Showing papers in "Acta Physiologica Scandinavica in 1985"
TL;DR: It was concluded that improvement in strength may be accounted for by neural factors during the course of very intensive strength training, especially in highly trained subjects.
Abstract: Eleven male subjects (20-32 years) accustomed to strength training went through progressive, high-load strength training for 24 weeks with intensities ranging variably between 70 and 120% during each month. This training was also followed by a 12-week detraining period. An increase of 26.8% (P less than 0.001) in maximal isometric strength took place during the training. The increase in strength correlated (P less than 0.05) with significant (P less than 0.05-0.01) increases in the neural activation (IEMG) of the leg extensor muscles during the most intensive training months. During the lower-intensity training, maximum IEMG decreased (P less than 0.05). Enlargements of muscle-fibre areas, especially of fast-twitch type (P less than 0.001), took place during the first 12 weeks of training. No hypertrophic changes were noted during the latter half of training. After initial improvements (P less than 0.05) no changes or even slight worsening were noted in selected force-time parameters during later strength training. During detraining a great (P less than 0.01) decrease in maximal strength was correlated (P less than 0.05) with the decrease (P less than 0.05) in the maximum IEMGs of the leg extensors. This period resulted also in decreases (P less than 0.05) of the mean muscle-fibre areas of both fibre types. It was concluded that improvement in strength may be accounted for by neural factors during the course of very intensive strength training. Selective training-induced hypertrophy also contributed to strength development but muscle hypertrophy may have some limitations during long-lasting strength training, especially in highly trained subjects.
758 citations
TL;DR: The same basic structure of the stride cycle as in other animals suggests similarities in the underlying neural control in human locomotion.
Abstract: Knowledge of adaptations to changes in speed and mode of progression (walking-running) in human locomotion is important for an understanding of underlying neural control mechanisms and allows a comparison with more detailed animal studies. Leg movements and muscle activity patterns were studied in ten healthy males (19-29 yr) during level walking (0.4-3.0 m X s-1) and running (1.0-9.0 m X s-1) on a motor-driven treadmill. Movements were recorded in the sagittal plane with a Selspot optoelectronic system. Recordings of EMG were made from seven different muscles of one leg by means of surface electrodes. Durations, amplitudes and relative phase relationships of angular displacements and EMG activity were analysed in relation to different phases of the stride cycle (defined by the leg movements). The durations of the entire stride cycle and of the support phase were found to decrease curvilinearly with velocity. Swing and support phase durations were linearly related to cycle duration in walking, and curvilinearly related in running. The characteristic occurrence of double support phases in walking was also seen in very slow running. Support length increased with speed up to about 1.2 m both in walking and running, but was longer in walking at the same velocity. Increases in net angular displacements were largest for hip movements and for knee flexion-extension during the swing phase in running. With increasing velocity a clear shift in relative rectus femoris activity occurred from knee extension to hip flexion. Gastrocnemius lateralis (LG) was co-activated with the other leg extensors prior to foot contact in running, whereas in walking LG was not turned on until later in the support phase. The ankle flexor tibialis anterior had its main peak of activity after touch-down in walking and before touch-down in running. The same basic structure of the stride cycle as in other animals suggests similarities in the underlying neural control. Human speed adaptation is distinguished primarily by an increase in both frequency and amplitude of leg movements and by a possibility of changing between a walking and a running type of movement pattern.
385 citations
TL;DR: The results indicate that the number of fibres activated from the start increase gradually in response to increased exercise intensity, and the rates of glycogen depletion in type I fibres suggest a progressive tension output of these fibres with increasing intensity.
Abstract: Glycogen depletion of muscle fibre types I, IIA, IIAB and IIB was studied during bicycle exercise at 43% (n = 5), 61% (n = 7) and 91% (n = 5) of VO2max. Glycogen content in individual fibres from vastus lateralis muscles was quantified as optical density of periodic acid-Schiff (PAS) stain. After 60 min at the lowest intensity, glycogen depletion was observed in almost all type I fibres and in about 20% of type IIA fibres. After 60 min exercise at 61% of VO2max, glycogen breakdown was observed in all type I fibres and in about 65% of type IIA fibres. During the first part of exercise at 91% of VO2max, glycogen breakdown was observed in all type I and IIA and in about 50% of type IIAB and IIB fibres. Muscle lactate concentration increased during the the first 5 min of exercise at 91% of VO2max to 15 mmol kg-1 (w/w) and remained thereafter at this level. From start of exercise the average rates of glycogen depletion in type I fibres were about 1.0, 2.0 and 4.3 mmol glucosyl units kg-1 (w/w) min-1 at 43%, 61% and 91% of VO2max. The depletion rates were almost constant with time at the two lower intensities. The results indicate that the number of fibres activated from the start increase gradually in response to increased exercise intensity. The rates of glycogen depletion in type I fibres suggest a progressive tension output of these fibres with increasing intensity.
