitch and fast‐twitch muscles.
Blood flow to the haemopoietic bone marrow
Authors: IVERSEN P. O.
Published: October 2003

IVERSEN, P. O. 1997. Blood flow to the haemopoietic bone marrow. Acta Physiol Scand159, 269–276. Received 25 September 1996, accepted 14 October 1996. ISSN 0001–6772. Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.

In order to maintain an adequate haemopoiesis, the bone marrow is dependent on a sufficient blood supply. Our understanding of the regulation of marrow perfusion remained patchy for several decades, mainly because of technological difficulties. Recent advances in methodology have permitted more detailed analyses of bone marrow perfusion.

Enhanced stimulation of erythropoietic or leucopoietic activity leads to increased blood flow to the bone marrow. There is evidence that this vasodilatory effect is mediated by the cytokines erythropoietin and granulocyte colony‐stimulating factor; however, a direct link has yet to be firmly established. The presence of receptors for several other cytokines on vascular endothelial and smooth muscle cells suggests that these may also have a regulatory role. The vasodilating factor nitric oxide (NO) regulates bone marrow blood flow both under normal conditions and during accelerated haemopoiesis, and NO is possibly induced via activation of cytokine receptors. There are conflicting reports as to how catecholamines affect marrow vascular tone. Although there is firm evidence that the bone marrow vasculature is innervated, no definite role of this innervation in vasoregulation has been documented.

Advances in bone marrow/blood stem cell transplantation technology and the development of other therapeutic strategies for bone marrow failure may in part be dependent on optimization of the blood supply to the haemopoietic bone marrow.
Global cerebral blood flow during infusion of adenosine in humans: assessment by magnetic resonance imaging and positron emission tomography
Authors: STÅNGE K. , GREITZ D. , INGVAR M. , HINDMARSH T. , SOLLEVI A.
Published: October 2003

Adenosine, an endogenous vasodilator, induces a cerebral vasodilation at hypotensive infusion rates in anaesthetized humans. At lower doses (< 100 μg kg−1 min−1), adenosine has shown to have an analgesic effect. This study was undertaken to investigate whether a low dose, causing tolerable symptoms of peripheral vasodilation affects the global cerebral blood flow (CBF). In nine healthy volunteers CBF measurements were made using axial magnetic resonance (MR) phase images of the internal carotid and vertebral arteries at the level of C2–3. Quantitative assessment of CBF was also obtained with positron emission tomography (PET) technique, using intravenous bolus []>
15O]butanol as tracer in four of the subject at another occasion. During normoventilation (5.4 ± 0.2 kPa, mean ± s.e.m.), the cerebral blood flow measured by magnetic resonance imaging technique, as the sum of the flows in both carotid and vertebral arteries, was 863 ± 66 mL min−1, equivalent to about 64 ± 5 mL 100 g−1 min−1. The cerebral blood flow measured by positron emmission tomography technique, was 59 ± 4 mL 100 g−1 min−1. All subjects had a normal CO2 reactivity. When adenosine was infused (84 ± 7 μg kg−1 min−1) the cerebral blood flow, measured by magnetic resonance imaging was 60 ± 5 mL 100 g−1 min−1. The end tidal CO2 level was slightly lower (0.2 ± 0.1 kPa) during adenosine infusion than during normoventilation. In the subgroup there was no difference in cerebral blood flow as measured by magnetic resonance imaging or positron emission tomography. In conclusion, adenosine infusion at tolerable doses in healthy volunteers does not affect global cerebral blood flow in unanaesthetized humans.
Effects of reduced muscle temperature on the oxygen uptake kinetics at the start of exercise
Authors: SHIOJIRI T. , SHIBASAKI M. , AOKI K. , KONDO N. , KOGA S.
Published: October 2003

SHIOJIRI, T., SHIBASAKI, M., AOKI, K., KONDO, N. & KOGA, S. 1997. Effects of reduced muscle temperature on the oxygen uptake kinetics at the start of exercise. Acta Physiol Scand 159, 327–333. Received 25 September 1995, accepted 5 November 1996. ISSN 0001–6772. Laboratory of Exercise and Sports Science, Yokohama City University; Division of Intelligence Science, Graduate School and Technology, Division of Education, Graduate School, Faculty of Human Development, Kobe University; and Applied Physiology Laboratory, Kobe Design University, Japan.

The purpose of this study was to examine the effects of reduced muscle temperature (Tm ) on gas exchange kinetics and haemodynamics at the start of exercise. Six male subjects performed moderate cycle exercise under reduced (C) and normal (N) Tm conditions. Tm and rectal temperature were significantly reduced by immersion in cold water (by 6.6 °C and 1.8 °C, respectively). The increases in oxygen uptake (V˙o2) and oxygen pulse (V˙o2/HR) during phase 1 (abrupt increase after the start of exercise) were significantly lower under C than under N. The time constant for O2 under C (36.0 ± 7.7 (SD) s) was significantly greater than under N (27.5 ± 4.4 s); however, the time constants of cardiac output under C (38.3 ± 16.6 s) and N (33.7 ± 18.5 s) were similar. These results suggest that the slower V˙o2 on‐response under reduced Tm conditions is caused by decreased O2 extraction in working muscle and/or by impairment of oxidative reactions by reduced muscle temperature.
The effects of triiodothyronine (T3) on heart rate, temperature and ECG measured with telemetry in freely moving mice
Authors: JOHANSSON C. , THORÉN P.
Published: October 2003

We have set up a telemetry system and recorded heart rate, electrocardiogram (ECG), body temperature and the locomotor activity in awake freely moving mice. The telemetry system (DATA Sciences, St Paul, MN, USA) comprises a transmitter implanted in the peritoneal cavity and a receiver (RA1010) placed underneath the home cage. The signal from the transmitter includes the electrical activity of the heart and the body temperature. The results show that four days after the surgical procedure the mice have recovered and regained a clear circadian rhythm. The heart rate varied under baseline conditions between 432 and 618 beats min−1 and the body temperature between 35.1 and 37.7 °C (based on 60 min mean values). A clear time correlation between heart rate, body temperature and locomotor activity was found. As an evaluation of the method we injected T3 s.c. during a period of 4 days. Further, we were interested in whether it was possible to measure an integrated physiological response to T3 and further investigate the time course for the effect. After one day of treatment with triiodothyronine there was a significant increase in body temperature and locomotor activity. The increase in heart rate was seen after 2 days. The ECG recording revealed a significantly shortened QTend‐ and QRS‐time. No significant difference in the PQ‐time was found. This method may be of great importance in studies of genetically manipulated mice.