Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many cross-sectional studies have demonstrated the influences of fitness level or the regional distribution of fat on lipid and carbohydrate metabolism; however, the relative contribution of these two variables in the same subjects has not been extensively examined. The purpose of this study was to determine the impact of regional adiposity on plasma lipids and carbohydrate metabolism in middle- to older-aged men with a wide range of fitness levels. Forty-six sedentary and exercise-trained men (age [mean +/- SE], 52.8 +/- 0.88 years) were included in this study. Fitness level was assessed by (a) time to exhaustion, and (2) maximal oxygen uptake achieved during an incremental treadmill test. Plasma lipid levels were determined in the basal, fasting state. Carbohydrate metabolism was evaluated by the glucose and insulin responses (total glucose and insulin areas under the curve, insulin sensitivity index [ISI]) to a 75-g, 2-hour oral glucose tolerance test (OGTT). Abdomen to hip ratio (AHR) was used as the index of regional adiposity. Multiple regression analysis indicated that fitness level and the percentage of body fat were significant predictors (approximately 56% of total variance) for total insulin area under the curve and the ISI. A comparison between the sedentary and trained subjects showed that training resulted in an improved ISI at an equal AHR. Fitness level was also the only significant multiple regression predictor for high-density lipoprotein (HDL)-cholesterol (25% of total variance) and accounted for the greatest amount of variance in triglyceride levels (34%), although AHR was also a significant predictor (6%).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of fitness level and the regional distribution of fat on carbohydrate metabolism and plasma lipids in middle- to older-aged men. 187 Apr 25

The effects of ingesting a mixed-snack food (CB), fructose (FRU), or placebo (PBO) prior to exercise (70% peak VO2) on the metabolic response during and after cycle exercise were studied in eight normal healthy volunteers with a wide range of peak VO2 (30-70 cc.kg-1.min-1). The study was designed to minimize the impact of confounding factors by using various strategies. First, the volunteers were grouped in teams with stratification by peak VO2, and the tests were randomized by a Latin-square design. Second, subjects received two acclimation trials in the cycle ergometer to diminish the effect of learning experiences and allow them to get used to the room and equipment. In addition, financial incentives were offered for team and individual endurance times. The test meals were administered 30 min prior to the beginning of exercise, and the subjects exercised to exhaustion, which was defined with clear-cut endpoints. Gas and blood samples were taken at regular intervals before, during, and for 60 min after each exercise bout. CB and FRU induced higher pre-exercise glucose and insulin concentrations. Blood lactate increased 100% with FRU ingestion. Despite these differences; endurance time, substrate, and hormone concentrations as well as rates of substrate oxidation during exercise were identical among the three conditions. During the post-exercise recovery period, PBO was associated with a starvation-like pattern of substrate utilization in which lipid oxidation was 60% greater and carbohydrate oxidation 50% less than following either CB (75 +/- 11, 248 +/- 27 mg.min-1, P less than 0.05) or F ingestion (93 +/- 4, 221 +/- 14 mg.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Pre-exercise feeding does not affect endurance cycle exercise but attenuates post-exercise starvation-like response. 192 74

Most incidence studies indicate that baseline plasma glucose, either fasting or post-glucose load, is the best predictor of progression to non-insulin-dependent diabetes mellitus (NIDDM)--the higher the level, the higher the risk. Elevated serum insulin concentrations in the presence of normal fasting plasma glucose levels reflect the presence of insulin resistance and they have also been shown to predict deterioration to NIDDM in a number of populations. Hyperinsulinaemia is a notable characteristic of populations with a high prevalence of NIDDM such as Micronesian Nauruans, American Pima Indians, Mexican-Americans and Asian Indians. In Nauruans and Pima subjects with normal glucose tolerance, those with higher post-load (2-hour) serum insulin at baseline were more likely to progress to either impaired glucose tolerance (IGT) or NIDDM. Conversely, amongst subjects with IGT, progression to NIDDM was predicted by lower (but still high relative to normal) baseline insulin responsiveness. Similar results for subjects with IGT have been described in Japanese. It appears from longitudinal studies that baseline insulin and glucose levels explain much of the association of obesity with risk of NIDDM. It remains to be resolved whether obesity itself may be a manifestation of an underlying defect (such as primary hyperinsulinaemia) which leads to both obesity and NIDDM. The possible sequence of events for the development of NIDDM includes a genetic defect resulting in hyperinsulinaemia and/or insulin resistance and leading ultimately to secondary pancreatic exhaustion with an insulin secretory defect which may also be genetically determined or the result of glucotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hyperinsulinaemia is a predictor of non-insulin-dependent diabetes mellitus. 193 64