286 citations
TL;DR: It is suggested that the facilitated induction of LLP in the presence of GABA antagonists is related to a facilitated activation of these NMDA receptor channels which is secondary to the higher levels of dendritic depolarization attained during tetanization under conditions of reduced postsynaptic inhibition.
Abstract: Long-lasting potentiation (LLP) of synaptic transmission in the CAI region of the hippocampal slice preparation has been examined. The effects of reduced postsynaptic inhibition given by application of gamma-aminobutyric acid (GABA) antagonists (mainly picrotoxin) on the generation of LLP were investigated. It was first demonstrated that picrotoxin had little effect on excitatory synaptic transmission itself as judged by the rising phase of the field EPSP. Moreover, there were largely no actions on short-lasting synaptic effects such as paired pulse facilitation and frequency potentiation. On the other hand, following drug application, much fewer afferent volleys were needed to generate a given amount of LLP. Long-lasting potentiation could be produced by trains containing as few as 2-5 impulses, trains that normally give rise to only short-lasting effects. There was no apparent difference in the maximal amount of LLP that could be produced for a given input, suggesting that the GABA antagonists do not operate by enhancing the capacity for LLP production but by facilitating its induction. As in normal solution, the LLP in the presence of the drugs was confined to the tetanized pathway. Tetanization in the treated slices was associated with enhanced somatic firing as well as an increase of the negative extracellular potential recorded in the dendritic layer. It is proposed that part of this increased negativity represents current through synaptically opened N-methyl-D-aspartate (NMDA) receptor channels. Furthermore, it is suggested that the facilitated induction of LLP in the presence of GABA antagonists is related to a facilitated activation of these NMDA receptor channels which is secondary to the higher levels of dendritic depolarization attained during tetanization under conditions of reduced postsynaptic inhibition.
232 citations
TL;DR: It may be suggested that NPY is involved in the regulation of NA release as well as the sympathetic control of atrial contractility and coronary blood flow.
Abstract: The effects of neuropeptide Y (NPY) on contractility of the spontaneously beating guinea-pig atrium and transmural nerve stimulation (TNS)-induced efflux of tritium-noradrenaline (3H-NA) were studied in vitro. NPY induced a moderate positive chronotropic and inotropic atrial response, which was resistant to metoprolol. TNS at 2 Hz for 2 s caused an increase in rate and contractile force. These effects were significantly reduced by NPY. NPY also reduced the TNS induced (2 Hz for 20 s), fractional [3H]NA release by 40% without affecting the contractile response. The contractile effects of exogenous NA on the guinea-pig atrium were not affected by NPY. NPY caused a long-lasting increase in coronary perfusion pressure, and also, in high doses, an inhibition of ventricular contractility in the isolated, perfused guinea-pig heart. The perfusion pressure increase to NPY, which most likely reflects coronary vasoconstriction, was resistant to alpha- and beta-adrenoceptor blockade but sensitive to the calcium antagonist nifedipine. A 50% reduction of the vascular NPY response occurred at 10(-9) M nifedipine, which did not influence cardiac contractility per se or the contractile effects of NA. NPY did not modify the increase in ventricular contractility induced by NA. Noradrenaline did not influence coronary perfusion pressure after beta-blockade. Since NPY is present together with NA in cardiac nerves, it may be suggested that NPY is involved in the regulation of NA release as well as the sympathetic control of atrial contractility and coronary blood flow.
144 citations
TL;DR: The results indicate that there are adenosine receptors modulating the efflux of glutamate in field stimulated hippocampal slices and that there is a role for L-PIA in this response.
Abstract: Hippocampal slices were labelled with [3H]glutamate. Evoked release, which was calcium-dependent and inhibited by tetrodotoxin, could be reduced concentration-dependently by L-PIA. The effect of L-PIA was blocked by 10 microM 8-phenyltheophylline. The results indicate that there are adenosine receptors modulating the efflux of glutamate in field stimulated hippocampal slices.
141 citations
137 citations
126 citations
TL;DR: The present data suggest that NPY, a peptide with sympathoactive actions, is co-stored with NA in heavy fractions corresponding to large dense-cored vesicles, while light fractions with small dense-dense vesicle probably contain NA but not NPY-LI.
