bluuebunny/crossref_metadata_2025 huggingface dataset:
Changes in the chemical composition of soil organic matter after application of compost
Authors: Leifeld J. , Siebert S. , Kögel‐Knabner I.
Published: March 2003

Is the composition of soil organic matter changed by adding compost? To find out we incubated biowaste composts with agricultural soils and a humus‐free mineral substrate at 5°C and 14°C for 18 months and examined the products. Organic matter composition was characterized by CuO oxidation of lignin, hydrolysis of cellulosic and non‐cellulosic polysaccharides (CPS and NCPS) and 13C cross‐polarization magic angle spinning nuclear magnetic resonance (CPMAS 13C‐NMR) spectroscopy. The lignin contents in the compost‐amended soils increased because the composts contained more lignin, which altered little even after prolonged decomposition of the composts in soil. A pronounced decrease in lignin occurred in the soils amended with mature compost only. Polysaccharide C accounted for 14–20% of the organic carbon at the beginning of the experiment for both the compost‐amended soils and the controls. During the incubation, the relative contents of total polysaccharides decreased for 9–20% (controls) and for 20–49% (compost‐amended soils). They contributed preferentially to the decomposition as compared with the bulk soil organic matter, that decreased between < 2% and 20%. In the compost‐amended agricultural soils, cellulosic polysaccharides were decomposed in preference to non‐cellulosic ones. The NMR spectra of the compost‐amended soils had more intense signals of O–alkyl and aromatic C than did those of the controls. Incubation for 18 months resulted mainly in a decline of O–alkyl C for all soils. The composition of the soil organic matter after compost amendment changed mainly by increases in the lignin and aromatic C of the composts, and compost‐derived polysaccharides were mineralized preferentially. The results suggest that decomposition of the added composts in soil is as an ongoing humification process of the composts themselves. The different soil materials affected the changes in soil organic matter composition to only a minor degree.
Modelled changes in arctic tundra snow, energy and moisture fluxes due to increased shrubs
Authors: Liston Glen E. , Mcfadden Joseph P. , Sturm Matthew , Pielke Roger A.
Published: March 2003

In arctic tundra, shrubs can significantly modify the distribution and physical characteristics of snow, influencing the exchanges of energy and moisture between terrestrial ecosystems and the atmosphere from winter into the growing season. These interactions were studied using a spatially distributed, physically based modelling system that represents key components of the land–atmosphere system. Simulations were run for 4 years, over a 4‐km2 tundra domain located in arctic Alaska. A shrub increase was simulated by replacing the observed moist‐tundra and wet‐tundra vegetation classes with shrub‐tundra; a procedure that modified 77% of the simulation domain. The remaining 23% of the domain, primarily ridge tops, was left as the observed dry‐tundra vegetation class. The shrub enhancement increased the averaged snow depth of the domain by 14%, decreased blowing‐snow sublimation fluxes by 68%, and increased the snowcover's thermal resistance by 15%. The shrub increase also caused significant changes in snow‐depth distribution patterns; the shrub‐enhanced areas had deeper snow, and the non‐modified areas had less snow. This snow‐distribution change influenced the timing and magnitude of all surface energy‐balance components during snowmelt. The modified snow distributions also affected meltwater fluxes, leading to greater meltwater production late in the melt season. For a region with an annual snow‐free period of approximately 90 days, the snow‐covered period decreased by 11 days on the ridges and increased by 5 days in the shrub‐enhanced areas. Arctic shrub increases impact the spatial coupling of climatically important snow, energy and moisture interactions by producing changes in both shrub‐enhanced and non‐modified areas. In addition, the temporal coupling of the climate system was modified when additional moisture held within the snowcover, because of less winter sublimation, was released as snowmelt in the spring.
Influence of atmospheric CO2 enrichment on methane consumption in a temperate forest soil
Authors: Phillips Rebecca L. , Whalen Stephen C. , Schlesinger William H.
Published: March 2003

Rates of atmospheric CH4 consumption of soils in temperate forest were compared in plots continuously enriched with CO2 at 200 µL L−1 above ambient and in control plots exposed to the ambient atmosphere of 360 µL CO2 L−1. The purpose was to determine if ecosystem atmospheric CO2 enrichment would alter soil microbial CH4 consumption at the forest floor and if the effect of CO2 would change with time or with environmental conditions. Reduced CH4 consumption was observed in CO2‐enriched plots relative to control plots on 46 out of 48 sampling dates, such that CO2‐enriched plots showed annual reductions in CH4 consumption of 16% in 1998 and 30% in 1999. No significant differences were observed in soil moisture, temperature, pH, inorganic‐N or rates of N‐mineralization between CO2‐enriched and control plots, indicating that differences in CH4 consumption between treatments were likely the result of changes in the composition or size of the CH4‐oxidizing microbial community. A repeated measures analysis of variance that included soil moisture, soil temperature (from 0 to 30 cm), and time as covariates indicated that the reduction of CH4 consumption under elevated CO2 was enhanced at higher soil temperatures. Additionally, the effect of elevated CO2 on CH4 consumption increased with time during the two‐year study. Overall, these data suggest that rising atmospheric CO2 will reduce atmospheric CH4 consumption in temperate forests and that the effect will be greater in warmer climates. A 30% reduction in atmospheric CH4 consumption by temperate forest soils in response to rising atmospheric CO2 will result in a 10% reduction in the sink strength of temperate forest soils in the atmospheric CH4 budget and a positive feedback to the greenhouse effect.
Aurora‐B phosphorylates Histone H3 at serine28 with regard to the mitotic chromosome condensation
Authors: Goto Hidemasa , Yasui Yoshihiro , Nigg Erich A. , Inagaki Masaki
Published: March 2003

Background:  Histone H3 (H3) phosphorylation plays important roles in mitotic chromosome condensation. We reported that H3 phosphorylation occurs at Ser28, as well as at Ser10 during mitosis, at least in mammals. Aurora B was recently demonstrated to be responsible for Ser10 phosphorylation in S. cerevisiae, C. elegans, Drosophila and Xenopus egg extract.

