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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Detraining is the partial or complete loss of training-induced adaptations, in response to an insufficient training stimulus. Detraining characteristics may be different depending on the duration of training cessation or insufficient training. Short term detraining (less than 4 weeks of insufficient training stimulus) is analysed in part I of this review, whereas part II will deal with long term detraining (more than 4 weeks of insufficient training stimulus). Short term cardiorespiratory detraining is characterised in highly trained athletes by a rapid decline in maximal oxygen uptake (VO2max) and blood volume. Exercise heart rate increases insufficiently to counterbalance the decreased stroke volume, and maximal cardiac output is thus reduced. Ventilatory efficiency and endurance performance are also impaired. These changes are more moderate in recently trained individuals. From a metabolic viewpoint, short term inactivity implies an increased reliance on carbohydrate metabolism during exercise, as shown by a higher exercise respiratory exchange ratio, and lowered lipase activity, GLUT-4 content, glycogen level and lactate threshold. At the muscle level, capillary density and oxidative enzyme activities are reduced. Training-induced changes in fibre cross-sectional area are reversed, but strength performance declines are limited. Hormonal changes include a reduced insulin sensitivity, a possible increase in testosterone and growth hormone levels in strength athletes, and a reversal of short term training-induced adaptations in fluid-electrolyte regulating hormones.
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PMID:Detraining: loss of training-induced physiological and performance adaptations. Part I: short term insufficient training stimulus. 1096 48

We encountered a case with long-term remission of Cushing's disease due to pituitary apoplexy. The apoplexy of pituitary adenoma secreting adrenocorticotropin hormone was diagnosed by successive and timely magnetic resonance imaging when the symptoms of the patient were not yet severe and anterior pituitary dysfunction was only a transient reduction of growth hormone secretion. Seven years after the first episode of pituitary apoplexy, hypercorticism recurred, and pituitary magnetic resonance imaging showed a regrowth of the pituitary adenoma. A spontaneous remission of Cushing's disease without significant visual, neurologic or hormonal defects seems to be a much more common phenomenon than has been previously suggested. Cases with relapse after spontaneous remission of Cushing's disease are rare and the duration of remission in previous reports was within 5 years. We observed such a patient with a 7 year-remission caused by pituitary apoplexy. We consider that a careful long-term follow-up is required for patients with Cushing's disease whose remission was due to pituitary apoplexy.
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PMID:Recurrence of Cushing's disease after long-term remission due to pituitary apoplexy. 1122 56

To investigate hemodynamic and hormonal effects of ghrelin, a novel growth hormone (GH)-releasing peptide, we gave six healthy men an intravenous bolus of human ghrelin (10 microg/kg) or placebo and vice versa 1-2 wk apart in a randomized fashion. Ghrelin elicited a marked increase in circulating GH (15-fold). The elevation of GH lasted longer than 60 min after the bolus injection. Injection of ghrelin significantly decreased mean arterial pressure (-12 mmHg, P < 0.05) without a significant change in heart rate (-4 beats/min, P = 0.39). Ghrelin significantly increased cardiac index (+16%, P < 0.05) and stroke volume index (+22%, P < 0.05). We also examined ghrelin receptor [GH secretagogues receptor (GHS-R)] gene expression in the aortas, the left ventricles, and the left atria of rats by RT-PCR. GHS-R mRNA was detectable in the rat aortas, left ventricles, and left atria, suggesting that ghrelin may cause cardiovascular effects through GH-independent mechanisms. In summary, human ghrelin elicited a potent, long-lasting GH release and had beneficial hemodynamic effects via reducing cardiac afterload and increasing cardiac output without an increase in heart rate.
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PMID:Hemodynamic and hormonal effects of human ghrelin in healthy volunteers. 1129 72