Abstract: The subcellular storage of neuropeptide Y-like immunoreactivity (NPY-LI) in peripheral sympathetic neurons and adrenal gland as well as its axonal transport in the sciatic nerve was studied in relation to catecholamines in the cat. In the subcellular fractions from different parts of sympathetic neurons, i.e. cell bodies (coeliac ganglia), axons (sciatic nerve) and terminals (spleen), the NPY-LI was found together with noradrenaline (NA) in heavy fractions assumed to contain large dense-cored vesicles. In addition, minor lighter fractions in the coeliac ganglion contained NPY-LI. The molar ratio between vesicular NA and NPY was high in the terminal regions (150 to 1) and much lower in axons and cell bodies (10 to 1), thus reflecting the different mechanisms of resupply for classical transmitter and peptide. In the adrenal gland the NPY-LI was mainly located in the catecholamine-storing chromaffin-granule fraction and also to a smaller extent in lighter fractions. Using reversed-phase HPLC, one molecular form of NPY-LI corresponding to porcine NPY was found in the coeliac ganglion, while the adrenal medulla also contained minor peaks with NPY-LI in addition to the main form, which co-eluted with porcine NPY. NA was stored both in light and heavy fractions in the spleen, while it was mainly found in heavier fractions in the sciatic nerve. In the coeliac ganglion, most of the noradrenaline was present in a non-particulate form. The anterograde transport rate for NPY-LI in the sciatic nerve was estimated to be about 9 mm h-1. A minor retrograde transport of NPY-LI was also detected. In conclusion, the present data suggest that NPY, a peptide with sympathoactive actions, is co-stored with NA in heavy fractions corresponding to large dense-cored vesicles, while light fractions with small dense-cored vesicles probably contain NA but not NPY-LI. The main resupply of NPY to terminals is, in contrast to NA, most likely by axonal transport, which implicates differences in the storage, turnover and release of these co-existing substances in the sympathoadrenal system.
117 citations
116 citations
TL;DR: ST subjects were capable of accumulating more lactate in blood compared with ET subjects, but at the expense of a lower pH, since the buffer capacity seemed to be the same for the two groups.
Abstract: High ability to perform strenuous exercise of short duration is accompanied by a large lactate formation in the exercising muscles, but the disturbances in extracellular acid-base and electrolyte balance might be attenuated compared to subjects with less ability to perform intense exercise. To study this, oxygen deficit, changes in arterial blood acid-base status and plasma electrolytes were studied in six-endurance trained (ET) and six sprint-trained (ST) subjects who exercised on a treadmill at a speed which led to exhaustion within 1 min. During exercise the ET and ST subjects developed an oxygen deficit of 41 and 56 ml oxygen units kg-1 respectively, whereas peak blood lactate concentration post exercise averaged 12.5 and 16.7 mmol l-1. Blood pH followed lactate concentration closely, reaching nadir values of 7.175 and 7.065 for ET and ST subjects respectively. Respiratory compensation and changes in blood bicarbonate and standard base deficit (SBD) concentrations for a given lactate concentration were the same for the two groups, amounting to a change in PCO2 of 0.12 kPa, in bicarbonate concentration of 1.09 mmol l-1 and in SBD of 1.44 mmol l-1 mM-1 change in blood lactate concentration. During exercise the increase in haematocrit, from to 43 to 45% for the ET subjects and from 46 to 50% for the ST subjects, was accompanied by almost parallel relative changes in plasma chloride and sodium concentrations. Whereas haematocrit continued to increase post exercise and followed blood lactate concentration closely, plasma sodium and chloride concentrations decreased to pre-exercise values within 9 min of recovery. The anion gap increased significantly more than blood lactate concentration. Thus, ST subjects were capable of accumulating more lactate in blood compared with ET subjects, but at the expense of a lower pH, since the buffer capacity seemed to be the same for the two groups. The acidosis, which was larger than could be accounted for by lactic acid, was associated with an inexplicably large anion gap.
TL;DR: The results show that not only the number of impulses, but also their pattern of occurrence, may influence the degree of vasoconstriction, and the normal irregular sympathetic discharge pattern in itself has a bearing on the physiology of neuro-effector control mechanisms.
Abstract: Contractile responses to electrical field stimulation of excised small mesenteric arteries and veins of the rat were compared when stimuli were delivered in irregular bursts or at regular intervals. Spontaneously occurring skin vasoconstrictor impulses in a few-unit median nerve recording in man were stored on tape and used to trigger a stimulator. Two irregular stimulation sequences at average frequencies of 1.6 and 1.8 Hz, respectively, were used. In the arteries, average contractile responses were significantly greater at an irregular than at an even stimulation frequency, but in the veins, similar degrees of contraction were obtained with the two modes of stimulation. The frequency-response relationships to continuous regular stimulation showed the artery to respond less than the vein at low frequencies. This apparently explains the differences in behaviour between the vessels to irregular stimulation. The results show that not only the number of impulses, but also their pattern of occurrence, may influence the degree of vasoconstriction. Thus, the normal irregular sympathetic discharge pattern in itself has a bearing on the physiology of neuro-effector control mechanisms.
TL;DR: The data suggest that NPY mediates contraction of cerebrovascular smooth muscle via a mechanism that is dependent on the concentration of extracellular calcium.