Results:  We compared the distribution of Aurora‐B with that of H3 phosphorylation. Aurora‐B was primarily localized in the heterochromatin of late G2 phase cells, where only Ser10 phosphorylation was observed. The treatment of such cells with calyculin A induced Ser28 phosphorylation in the Aurora‐B‐localized area. During prophase to metaphase, Aurora‐B was distributed in condensing chromosomes where Ser10 and Ser28 were phosphorylated. Aurora‐B can phosphorylate H3‐Ser10 and ‐Ser28 in nucleosomes in vitro. Transfection of a dominant‐negative mutant of Aurora‐B resulted in a reduction of H3 phosphorylation, not only at Ser10 but also Ser28, during mitosis.

Conclusions:  With regard to mitotic chromosome condensation, Aurora‐B directly phosphorylated H3, not only at Ser10 but also at Ser28. The level of Ser28 phosphorylation is diminished to undetectable levels by PP1 phosphatase prior to entry into mitosis.
Neural and non‐neural activation of electrogenic secretion by 5‐hydroxytryptamine in the rat ileum in vitro
Authors: ROLFE  , LEVIN
Published: March 2003

5‐hydroxytryptamine (5‐HT) stimulates electrogenic Cl−secretion in rat ileum stripped of its outer smooth musculature and myenteric plexus. The myenteric plexus, however, is a site of 5‐HT synthesis in the gut, and the plexus mediates electrogenic ion secretion activated by luminal enterotoxin STa and taurocholate. Thus, we investigated the role of the myenteric plexus in 5‐HT‐induced electrogenic secretion in vitro by measuring short‐circuit current (Isc, microamps) with voltage‐clamp apparatus as an index of electrogenic Cl−secretion in rat ileum which was either stripped of the myenteric plexus or was left intact. Serosally added 5‐HT stimulated electrogenic Cl−secretion in muscle‐stripped and intact ileum in a concentration‐dependent manner. Pre‐treatment of stripped ileum with atropine (1 μm), hexamethonium (100 μm), tetrodotoxin (1.25 μm) and capsaicin (1 μm) for 15 min did not effect the maximum Isc induced by 5‐HT which would implicate a direct action on the enterocyte. In intact ilea, however, tetrodotoxin (TTX) and capsaicin reduced significantly the maximum values of Isc stimulated by 5‐HT, and the nitric oxide synthase inhibitor Nω‐nitro‐
L‐arginine methyl ester (
L‐NAME) caused a significant decrease in the maximum response to 5‐HT. These results suggest that electrogenic secretion induced by 5‐HT in rat ileum in vitro occurs partly by activation of a non‐neural pathway probably involving a direct interaction with the enterocyte, and partly via a nitrinergic‐myenteric secretory reflex activated by sensory afferent fibres. These data highlight the danger of characterising intestinal secretory activity from in vitro experiments by using muscle‐stripped tissue only.
Growth hormone induces muscle fibre type transformation in growth hormone‐deficient rats
Authors: DAUGAARD  , LAUSTSEN  , HANSEN  , RICHTER
Published: March 2003

The effect of recombinant human growth hormone (rhGH) on growth and composition of muscle was studied in growth hormone‐deficient rats (dw/dw) treated for 10 days with either rhGH (GH) or with placebo (PLA). Age‐matched control rats (DW/dw) (AGE) were treated as PLA. Growth rate increased (P < 0.05) when rats were treated with rhGH and plasma insulin‐like growth factor‐1 concentration was higher (P < 0.05) in GH and AGE than in PLA. The wet weight of the soleus (SOL) and the extensor digitorum longus muscles (EDL) was less in PLA compared to GH and AGE (P < 0.05). In the SOL, the amount of myosin heavy chain (MHC) I was lower (69.1 ± 1.7%) (Mean ± SEM) in PLA compared to both GH (85.3 ± 2.3%) and AGE (76.4 ± 1.6%) (P < 0.05). At the same time the amount of MHC IIA/IIX was higher (30.9 ± 2.2%) in PLA compared to GH (14.7 ± 2.3%) and AGE (23.6 ± 1.6% (P < 0.05)). In EDL, treatment with rhGH did not significantly affect MHC‐isoforms or the fibre type composition, but 11% more MHC IIB and 11% less MHC IIA/IIX was observed in PLA compared to AGE (P < 0.05) suggesting a long‐term effect of growth hormone. MHC‐isoform data were confirmed using histochemistry. In addition, in the SOL, the maximal activity of 3‐hydroxyacyl‐CoA dehydrogenase (HAD) in GH and AGE was higher (22 and 27%, respectively) than in PLA (P < 0.05). In the EDL, no differences were observed in maximal activity of HAD. In conclusion, the data support a role for growth hormone in muscle fibre growth and differentiation.
Normovolaemic haemodilution and hyperoxia have no effect on fractal dimension of regional myocardial perfusion in dogs
Authors: KLEEN  , HABLER  , HUTTER  , PODTSCHASKE  , TIEDE  , KEMMING  , WELTE  , KEIPERT  , BATRA  , FAITHFULL  , CORSO  , MESSMER
Published: March 2003