To test the hypotheses that short-term bed-rest (BR) deconditioning influences metabolic, cardiorespiratory, and neurohormonal responses to exercise and that these effects depend on the subjects' training status, 12 sedentary men and 10 endurance- and 10 strength-trained athletes were submitted to 3-day BR. Before and after BR they performed incremental exercise test until volitional exhaustion. Respiratory gas exchange and heart rate (HR) were recorded continuously, and stroke volume (SV) was measured at submaximal loads. Blood was taken for lactate concentration ([LA]), epinephrine concentration ([Epi]), norepinephrine concentration ([NE]), plasma renin activity (PRA), human growth hormone concentration ([hGH]), testosterone, and cortisol determination. Reduction of peak oxygen uptake (VO(2 peak)) after BR was greater in the endurance athletes than in the remaining groups (17 vs. 10%). Decrements in VO(2 peak) correlated positively with the initial values (r = 0.73, P < 0.001). Resting and exercise respiratory exchange ratios were increased in athletes. Cardiac output was unchanged by BR in all groups, but exercise HR was increased and SV diminished in the sedentary subjects. The submaximal [LA] and [LA] thresholds were decreased in the endurance athletes from 71 to 60% VO(2 peak) (P < 0.001); they also had an earlier increase in [NE], an attenuated increase in [hGH], and accentuated PRA and cortisol elevations during exercise. These effects were insignificant in the remaining subjects. In conclusion, reduction of exercise performance and modifications in neurohormonal response to exercise after BR depend on the previous level and mode of physical training, being the most pronounced in the endurance athletes.
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PMID:Effects of 3-day bed rest on physiological responses to graded exercise in athletes and sedentary men. 1140 37

In adults, abdominal visceral adiposity is related to an increased risk of cardiovascular diseases, Type 2 diabetes mellitus, and stroke. The antecedents of these conditions likely begin with the alterations in body fat distribution during childhood and adolescence. The sexually dimorphic alterations in fat distribution are influenced by sex differences in hormone concentrations, anatomical differences in the number and density of specific hormone receptors, capillary blood flow, and the activity of enzymes promoting lipid synthesis or degradation. Hormones influencing the amount and regional distribution of adipose tissue during puberty include cortisol, insulin, growth hormone, and the sex steroids. Cortisol and insulin promote fat deposition while the sex steroids and GH stimulate lipolysis. An overly sensitive hypothalamic-pituitary-adrenal axis may exist in obesity and disrupt the balance between the lipogenic effects of cortisol and insulin and the lipolytic effects of sex steroids and growth hormone. Leptin is released from the adipocytes and may act as a metabolic signal to the hypothalamic areas controlling satiety, energy expenditure, and the regulation of cortisol, insulin, sex steroid and growth hormone release. The complex issues of the hormonal control of alterations in body fat distribution during puberty are developed and a working model is proposed. Am. J. Hum. Biol. 11:209-224, 1999. Copyright 1999 Wiley-Liss, Inc.
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PMID:Hormonal changes during puberty and their relationship to fat distribution. 1153 45

Accumulating data show that growth hormone (GH) and insulin-like growth factor-I (IGF-I) have major effects on the cardiovascular system. In the present study we have directly compared GH and IGF-I in an in vivo rat model of experimental myocardial infarction. Four weeks after ligation of the left coronary artery, male rats were treated with recombinant human (rh) GH 1.1 mg/kg per day, rhIGF-I 3.0 mg/kg per day or saline s.c. for 2 weeks. Transthoracic echocardiography was performed before and after the treatment period. Both GH and IGF-I reduced total peripheral resistance (P< 0.01), end-systolic wall stress (P< 0.01) and end-systolic short-axis area (P< 0.001 and P< 0.05). GH also increased area fractional shortening (P< 0.05). Stroke volume (SV) and SV index were improved by IGF-I (P< 0.0001), and SV tended to be increased by GH (P= 0.12). In conclusion, GH and IGF-I had similar beneficial effects on systolic function and peripheral resistance after experimental myocardial infarction.
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PMID:Similar cardiovascular effects of growth hormone and insulin-like growth factor-I in rats after experimental myocardial infarction. 1173 33

Several issues have to be considered when taking care of girls and women with Turner syndrome. During childhood, short stature is the primary concern and treatment with growth hormone (GH) is now widely used, often in conjunction with the androgen, oxandrolone. Recent studies indicate that doses used previously in the treatment of short stature have been too small. Induction of puberty should be performed at an appropriate age with reference to the peers of the patient. In adulthood, female sex hormone substitution should be offered to possibly prevent the increased morbidity seen in Turner syndrome, which consists of increased risk of fractures and osteoporosis, a clustering of diseases like ischaemic heart disease, hypertension, stroke and Type 2 diabetes, the latter entities being involved in the insulin resistance syndrome. Furthermore, hypothyreosis are often seen and the risk of Type 1 diabetes may also be increased. Congenital malformations of the heart are frequently seen in Turner syndrome, possibly increasing the risk of dissecting aorta aneurism. Liver enzymes are often elevated in Turner syndrome and there may be an increased risk of cirrhosis of the liver. Mortality does seem to be increased in Turner syndrome and women with the 'pure' 45,X karyotype do seem to be most severely affected. In the clinical practice of Turner syndrome, a careful monitoring of glucose and bone metabolism, weight, thyroid function and blood pressure should be performed. A cardiovascular risk profile should be determined and the patient informed concerning risks and benefits from sex hormone replacement therapy. Based on the available literature, sex hormone replacement therapy is highly recommended, although at present there are no longitudinal data documenting the long-term positive effect of sex steroid substitution. However, hypogonadism is expected to explain at least part of the decreased lifespan found in Turner syndrome. Since general physicians encounter Turner patients infrequently, it is recommended that the care and treatment of Turner syndrome is centralised.
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PMID:Aspects of the treatment of Turner syndrome. 1182 6