Abstract: The action of neuropeptide Y (NPY), which coexists with noradrenaline (NA) in perivascular sympathetic nerves, has been examined on feline cerebrovascular smooth muscle using a sensitive in vitro. system. The direct cerebrovascular responses of peptides with structural similarities with NPY, peptide YY (PYY), avian (APP), and bovine (BPP) and human (HPP) pancreatic polypeptides, have been compared with that of NPY on isolated feline cerebral arteries. The relative potency for contractions induced by the peptides is: NPY, PYY > APP > BPP, HPP. The alpha-adrenoceptor antagonist rauwolscine, which blocked the response to noradrenaline (NA), had no effect on NPY-induced contractions. Neuropeptide Y significantly potentiated contractions induced by 10-6 M NA, but not by 10-5 M. Withdrawal of Ca2+ from the extracellular medium for 30 min reduced the contractile response to NPY in cerebral vessels by about 80%. Subsequent readdition of Ca2+ caused reproducible contractions which were inhibited by the calcium entry blocker nimodipine. Nimodipine also relaxed isolated middle cerebral artery segments contracted by NPY and NA in a concentration-dependent manner. The data suggest that NPY mediates contraction of cerebrovascular smooth muscle via a mechanism that is dependent on the concentration of extracellular calcium.
TL;DR: The results indicate that oxygen radicals generated by xanthine oxidase are very important, but not the only significant factor in the small intestinal reperfusion damage.
Abstract: Characteristic mucosal lesions develop in the small intestine during ischaemia and hypotension. This tissue damage can be further aggravated in the immediate reperfusion phase, presumably secondary to the generation of oxygen free radicals which have been proposed to be generated in this situation through the hypoxanthine-xanthine oxidase system. This was further investigated in the cat small intestine using a standardized regional intestinal hypotension model in which the effects of allopurinol (a xanthine oxidase inhibitor) were compared to those of an exogenous supply of inosine. The grade of mucosal damage, the nucleotide levels, the concentrations of hypoxanthine, total and oxidized glutathione, and of conjugated dienes were measured in the intestinal tissue. The results indicate that oxygen radicals generated by xanthine oxidase are very important, but not the only significant factor in the small intestinal reperfusion damage.
TL;DR: It is suggested that the likely mechanism for activation of the vagal afferents is a squeezing of the myocardium when the heart has to contract around an almost empty chamber, and that this sympathoinhibition is mediated primarily by mechanically sensitive cardiac vagalafferents.
Abstract: SKOOG, P., MANSSON, J. & THOREN, P. 1985. Changes in renal sympathetic outflow during hypotensive haemorrhage in rats. Acta Physiol Scand 125, 655–660. Received 11 February 1985, accepted 13 June 1985. ISSN 0001–6772. Department of Physiology, University of Goteborg, Sweden.
The goal of this study was to investigate changes in renal sympathetic outflow during hypotensive haemorrhage. Normotensive Wistar-Kyoto rats were anaesthetized with chloralose (50 mg kg-1) and bled to an arterial blood pressure of 50 mmHg for 30 min. Changes in heart rate (HR) and renal nerve activity (RNA) were registered. The hypotensive haemorrhage induced a short-lasting sympathetic excitation that was followed within 5–10 min by a powerful sympathetic inhibition and bradycardia. The average maximal decrease in sympathetic activity was 65% and the maximal decrease in heart rate was 45 beats min-1. There was a close correlation between changes in heart rate and renal sympathetic activity.
The marked depressor response was due at least in part to activation of vagal afferents because the depressor responses were acutely reversed by bilateral cervical vagotomy.
As cardiac afferents are known to be activated by prostaglandins and bradykinins, and these agents are released by myocardial ischaemia, haemorrhage was repeated after use of indomethacin and aprotinin (a protein inhibitor decreasing bradykinin formation), and a marked sympathetic inhibition could still be elicited upon haemorrhage. We therefore suggest that the likely mechanism for activation of the vagal afferents is a squeezing of the myocardium when the heart has to contract around an almost empty chamber. In conclusion, this study demonstrated that hypotensive haemorrhage triggers profound inhibition of RNA in rats and that this sympathoinhibition is mediated primarily by mechanically sensitive cardiac vagal afferents.
TL;DR: Human mixed saliva extracted with chloroform was found to contain immunoreactive melatonin which eluted in HPLC as synthetic melatonin, and there was a clear diurnal rhythm in saliva melatonin with low day and high night levels.
Abstract: Human mixed saliva extracted with chloroform was found to contain immunoreactive melatonin which eluted in HPLC as synthetic melatonin. There was a clear diurnal rhythm in saliva melatonin with low day and high night levels. A similar rhythm was observed in serum. The high night levels in saliva were lower than the corresponding levels in serum. The calculated secretion rate of melatonin into saliva was less than 0.5-0.9 pmol X h-1 during the day and 1.0-2.4 pmol X h-1 during the night. Saliva sampling can be used as a simple and non-invasive way of studying melatonin secretion in human body.
TL;DR: The vasoconstrictor response in the dental pulp and oral mucosa caused by activation of sympathetic nerves is more resistant to phentolamine than the response induced by infusion of exogenous noradrenaline.
