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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After prolonged (8 hrs) swimming, the level of corticosteroids was reduced and the contents of aldosterone and DOC in the blood was increased in the rats. At incubation of these rats' adrenals in the L-thyrosine substratum the synthesis of adrenaline was reduced. Addition of hydrocortisone, prednisolone and corticosterone into the medium as well as in vivo administration of these increased the adrenaline synthesis in swimming rats and did not alter it in intact rats. Neither in vitro addition of aldosterone nor in vivo administration of ACTH activated the process. The activating effect of glucocorticoids was absent at incubation of the adrenals with L-DOPA and L-noradrenaline. Synthesis of cathecholamines in the heart of swimming rats in the presence of L-thyrosine and L-DOPA as precnrsors was suppressed; neither was it restored by administration of corticosteroids both in vitro and in vivo. This suggests that one of the reasons for suppression of the catecholamine synthesis in adrenals at obvious physical fatigue is the decrease of the glucocorticoid activity.
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PMID:[Interaction of catecholamines and corticosteroids during the process of muscle fatigue]. 20 48

[3H]adenine was taken up by a crude hypothalamic synaptosomal fraction and incorporated into mainly nucleotides. The synaptosomes were superfused and after the initial washout a steady fractional release rate of 0.5-1% of the content/min was found. Electrical pulses (2 ms, 50 Hz, 10-20 mA, 4 min) and veratridine (10 microM, 4 min) induced a Ca++-dependent increase in purine release rate. K+ (30 mM, 4 min) caused a largely Ca++-independent increase. Most of the released material co-chromatographed with adenosine, inosine and hypoxanthine, while little or no nucleotide material was detected. Release of endogenous adenosine, inosine and hypoxanthine was detected by high performance liquid chromatography. However, following hypo-osmotic shock most of the released material was in nucleotides. The removal of glucose from the medium increased the fractional release rate 2-3 fold. Histamine, acetylcholine and glutamate were without effect. High amounts of noradrenaline caused an EGTA-inhibited release of purines, which was un-affected by propranolol or phentolamine. It is suggested that purines are released from neuronal structures and that the release reflects increased energy consumption and/or decreased energy production.
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PMID:Release of 3H-nucleosides from 3H-adenine labelled hypothalamic synaptosomes. 22 29

12 healthy male volunteers spent 64 h of continuous waking under strictly controlled environmental conditions (light, food, drink, activity) in isolation from the external world. Before and after the vigil the subjects slept in the laboratory. An additional group of five participated only during day time and spent the intervening night period asleep at home. Measurements were carried out in 3 h intervals except for sleep periods. Shortly before the circadian trough and peak of adrenaline excretion respectively, the subjects were exposed to a performance stressor. Results from the vigil showed a very pronounced circadian rhythm for adrenaline excretion but none for noradrenaline excretion. For adrenaline, night-time sleep reduced excretion levels, causing an even more pronounced circadian pattern. For noradrenaline, night-time sleep caused a drop in excretion giving the impression of a circadian rhythm. These and previous results led to the conclusion that the excretion of adrenaline exhibits a self-sustained rhythm while a rhythm in noradrenaline excretion is found only when caused by external synchronizers such as sleep-wake alternation. No difference in magnitude of stress response between peak and trough was observed for any of the catecholamines. Night-time (trough) exposure completely obliterated the circadian rhythm of adrenaline excretion for the duration of the exposure. It was concluded that the normal pronounced night-time trough of adrenaline cannot be due to unavailability of adrenaline in the medulla. With respect to sleep deprivation, no effect was found on excretion levels during waking, during sleep, or in response to the stressor as deprivation progressed. Finally, there was also found to be a close temporal covariation between adrenaline excretion and both rectal temperature and self-rated fatigue (neg.).
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PMID:Sleep and stressor exposure in relation to circadian rhythms in catecholamine excretion. 46 21

Alterations in metabolism of catecholamines were studied in sportsmen after development of acute fatigue as a result of the test physical loading. Three types of the alterations were characterized on the basis of differences in excretion with urine of free and sulphate-bound adrenaline, noradrenaline, of their precursors DOPA and dopamine as well as acid metabolites (vanillyl mandelic acid). The first type of the alterations in catecholamines metabolism comprized the cases, when excretion of catecholamines, their precursors and metabolites did not increase; this appears to relate to the partial exhaustion of hormones and peripheric mediators of sympathoadrenal system. The second type was characterized by decreased excretion of the substances studied, by development of the "perversed" reactions due to modifications in the regulatory system, which led to the inhibition of the system instead of its stimulation. The third type was manifested as the hyperfunction of the system. The increased synthesis of catecholamines during the hyperfunction suggests that this process serves as a compensatory reaction to their preceding elevated secretion; the phenomenon appears to depend on the increased secretion of the newly formed catecholamines. Excretion of catecholamines and their precursors was decreased for a long time after development of chronic fatigue in the resting state and the increase in excretion of the substances studied was not observed after physical loading.
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PMID:[Catecholamines, their precursors and metabolites in human fatigue after exertion]. 88 3