Hypervolaemic haemodilution makes myocardial perfusion more homogenous as reflected by reduced fractal dimension of regional myocardial perfusion. The clinically more commonly performed acute normovolaemic haemodilution, however, has not yet been studied in this respect. Hyperoxic ventilation with 100% oxygen is used in conjunction with haemodilution to compensate for low oxygen content by increasing physically dissolved oxygen in plasma. Since hyperoxia is known to cause disturbance in microcirculatory regulation we studied the effects of acute normovolaemic haemodilution to haematocrit (hct) 20 ± 1% and hyperoxia on regional myocardial perfusion heterogeneity in 22 anaesthetized dogs using fractal and correlation analysis. Regional myocardial perfusion was assessed with radioactive microspheres. The results of the study were that heart rate, blood volume and arterial pressure were unchanged during haemodilution. Cardiac index was 3.6 ± 0.7 L min−1 m−2 before and 4.6 ± 0.7 L min−1 m−2 after haemodilution (P < 0.05). Fractal dimension (D) of regional myocardial perfusion was 1.17 ± 0.10 at baseline. Neither haemodilution (D = 1.19 ± 0.10) nor hyperoxia (D = 1.17 ± 0.10) altered fractal properties of regional myocardial perfusion. Spatial correlation of blood flow to adjacent tissue samples before haemodilution was 0.58 ± 0.15. Haemodilution and hyperoxia did not significantly influence spatial correlation (0.57 ± 0.12 vs. 0.60 ± 0.09; ns). We conclude that neither acute normovolaemic haemodilution nor haemodilution in combination with hyperoxic ventilation alter physiological myocardial perfusion heterogeneity.
Effects of physical activity and acupuncture on calcitonin gene‐related peptide immunoreactivity in different parts of the rat brain and in cerebrospinal fluid, serum and urine
Authors: WYON  , HAMMAR  , THEODORSSON  , LUNDEBERG
Published: March 2003

Calcitonin gene‐related peptide (CGRP) is a very potent vasodilator in the nervous system, and maybe involved in hot flushes experienced by most women around menopause. Flushing post‐menopausal women had higher urinary excretion of CGRP before than after successful treatment of their flushes with acupuncture.The prevalence of vasomotor symptoms is lower in physically active women. In a rat model we therefore intended to assess whether acupuncture and exercise affected CGRP concentrations in different parts of the brain and peripherally. The aim of the study was to elucidate the short‐ and long‐term effects of exercise and acupuncture on CGRP concentrations in the nervous system of normal adult rats. In a rat model, we examined the effects of single interventions and long‐term treatment with physical exercise and manual or electro‐acupuncture on CGRP concentrations in urine, cerebrospinal fluid and serum and different parts of the brain. In all compartments studied, but significantly only in the cerebrospinal fluid, CGRP increased after a single session of physical exercise or electro‐acupuncture. Manual acupuncture did not change CGRP concentrations in any compartment. Rats had the highest concentrations of CGRP in the pituitary and hypothalamus but the concentrations did not differ significantly between control rats and those subjected to long‐term treatment with manual or electro‐acupuncture or running rats. Rats treated with electro‐acupuncture had twice the CGRP concentration in the frontal cortex compared to control rats, albeit the difference did not reach statistical significance. Evidently manual and electro‐acupuncture have different effects, whereas electro‐acupuncture and physical exercise have more similar effects on CGRP production and/or release. To elucidate the role of CGRP in vasomotor symptoms, further studies with older flushing rats should be performed.
Body core temperature during food restriction in rats
Authors: SEVERINSEN  , MUNCH
Published: March 2003

Deep body temperature and locomotor activity of rats fed a reduced food amount (n = 9) and of starved rats (n = 9), were measured by implanted transmitters. Both groups were then refed ad libitum. The reduction in body temperature was significant for both groups, but larger in the starved rats than in the food restricted rats. There was a displacement of the circadian temperature rhythm in the starved rats. There were no significant differences in locomotor activity between groups until the start of refeeding. Rats fed reduced food amounts rapidly increased their activity, while the starved group retained a low activity for several days. Thermal conductance was reduced by 30% in both groups. This reduction in thermal conductance may explain how starving and semistarving rats are able to maintain core temperatures close to normal, even if resting metabolic rates are drastically reduced. The measured reduction in body core temperature signifies a change in the thermoregulatory `set‐point' during starvation.
Bradykinin elevates cytosolic Ca2+ concentration in smooth muscle cells isolated from rat duodenum
Authors: WASSDAL  , LARSEN  , IVERSEN
Published: March 2003

