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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute physiological responses to the "PO2-Aerobic Exerciser" (AE), a partial rebreathing device designed to stimulate training at altitudes, were studied in seven healthy men [mean VO2max = 56.1 +@- 10.1 (SD) ml X kg-1 X min-1] who performed cycle ergometer exercise to exhaustion in three experimental situations: a control test (C) breathing normal atmosphere: a test with the device (AE); and a test with the AE air supplemented with oxygen (AEO2'). Arterial oxygen saturation at rest for C, AE, and AEO2' studies was 97 +/- 1, 95 +/- 2, and 97 +/- 1%, respectively (P less than 0.05 for C vs AE and AE vs AEO2'), while at exhaustion it was 95 +/- 1, 87 +/- 2, and 95 +/- 1%, respectively (P less than 0.05 for C vs AE and AE vs AEO2'). Maximum work rate decreased from a control value of 1738 +/- 184 kg X min-1 to 1371 +/- 147 kg X min-1 during AE and remained below control levels during AEO2'; 1554 +/- 110 kg X min-1 (P less than 0.05). Beyond 60% of maximum work rate during AE, inspired CO2 increased to 0.026 +/- 0.005. Mouth pressure swings of up to -19.2 +/- 10.2 and 12.7 +/- 5.7 cm H2O were recorded during AE. While the PO2 aerobic exerciser induced a hypoxic stress, the pertubation imposed was not explained fully by arterial oxygen desaturation. Other factors such as hypercapnia and a flow resistive increase in the work of breathing appear to have influenced work capacity during the use of the device.
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PMID:Influence of supplemental oxygen on the physiological response to the PO2 aerobic exerciser. 370 49

The purpose of this study was to examine plasma and intraerythrocyte lactate concentrations during graded exercise in humans. Seven adult volunteers performed a maximum O2 uptake (VO2max) test on a cycle ergometer. Plasma and intraerythrocyte lactate concentrations (mmol . L-1 of plasma or cell water) were determined at rest, during exercise, and at 15-min post-exercise. The results show that plasma and intraerythrocyte lactate concentrations were not significantly different from each other at rest or moderate (less than or equal to 50% VO2max) exercise. However, the plasma concentrations were significantly increased over the intraerythrocyte levels at 75% and 100% VO2max. The plasma to red cell lactate gradient reached a mean (+/- SE) 1.7 +/- 0.4 mmol . L-1 of H2O at exhaustion, and was linearly (r = 0.84) related to the plasma lactate concentration during exercise. Interestingly, at 15-min post-exercise the direction of the lactate gradient was reversed, with the mean intraerythrocyte concentration now being significantly increased over that found in the plasma. These results suggest that the erythrocyte membrane provides a barrier to the flux of lactate between plasma and red cells during rapidly changing blood lactate levels. Furthermore, these data add to the growing body of research that indicates that lactate is not evenly distributed in the various water compartments of the body during non-steady state exercise.
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PMID:Intraerythrocyte and plasma lactate concentrations during exercise in humans. 373 60

Heavy dynamic exercise using both arm and leg muscles was performed to exhaustion by seven well-trained subjects. The aerobic and anaerobic energy utilization was determined and/or calculated. O2 uptake during exercise and during 1 h of recovery was measured as well as splanchnic and muscle metabolite exchange. Glycogen and lactate content in the quadriceps femoris was determined before exercise, immediately after exercise, and after a recovery period. In four male subjects the estimated mean lactate production during exercise was 830 mmol. The splanchnic uptake of lactate during recovery was 80 mmol, and the calculated maximum amount oxidized during the recovery period was 330 mmol. About 60 mmol were accounted for in the body water at the end of the rest period. The remaining 360 mmol of lactate were apparently resynthesized into glycogen in muscle via gluconeogenesis. It is concluded that approximately 50% of the lactate formed during heavy exercise is transformed to glycogen via glyconeogenesis in muscle during recovery and that lactate uptake by the liver is only 10%.
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PMID:Disposal of lactate during and after strenuous exercise in humans. 373 22

We have recently reported that acute intraperitoneal administration of pyridostigmine bromide to rats resulted in significant decrements in physical performance in the heat, adverse thermoregulatory effects, and exacerbated elevations in several indices of heat/exercise injury. Since it will be consumed orally as a prophylaxis for organophosphate poisoning, pyridostigmine was dissolved in the drinking water of rats. Consumption of pyridostigmine for 7 days (n = 34, 6.6 mg/day) resulted in a 23% (p less than 0.001) reduction of circulating cholinesterase when compared with a control group (n = 31) while ingestion for 14 days (n = 35, 8.9 mg/day) elicited a 39% (p less than 0.001) inhibition of circulating cholinesterase when compared to a second control group (n = 33). Water and food consumption, rate of weight gain, and overt behavior were unaffected by pyridostigmine consumption. When approximately half the animals in each group were exercised (9.14 m/min) in the heat (35 degrees C) to hyperthermic exhaustion (Tre = 42.5-43 degrees C, rats unable to right themselves), pyridostigmine consumption for 14 days effected a significantly (p less than 0.05) increased rate of weight loss, but no further effects on thermoregulation or performance were noted. Several minor increments were observed in clinical indices of heat/exercise injury in rats consuming pyridostigmine for 14 days. These data indicate that oral dosages of pyridostigmine can probably be titrated to levels of cholinesterase inhibition which are efficacious in prophylaxis against organophosphate toxicity without significant effects on selected physiologic and metabolic processes.
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PMID:Oral pyridostigmine administration in rats: effects on thermoregulation, clinical chemistry, and performance in the heat. 378 59

