Operation Everest III: role of plasma volume expansion on VO(2)(max) during prolonged high-altitude exposure.
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We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O(2) uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively. VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery of VO(2)(max). (+info)
Influence of cholesterol status on blood lipid and lipoprotein enzyme responses to aerobic exercise.
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To compare postexercise changes in plasma lipids and lipoprotein enzymes in 13 hypercholesterolemic (HC) and 12 normocholesterolemic men [total cholesterol (TC) 252 +/- 5 vs. 179 +/- 5 mg/dl], fasting blood samples were obtained 24 h before, immediately, 24, and 48 h after a single bout of treadmill walking (70% peak O(2) consumption, 500 kcal expenditure). Significant findings (P < 0.05 for all) for plasma volume-adjusted lipid and enzyme variables were that TC, low-density-lipoprotein cholesterol, and cholesterol ester transfer protein activity were higher in the HC group but did not influence the lipid responses to exercise. Across groups, TC was transiently reduced immediately after exercise but returned to baseline levels by 24 h postexercise. Decreases in triglyceride and increases in high-density-lipoprotein cholesterol (HDL-C) and HDL(3)-C were observed 24 h after exercise and lasted through 48 h. Lipoprotein lipase activity was elevated by 24 h and remained elevated 48 h after exercise. HDL(2)-C, cholesterol ester transfer protein activity, hepatic triglyceride lipase, and lecithin: cholesterol acyltransferase activities did not change after exercise. These data indicate that the exercise-induced changes in HDL-C and triglyceride are similar in HC and normocholesterolemic men and may be mediated, at least in part, by an increase in lipoprotein lipase activity. (+info)
High dose angiotensin-converting enzyme inhibition prevents fluid volume expansion in heart transplant recipients.
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OBJECTIVES: We sought to test the hypothesis that plasma volume (PV) expansion in heart transplant recipients (HTRs) is caused by failure to reflexively suppress the renin-angiotensin-aldosterone (RAA) axis. BACKGROUND: Extracellular fluid volume expansion occurs in clinically stable HTRs who become hypertensive. We have previously demonstrated that the RAA axis is not reflexively suppressed by a hypervolemic stimulus in HTRs. METHODS: Plasma volume and fluid regulatory hormones were measured in eight HTRs (57+/-6 years old) both before and after treatment with captopril (225 mg/day). Antihypertensive and diuretic agents were discontinued 10 days before. The HTRs were admitted to the Clinical Research Center (CRC), and, after three days of a constant diet containing 87 mEq/day of Na+, PV was measured by using the modified Evans blue dye dilution technique. After approximately four months (16+/-5 weeks), the same HTRs again discontinued all antihypertensive and diuretic agents; they were progressed to a captopril dose of 75 mg three times per day over 14 days, and the CRC protocol was repeated. RESULTS: Captopril pharmacologically suppressed (p<0.05) supine rest levels of angiotensin II (-65%) and aldosterone (-75%). The reductions in vasopressin and atrial natriuretic peptide levels after captopril did not reach statistical significance. The PV, normalized for body weight (ml/kg), was significantly reduced by 12% when the HTRs received captopril. CONCLUSIONS: Extracellular fluid volume is expanded (12%) in clinically stable HTRs who become hypertensive. Pharmacologic suppression of the RAA axis with high-dose captopril (225 mg/day) returned HTRs to a normovolemic state. These findings indicate that fluid retention is partly engendered by a failure to reflexively suppress the RAA axis when HTRs become hypervolemic. (+info)
Procainamide and phenytoin. Comparative study of their antiarrhythmic effects at apparent therapeutic plasma levels.