Circadian rhythms in urinary catecholamine excretion, performance and self-ratings were studied in two experiments with a total of 29 subjects who were deprived of sleep for 72 hr. Adrenaline excretion and fatigue ratings showed the most consistent circadian variations; noradrenaline and performance rhythms were more irregular. The average crest phase for adrenaline excretion was around 1400 hr, for noradrenaline about 0800 hr, for performance 1700 hr and for fatigue 0500 hr. Twenty-four hour levels of performance and 'subjective arousal' decreased over the three days of sleep deprivation, while adrenaline excretion levels increased.
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PMID:Circadian rhythms of catecholamine excretion, shooting range performance and self-ratings of fatigue during sleep deprivation. 113 17

Caffeine is the most widely consumed central-nervous-system stimulant. Three main mechanisms of action of caffeine on the central nervous system have been described. Mobilization of intracellular calcium and inhibition of specific phosphodiesterases only occur at high non-physiological concentrations of caffeine. The only likely mechanism of action of the methylxanthine is the antagonism at the level of adenosine receptors. Caffeine increases energy metabolism throughout the brain but decreases at the same time cerebral blood flow, inducing a relative brain hypoperfusion. Caffeine activates noradrenaline neurons and seems to affect the local release of dopamine. Many of the alerting effects of caffeine may be related to the action of the methylxanthine on serotonin neurons. The methylxanthine induces dose-response increases in locomotor activity in animals. Its psychostimulant action on man is, however, often subtle and not very easy to detect. The effects of caffeine on learning, memory, performance and coordination are rather related to the methylxanthine action on arousal, vigilance and fatigue. Caffeine exerts obvious effects on anxiety and sleep which vary according to individual sensitivity to the methylxanthine. However, children in general do not appear more sensitive to methylxanthine effects than adults. The central nervous system does not seem to develop a great tolerance to the effects of caffeine although dependence and withdrawal symptoms are reported.
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PMID:Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. 135 51

To evaluate physical and mental workload in middle-aged workers, urinary excretion of catecholamines and cortisol and self-reported scores of fatigue, stress and arousal in middle-aged steel workers were compared with those in young steel workers. Noradrenaline excretion in daytime of the day-off was higher in middle-aged workers than that in young workers. In the work days, noradrenaline excretion during working hours increased in both age groups when compared with that in the day-off. The work-related increase in noradrenaline excretion was more evident in the middle-aged group than in the young group. Adrenaline excretion during working hours was greater in the middle-aged group than that in the young group, whereas the adrenaline value in the day-off was almost the same in the two age-groups. Age-difference was hardly observed in dopamine and cortisol excretion. These findings suggest that the workload in middle-aged workers was greater than that in young workers. However, self-reported scores of fatigue and stress in middle-aged workers were less than those in young workers, suggesting inconsistency between subjective score of workload and urinary levels of catecholamines. These age-related differences in urinary levels of noradrenaline and adrenaline were not so obvious in workers engaged in automated and mechanized work (vigilance task) when compared to workers engaged in less automated and less mechanized work. It is considered that factory automation might reduce the workload in middle-aged workers.
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PMID:[Evaluation of workload in middle-aged steel workers by measuring urinary excretion of catecholamines and cortisol]. 177 Jun 15

Recent studies have shown that diaphragm fatigue can be reversed by mechanical augmentation of phrenic arterial flow. The purpose of the present experiment was to determine whether it was possible to pharmacologically augment diaphragm blood flow and reverse fatigue by the administration of norepinephrine. Four groups of studies were performed, all employing our previously described in situ isometric canine diaphragm strip preparation (Supinski et al., J. Appl. Physiol. 60: 1789-1796, 1986). Group I studies examined the effects of norepinephrine on the contractility of the nonfatigued diaphragm in normotensive dogs, group II studies examined the effects of this drug on the contractility of the fatigued diaphragm in normotensive animals, and group III studies examined the effect of this drug on the contractility of the fatigued diaphragm in hypotensive animals. Group IV studies examined the effect of norepinephrine in normotensive animals in which the phrenic artery was cannulated and pump perfused at constant flow. Fatigue was induced in group II, III, and IV studies by rhythmically stimulating the diaphragm via intramuscular electrodes. Norepinephrine had no effect on the contractility of the nonfatigued diaphragm (group I). In normotensive (group II) and hypotensive animals (group III), norepinephrine elicited dramatic increases in arterial blood pressure and phrenic arterial flow and produced a significant upshift in the force-frequency curve of the fatigued diaphragm. However, when phrenic flow was held constant (group IV experiments), norepinephrine failed to augment the contractility of the fatigued diaphragm. These results indicate that 1) norepinephrine can increase phrenic blood flow and augment the contractility of the fatigued diaphragm in both normotensive and hypotensive conditions and 2) this effect of norepinephrine to partially reverse fatigue is secondary to its action to augment diaphragmatic blood flow.
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PMID:Effect of norepinephrine on diaphragm contractility and blood flow. 207 96