Abstract: Neuropeptide Y (NPY) immunoreactivity (-IR) was found to be present in perivascular nerves in the cat dental pulp and oral mucosa. Many ganglion cells in the superior cervical ganglion also contained NPY-IR. Ligation of the inferior alveolar or lingual nerves produced an accumulation of NPY-IR in axons proximal to the site of ligation, suggesting an anterograde axonal transport of the peptide. After unilateral sympathectomy the NPY-IR disappeared in the dental pulp and oral mucosa on the ipsilateral side. Reversed phase high performance liquid chromatography showed that the main peak of NPY-like immunoreactivity found in the superior cervical ganglion co-chromatographed with synthetic porcine NPY. Changes in blood flow in dental pulp or oral mucosa were measured indirectly by recording local clearance of 125I during electrical stimulation of the sympathetic nerve or during close intra-arterial infusion of noradrenaline or NPY. All three procedures resulted in a pronounced decrease in local blood flow of a similar magnitude in both tissues. After alpha-adrenoceptor blockade with phentolamine, the vasoconstrictor effect of noradrenaline was abolished. However, the effect of sympathetic stimulation after phentolamine was only partially reduced (23-54%) and the response to NPY was almost unaffected by the alpha-receptor blockade. The remaining effect of sympathetic stimulation after phentolamine was abolished by guanethidine. However, the response to NPY was not changed by the latter drug. In conclusion, the vasoconstrictor response in the dental pulp and oral mucosa caused by activation of sympathetic nerves is more resistant to phentolamine than the response induced by infusion of exogenous noradrenaline. Since NPY is probably co-localized with noradrenaline in the sympathetic perivascular nerves and NPY reduces local blood flow, it is proposed that this peptide is involved in sympathetic vascular control in oral tissues.
TL;DR: The results suggest that the structures in the deep, ventro-lateral aspect of rostral medulla, from which apnoea can be induced, correspond partly to the nucleus paragigantocellularis lateralis (nPGL) and the nucleus preolivaris, which appear to be relevant for the drive inputs necessary for respiratory rhythmogenesis.
Abstract: Unilateral focal cold blocks (20 degrees C) in structures located ventrolaterally in rostral medulla consistently caused apnoea or deep depression of inspiratory motor output. The inhibitory effect could be correlated with the cooling temperature. Apnoeic response occurred either with complete absence of any inspiratory activity or combined with low level tonic inspiratory motor activity ('tonic apnoea'). The appearance of apnoea was CO2-independent, whereas the tonic component of the latter increased with increasing levels of PCO2. The results suggest that the structures in the deep, ventro-lateral aspect of rostral medulla, from which apnoea can be induced, correspond partly to the nucleus paragigantocellularis lateralis (nPGL) and the nucleus preolivaris. These structures appear to be relevant for the drive inputs necessary for respiratory rhythmogenesis. Unilateral focal cooling in the rostral medulla, including the 'Botzinger Complex', caused increments in respiratory rate both in vagotomized and non-vagotomized animals. The increase in respiratory rate in response to cooling in the region of the 'Botzinger Complex' was combined with either an enhancement or some depression of respiratory motor output. This area in the rostral part of the ventral respiratory group (VRG) seems not to be crucial for respiratory rhythmogenesis, but to play a role in determining both the intensity and timing of the respiratory activity. All effects of unilateral cold block were bilaterally symmetrical.
Journal Article•
TL;DR: This thesis has analyzed the role of brain serotonergic (5-HT) neurotransmission in avoidance learning in the male rat using neurochemical, pharmacological and behavioural approaches and found that serotonin also has a role in associative learning processes.
