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Query: UMLS:C0015672 (
fatigue
)
51,768
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The present study examined the relationships between changes in intra- and extracellular concentrations of strong ions, the appearance of nonvolatile acid (NVA) in venous perfusate, and skeletal muscle
fatigue
during intense electrical stimulation. A one-pass system was used to perfuse an isolated rat hindlimb during 5 min of intermittent tetanic contractions. Initial isometric tensions averaged 2.85 kg/hindlimb and declined by 45% during 5 min. During stimulation, intracellular lactate concentration ([La-]i) increased by 2, 13, 15, and 21 meq/l of intracellular fluid in the soleus, plantaris, and red and white gastrocnemius. This was associated with a proportionate decrease in intracellular K+ ([K+]i) and Mg2+([Mg2+]i) concentrations and increased intracellular
Na+
([
Na+
]i) and Cl-([Cl-]i) concentrations. A stoichiometrically equivalent uptake of
Na+
and Cl- from the perfusate peaked at 8.5 mu eq.min-1.g-1 at the end of the 5th min. The increase in plasma [K+] during the last 4 min of stimulation was constant at 0.5 mu eq.min-1.g-1. A significant reduction in intracellular strong ion difference of all muscles contributed directly to an increase in [H+] during stimulation. After the 1st min of stimulation the rate of appearance of NVA in venous perfusate exceeded that of the increase in venous plasma [La-] by 12-fold; this decreased to 2.7-fold at the end of 5 min. La- release and NVA appearance in venous perfusate was maximal at 3.1 and 9.7 mu eq.min-1.g wet wt-1 during the 4th min of stimulation. It is concluded that the changes in the intracellular concentrations of strong ions during intense contractile activity are the primary factors contributing to skeletal muscle
fatigue
.
...
PMID:Ion fluxes during tetanic stimulation in isolated perfused rat hindlimb. 333 65
Muscle phosphorylase deficiency (McArdle's disease) has conventionally been considered a disorder of glycogenolysis, and the associated impairment in oxidative metabolism has been largely overlooked. Muscle glycogen normally is the primary oxidative fuel at exercise work loads requiring more than 75-80% of maximal O2 uptake (VO2max). Evidence is presented to support the hypothesis that a limited flux through the Embden-Myerhof pathway in McArdle's disease reduces the capacity to generate NADH required to support a normal VO2max. The extent of the oxidative defect is substrate dependent; i.e., it can be partially corrected by increasing the availability of alternative oxidative substrates (e.g., glucose, free fatty acids) to working muscle. Experiments employing modification of substrate availability closely link the hyperkinetic circulatory response to exercise (i.e., an abnormally large increase in O2 transport to skeletal muscle) and the premature muscle
fatigue
and cramping of McArdle patients with their oxidative impairment and suggest that a metabolic common denominator in these abnormal responses may be a pronounced decline in the muscle phosphorylation potential ([ATP]/[ADP][Pi]). The hyperkinetic circulation likely is mediated by the local effects on metabolically sensitive skeletal muscle afferents and vascular smooth muscle of K+, Pi, or adenosine or a combination of these substances released excessively from working skeletal muscle. The premature muscle
fatigue
and cramping of McArdle patients does not appear to be due to depletion of ATP but is associated with an increased accumulation of Pi and probably ADP in skeletal muscle. Accumulations of Pi and ADP are known to inhibit the myofibrillar, Ca2+, and
Na+
-K+-ATPase reactions.
...
PMID:The pathophysiology of McArdle's disease: clues to regulation in exercise and fatigue. 352 13
Thirty-one patients with primary dysmenorrhoea were treated in a double-blind, six-period, cross-over clinical trial with tiaprofenic acid, naproxen
sodium
and a placebo in randomized order, each for 2 consecutive cycles. Complete disappearance of the symptoms or pronounced therapeutic effects were obtained with tiaprofenic acid, naproxen
sodium
and the placebo in 74%, 65% and 35% of cases, respectively, while these treatments were ineffective in 3%, 6% and 38% of cases, respectively. Tiaprofenic acid was superior to the placebo for relieving pelvic pain and overall discomfort and for reducing the need for bed-rest. Naproxen sodium compared favourably with the placebo with respect to pelvic pain and overall discomfort. The effects of tiaprofenic acid and naproxen
sodium
were not significantly different. Tiaprofenic acid had no side-effects, whereas
tiredness
was experienced in 3 cases of naproxen
sodium
treatment. The results indicate that tiaprofenic acid is a useful alternative for the treatment of primary dysmenorrhoea.
...