Two pediatric patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes were diagnosed with growth hormone deficiency with the primary lesion identified as the growth hormone-releasing factor producing cells of the hypothalamus. Stimulation tests with insulin, levodopa and sleep did not overcome the deficient pattern of growth hormone secretion. By comparison, the growth hormone-releasing factor stimulation test generated a normal growth hormone response in these two patients. Growth hormone supplementary therapy was effective in terms of growth gain without adverse effects.
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PMID:Hypothalamic growth hormone deficiency and supplementary GH therapy in two patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. 1253 71

Incidence of CVD in diabetic men was reported to be twice as that of non-diabetics and almost three times greater in diabetic women in the Framingham Study. It is postulated that excessive glycation and oxidation, endothelial dysfunction and increased platelet aggregation may be responsible for endothelial proliferation and thickening of plasmatic membrane in small blood vessels ('lipohyalinosis') leading to lacunar infarction. Prothrombotic state may precipitate a stroke, however, platelet aggregability, elevated fibrinopeptide A (FPA) and D-dimer were not significantly related to stroke in diabetic mellitus (DM), whereas suppressed fibrinolytic activity was a common finding. Of many unknown factors in pathogenesis, the deficient insulin secretion, resistance to action of insulin at level of 'insulin receptors', changes in counter regulatory hormones (e.g. glucagon, pancreatic polypetides, growth hormone, catecholamines, etc.) and decrease in the hepatic sensitivity to insulin action in suppressing glucose output have received more attention. Hyperosmolar state can simulate stroke syndromes. Early recognition and treatment of risk factors such as hypertension or better glycemic control, correction of hyperlipidemia or obesity in diabetic population are important. In diabetic subjects already showing recurrent transient cerebral ischemic attacks (TIAs) or minor strokes, the benefit of antiplatelet agents or antithrombotic therapy in prevention of major strokes is well established. Ramipril has been found to be effective in reducing stroke risk by 33% in diabetic patinets in HOPE study.
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PMID:Cerebrovascular disease in type 2 diabetes mellitus. 1257 84

Multidirectional changes in the natural history of many cardiovascular syndromes have been linked to different levels of daily and monthly geomagnetic activity (GMA). Previous studies have found that in periods of high GMA, there were more admissions for acute myocardial infarction and more cases of anterior wall myocardial infarction. Results also indicated: higher out-patient mortality and a trend towards higher hospital mortality from acute myocardial infarction; higher diastolic arterial pressure in healthy subjects and in treated hypertensive patients; higher prolactin and 17-corticosteroid levels in the peripheral blood; more severe migraine attacks and more admissions for CVA and cerebrovascular insufficiency in male patients; changes in many blood coagulation cellular gradients (platelet count, basophils in the peripheral blood), a rise in platelet aggregation, fibrinogen level and a drop in leukocyte adhesiveness. Periods of low GMA showed a related increase (negative correlation) in in-hospital non-myocardial infarction-related cardiovascular deaths. Only in times of lowest GMA did inferior wall myocardial infarction exceed anterior wall myocardial infarction. Low GMA was also associated with higher levels of growth hormone and 11-ketosteroids in the peripheral blood, more sudden deaths, some increase in electrical heart instability number of ventricular and supraventricular extrasystoles and higher rate of ventricular tachycardia. The monthly occurrence of pregnancy-induced hypertension was negatively correlated with GMA level. Gender differences were noted in some of the parameters. Other studied parameters did not show changes related to GMA. These included hemoglobin level, electrolyte level, heart beat and pulse rate. Moreover, some observed cardiovascular fluctuations that were related to the level of GMA, also showed differences in the rising and dropping parts of the 11-year cycle of solar activity. It has been suggested that some of the changes observed in many clinical syndromes may be related to the concomitant activation of the serotoninergic system.
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PMID:The effect of geomagnetic activity on cardiovascular parameters. 1265 77


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