Abstract: This thesis has analyzed the role of brain serotonergic (5-HT) neurotransmission in avoidance learning in the male rat using neurochemical, pharmacological and behavioural approaches. The acute and long-term effects of p-chloroamphetamine (PCA) on one-way and two-way active avoidance (AA) acquisition and retention and passive avoidance (PA) retention and on central monoamine concentrations were examined in the male rat. The effects of PCA were compared with the 5-HT synthesis inhibitor p-chlorophenylalanine (PCPA). To characterize the effects of PCA the following neurotoxins were used: 5,6- and 5,7-dihydroxytryptamine (5,6- and 5,7-DHT) and N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4). The concentrations of biogenic monoamines and their metabolites in discrete brain regions were determined by high pressure liquid chromatography with or without electrochemical detection. The effects on 5-HT receptors in vitro and in vivo were measured by ligand binding studies (using 3H-5-HT and 3H-ketanserin as radioligands) and with behavioural techniques, respectively. Administration of the 5-HT releasing compound PCA prior to training (pre-training) produced a dose- and time-related impairment of one-way AA acquisition and retention and PA retention. A series of studies indicated that the avoidance learning deficits caused by PCA are produced by release of 5-HT, resulting in stimulation of postsynaptic 5-HT receptors. For instance, the avoidance deficit was blocked by pretreatment with the 5-HT uptake inhibitors alaproclate and zimeldine, which inhibit the 5-HT release induced by PCA. The avoidance deficits could not be related to changes (direct or indirect) in NA and DA transmission. Lesion experiments in combination with biochemical analyses provided evidence that the avoidance deficit caused by PCA involves 5-HT terminals of the forebrain, while the descending 5-HT projections seem to play a minor role. The AA acquisition deficit induced by PCA appears to be mediated via stimulation of 5-HT2 receptors, whereas the PA retention is mediated via 5-HT1 receptors. Analysis of the PCA-induced AA deficit indicated that it is mediated by non-associative factors. Thus, the performance of the PCA-treated rats was susceptible to interference from extratask contextual stimuli. Pre-training administration of PCA was found to produce a time-dependent loss in memory retention (PA retention) in animals which had acquired the response. This finding indicates that serotonin also has a role in associative learning processes e.g. in the way information is processed in the rat brain following acquisition.(ABSTRACT TRUNCATED AT 400 WORDS)
TL;DR: Electromyographic activity of the knee extensor and triceps surae musculature was studied in ergometer bicycling at five different power outputs around aerobic (AerT) and anaerobic (AnT) thresholds to suggest the integral of EMG activity could serve as an indicator of the aerobic threshold of an individual muscle.
Abstract: Electromyographic activity (EMG) of the knee extensor musculature (m. vastus lateralis, m. vastus medialis, m. rectus femoris), triceps surae (m. gastrocnemius, m. soleus) and m. tibialis anterior was studied in ergometer bicycling at five different power outputs around aerobic (AerT) and anaerobic (AnT) thresholds. EMGs were sampled with surface electrodes for ten revolutions at the beginning, in the middle and at the end of each work load and integrated (IEMG) separately for each of the muscles and for the descending (work) and ascending (rest) phase of the revolution. The mean power frequency (MPF) of the power spectral density function for the descending periods was also calculated. The first work load was 50% of the maximal load, the second at the level of AerT, the third at the AnT, the fourth between the AnT and the maximal load and the fifth load was maximal. The AerT and AnT were determined using blood lactate, ventilation volume and oxygen consumption. Five males from 21 to 38 years of age volunteered as subjects. When the IEMGs of the knee extensor and triceps surae musculature were related to the work load a nonlinearity was found at the aerobic threshold while no further change in the linearity was found at the AnT. The non-linear increase of the IEMG at the AerT was found both for the working (descending) and resting (ascending) phases of the cycling. In the MPF no difference below and above the AnT was found. It was thought that the integral of EMG activity could serve as an indicator of the aerobic threshold of an individual muscle.
TL;DR: Evidence is presented that it is the positive charge of protamine that is a major factor underlying the barrier opening, and whether barrier opening through transendothelial vesicular or channel transport occurs only at locations on the cell membrane deprived of negative surface charge areas.
Abstract: Recent evidence points to the negative surface charge of the luminal endothelial membrane of brain vessels as one determinant for morphologic blood-brain barrier function. The present study evaluates, in awake rats, how barrier function is affected by the polycation protamine to neutralize the negatively charged groups. High local doses of protamine, as infused intracarotideally, are able to substantially impair barrier capacity against albumin and inulin, which normally do not pass the blood-brain barrier. Evidence is presented that it is the positive charge of protamine that is a major factor underlying the barrier opening. However, when comparing the barrier opening obtained by corresponding concentration of the polycation lysine, it was obvious that another property of protamine contributed. This property was not linked to hyperosmolar, hypertensive or vasodilatory barrier opening, but may be a direct, cytotoxic effect of protamine. It is discussed whether barrier opening through transendothelial vesicular or channel transport occurs only at locations on the cell membrane deprived of negative surface charge areas.
TL;DR: A model is presented for the contribution of the chromogranins to osmotic pressure regulation in the bovine adrenomedullary catecholamine-storing granules.
Abstract: The soluble proteins (chromogranins) of bovine chromaffin granules have been studied by micro-osmometry with semi-permeable membranes (UM2, PM10 and PM30 with cut-offs greater than 1, greater than 10 and greater than 30 kD, respectively) at 1 = 0.15 and pH 5-8 for protein concentrations up to 20 mg X ml-1. After lysis of chromaffin granules in phosphate buffer pH 6, the released chromogranins behaved as aggregating solutes, consistent with an inconspicuous osmotic pressure contribution from the chromogranins at the protein concentration of the intact granules. Thus, in the presence of phosphate about 90% of the molecules behaved as colloids with Mr = 30,300 at c = o. After lysis in phosphate-free buffers the chromogranins behaved as highly non-ideal solutes in a manner which was incompatible with isotonicity at the protein concentration of the intact granules. About two-thirds of the molecules in the lysates in Na-succinate pH 5-6 and K-acetate pH 6 exhibited Mr = 66,000 and 79,000, respectively. In dilute solutions (less than 12 mg protein X ml-1) and ATP/protein ratios corresponding to those in the intact granules, the UM2 pressures were markedly increased, indicating release of polypeptides with Mr 2000-3000 from aggregates. CaCl2 was without specific effect on the colloid osmotic pressures but reduced the ATP-dependent increase in pressure, suggesting release of molecules twice the size of those released by ATP alone. A model is presented for the contribution of the chromogranins to osmotic pressure regulation in the bovine adrenomedullary catecholamine-storing granules.