PMID:Tiaprofenic acid in the treatment of primary dysmenorrhoea. 353 72
Patients with axillary-subclavian vein thrombosis often have a poor outcome when treated with intravenous heparin
sodium
and oral warfarin
sodium
. Four patients were therefore treated with thrombolytic therapy. Good initial and excellent long-term results were achieved. In follow-up that has ranged up to four years, these patients do not have the common complaints of edema,
fatigue
, cramping, or weakness seen after traditional anticoagulation. Patients have returned to their previous occupations and have normal arm function. Noninvasive Doppler vascular laboratory studies suggest continued patency of axillary veins. Thrombolytic therapy should be considered in the treatment of spontaneous axillary-subclavian vein thrombosis.
...
PMID:Thrombolytic therapy of axillary-subclavian venous thrombosis. 361 22
The diaphragm, a ventilatory muscle, has abundant sensory innervation. The effects of phrenic afferent activation on ventilation have been varied. In this study the proximal end of the phrenic nerve was electrically stimulated, and the effects on ventilation were measured in supine dogs anesthetized with either alpha-chloralose or pentobarbital
sodium
. We found a maximum increase in ventilation of 45 +/- 4% in the alpha-chloralose group and an increase in mean arterial blood pressure of 18 +/- 4%. This response was obtained at high stimulus intensities (60 times twitch threshold). Stimulation of the proximal end of the gastrocnemius nerve produced a similar ventilatory response (61 +/- 10%) but at lower stimulus intensities. During pentobarbital
sodium
anesthesia both the hyperventilation and the pressor response were produced; however, ventilation was increased by an increase in respiratory frequency. The reflex was abolished by sectioning of the cervical dorsal roots (C4-C7). Proximal cold blockade of the nerve abolished the response at a perineural temperature of 1.35 +/- 0.64 degrees C. The main effect of activation of phrenic afferents was an increase in ventilation and blood pressure that was mediated by unmyelinated fibers and possibly thin myelinated fibers. This response is similar to skeletal muscle afferent activation and may play a role in ventilatory drive during such conditions as exercise and respiratory muscle
fatigue
.
...
PMID:Ventilatory effects of stimulation of phrenic afferents. 365 54
Intracellular potassium ([K+]i), interstitial potassium ([K+]inter), intracellular
sodium
([
Na+
]i), and resting membrane potential (RMP) were measured before and after repetitive stimulation of mouse soleus and EDL (extensor digitorum longus) muscles. At rest, RMP was -69.8 mV for soleus and -74.9 mV for EDL (37 degrees C). [K+]i was 168 mM and 182 mM, respectively. In soleus, free [
Na+
]i was 12.7 mM. After repetitive stimulation (960 stimuli) RMP had decreased by 11.9 mV for soleus and by 18.2 mV for EDL. [K+]i was reduced by 32 mM and 48 mM, respectively, whereas [K+]inter was doubled. In soleus [
Na+
]i had increased by 10.6 mM, demonstrating that the [K+]i-decrease is three times higher than the [
Na+
]i-increase. It is concluded that this difference reflects different activity induced movements of Na and K, and that the difference is not due to the Na/K pumping ratio. The possible involvement of the potassium loss in muscle
fatigue
is discussed. After stimulation RMP recovered with a time constant of 0.9 min for soleus and 1.5 min for EDL. Within the first minutes after stimulation the intracellular potassium concentration increased by 20.4 mM/min for soleus and 21.7 mM/min for EDL. Free [
Na+
]i decreased with less than 10 mM/min. The mechanisms underlying the different rate of changes are discussed.
...
PMID:Potassium and sodium shifts during in vitro isometric muscle contraction, and the time course of the ion-gradient recovery. 371 46
Torasemide 40 mg/day p.o. was administered for 21 days to 8 healthy volunteers to investigate its pharmacodynamics, pharmacokinetics and safety on chronic administration. It induced a highly significant initial increase in 24-h urinary volume and 24-h excretion of
sodium
and chloride, but its affect diminished after the first days. On Days 0, 1, 10 and 21 the experiment was divided in 3 clearance phases, extending from 0 to 2 h, 2 to 6 h and 6 to 24 h after dosing. The fractional excretion of
sodium
, chloride, potassium, calcium, magnesium and inorganic phosphates peaked during the first 2 h and returned almost to the control value during the following two clearance phases. The phase-dependent changes were significant for all electrolytes, except for potassium and inorganic phosphate. Plasma electrolyte levels remained constant throughout the study, except for a small decrease in chloride and potassium and for an increase in calcium and magnesium. Fasting blood glucose and glucose tolerance test were unaffected. A small but significant decrease in LDL-cholesterol was observed on Day 10. Other plasma lipid components showed minor changes. Plasma uric acid levels were moderately increased. There was no significant change of the creatinine clearance. Body weight fell significantly (by about 2 kg) during the study. Tonal audiometry was normal before and after the study. There was no significant difference between the plasma levels of torasemide on Days 1, 10 and 21, nor between its elimination half-life on Days 1 and 21. Side-effects consisted mainly of
fatigue
and low-back pain on days of intense diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Diuretic activity, safety and pharmacokinetics of torasemide during chronic treatment in normal subjects. 378 Aug 35
Nine semi-professional football players have been studied during a pre-championship retreat in a hilly area with their team. The nine athletes drank "Amorosa" oligo mineral water for three weeks and various haematochemical parameters (such as uricaemia, creatinemia, azotemia,
sodium
content) both before and after the retreat, have been evaluated. Furthermore, LDH and CPK were monitored before and after an exertion test on an exercise bicycle after hydropinic ingestion. The results obtained fully confirm the diuretic and cathartic properties of the water and its property of mobilization of hydroelectrolytic system which are even more useful in subjects needing a rapid elimination of metabolic wastes accumulated during muscle
fatigue
.