The possible involvement of neuropeptide Y (NPY) in sympathetic control of renal blood flow was investigated in the pig in vivo. Exogenous NPY caused renal vasoconstriction with a threshold effect at an arterial plasma concentration of 164 pmol 6(-1). Stimulation of the renal nerves (0.59, 2 and 10 Hz) in control animals evoked rapid and frequency-dependent reduction in renal blood flow and overflow of NPY-like immunoreactivity (NPY-LI) and noradrenaline (NA) from the kidney, suggesting co-release from sympathetic nerves. Following the administration of the alpha- and beta-adrenoceptor antagonists phenoxybenzamine and propranolol, the vasoconstrictor response to exogenous NA was reduced by 98%, whereas that of NPY was unaltered. The response to nerve stimulation with 0.59 Hz was abolished, whereas relatively slowly developing reductions in renal blood flow by 7 and 28% were obtained upon stimulation with 2 and 10 Hz respectively. The nerve stimulation-evoked overflow of NA at 0.59 and 2 Hz, but not at 10 Hz and not that of NPY-LI, was enhanced after adrenoceptor blockade. Twenty-four hours after reserpine treatment (1 mg kg-1 i.v.) the contents of NPY-LI and NA in the renal cortex were reduced by 80 and 98% respectively. Sectioning of the renal nerves largely prevented the reserpine-induced depletion of NPY-LI, but not that of NA. Nerve stimulation of the denervated kidney with 2 and 10 Hz 24 h after reserpine treatment evoked slowly developing and long-lasting reductions in renal blood flow by 6 and 52% respectively. These responses were associated with overflow of NPY-LI, which was similar to and threefold higher than that observed in controls at 2 and 10 Hz respectively, while no detectable overflow of NA occurred. Repeated stimulation with 10 Hz resulted in a progressive fatigue of the vasoconstrictor response and the associated overflow of NPY-LI, giving a high correlation (r = 0.86, P less than 0.001) between the two parameters. It is concluded that NPY is a potent constrictor of the renal vascular bed. Furthermore, although NA is the likely transmitter mediating most of the responses to low to moderate nerve activation under control conditions, the data suggest that NPY may mediate the non-adrenergic reductions in renal blood flow evoked by high-frequency sympathetic nerve stimulation after reserpine treatment.
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PMID:Release and vasoconstrictor effects of neuropeptide Y in relation to non-adrenergic sympathetic control of renal blood flow in the pig. 257 Dec 35

The present study was conducted to estimate the effects of the physical load of instructors during ice skating camp. The subjects were 9 instructors aged from 20 to 24. To discover measures to relieve the physical load, we measured 1) urinary excretion of catecholamine (noradrenaline; NA, adrenaline; A), 17-OHCS, creatinine and nitrogen; N each day, 2) subjective symptoms of fatigue three time a day (morning, after skating, and at night), 3) nutrient intakes, 4) performed a time study and 5) measured the heart rate during skating instruction. The main results obtained were as follows: 1) The mean heart rate during skating instruction was 98.4-113.1 beats/min. 2) Urinary excretions of NA, A, and 17-OHCS were observed to have increased gradually during skating camp. The values of NA, A and 17-OHCS in the skating camp period were significantly higher than those of daily life. Subjective symptoms of fatigue were also increased gradually. The construction of symptom clusters was of the I-dominant type (I greater than III greater than II) at each point. 3) Intakes of energy, carbohydrate, protein and fat during the skating camp period were higher in comparison with those of daily life. 4) Urinary-N and creatinine levels during the skating camp period showed no changes. N-intake/urinary-N of the skating camp period tended to be higher than that of daily life. 5) In the time study, mean energy consumption was 3300-3400 kcal/day. The mean time of skating instruction was 218-227 min. The sleeping time was observed to have decreased gradually.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A study on the effects of the physical load of instructors during ice skating camp]. 263 76


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