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The antiarrhythmic effects of procainamide and phenytoin were studied in 81 patients admitted to the coronary care unit at the University Hospital in Linkoping because of a suspected or proven diagnosis of acute myocardial infarction, and who developed ventricular arrhyhmias, requiring treatment, during the first 8 hours in hospital. Patients were randomly allocated to a procainamide of phenytoin group. The drugs were given as intravenous and oral loading doses followed by oral maintenance therapy. Plasma levels of the two druge were frequently determined and the electrocardiogram was continuously recorded during the 24-hour trial and analysed minute by minute. A significantly higher frequency of therapeutic failure was found in the phenytoin group (23 of 35 patients)compared to the procainamide group(13 of 39 aptients) during the first 2 hours after initiation of therapy. Four patients in the phenytoin group and 2 in the procainamide group developed symptoms probably caused by the trial drugs, necessitating discontinuation of therapy. The mean plasma levels were usually within the apparent therapeutic range (for phenytoin 40-72 mumol/l (10-18 mug/ml), and for procainamide 17-34 mumol/l (4-8 mug/ml). Seventeen patients (68%) in the phenytoin group and 10 patients (48%) in the procainamide group had plasma concentrations within this range when the therapeutic failure was observed. Nine patients died in hospital but only one of them during the trial. The results of this investigation clearly demonstrate the overall superiority of procainamide over phenytoin as an antiarrhythmic drug in short-term therapy after acute myocardial infarction. (+info)
Left ventricular diastolic filling and cardiovascular functional capacity in older men.
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We investigated anaerobic threshold (< theta(L)) gas exchange kinetics and maximal oxygen uptake (VO2,max) among older men with reduced left ventricular end-diastolic filling (LVDF). Ten men (mean age, 73 years) with LVDF impairment and low fitness, but without other cardiovascular dysfunction were studied. Treatments compared to control included: 5 days, high intensity exercise training protocol; 5 days, calcium channel blockade (240 mg verapamil); 21 days, detraining/washout; and 5 days, combined treatments. Results indicated no changes in resting left ventricular systolic function with any treatment. Significant resting diastolic function changes included increased early:late flow velocity (control, 0.87; training, 1.28; verapamil, 1.32), and a decreased isovolumic relaxation time (control, 0.10 s; training, 0.08 s; verapamil, 0.08 s). The combined treatments were not additive. Sub-threshold oxygen uptake kinetics (tauVO2, s) were significantly faster following either training or verapamil (tauVO2,control, 62+/-12; tauVO2,training, 44+/-9; tauVO2,verapamil, 48+/-10) and combined treatments (tauVO2, 41+/- 8). V O2,max (ml kg(-1) min(-1)) was significantly increased (control, 21.8+/-2.2; training, 27.3+/-2.2; verapamil, 25.2+/-3.4; combined treatments, 26.9+/-2.3). Increasing ventricular preload with either exercise training or calcium channel blockade was coincident with faster tauVO2 and increased VO2,max. (+info)
Effect of carbohydrate ingestion on glucose kinetics and muscle metabolism during intense endurance exercise.
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There has been recent interest in the potential performance and metabolic effects of carbohydrate ingestion during exercise lasting approximately 1 h. In this study, 13 well-trained men ingested in randomized order either a 6% glucose solution (CHO trial) or a placebo (Con trial) during exercise to exhaustion at 83+/-1% peak oxygen uptake. In six subjects, vastus lateralis muscle was sampled at rest, at 32 min, and at exhaustion, and in six subjects, glucose kinetics was determined by infusion of [6,6-(2)H]glucose in both trials and ingestion of [6-(3)H]glucose in the CHO trial. Of the 84 g of glucose ingested during exercise in the CHO trial, only 22 g appeared in the peripheral circulation. This resulted in a small (12 g) but significant (P<0.05) increase in glucose uptake without influencing carbohydrate oxidation, muscle glycogen use, or time to exhaustion (CHO: 68.1+/-4.1 min; Con: 69.6+/-5.5 min). Decreases in muscle phosphocreatine content and increases in muscle inosine monophosphate and lactate content during exercise were similar in the two trials. Although endogenous glucose production during exercise was partially suppressed in the CHO trial, it remained significantly above preexercise levels throughout exercise. In conclusion, only 26% of the ingested glucose appeared in the peripheral circulation. Glucose ingestion increased glucose uptake and partially reduced endogenous glucose production but had no effect on carbohydrate oxidation, muscle metabolism, or time to exhaustion during exercise at 83% peak oxygen uptake. (+info)
Renal responsiveness to aldosterone during exposure to simulated microgravity.