The effect of bradykinin on the cytosolic Ca2+ concentration were measured in single, Fura‐2 loaded, smooth muscle cells isolated from rat duodenum. All cells responded with a Ca2+ signal when exposed to bradykinin. The bradykinin response consisted of an initial Ca2+ spike followed by a plateau. Pre‐treatment of single muscle cells with either the phospholipase C blocker U‐73122 or thapsigargin, which is a potent inhibitor of the endoplasmic reticulum Ca2+‐ATPase, inhibited the response to bradykinin. Pre‐treatment of the cells with EGTA or La3+ to inhibit the Ca2+ influx, abolished the response induced by bradykinin. We conclude that bradykinin applied to single smooth muscle cells from rat duodenum, increases cytosolic Ca2+ by emptying intracellular Ca2+ stores, and by contribution from extracellular Ca2+. In contrast to bradykinin‐induced response in isolated rat duodenum (a relaxation followed by a contraction), we did not observe a biphasic effect of bradykinin on cytosolic Ca2+ in single muscle cells. Bradykinin may thus cause relaxation of duodenal smooth muscle indirectly through an effect on neighbouring cells as dilatation is brought about by this agent in blood vessels.
Effects of anabolic/androgenic steroids on regenerating skeletal muscles in the rat
Authors: Ferry  , Noirez  , Page C. Le , Salah I. Ben , Daegelen  , Rieu
Published: March 2003

We have examined the effect of male sexual hormones on the regeneration of skeletal muscles. Degeneration/regeneration of the left soleus and extensor digitorum longus muscles (EDL) of Wistar male rats was induced by an injection of snake venom (2 μg, Notechis scutatus scutatus). During the muscle regeneration (25 days), rats were treated with either oil (CON), nandrolone (NAN), NAN combined with exercise (NAN + EXE) or were castrated (CAS). Muscle growth and myosin heavy chain (MyHC) isoform content of regenerating muscles were studied. Castration altered the concentrations of MyHC in venom‐treated EDL (P < 0.01) and soleus (P < 0.05). NAN increased the mass (P < 0.01) of regenerating soleus and decreased the relative amount of fast MyHC protein (% of total, P < 0.05). The effect of NAN + EXE on the fast MyHC proteins of venom‐treated soleus was opposite (P < 0.05). NAN and NAN + EXE were without effect on the regenerating EDL (P > 0.05). In conclusion, it is possible that male sexual hormones play a role in the growth (synthesis of contractile proteins) of regenerating muscles in rat. In addition, contrary to NAN + EXE, NAN could be beneficial to soleus regeneration.
Ageing alters aortic antioxidant enzyme activities in Fischer‐344 rats
Authors: Demaree  , Lawler  , Linehan  , Delp
Published: March 2003

Oxidative stress imposed by reactive oxygen species is now believed to contribute to hypertension, atherosclerosis and ageing of the vasculature all involving a loss of relaxation. The antioxidant enzymes glutathione peroxidase, superoxide dismutase and catalase play a crucial role in defending against the ravages of oxidative stress. Our purpose was to characterize age‐related changes in glutathione peroxidase, superoxide dismutase and catalase in the rat aorta. Aortas were extracted from seven young (4 months), seven middle aged (18 months) and seven old (24 months) animals. Analysis of variance was used with Fisher‐LSD post hoc to determine mean differences among glutathione peroxidase, superoxide dismutase and catalase. Aortic glutathione peroxidase activities rose steadily with age expressed in μmol mg protein−1 min−1± SEM (young: 141 ± 22; middle aged: 198 ± 18; old: 229 ± 26) reaching significance between young and old. Superoxide dismutase activities significantly decreased in middle aged when compared with young (young: 22 ± 2 vs. middle aged: 15 ± 2 U mg protein−1) before trending upward again in old age (19 ± 2). Catalase activities dropped significantly between young and old when expressed in mU mg protein−1 (young: 230 ± 30; middle aged: 173 ± 18; old: 144 ± 23). Ratios for the various enzymes indicate a shrinking contribution of catalase with ageing, with an enhanced role for glutathione peroxidase in the antioxidant defence. These data in aortas of ageing rats show a complex alteration of the antioxidant profile.
Impact of testosterone and oestradiol on region specificity of skeletal muscle‐ATP, creatine phosphokinase and myokinase in male and female Wistar rats
Authors: Ramamani  , Aruldhas  , Govindarajulu
Published: March 2003

The main aim of the present study was to test the hypothesis that skeletal muscle ATP concentration, creatine phosphokinase and myokinase enzyme activities are stimulated by the sex steroids in both male and female rats (animals were not subjected to any kind of exercise or any training). To test the hypothesis healthy mature (90–120 days old, weighing about 160–180 g) male and female rats were gonadectomized. Gonadectomized male and female rats were administered with testosterone (Sigma Chemical, St Louis, MO, USA) at a dose of 100 μg (100 g body weight)–1 day–1 for males and 5 μg (100 g body weight)–1day–1 for females for 30 days from day 31 post‐castration onwards; and oestradiol at a dose of 5 μg (100 g body weight)–1day–1 for 30 days from day 31 post‐castration onwards for both males and females (17β oestradiol, Sigma Chemical Company, St Louis, MO, USA). The ATP content, creatine phosphokinase and myokinase enzyme activities of skeletal muscles were significantly higher than that of skeletal muscles of female control rats. Gonadectomy resulted in a significant decrease in ATP content and creatine phosphokinase myokinase enzyme activities in both male and female rats. Testosterone treatment to gonadectomized male rats brought back the parameters to normalcy whereas the same to the female rats enhanced the enzyme activities and ATP contents to the level of control male rats. Oestradiol treatment to castrated male rats did not bring about any significant alterations whereas the same in gonadectomized female rats brought them back to normalcy. Therefore from the present study it is concluded that testosterone is effective in both males and females whereas oestradiol was effective only in the females in enhancing skeletal muscle energy metabolism.
Physiological aspects of exocytosis in chromaffin cells of the adrenal medulla
Authors: Aunis  , Langley
Published: March 2003