Six subjects performed one-legged dynamic knee-extension. Blood samples were drawn from the femoral artery and vein, and muscle biopsies were obtained from the quadriceps muscle. Leg blood flow was measured by the thermodilution technique, and 3H-inulin was infused for determination of extra- and intracellular muscle water shifts. During the submaximal work load (S) muscle lactate increased, whereas muscle pH remained almost constant; after maximal exercise (M) the values markedly increased for lactate and decreased for pH. Except for a release of lactate from the exercising muscles, K was continuously released throughout S, and this release increased during M. Immediately when the muscles relaxed, the K release was converted to a K re-uptake. The calculated K loss, based on v- a and flow values, agreed with the decrease in muscle K content from 458 mmol/kg dw at rest to 414 mmol/kg dw at exhaustion (P less than 0.05), as analyzed on the muscle biopsies. Muscle water content increased during S mainly because of an increased extracellular H2O, whereas during M the largest increase occurred in intracellular H2O (H2Oi). Because of the simultaneous K loss and H2Oi increase in the exercising muscle the intracellular [K] was calculated to decrease from 165 mM at rest to 129 mM at exhaustion. This decrease and an increase in extracellular [K] from 4.5 mM at rest to greater than 6.0 mM at exhaustion affects the muscle membrane excitability. Muscle fatigue may thus not only be caused by changes within the cell, affecting energy metabolism or actin-myosin reaction, but may be located at the membrane protecting the cell against overload.
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PMID:Water and ion shifts in skeletal muscle of humans with intense dynamic knee extension. 397 Feb 34

A diuretic drug (40 mg of furosemide) was utilized to study the effects of dehydration (D) on competitive running performance, without prior thermal or exercise stress. Eight men competed in randomized races of 1,500, 5,000, and 10,000 m, while normally hydrated (H) and with mean plasma volume reductions of 9.9, 12.3, and 9.9%, respectively. As a result of the reduced body water (change in body weight = -1.9, -1.6, and -2.1%), mean outdoor performance times on a running track increased 0.16 min, 1.31 min (P less than 0.05), and 2.62 min (P less than 0.05) in the 1,500-m, 5,000-m, and 10,000-m trials. Running performance decrements due to dehydration were more strongly correlated with changes in body weight (r = -0.79, -0.65, and -0.40) than with urine volume or plasma volume differences. In addition, subjects were studied during submaximal and maximal treadmill exercise while H and D (mean change in plasma volume = -7.1%). Neither submaximal nor maximal oxygen uptake was significantly altered (P greater than 0.05) as a consequence of D. Mean treadmill run time to volitional exhaustion was reduced by 41.4 s (P less than 0.05) during the D treadmill trial. Therefore, it appears that competitive performance in trials of long duration (5,000 and 10,000 m) was affected to a greater extent by D than the shorter 1,500-m event, even though submaximal and maximal oxygen uptake was not altered.
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PMID:Influence of diuretic-induced dehydration on competitive running performance. 403 1

Nine men were studied during three 4-h cycling bouts to determine the effect of frequency and dosage of solid carbohydrate (CHO) feedings (86 g) on muscle glycogen utilization and exercise performance. In the frequency trial (F), the subjects ingested 10.75 g of CHO along with 200 ml of water at 30-min intervals; in the dosage trial (D), the subjects ingested 21.5 g of CHO with 400 ml of water at 60-min intervals. During the control trial (C), the subjects ingested 400 ml of an artificially sweetened placebo at 60-min intervals. Respiratory exchange ratios were significantly elevated in both trials D and F (P less than 0.05). Blood glucose was significantly elevated in trial D 20 min post-feeding but had returned to control levels by 50 min. In trial F, blood glucose was maintained at a constant level throughout the entire 4 h. In trial C, blood glucose declined steadily during the entire 4 h. Despite the differences in blood glucose levels between the three trials, there were no significant differences in the rate of muscle glycogen utilization in any of the trials (D = 82.9 +/- 6.6 [SE] mmol X kg-1 vs C = 80.9 +/- 6.9 mmol X kg-1 vs F = 74.4 +/- 12.2 mmol X kg-1). In a sprint ride (100% VO2max) to exhaustion at the end of each trial, the subjects performed significantly longer in trial F compared to C (120.97 +/- 9.6 vs 81.0 +/- 7.1 s).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of carbohydrate feeding frequencies and dosage on muscle glycogen use during exercise. 403 4