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We measured renal functions and hormones associated with fluid regulation after a bolus injection of aldosterone (Ald) during head-down tilt (HDT) bed rest to test the hypothesis that exposure to simulated microgravity altered renal responsiveness to Ald. Six male rhesus monkeys underwent two experimental conditions (HDT and control, 72 h each) with each condition separated by 9 days of ambulatory activities to produce a crossover counterbalance design. One test condition was continuous exposure to 10 degrees HDT; the second was a control, defined as 16 h per day of 80 degrees head-up tilt and 8 h prone. After 72 h of exposure to either test condition, monkeys were moved to the prone position, and we measured the following parameters for 4 h after injection of 1-mg dose of Ald: urine volume rate (UVR); renal Na(+)/K(+) excretion ratio; renal clearances of creatinine, Na(+), osmolality, and free water; and circulating hormones [Ald, renin activity (PRA), vasopressin (AVP), and atrial natriuretic peptide (ANP)]. HDT increased Na(+) clearance, total renal Na(+) excretion, urine Na(+) concentration, and fractional Na(+) excretion, compared with the control condition, but did not alter plasma concentrations of Ald, PRA, and AVP. Administration of Ald did not alter UVR, creatinine clearance, Ald, PRA, AVP, or ANP but reduced Na(+) clearance, total renal Na(+) excretion, urinary Na(+)/K(+) ratio, and osmotic clearance. Although reductions in Na(+) clearance and excretion due to Ald were greater during HDT than during control, the differential (i.e., interaction) effect was minimal between experimental conditions. Our data suggest that exposure to microgravity increases renal excretion of Na(+) by a natriuretic mechanism other than a change in renal responsiveness to Ald. (+info)
Prolonged exercise after diuretic-induced hypohydration: effects on substrate turnover and oxidation.
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To determine the influence of a diuretic-induced reduction in plasma volume (PV) on substrate turnover and oxidation, 10 healthy young males were studied during 60 min of cycling exercise at 61% peak oxygen uptake on two separate occasions > or =1 wk apart. Exercise was performed under control conditions (CON; placebo), and after 4 days of diuretic administration (DIU; Novotriamazide; 100 mg triamterene and 50 mg hydrochlorothiazide). DIU resulted in a calculated reduction of PV by 14.6 +/- 3.3% (P < 0.05). Rates of glucose appearance (R(a)) and disappearance (R(d)) and glycerol R(a) were determined by using primed constant infusions of [6,6-(2)H]glucose and [(2)H(5)]glycerol, respectively. No differences in oxygen uptake during exercise were observed between trials. Main effects for condition (P < 0.05) were observed for plasma glucose and glycerol, such that the values observed for DIU were higher than for CON. No differences were observed in plasma lactate and serum free fatty acid concentrations either at rest or during exercise. Hypohydration led to lower (P < 0.05) glucose R(a) and R(d) at rest and at 15 and 30 min of exercise, but by 60 min, the effects were reversed (P < 0. 05). Hypohydration had no effect on rates of whole body lipolysis or total carbohydrate or fat oxidation. A main effect for condition (P < 0.05) was observed for plasma glucagon concentrations such that larger values were observed for DIU than for CON. A similar decline in plasma insulin occurred with exercise in both conditions. These results indicate that diuretic-induced reductions in PV decreases glucose kinetics during moderate-intensity dynamic exercise in the absence of changes in total carbohydrate and fat oxidation. The specific effect on glucose kinetics depends on the duration of the exercise. (+info)