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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine subjects (VO2max 65 +/- 2 ml.kg-1.min-1, mean +/- SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g.kg-1 body mass) or a sodium chloride placebo (P, 0.045 g.kg-1 body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% VO2max, followed by exercise to exhaustion at 95% VO2max. Pre-exercise arterialized-venous [H+] was lower in C (36.2 +/- 0.5 nmol.l-1; pH 7.44) than P (39.4 +/- 0.4 nmol.l-1; pH 7.40); the plasma [H+] remained lower and [HCO3-] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% VO2max was similar in C (310 +/- 69 s) and P (313 +/- 74 s). Cardiorespiratory variables (ventilation, VO2, VCO2, heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195 +/- 19 mumol.l-1; P, 81 +/- 7 mumol.l-1) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% VO2max. Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.
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PMID:The effect of citrate loading on exercise performance, acid-base balance and metabolism. 276 67

The effect of physical exercise on atrial natriuretic peptide (ANP) was studied in 10 healthy young volunteers. The subjects were exercised on a bicycle ergometry until exhaustion. Blood samples were drawn at rest, at maximal load and in the following resting period. ANP concentrations were measured by radio-immunoassay. The level of ANP rose from 6.7 +/- 0.5 at rest to 33.2 +/- 7.0 pmol/l (mean +/- SEM) (p less than 0.05) at maximal load and returned to normal after 45 min. It was not possible to demonstrate a correlation between a change in ANP concentration and changes in pulse rate, blood pressure, maximal physical load, volume of urine, the amount of urine sodium, urine potassium or urine creatinine during the exercise load.
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PMID:Atrial natriuretic peptide in relation to physical exercise. 296 Oct 45

Although the menopause is generally considered to be the consequence of follicular exhaustion, the relationship between follicle number and the menopausal transition has not been explicity studied. We addressed this question in 17 women, aged 45-55 yr, who were undergoing elective total abdominal hysterectomy and salpingo-oophorectomy. The women were divided into 3 groups according to their menstrual history: 1) menstruating regularly (n = 6), 2) perimenopausal (irregular menses; n = 7), and 3) postmenopausal (greater than 1 yr since last menses; n = 4). The mean ages of the 3 groups were similar. Menstrual histories were confirmed by plasma hormone levels and endometrial histology. One ovary from each woman was serially sectioned for determination of follicle numbers. The mean number of primordial follicles in the ovaries of women who were still menstruating regularly was 10-fold higher than that in perimenopausal women [1392 +/- 355 (+/- SEM) vs. 142 +/- 72]. Follicles were virtually absent in the postmenopausal ovaries. Comparison of these data with those obtained by others in younger women suggests that follicular depletion accelerates dramatically in the last decade of menstrual life. These results support the view that declining follicular reserve is the immediate cause of both the perimenopausal and menopausal transitions, and indicate that the rate and, therefore, the regulation of follicular depletion change during the final phase of reproductive life.
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PMID:Follicular depletion during the menopausal transition: evidence for accelerated loss and ultimate exhaustion. 311 54

Plasma catecholamine concentrations were measured in 15 patients (six male) aged 14-63 years attending the casualty department with acute severe asthma (peak expiratory flow 27% (SEM 3%) of predicted). Nine patients were admitted and six were not. The plasma noradrenaline concentration, reflecting sympathetic nervous discharge, was two to three times normal in all patients and was significantly higher in those who required admission compared with those discharged home (mean 7.7 (SEM 0.6) v 4.7 (0.5) nmol/l (1.3 (SEM 0.1) v 0.8 (0.08) ng/ml); p less than 0.001). Plasma adrenaline concentration, however, was not increased in any patient. This surprising failure of the plasma adrenaline concentration to increase during the stress of an acute attack of asthma was unexplained and contrasts with the pronounced rise in plasma adrenaline and noradrenaline concentrations in acute myocardial infarction, heart failure, and septicaemia. The failure of plasma adrenaline concentration to increase in acute asthma is unlikely to be explained by adrenal exhaustion, but it may be another example of impaired adrenaline secretion in asthma.
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PMID:Circulating catecholamines in acute asthma. 391 81