TL;DR: The aim of the study was to determine the distribution, total number and size of different types of fibres in whole cross-sections of female m tibialis anterior and to compare these data with previous results obtained from male skeletal muscles as well as with data obtained by biopsy technique.
Abstract: The aim of the study was to determine the fibre size distribution within the human m tibialis anterior. Ten-micron thick cross-sections of the whole muscle were enzyme histochemically stained for myofibrillar ATPase at pH 9.4. The cross-sectional area of 100 fibres with low (type 1) ATPase and high (type 2) ATPase activity was measured in three different regions (superficial, central and deep). Both the type 1 and type 2 fibres were found to be larger in the deep region than in the central or superficial regions. The variation in fibre size could not be explained by the cryofixation or cryo-embedding techniques used. The data suggest that muscle adaptation to physical demands may not only occur by means of variation in types and number of muscle fibres, but also by variation in fibre size over the muscle cross-section.
TL;DR: The present findings indicate the existence of a sympathetic nonadrenergic neuronal mechanism mediating vasoconstriction and inhibition of colonic motility in the cat, and suggest NPY may be released from noradrenaline neurons to act on colonic smooth muscle and vessels.
Abstract: The present study investigated sympathetic mechanisms involved in the regulation of colonic motility and blood flow in the cat. Infusion of neuropeptide Y (NPY) close i.a. produced an inhibition of colonic motility and a vasoconstriction of long duration but no post-infusion vasodilatation. In contrast to NPY, porcine pancreatic polypeptide did not evoke any vascular or motility response. On a molar basis, NPY was 25 times more potent than noradrenaline in producing 50% reduction of the colonic blood flow. These vascular and motility effects of NPY were resistant to guanethidine, phentolamine, phenoxybenzamine and propranolol. Thus, the action of NPY on vascular and colonic smooth muscle did not seem to be mediated via adrenergic receptors. Noradrenaline administered close i.a. produced inhibition of colonic motility, and vasoconstriction followed by a rapid vasodilatation. These effects were completely blocked by combined alpha- and beta-adrenoceptor blockade. Electrical stimulation of the splanchnic and lumbar colonic nerves produced an overall inhibition of colonic motility, and vasoconstriction of the proximal and distal colon, respectively, with a rapid post-stimulatory vasodilatation. After combined alpha- and beta-adrenoceptor blockade the inhibitory effect of the nerve stimulations on colonic motility partly remained together with a marked vasoconstriction, which was most pronounced upon lumbar colonic nerve stimulation. All vascular effects of sympathetic nerve stimulation were eradicated by guanethidine, which also abolished the inhibitory motility response to splanchnic nerve stimulation. However, lumbar colonic nerve stimulation elicited a colonic contraction, possibly due to stimulation of afferent C-fibres. The present findings indicate the existence of a sympathetic nonadrenergic neuronal mechanism mediating vasoconstriction and inhibition of colonic motility in the cat. Thus, NPY may be released from noradrenergic neurons to act on colonic smooth muscle and vessels.
TL;DR: The distribution of carbonic anhydrase in cerebrum, cerebellum and medulla oblongata of the cat brain has been examined by a histochemical method andNeuron cell bodies and dendrites are stained in some locations and the localization of the enzyme shows regional differences.
Abstract: The distribution of carbonic anhydrase (CA) in cerebrum, cerebellum and medulla oblongata of the cat brain has been examined by a histochemical method. Neuron cell bodies and dendrites are stained in some locations. Many axons are distinctly stained and different intensities of staining can be seen even in adjacent axons. One of the most intensely stained structures is the capillary endothelium and stained capillaries are found in all parts examined. Glial cells are intensely stained in agreement with biochemical and earlier histochemical works. Myelin sheaths are never stained, possibly due to enzyme loss during embedding. The localization of the enzyme shows regional differences. In this respect, the medulla oblongata has been examined in more detail. A small area close to the ventral surface, medial to the roots of the hypoglossal nerve, is characterized by a high CA staining of the neuropil. The cell membrane of some large neurones and the capillary endothelium in this area were also stained. With regard to position and CA content, this area corresponds well to the characteristics of the medullary chemosensitive area as defined by previous experimental studies.
TL;DR: The age-related coronary flow reduction and the consistently reduced flow inSHR indicate a structural narrowing of the coronary vascular bed, particularly in SHR.