The adrenal medulla is composed principally of groups of adrenergic and noradrenergic chromaffin cells, with minor populations of small intensely fluorescent cells and ganglionic neurones. Different molecular stimuli evoke distinct secretory events in the gland, involving the release of either adrenaline or noradrenaline together with various neuroactive peptides. The nature of the secretory response can be controlled at a central level or regulated locally within the gland. Specific innervation patterns to the different types of chromaffin cell have been implicated in central regulatory mechanisms, while several explanations for regulating secretion locally have been proposed. The differential distribution of various types of receptors between cell phenotypes, such as muscarinic or nicotinic acetylcholine receptors, histamine receptors, angiotensin receptors and different classes of opiate receptors between the two principal chromaffin cell populations could be involved in local control. In addition exocytosis parameters could be modulated differently in adrenergic and noradrenergic cells by phenotype‐specific mechanisms, possibly involving molecules like Growth Associated Protein‐43, Synaptosomal Associated Protein‐25 isoforms or the p11 annexin subunit. The distribution of the various types of calcium channels is also known to vary between chromaffin cell subtypes. This short review examines possible ways in which specific innervation patterns in the adrenal gland could be programmed and discusses exocytosis mechanisms that could differ between chromaffin cell phenotypes. Data reviewed here suggest that the adrenal medulla should no longer be viewed as a homogeneous entity but as consisting of an ensemble of individual cell subpopulations each with a distinct secretory response that could in part reflect its local history.
Heart rate variability in healthy volunteers during normobaric and hyperbaric hyperoxia
Authors: Lund  , Kentala  , Scheinin  , Klossner  , Helenius  , Sariola‐Heinonen  , Jalonen
Published: March 2003

Inhaled supranormal partial pressure of oxygen induces bradycardia and peripheral vasoconstriction. The exact mechanism of the decreasing heart rate is not clear, but the autonomic nervous system is partly involved. In the present study the role of the autonomic nervous system in hyperoxic bradycardia was evaluated by using the power spectral analysis of heart rate variability. Ten healthy volunteers participated in four experiments: (i) hyperbaric oxygen treatment (100% oxygen at 2.5 ATA), (ii) hyperbaric air treatment (O2 21% at 2.5 ATA), (iii) oxygen treatment at normal pressure (100% O2, 1 ATA) and (iv) air breathing at normal pressure (21% O2, 1 ATA). During the experiments, ECG was registered and subjected to power spectral analysis. The volunteers rated their perception of temperature, ear discomfort, sweating and excitement on a visual analogue scale. Statistical comparison of the results of the four trials was conducted with a two‐way
ANOVA for repeated measurements. Heart rate decreased during all interventions, but there were no statistically significant differences between the sessions. High frequency variability of heart rate variability and Hayano’s index of HF power increased and LF/HF ratio decreased with increasing partial pressure of oxygen. Our results suggest, that normobaric and hyperbaric hyperoxia increase parasympathetic influence in the regulation of the heart.
Effect of training on the activity of five muscle enzymes studied on elite cross‐country skiers
Authors: Evertsen  , Medbø  , Jebens  , Gjøvaag
Published: March 2003

This study examines the effect of training intensity on the activity of enzymes in m. vastus lateralis. Elite junior cross‐country skiers of both sexes trained 12–15 h weeks–1 for 5 months at either moderate (60–70% of VO2max, MIG) or high training intensity (80–90% of the VO2max, close to the lactate threshold; HIG). Muscle biopsies for enzyme analyses and fibre typing were taken before and after the training period. Histochemical analyses on single fibres were done for three enzymes (succinate dehydrogenase [SDH], hydroxybutyrate dehydrogenase [HBDH], glycerol‐3‐phosphate dehydrogenase [GPDH]), while the activity of citrate synthase [CS] and phosphofructokinase [PFK] was measured on whole biopsies. The activity of GPDH was low in ST fibres and high in FT fibres. The activity of SDH and HBDH was high in both ST and FTa fibres but low in the FTb fibres. The HIG increased their performance more than the MIG did during the training period as judged from scores on a 20‐min run test. The SDH activity rose by 6% for the HIG (P < 0.02). No effects of training were found in the activities of CS, HBDH or GPDH, neither in the two training groups nor for the two genders (P ≥ 0.16). The PFK activity fell by 10% for the HIG (P=0.02), while no change was found for the MIG. For GPDH, CS and SDH the women’s activity was ≈20% less than the value for the men (P < 0.03). For PFK and HBDH there was no sex difference (P ≥ 0.27). There were positive correlations between the activity of three of the enzymes (CS, SDH and GPDH) and the performance parameters (VO2max, cross‐country skiing and running performance; r ≥ 0.6, P < 0.01). No correlations were found between the PFK or HBDH activities and the performance parameters (r ≤ 0.16, P > 0.05). This study suggests that intensities near the lactate threshold affect biochemical and physiological parameters examined in this study as well as the performance of elite skiers, and that the rate‐limiting enzymes may be more sensitive to training than non‐rate‐limiting enzymes.
Modulation of volume‐sensitive Cl – channels and cell volume by actin filaments and microtubules in human cervical cancer HT‐3 cells
Authors: Shen  , Chou  , Hsu  , Hsu  , Wu
Published: March 2003