The effect of intravenous pindolol (0.0256 mg/kg) on changes in plasma arachidonic acid (AA), some of its metabolites, and catecholamines induced by submaximal exercise was studied in six healthy male volunteers. Exercise resulted in markedly increased plasma concentrations of thromboxane B2 (TxB2) from 0.13 +/- 0.01 to 0.27 +/- 0.02 pmol/ml (mean +/- SEM; p less than 0.05) and AA from 4.1 +/- 0.6 to 8.0 +/- 0.9 mumol/l (p less than 0.005). No significant changes were seen in plasma concentrations of 6-keto-PGF1 alpha or PGE2 during exercise. A marked increase in plasma noradrenaline was seen already at 15 min of exercise, while the adrenaline concentration increased significantly at 30 min of exercise and a very marked increase in the adrenaline concentration was seen at exhaustion. A positive correlation (r = 0.54; p less than 0.05) was seen between plasma TxB2 and plasma adrenaline during exercise. The peak increase in both of these parameters was seen simultaneously at exhaustion. Pindolol treatment resulted in almost total inhibition of the increase in plasma TxB2 and AA during exercise. Pindolol treatment also resulted in a significantly higher adrenaline level at exhaustion. These data seem to indicate that an increased sympathetic tone may result in an increased release of arachidonic acid in the formation of vasoconstrictive thromboxane A2.
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PMID:The effect of pindolol on exercise-induced increase in plasma vasoactive prostanoids and catecholamines in healthy men. 393 85

Histamine (HA) may participate in the neuroendocrine regulation of pituitary hormone secretion. HA diphosphate infused iv for 120 min in a dose of 9, 18, 30, or 50 micrograms/kg BW.h to six normal men stimulated PRL secretion in a dose-dependent manner [absolute change in PRL (delta PRL) area = 52 X (HA dose) - 618; r = 0.9926; P less than 0.001]. The stimulatory effect of HA was modest and occurred during the second hour of infusion. This increase might be due to the opposing effects of HA on PRL secretion, specifically stimulation via H1 receptors and inhibition via H2 receptors. The PRL-releasing effect of 11 micrograms HA dihydrochloride was not significantly different from that of an equimolar dose of HA diphosphate (18 micrograms). Selective activation of H2 receptors by combined infusion of HA and the H1 receptor antagonist mepyramine inhibited PRL secretion compared to the effect of NaCl [delta PRL, -55 +/- 23 (+/- SEM) vs. -20 +/- 17 microIU/ml; P less than 0.01; n = 6). Mepyramine infused alone had no effect (delta PRL, -43 +/- 22 vs. -33 +/- 30 microIU/ml; n = 6). Selective activation of H1 receptors by combined infusion of HA and the H2 receptor antagonist cimetidine stimulated PRL secretion (delta PRL, 193 +/- 40 vs. -20 +/- 17 microIU/ml; P less than 0.0005; n = 6). When infused alone, cimetidine had only a modest and late stimulatory effect (delta PRL, 35 +/- 22 vs. -27 +/- 15; P less than 0.025; n = 6). Dopamine receptor blockade with metoclopramide (MET; 10 mg, three times daily, orally) did not prevent the PRL-inhibiting action of H2 receptor activation (delta PRL, -374 +/- 70 vs. -184 +/- 107 microIU/ml; P less than 0.01; n = 6), whereas the PRL-stimulating effect of H1 receptor activation was abolished by the drug (delta PRL, -249 +/- 64 vs. -174 +/- 54 microIU/ml; n = 6). The latter effect of MET was not due to exhaustion of the lactotrophs, since 200 micrograms TRH stimulated PRL secretion during MET treatment. These findings suggest that the H1 receptor-mediated PRL-stimulating effect of HA occurs through an inhibition of the dopaminergic system, whereas the H2 receptor-mediated PRL-inhibiting effect of HA does not involve dopaminergic neurons.
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PMID:Histaminergic regulation of prolactin secretion: dose-response relationship and possible involvement of the dopaminergic system. 394 33

It is not certain to what extent low frequency fatigue affects the performance of a muscle. We studied the endurance capacity of the sternomastoid muscle to undergo repetitive isometric neck flexion contractions for 2 s every 4 s at 35% of its maximal voluntary contraction force (MVC) in 5 normal subjects starting with different levels of fatigue. The endurance time, the duration the subjects were able to achieve the target force before exhaustion, was measured in each subject on 3 occasions: Study 1: in the fresh state, with a normal frequency/force curve and 20:50 ratio (ratio of force response at 20 Hz to that at 50 Hz) before the start of the endurance exercise; Study 2: with a moderately reduced 20:50 ratio before the start of endurance exercise (mean +/- SEM reduction in 20:50 ratio 11.4 +/- 0.8%); Study 3: with a substantially reduced 20:50 ratio before the start of the endurance exercise (29.2 +/- 3.7%). These reductions in 20:50 ratio were produced by the subjects performing 150 isometric neck flexion contractions at 50% of their MVC, followed by a period of rest to allow the 20:50 ratio to recover to approximately 10% of the starting value in Study 2, and to within 20 to 40% of the starting value in Study 3. Endurance exercise was then carried out.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of low frequency fatigue on endurance exercise in the sternomastoid muscle of normal humans. 396 31