Despite intensive research effort, the aetiology of non-insulin dependent diabetes mellitus remains unknown. In this disorder, hyperglycaemia results from three defects: impaired suppression of hepatic glucose production; reduced peripheral clearance of glucose; and impaired glucose-mediated insulin secretion. It has been proposed that reduced peripheral glucose clearance is the primary or inherited defect and that hyperinsulinaemia secondary to this eventually leads to beta cell exhaustion and impaired insulin secretion. Other authors have proposed that the initial defect is an abnormality in the first phase of insulin secretion. In this paper it is proposed that the primary abnormality is failure of hepatic gluconeogenesis to suppress adequately and that the resulting excess glucose flux results in peripheral insulin resistance and in a defect of glucose-mediated insulin secretion. This hypothesis is supported by recent data showing the glucose per se can induce defects in insulin action and insulin secretion.
 ...
PMID:The aetiology of non-insulin-dependent diabetes mellitus: is abnormal suppression of hepatic gluconeogenesis the primary event? 194 65

To explain mechanisms responsible for derangement of insulin release in uremia, we investigated glucose metabolism through three different tests in 14 patients with end-stage chronic renal failure. These tests were: intravenous glucose tolerance test with 0.33 g/kg of glucose solution (IVGTT); IVGTT with 0.5 g/kg of glucose solution (IVGTT2); IVGTT during aminophylline infusion (IVGTT + A). Twelve of the patients had IVGTT repeated after two to four months of thrice-weekly regular hemodialysis (IVGTT3). In each test we measured plasma glucose (G), immunoreactive insulin (IRI) and C-peptide. We also calculated glucose constant decay (K), insulin production (IRI area), insulinogenic index (IGI), and insulin resistance index (RI). Twenty-nine healthy volunteers formed the normal controls for IVGTT. As compared to controls, during IVGTT uremic patients showed significantly lower values in K, IRI area and IGI, and showed a significant RI value increase. During IVGTT2, IRI are values were higher than during IVGTT but IGI and K values were unchanged. During IVGTT + A both IRI area and IGI values were higher than during IVGTT. After hemodialysis treatment (IVGTT3) K, IRI areas and IGI increased significantly as compared to the predialysis period. K increase after hemodialysis correlated directly to IGI increase and inversely to RI changes. IGI increase during IVGTT3 was directly correlated to IGI rise during IVGTT + A. From these data we infer that defective insulin release in uremia is due to a decrease of beta-cell glucose sensitivity rather than to their functional exhaustion. An impaired adenyl cyclase-cAMP system may have an important role in the pathogenesis of this abnormality.
 ...
PMID:Glucose-induced insulin secretion in uremia: effects of aminophylline infusion and glucose loads. 196 48

Diagnostic electrocardiostimulation (ECS) of the right atrium with evaluation of the functional state of the heart conduction system and coronary reserve was carried out in 177 patients. The level of blood catecholamines, activity of cholinesterase and content of destroyed acetylcholine, cortisol, free fatty acids, glucose, insulin, thyroxine, triiodothyronine, renin, testosterone, calcium was determined before and at the height of diagnostic ECS. In cases with a tendency to bradycardia one could note compensatory tension of the sympathetic-adrenal system and mechanisms of general adaptation. In organic weakness of the sinus node with stable bradysystole there were signs of exhaustion of the adrenal reserves of catecholamines and cortisol manifested in paradoxic reduction of them in the blood in response to frequent ECS and corresponding changes of energy provision.
 ...
PMID:[The neurohumoral regulation and energy support of the myocardium in patients with heart rhythm disorders]. 197 44