...
PMID:[Clinical experience with the use of Amorosa, a low-mineral water, in athletes]. 380 92
The winter athlete has several potential tactics for sustaining body temperature in the face of severe cold. An increase in the intensity of physical activity may be counter-productive because of increased respiratory heat loss, increased air or water movement over the body surface, and a pumping of air or water beneath the clothing. Shivering can generate heat at a rate of 10 to 15 kJ/min, but it impairs skilled performance, while the resultant glycogen usage hastens the onset of
fatigue
and mental confusion. Non-shivering thermogenesis could arise in either brown adipose tissue or white fat. Brown adipose tissue generates heat by the action of free fatty acids in uncoupling mitochondrial electron transport, and by noradrenaline-induced membrane depolarisation and
sodium
pumping. The existence of brown adipose tissue in human adults is controversial, and although there are theoretical mechanisms of heat production in white fat, their contribution to the maintenance of body temperature is small. Acclimatisation to cold develops over the course of about 10 days, and in humans the primary change is an insulative, hypothermic type of response; this reflects the intermittent nature of most occupational and athletic exposures to cold. Nevertheless, with more sustained exposure to cold air or water, humans can apparently develop the humoral type of acclimatisation described in small mammals, with an increased output of noradrenaline and/or thyroxine. The associated mobilisation of free fatty acids suggests the possibility of using winter sport as a pleasant method of treating obesity. In men, a combination of moderate exercise and facial cooling induces a substantial fat loss over a 1- to 2-week period, with an associated ketonuria, proteinuria, and increase of body mass. Possible factors contributing to this fat loss include: (a) a small energy deficit; (b) the energy cost of synthesising new lean tissue; (c) energy loss through the storage and excretion of ketone bodies; (d) catecholamine-induced 'futile' metabolic cycles with increased resting metabolism; and (e) a specific reaction to cold dehydration. Current limitations for the clinical application of such treatment include uncertainty regarding optimal environmental conditions, concern over possible pathological reactions to cold, and suggestions of a less satisfactory fat mobilisation in female patients. Possible interactions between physical fitness and metabolic reactions to cold remain controversial.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Adaptation to exercise in the cold. 388 60
Hemodynamic and metabolic effects of fructose-1,6-diphosphate (F.D.P.) and dichloroacetate
sodium
(D.C.A.) administration were studied in 17 mongrel dogs during experimentally induced hemorrhagic shock using a modified Wigger's technique. During the oligemic period, which was maintained for 3 hours, a control group of animals (A) received a 5% glucose solution at a rate of 3 mg/kg/min, while the treated group (B) received D.C.A. (175 mg/kg for 30 minutes) and F.D.P. (5 mg/kg/min) as aqueous solutions. After retransfusion of the shed blood, both groups of animals were left to recover. All eight dogs of the control group died within 3 hours following the experiment, while six out of the nine treated dogs survived during a week of follow-up (p = 0.007). Two hours after retransfusion, blood pressure and cardiac index in group B returned to control levels (115 +/- 4.8 mmHg and 0.097 +/- 0.008 liters/min/kg), while group A demonstrated a rapid and progressive deterioration (64 +/- 9.7 mmHg and 0.041 +/- 0.005 liters/min/kg). Severe core hypothermia (down to 33.3 degrees C) developed in group A dogs despite retransfusion, while a normal core temperature was maintained in the treated dogs. Calculated oxygen consumption during the oligemic period was significantly higher in group B animals despite similar calculated oxygen delivery in both groups of animals. Hyperlactemia was significantly lower in group B animals despite F.D.P. administration. This can be attributed to the addition of D.C.A. to the treatment. F.D.P. and D.C.A. administration prevented the occurrence of respiratory failure resulting, most probably, from respiratory muscle
fatigue
owing to depressed metabolic rate and increased lactate formation in these muscles during the shock period. It is suggested that administration of F.D.P. and D.C.A. during hemorrhagic shock in dogs has a favorable effect on the outcome of this life-threatening condition.
...
PMID:Successful treatment of irreversible hemorrhagic shock in dogs with fructose-1,6 diphosphate and dichloroacetate. 397 67
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