Hypotonicity activates volume‐sensitive Cl– currents, which are implicated in the regulatory volume decrease (RVD) responses and transport of taurine in human cervical cancer HT‐3 cells. In this study, the role of cytoskeleton in the regulation of volume‐sensitive Cl– channels and RVD responses in HT‐3 cells was studied. Cells were incubated with various compounds, which depolymerized or polymerized cytoskeletal elements, i.e. actin filaments and microtubules. The hypotonicity‐induced changes in Cl– conductance and in cell volume were measured by whole‐cell voltage clamping and cell size monitoring, respectively. Our results show that in HT‐3 cells hypotonicity activated an outward rectified Cl– current that was abrogated by Cl– channel blockers. Cytochalasin B, an actin‐depolymerizing compound, induced a substantial increase in Cl– conductance under isotonic condition and potentiated the expression of Cl– currents in hypotonic stress. Phorbol 12‐myristate 13‐acetate (PMA) significantly inhibited the cytochalasin B‐induced activation of Cl– conductance under isotonic condition. On the other hand, treatment with cytochalasin B significantly prolonged the RVD responses. Phalloidin, a stabilizer of actin polymerization, did not change the basal currents under isotonic condition, but completely abolished the increase in whole‐cell Cl– conductance elicited by hypotonicity and retarded the cell volume recovery. Colchicine, a microtubule‐assembly inhibitor, had no effect on either basal Cl– conductance or volume‐sensitive Cl– current and was unable to inhibit the RVD responses. Taxol, a microtubule‐stabilizing compound, did not alter the basal Cl– conductance, but inhibited the activation of volume‐sensitive Cl– channels as well as the process of RVD in a dose‐dependent manner. These data support the notion that functional integrity of actin filaments and microtubules plays critical roles in maintaining the RVD responses and activation of Cl– channels in human cervical cancer HT‐3 cells.
Intracellular acidosis modulates the stretch‐induced changes in E–C coupling of the rat atrium
Authors: Tavi  , Han  , Weckström
Published: March 2003

By inducing a small reduction of the intracellular pH (0.18 units) with 20 mmol L–1 propionate we demonstrated that acidification changed the responses of isolated rat atria to stretch. Stretch (increase of the intra‐atrial pressure) in normal pH increased the Ca2+ transients’ amplitude (Indo‐1 fluorescence) from 0.26 ± 0.09 in 1 mmHg to 0.36 ± 0.13 in 4 mmHg (P < 0.05, n=6), without affecting the diastolic [Ca2+]i level (n.s. n=6). The changes in Ca2+ balance during stretch were accompanied by a biphasic increase in the contraction force. Five minutes of continuous stretch increased the action potential duration (APD90%, P < 0.01, n=13) and decreased the APD15% (P < 0.001, n=13). During acidosis, the stretch‐induced increase of the Ca2+ transient amplitude (0.4 ± 0.13 vs. 0.3 ± 0.08, P < 0.05, n=6) was accompanied by the increase of the diastolic [Ca2+]i (1.16 ± 0.07, P < 0.05, n=6) compared with non‐acidotic control (1.06 ± 0.06, n=6). Acidic intracellular pH also inhibited the stretch‐induced changes in the action potentials (n=10) and slowed down the development of the contractile force during stretch. The results showed that acidosis modulates the mechanotransduction. It does this by interfering with the intracellular Ca2+ balance, inhibiting the Ca2+ extrusion mechanisms and reducing the Ca2+‐buffering power of the cells. The physiological and pathological processes associated with stretch are therefore modulated by intracellular pH owing to its concerted effects on intracellular Ca2+ handling caused by a competitive inhibition of various Ca2+‐binding molecules.
Plasma from ESRD patients inhibits nitric oxide synthase activity in cultured human and bovine endothelial cells
Authors: Xiao  , Schmidt  , Baylis
Published: March 2003

Our recent observations of reduced total nitric oxide synthesis in renal failure patients on peritoneal dialysis and haemodialysis suggest that hypertension in end‐stage renal disease involves lack of vasodilatory endothelial NO. To directly test this, uraemic plasma was obtained from dialysis patients and incubated with cultured vascular endothelial cells, to determine the effect on nitric oxide synthase (NOS) activity in comparison with plasma from subjects with normal renal function. After incubation for 6 h with 20% uraemic plasma from peritoneal dialysis and immediately prehaemodialysis patients, NOS activity was reduced in human dermal microvascular endothelial cells. Haemodialysis did not remove the NOS‐inhibitory activity of uraemic plasma nor did it activate inducible NOS, as NOS activity was always similar in control and dexamethasone pretreated cells. Nitric oxide production (accumulation of nitrite and nitrate) was lower in cells incubated with uraemic vs. normal plasma and excess arginine increased nitric oxide production by cells previously exposed to uraemic medium. This inhibitory effect was not associated with co‐factor deficiency but did correlate with plasma concentrations of endogenous NOS inhibitors. These in vitro findings suggest that low endothelial NOS activity may contribute to hypertension in end stage renal disease patients.
Abnormal pressure–natriuresis in hypertension: role of nitric oxide
Authors: Granger  , Alexander
Published: March 2003