Life-long sequential changes in glucose tolerance and insulin secretion were investigated in genetically obese Zucker rats (fa/fa) fed a diabetogenic diet rich in lard and sucrose. Comparisons were made with lean littermates (Fa/-) receiving normal chow diet. At 3-month intervals, seven to nine lean and obese rats had two permanent venous catheters implanted, allowing stress- and pain-free sampling of blood before, during, and after substrate administration. Intravenous glucose, iv arginine, and oral glucose tolerance were tested. The obese rats progressively developed hyperglycemia and severe hyperinsulinemia; their basal glycemia reached 8.8 +/- 1.1 vs. 5.8 +/- 0.2 mmol/liter in the lean rats at 46 weeks of age; respective insulinemia was 287.7 +/- 61.9 and 18.1 +/- 2.8 mU/liter (mean +/- SD). In the obese rats a distinct loss in glucose tolerance was seen with progression of age in spite of rising stimulated insulin secretion, which suggests progressive development of insulin resistance without exhaustion of B-cell secretory capacity. Absence of insulin deficiency was also suggested by immunohistochemical staining of pancreatic tissue specimens from obese rats, which showed large populations of insulin-containing cells. Like the obese animals, lean rats exhibited a decrease in insulin sensitivity with age. Relating basal individual glycemia and insulinemia, a rise by 1 mmol/liter in glycemia was associated with a 8.8-fold rise in basal insulinemia in lean rats, but only with a 1.8-fold increase in obese rats. Similar correlations for stimulated glycemia and insulinemia suggest impaired glucose sensitivity of pancreatic B-cells in obese vs. lean rats. In conclusion, hyperglycemia and hyperinsulinemia in insulin-resistant obese Zucker rats on a diabetogenic diet are not characterized by quantitatively deficient B-cell secretory capacity, but, rather, by impaired B-cell sensitivity to glucose with qualitatively intact regulation of glycemia and insulinemia at elevated plasma concentrations.
 ...
PMID:Lifelong sequential changes in glucose tolerance and insulin secretion in genetically obese Zucker rats (fa/fa) fed a diabetogenic diet. 198 47

The effects of a single bout of exercise to exhaustion on pancreatic insulin secretion were determined in seven untrained men by use of a 3-h hyperglycemic clamp with plasma glucose maintained at 180 mg/100 ml. Clamps were performed either 12 h after an intermittent treadmill run at approximately 77% maximum O2 consumption or without prior exercise. Arterialized blood samples for glucose, insulin, and C-peptide determination were obtained from a heated hand vein. The peak insulin response during the early phase (0-10 min) of the postexercise clamp was higher (81 +/- 8 vs. 59 +/- 9 microU/ml; P less than 0.05) than in the nonexercise clamp. Incremental areas under the insulin (376 +/- 33 vs. 245 +/- 51 microU.ml-1.min) and C-peptide (17 +/- 2 vs. 12 +/- 1 ng.ml-1.min) curves were also greater (P less than 0.05) during the early phase of the postexercise clamp. No differences were observed in either insulin concentrations or whole body glucose disposal during the late phase (15-180 min). Area under the C-peptide curve was greater during the late phase of the postexercise clamp (650 +/- 53 vs. 536 +/- 76 ng.ml-1.min, P less than 0.05). The exercise bout induced muscle soreness and caused an elevation in plasma creatine kinase activity (142 +/- 32 vs. 305 +/- 31 IU/l; P less than 0.05) before the postexercise clamp. We conclude that in untrained men a bout of running to exhaustion increased pancreatic beta-cell insulin secretion during the early phase of the hyperglycemic clamp. Increased insulin secretion during the late phase of the clamp appeared to be compensated by increased insulin clearance.
 ...
PMID:Effects of treadmill exercise to exhaustion on the insulin response to hyperglycemia in untrained men. 201 Mar 82