Abstract: The aim of the present study was to assess the influence of ageing on cardiac function and coronary flow in Wistar Kyoto normotensive rats (WKY, 16 and 78 weeks of age) and spontaneously hypertensive rats (SHR) of the same age. Cardiac function was determined on isolated hearts by means of an antegrade heart perfusion technique. Left atrial pressure and peak aortic pressure could be altered independently of each other. Recordings of cardiac output and coronary flow were then obtained at both normotensive and hypertensive levels of peak aortic pressures. Peak stroke volume (SV) was reduced with age in both WKY and SHR. Peak SV determined at normotensive pressure loads became diminished with age in WKY, while it at hypertensive pressure loads showed a small decline with age, since peak SV was low as early as 16 weeks of age. The age-dependent fall in cardiac performance was greater in SHR than in WKY, due to the enhanced peak SV in 16-week-old SHR at hypertensive pressure loads. Peak SV was markedly decreased at normotensive pressure levels in both 16- and 78-week-old SHR v. age-matched WKY. Coronary flow per unit tissue declined with age both in WKY and SHR. Coronary flow was also lower in SHR compared to age-matched WKY. With ageing this elevated performance was reduced down to the same level as in 78-week-old WKY. The age-related coronary flow reduction and the consistently reduced flow in SHR indicate a structural narrowing of the coronary vascular bed, particularly in SHR.
TL;DR: A fatigue test showed that the EDL became less fatigable and the soleus less fatigue resistant after denervation, which is taken as an indication that the contractile proteins are affected.
Abstract: The contractile properties of the fast-twitch m. extensor digitorum longus (EDL) and the slow-twitch m. soleus were examined after 5 days of denervation. An increase in twitch time to peak, twitch half relaxation time and twitch/tetanus ratio was observed. The EDL also showed a moderate decrease in maximal isotonic shortening velocity, which is taken as an indication that the contractile proteins are affected. A fatigue test showed that the EDL became less fatigable and the soleus less fatigue resistant after denervation.
TL;DR: Feed intake of both Svalbard and Norwegian reindeer was maximal in August, but declined thereafter, reaching minimum values in January (NR) and March (SR), 55 and 69% below the August value, respectively.
Abstract: Arctic reindeer exhibit marked seasonal changes in fat deposition and mobilization. At intervals throughout the year, therefore, we have measured feed intake of both Svalbard (SR) and Norwegian reindeer (NR) together with the seasonal changes in size, lipogenic and lipolytic capacity of isolated adipocytes from both sub-species. Feed intake of both NR and SR was maximal in August, but declined thereafter, reaching minimum values in January (NR) and March (SR), 55 and 69% below the August value, respectively. NR and SR adipocyte volume changed in parallel and were reduced to the same extent (69%) from their maximum in August to their minimum in May. Adipocyte lipogenic capacity, measured as acetate incorporation into cellular lipid at saturated acetate concentrations, was lowest in January (NR adipocytes) and March (SR adipocytes), 92 and 90%, respectively, below the maximum values, which were obtained in August. Lipolytic capacity, measured as maximum adrenaline-stimulated glycerol release, was high in SR adipocytes from March through to October and in NR adipocytes from July through to January. Minimum lipolytic capacity, on the other hand, was found in January (SR adipocytes) and March (NR adipocytes). The present findings may be explained by alterations in lipogenic enzyme activity and in the lipolytic activation system.
TL;DR: The present results demonstrate that trunk movements are generated and controlled by specific patterns of muscle coordination that are specific adaptations of the motor program to balance changes in mechanical conditions, such as angular acceleration, moment arm for the gravitational force, and intrinsic forces of active and passive structures surrounding the spine and pelvis.
Abstract: The pattern of activity in different trunk muscles during voluntary trunk movements was studied in the standing position in man. The electromyographic activity from ventral and dorsal trunk muscles on the left and right sides were recorded together with the movements in the sagittal and frontal planes (Selspot optoelectronic system). Movement direction, amplitude, velocity and initial posture were varied. In all movements there was a basic pattern of alternation between antagonist muscle groups. Fast movements were initiated by a sharp burst of activity, whereas slow flexions and side bendings resulted from a decrease in antigravity muscle activity. Movement amplitude was related to the magnitude of the initiating burst, and also to the time of onset of antagonist muscle activity with a braking effect. The contribution of passive internal forces in the braking of a movement was indicated by the myoelectrical pattern of activity, particularly in slow large side bendings, where ipsilateral activity was present at the end of the movement. Sagittal movements starting at different initial trunk inclinations resulted in shifts in onset time and duration between antagonist muscles. The observed modifications are specific adaptations of the motor program to balance changes in mechanical conditions, such as angular acceleration, moment arm for the gravitational force, and intrinsic forces of active and passive structures surrounding the spine and pelvis. In conclusion, the present results demonstrate that trunk movements are generated and controlled by specific patterns of muscle coordination.