The kidneys have a critical role in long‐term control of arterial pressure by regulating extracellular fluid and plasma volume. According to the renal body fluid feedback mechanism for long‐term control, persistent hypertension can only occur as a result of a reduction in renal sodium excretory function or a hypertensive shift in the pressure–natriuresis relationship. Although an abnormal relationship between renal perfusion pressure and renal sodium excretion has been identified in every type of hypertension where it has been sought, factors responsible for this effect are still unclear. Nitric oxide (NO) is produced within the kidney and plays an important role in the control of many intrarenal processes which regulate the renal response to changes in perfusion pressure and thus, help determine plasma volume and blood pressure. Numerous studies have shown that long‐term inhibition of NO synthesis results in a chronic rightward shift and marked attenuation in renal pressure–natriuresis. Recent studies have shown that certain animal models of genetic hypertension and forms of human hypertension areas are associated with a decrease in NO synthesis. Reductions in NO synthesis reduces renal sodium excretory function not only through direct actions on the renal vasculature, but through modulation of other vasoconstrictor processes and through direct and indirect alterations in tubular sodium transport. The causes and consequences of the dysregulation of NO in hypertension and other renal disease processes remain an important area of investigation.
Role of nitric oxide in haemodialysis hypotension
Authors: Nishimura  , Takahashi  , Yoshimura
Published: March 2003

To investigate the possible involvement of nitric oxide (NO) in haemodialysis hypotension, we measured plasma concentrations of nitrate anion (NO3–), a metabolite of NO, in 114 patients undergoing maintenance haemodialysis. Mean plasma NO3– concentrations before dialysis were greater in subjects with lower blood pressure (155 ± 16 μmol L–1) than in those with middle (117 ± 8 μmol L–1) or higher blood pressure (105 ± 12 μmol L–1) before dialysis. Further, mean plasma NO3– concentrations before dialysis were greater in subjects with lower blood pressure (186 ± 13 μmol L–1) than in those with middle (112 ± 7 μmol L–1) or higher blood pressure (64 ± 11 μmol L–1) after dialysis. Plasma NO3– concentrations before dialysis were inversely correlated with mean blood pressure before dialysis (r=0.318, P=0.0006), and showed a strong inverse correlation with mean blood pressure after dialysis (r=0.608, P=0.0001). In the selected participants who had equal range of mean blood pressure before dialysis, mean plasma NO3– concentrations were greater in subjects with severe hypotension during dialysis (180 ± 14 μmol L–1) than in those with mild hypotension (99 ± 11 μmol L–1) or without hypotension (53 ± 12 μmol L–1); plasma NO3– concentrations before dialysis were inversely correlated with changes in mean blood pressure during dialysis and mean blood pressure after dialysis. Results indicate that enhanced NO production may be involved in acute hypotension during dialysis, and suggest the possible involvement of NO in the pathogenesis of chronic hypotension associated with maintenance haemodialysis.
Tyramine‐induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats
Authors: Takauchi  , Yamazaki  , Akiyama
Published: March 2003

With the use of dialysis technique, the effects of tyramine on in situ cardiac sympathetic nerve endings were examined in anaesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and the concentration of dialysate noradrenaline (NA) served as an indicator of NA output at the cardiac sympathetic nerve ending. Locally applied tyramine (600 μM) increased dialysate NA levels from 17 ± 1 (pg mL−1) to 3466 ± 209 (pg mL−1). Pretreatment with reserpine (vesicle transport NA blocker 1 μM) did not affect tyramine‐induced NA efflux. The tyramine‐induced NA efflux was augmented by pretreatment with pargyline (1 m
M) but suppressed by pargyline (10 m
M). Pretreatment with α‐methyl‐tyrosine suppressed NA efflux evoked by tyramine. These pretreatments did not affect the time course of NA efflux but only altered peak height of NA efflux. The efflux of NA evoked by tyramine was not associated with any reduction of dihydroxyphenylglycol (DHPG). In contrast, in the pretreatment with reserpine, the efflux of NA was associated with a reduction of DHPG. This result suggests that NA graduation between axoplasm and stored vesicle contributes to maintaining the axoplasmic NA level during carrier‐mediated outward NA transport. The tyramine‐induced NA efflux provides a close reflection of the NA content at the nerve ending. With the use of dialysis, this experimental model is suitable for studying the mechanism of sympathomimetic amine‐induced neurotransmitter efflux.
Changes in height of jump, maximal voluntary contraction force and low‐frequency fatigue after 100 intermittent or continuous jumps with maximal intensity
Authors: Skurvydas  , Jascaninas  , Zachovajevas
Published: March 2003

Healthy untrained males (age 25.4 ± 1.7 years, n=12) gave their informed consent to take part in all experiments within the study. After 100 intermittent (every 20 s) drop jumps from the height of 0.4 m, jumps with counter‐movement to 90° angle in the knee and immediate maximal rebound (eccentric–concentric exercise; E–C) and 100 continuous jumps (five bouts of 20 jumps with counter‐movement to 90° angle in the knee with 10 s between bouts) (maximal exercise; M) with maximal intensity, the height of vertical jump decreased in a similar way, and this decrease did not depend on the performance mode of jumps. After E–C and M jumping exercises, there was a significant (P < 0.001) decrease in maximal voluntary contraction force, as well in the force generated by electrical stimulation at all stimulation frequencies, and these values were not restored to the initial level even after 24 h. After the E–C exercise, however, the muscle contraction force generated at different stimulation frequencies and, especially, at low‐stimulation frequencies (1–20 Hz) decreased to a significantly (P < 0.05–0.001) greater extent than after M exercise. Twenty minutes after the end of M exercise, there was still a greater increase in low‐frequency fatigue (LFF) and it was no different from the LFF registered 20 min after the end of E–C exercise. Twenty‐four hours after the M exercise, however, LFF was smaller than its respective value after E–C exercise. There was no significant relationship between the values of LFF after E–C and M exercises. This may indicate that there are differences in the origin of the LFF after the E–C and M exercises.
Neurogenic vasodilation in human skeletal muscle: possible role in contraction‐induced hyperaemia
Authors: Joyner M.J. , Halliwill J.R.
Published: March 2003