The importance of carbohydrates as a fuel source during endurance exercise has been known for 60 years. With the advent of the muscle biopsy needle in the 1960s, it was determined that the major source of carbohydrate during exercise was the muscle glycogen stores. It was demonstrated that the capacity to exercise at intensities between 65 to 75% VO2max was related to the pre-exercise level of muscle glycogen, i.e. the greater the muscle glycogen stores, the longer the exercise time to exhaustion. Because of the paramount importance of muscle glycogen during prolonged, intense exercise, a considerable amount of research has been conducted in an attempt to design the best regimen to elevate the muscle's glycogen stores prior to competition and to determine the most effective means of rapidly replenishing the muscle glycogen stores after exercise. The rate-limiting step in glycogen synthesis is the transfer of glucose from uridine diphosphate-glucose to an amylose chain. This reaction is catalysed by the enzyme glycogen synthase which can exist in a glucose-6-phosphate-dependent, inactive form (D-form) and a glucose-6-phosphate-independent, active form (I-form). The conversion of glycogen synthase from one form to the other is controlled by phosphorylation-dephosphorylation reactions. The muscle glycogen concentration can vary greatly depending on training status, exercise routines and diet. The pattern of muscle glycogen resynthesis following exercise-induced depletion is biphasic. Following the cessation of exercise and with adequate carbohydrate consumption, muscle glycogen is rapidly resynthesised to near pre-exercise levels within 24 hours. Muscle glycogen then increases very gradually to above-normal levels over the next few days. Contributing to the rapid phase of glycogen resynthesis is an increase in the percentage of glycogen synthase I, an increase in the muscle cell membrane permeability to glucose, and an increase in the muscle's sensitivity to insulin. The slow phase of glycogen synthesis appears to be under the control of an intermediate form of glycogen synthase that is highly sensitive to glucose-6-phosphate activation. Conversion of the enzyme to this intermediate form may be due to the muscle tissue being constantly exposed to an elevated plasma insulin concentration subsequent to several days of high carbohydrate consumption. For optimal training performance, muscle glycogen stores must be replenished on a daily basis. For the average endurance athlete, a daily carbohydrate consumption of 500 to 600g is required. This results in a maximum glycogen storage of 80 to 100 mumol/g wet weight.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Muscle glycogen synthesis before and after exercise. 201 84

Regular physical activity can improve cardiovascular fitness and may reduce the likelihood and debilitating effects of cardiovascular disease. Weight-training has generally been believed to have limited value in modifying risks of cardiovascular disease. Effects shown of resistance training on parameters associated with cardiovascular fitness and disease include: heart rate decreases for maximal work and recovery from short term weight-training, increased ventricular mass, and increased ventricular wall and septum thickness. Studies suggest that myocardial hypertrophy resulting from resistive training can be accompanied by positive myocardial adaptations. Blood pressure response considerations to resistive training include: similarity of resistive exercise peak response to other forms of high intensity exercise, highest blood pressures occur at or near exhaustion during maximum lifts, training appears to reduce the exercise blood pressure. Given the blood pressure responses caution is required for individuals with cardiovascular disease. Studies of high-volume weight-training indicate that small to moderate increases in aerobic power can occur in relatively short periods of time. The mechanisms by which weight-training increases VO2max is unclear. Resistive training may produce positive changes in serum lipids with the volume of training being the dependent factor. Cross-sectional and longitudinal studies of bodybuilders suggest that weight-training may beneficially alter glucose tolerance and insulin sensitivity. It appears that weight-training can increase short term high intensity endurance without a concomitant loss in performance. Resistive training increases power output and performance. Body composition has important relationships to cardiovascular fitness, strength and flexibility. It is likely that it can be affected and controlled by use of large body mass during exercise depending on training volume.
 ...
PMID:Health- and performance-related potential of resistance training. 201 69


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>