The influence of high-intensity bicycle exercise on the redox level and lactate accumulation in skeletal muscle (m. quadriceps femoris) of man has been investigated. Six subjects exercised to exhaustion at a load corresponding to 100% VO2max. Muscle content of NADH, determined by the bioluminescence technique, increased from (means +/- SEM) 0.089 +/- 0.007 mmol/kg dry wt. at rest to 0.190 +/- 0.031 after 2 min of exercise (P less than 0.05) and to 0.213 +/- 0.021 at exhaustion (P less than 0.05). Values after 2 min exercise and at exhaustion were not statistically different (P greater than 0.05). Muscle lactate was increased 13-fold after 2 min of exercise and 22-fold at exhaustion as compared to the resting value. After 10 min recovery NADH was restored back to the pre-exercise level whereas muscle lactate was still elevated. The increase of muscle NADH during exercise is in contrast to earlier studies on isolated animal muscles, where an oxidation of NADH was observed during contractions. The difference might be due to the experimental model (isolated muscle vs. in vivo) or to the analytical method (qualitative data by reflectance fluorimetri from the surface of intact muscle vs. quantitative data from muscle extracts). Calculations of the cytosolic NADH concentration from the lactate dehydrogenase equilibrium show that 95% or more of the NADH is confined to the mitochondrial compartment. The observed increase of muscle NADH therefore imply that the redox potential of the mitochondria is decreased during intense exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:NADH in human skeletal muscle during short-term intense exercise. 398 70

Urinary N-acetyl-beta-D-glucosaminidase (NAG), a proximal tubule lysosomal enzyme, has been used as an indicator of subtle renal injury. Since it has been positively and significantly correlated with hemoglobin A1c and microalbuminuria, it has been suggested that this enzyme may also reflect metabolic control. Albumin excretion is exacerbated in adult diabetic individuals during exercise; such exercise-induced albuminuria may be a forerunner of diabetic nephropathy. Metabolic control, degree of exertion, and duration of diabetes have been suggested to influence this increase in albuminuria during exercise. Studies of children are few and have produced inconsistent results. Thus we studied 28 insulin-dependent diabetic children ranging in age from 5 yr to 16 yr and 27 age-matched controls using treadmill exercise; two exercise periods consisting of (1) graded increases in speed and grade at 3-min intervals until exhaustion and (2) a constant speed and grade necessary to produce 2/3-3/4 maximal heart rate for 30 min were performed. Capillary blood glucose, urinary NAG/creatinine (cr) ratios (UNAG/Ucr) and urinary albumin/creatinine ratio (Ualb/Ucr) were measured before and after each exercise period; hemoglobin A1c was also measured. The latter averaged 11.8 +/- 0.6% (mean +/- SEM); contrary to previous studies, this was not correlated with pre- or postexercise UNAG/Ucr. During both exercise periods, blood glucose dropped 271 +/- 19 mg/dl to 213 +/- 21 mg/dl (period 1) and 230 +/- 22 mg/dl to 157 +/- 21 mg/dl (period 2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of exercise on urinary N-acetyl-beta-D-glucosaminidase activity and albumin excretion in children with type I diabetes mellitus. 405 33

Repetitive flank-perineum palpation combined with probing the vaginal cervix in ovariectomized hormonally untreated rats elicited a mean of 4.2 +/- 0.2 (SEM) successive lordosis responses before the response was exhausted. Two days after a single injection of estradiol benzoate (100 micrograms/kg body wt) in ovariectomized rats, a significantly greater number (7.8 +/- 0.2) of lordosis responses could be elicited before the response was exhausted (P less than 0.01). After this exhaustion, recovery of lordosis responsiveness to this stimulation occurred significantly earlier in the estrogen-treated rats (6 hr) than in the oil-treated rats (60 hr) (P less than 0.01). Several possible mechanisms mediating these effects are proposed.
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PMID:Estrogen accelerates the recovery of the lordosis response after its exhaustion induced by cervical probing. 664 38


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