Whether or not neurally mediated vasodilation contributes to the rise in skeletal muscle blood flow during exercise in humans remains unknown. Such a mechanism might serve as an important ‘feed‐forward’ regulatory signal causing blood flow to rise prior to the development of a metabolic demand. Research in animal species has identified three neurally mediated vasodilating mechanisms with the potential to increase skeletal muscle blood flow during exercise. These include sympathetic vasodilator nerves, the potential for substances released by motor nerves to evoke vasodilation and the possibility of an ‘intrinsic’ vasodilator nerve system within the walls of blood vessels. In humans, sympathetic vasodilator nerves are present in several vascular beds (e.g. cutaneous). However, more recent information suggests that the human skeletal muscle is not innervated by this class of nerves. Along these lines, the vasodilator response to exercise is unaffected by sympathectomy or by blockade of the traditional transmitters associated with neurally mediated vasodilation. The possibility that spillover of substances released from motor neurones evokes vasodilation is provocative. For example, acetylcholine could produce both skeletal muscle contraction via nicotinic receptors and vasodilation via endothelial muscarinic receptors. However, in many species including humans, atropine has no effect on exercise hyperaemia. While the concept of an ‘intrinsic’ vasodilator pathway within the walls of the skeletal muscle vascular bed is fascinating, limited information is available on this mechanism in animals and none is available in humans. Taken together, the current information suggests that neurally mediated vasodilating mechanisms may not exist in human skeletal muscle. Additionally, even if such mechanisms exist, they do not play an obligatory role in governing the rise in muscle blood flow during exercise in humans.
Anaplerosis of the citric acid cycle: role in energy metabolism of heart and skeletal muscle
Authors: Gibala M.J. , Young M.E. , Taegtmeyer H.
Published: March 2003

Efficient energy transfer in heart and skeletal muscle requires a series of moiety‐conserved cycles. The intermediaries of the metabolic cycles are finely regulated to maintain a dynamic state of equilibrium. In heart muscle, depletion of the citric acid cycle (TCA cycle) through a block of 2‐oxoglutarate dehydrogenase results in a rapid decline of contractile function, which is reversed by the addition of substrates promoting flux through the carboxylating enzymes, malic enzyme, pyruvate carboxylase and propionyl‐CoA carboxylase. Anaplerosis describes a pathway, which replenishes a metabolic cycle. We show that enzymes for anaplerosis of the TCA cycle are expressed in heart and skeletal muscles. The role of anaplerosis of the TCA cycle in skeletal muscle is not entirely clear, but there is substantial evidence for its operational control during exercise. While the anaplerotic flux of carbon into the TCA cycle exceeds the removal of cycle intermediates, this process is only transient and reverses with prolonged exercise. It remains to be determined, however, whether the initial increase in TCA cycle intermediates is obligatory in order to attain high rates of TCA cycle flux, or primarily reflects a mass action phenomenon owing to increased substrate availability for anaplerotic pathways.
Nitric oxide as a competitive inhibitor of oxygen consumption in the mitochondrial respiratory chain
Authors: Brown G.C.
Published: March 2003

Nitric oxide (NO) and its derivatives inhibit mitochondrial respiration by various means. The author and others have shown that low (nanomolar) concentrations of NO immediately, specifically and reversibly inhibit cytochrome oxidase in competition with oxygen, in isolated cytochrome oxidase, mitochondria, nerve terminals, cultured cells and tissues. Primary astrocytes and a macrophage cell line, activated by cytokines and endotoxin to express the inducible isoform of NO synthase, strongly and reversibly inhibited their own respiration and that of co‐incubated cells by this means. Primary aortic endothelial cells transiently inhibited their own respiration when NO production was acutely stimulated with bradykinin or ATP, and basal NO release increased the apparent Km for oxygen of respiration in these cells. Thus the NO inhibition of cytochrome oxidase may be involved in the physiological and/or pathological regulation of respiration rate and its affinity for oxygen.
Ruled by waves? Intracellular and intercellular calcium signalling
Authors: Røttingen  , Iversen
Published: March 2003

The field of calcium signalling has evolved rapidly the last 20 years. Physiologists had worked with cytosolic Ca2+ as the coupler of excitation and contraction of muscles and as a secretory signal in exocrine glands and in the synapses of the brain for several decades before the discovery of cellular calcium as a second messenger. Development of powerful techniques for measuring the concentration of cytosolic free calcium ions in cell suspensions and later in single cells and even in different cellular compartments, has resulted in an upsurge in the knowledge of the cellular machinery involved in intracellular calcium signalling. However, the focus on intracellular mechanisms might have led this field of study away from physiology. During the last few years there is an increasing evidence for an important role of calcium also as an intercellular signal. Via gap junctions calcium is able to co‐ordinate cell populations and even organs like the liver. Here we will give an overview of the general mechanisms of intracellular calcium signalling, and then review the recent data on intercellular calcium signals. A functional coupling of cells in different tissues and organs by the way of calcium might be an important mechanism for controlling and synchronizing physiological responses