The kinetics underlying plasma epinephrine concentrations were studied. Six athletes (T) and six sedentary males (C) were given intravenous infusions of 3H-labeled epinephrine, after which arterial blood was drawn. They rested sitting and bicycled continuously to exhaustion (60 min at 125 W, 60 min at 160 W, 40 min at 200 W, and 240 W to the end). Work time was 154 +/- 13 (SE) (T) and 75 +/- 6 (C) min. At rest, epinephrine clearance was identical [28.4 +/- 1.3 (T) vs. 29.2 +/- 1.8 (C) ml . kg-1 . min-1], but plasma concentration [1.42 +/- 0.27 (T) vs. 0.71 +/- 0.16 (C) nmol . l-1] and, accordingly, secretion [2.9 +/- 0.7 vs. 1.5 +/- 0.4 nmol . min-1] were higher (P less than 0.05) in T than C subjects. Epinephrine clearance was closely related to relative work load, decreasing from 15% above the basal level at 30% of maximal O2 uptake (VO2 max) to 22% below at 76% of VO2 max. Epinephrine concentrations increased much more with work intensity than could be accounted for by changes in clearance and were, at exhaustion, higher (P less than 0.05) in T (7.2 +/- 1.6) than in C (2.5 +/- 0.7 nmol . l-1) subjects despite similar glucose, heart rate, and hematocrit values. At a given load, epinephrine clearance rapidly became constant, whereas concentration increased continuously. Forearm extraction of epinephrine invalidated use of blood from a cubital vein or a hand vein arterialized by hot water in turnover measurements. During exercise, changes in epinephrine concentrations reflect changes in secretion rather than in clearance. Training may increase adrenal medullary secretory capacity.
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PMID:Effect of exercise on epinephrine turnover in trained and untrained male subjects. 405 86

Fatigue till exhaustion and renunciation was caused in rats through forced loaded swimming performance. Changes in watersoluble protein, in its fractions separated by means of disk electrophoresis, as well as in the fractions of lactic dehydrogenase and non-specific esterases were searched for in the different organs. Insofar water-soluble protein is concerned, a statistically reliable increase was found in the liver and heart chamber musculature, and reduction - in the skeletal muscles. Changes in the brain and kidney were not recorded. Large protein fraction ammassments were observed in all the organs which interfered with the interpretation of electrophoregrams. Nevertheless, clear-cut changes after exertion were not disclosed. The isoenzymes of lactic dehydrogenase did not reveal alterations in the organs investigated after physical effort. A loss of non-specific esterase fractions at electrophoretic range from 0.4 to 0.6 was established in the liver of tired animals only.
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PMID:[The effect of acute fatigue on organ proteins and protein fractions]. 480 17

The number of reports concerning the chemical toxicology of metals which are released in the environment by natural as well as anthropogenic sources, have been increasing constantly. Lead, cadmium, and manganese have found a variety of uses in industry, craft, and agriculture owing to their physical and chemical properties. The environmental burden of heavy metals has been rising substantially by smelter emission in air and waste sewage in water. Further, organic compounds of lead and manganese used as antiknock substances in gasoline are emitted into the atmosphere by automobile exhaustion. Such environmental contamination of air, water, soil, and food is a serious threat to all living kinds. Although these metals are known to produce their toxic effects on a variety of body systems, much emphasis has been placed on their effects on the nervous system owing to apparent association of relatively low or "subclinical" levels of metallic exposure with behavioral and psychological disorders. Clinical and animal data on environmental exposure show that while lead and manganese are most toxic to the nervous system, cadmium exerts profound adverse effects on kidney and the male reproductive system. It appears that the consequences of exposure to lead in adults are less severe than the types of exposure associated with hyperactivity in neonates. Except for a few reports, hyperactivity has indeed been observed in animals exposed to either of these three metals. Experimental work has also shown that these metals produce behavioral changes by altering the metabolism of brain neurotransmitters, especially catecholamines. Recently, it is hypothesized that these metals exert their toxic effect by damaging biological defences which exist in the body to serve as protective mechanisms against exogenous toxins. A voluminous publication list with diverse opinions on the biological effects of metals is available and there is an urgent need to compile assessment of the existing literature to identify the future theme of research work. The problem of metal toxicity becomes even more complex owing to simultaneous or successive exposure of the general population to different physical, chemical, biological, and psychological factors in the environment. The net toxic manifestations produced by multiple exposure should, therefore, be different from those produced by a single factor as the result of their additive, synergistic or antagonistic action. Even though a metal may not exist in sufficient amounts to cause any disability, the toxicity could result when a second factor is also present.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The present status of biological effects of toxic metals in the environment: lead, cadmium, and manganese. 614 4


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