Transcapillary fluid responses to lower body negative pressure

The effect of lower body negative pressure (LBNP) on transcapillary fluid balance is unknown. Therefore, our objective was to assess leg interstitial fluid pressures (IFP), leg circumference, plasma volume (PV), and net whole body transcapillary fluid transport (TFT) during and after supine LBNP and to evaluate the addition of oral saline ingestion on transcapillary exchange. Six healthy men 23-41 yr old underwent 4 h of 30 mmHg LBNP, followed by 50 min of supine recovery on two separate occasions, once with and once without ingestion of 1 liter of isotonic saline. IFP was measured continuously in subcutis as well as superficial and deep regions of the tibialis anterior muscle by slit catheters. TFT was calculated by subtracting urine production and calculated insensible fluid loss from changes in PV. During exposure to LBNP, IFP decreased in parallel with chamber pressure, foot venous pressure did not change, leg circumference increased by 3 +/- 0.35% (SE) (P < 0.05), and PV decreased by 14 +/- 2.3%. IFP returned to near control levels after LBNP. At the end of minute 50 of recovery, PV remained decreased (by 7.5 +/- 5.2%) and leg circumference remained elevated (by 1 +/- 0.37%). LBNP alone produced significant movement of fluid into the lower body but no net TFT (-7 +/- 12 ml/h). During LBNP with saline ingestion, 72 +/- 4% of the ingested fluid volume filtered out of the vascular space (TFT = 145 +/- 10 ml/h), and PV decreased by 6 +/- 3%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Albuminuria and overall capillary permeability of albumin in acute altitude hypoxia

The mechanism of proteinuria at high altitude is unclear. Renal function and urinary excretion rate of albumin (Ualb) at rest and during submaximal exercise and transcapillary escape rate of 125I-labeled albumin (TERalb) were investigated in 12 normal volunteers at sea level and after rapid and passive ascent to 4,350 m. The calcium antagonist isradipine (5 mg/day; n = 6) or placebo (n = 6) was administered to abolish hypoxia-induced rises in blood pressure. Lithium clearance and urinary excretion of beta 2-microglobulin were used to evaluate renal tubular function. High altitude increased Ualb from 2.8 to > 5.0 micrograms/min in both groups (P < 0.05). In the placebo group, high altitude significantly increased filtration fraction (P < 0.05), but this response was abolished by isradipine. Lithium clearance and urinary excretion of beta 2-microglobulin remained unchanged by hypoxia in both groups. Exercise did not reveal any further renal dysfunction. In both groups, high altitude increased TERalb from 4.8 to > 6.7%/h (P < 0.05). In conclusion, acute altitude hypoxia increases Ualb despite unchanged tubular function and independent of effects of isradipine on filtration fraction. The elevated TERalb suggests an overall increase in capillary permeability, including the glomerular endothelium, as the critical factor in high-altitude induced albuminuria.     

Coexistence of both oleosin isoforms on the surface of seed oil bodies and their individual stabilization to the organelles

Increased urine albumin is associated with atherosclerotic disease and predicts cardiovascular morbidity and mortality in nondiabetic populations. This finding is frequently postulated to reflect the impact of atherosclerotic damage on glomerular and systemic capillary permeability, an interesting but as yet untested hypothesis. The transcapillary escape rate of albumin (TERalb, the 1-hour decline rate of intravenous 125I-albumin, a measure of capillary macromolecular permeability), albuminuria, lipid levels, echocardiographic wall thickness, and insulin responses to oral glucose were measured in 30 untreated dipstick-negative lean men and clinically stable atherosclerotic peripheral vascular disease; tolerance to oral glucose was a requirement for inclusion in the study. Because hypertension per se might influence TERalb, the sample included either normotensive (n=18, 118+/-6/72+/-7 mm Hg) or hypertensive (n=12, 141+/-7/84+/-6 mmHg by 24-hour blood pressure monitoring) arteriopathic patients; 11 normal age- and gender-matched subjects (121+/-7/76+/-5 mmHg) were used as control subjects. TERalb was higher in patients (10.7+/-3.2 versus 7.4+/-1.7%/h, P<0.013), a difference that persisted after postload glucose, insulin, and lipid levels were accounted for by covariance analysis; atherosclerosis and hypertension together did not further impair vascular permeation to albumin. In contrast with TERalb, albuminuria was elevated only in the hypertensive subgroup; the 2 variables showed no relationship, even when the data were analyzed separately in normotensive and hypertensive subgroups. Urine albumin correlated positively with 24-hour blood pressure and wall thickness. Thus, systemic capillary permeability is altered in nondiabetic atherosclerotic patients independently from blood pressure levels, but this abnormality is not reflected by proportionate changes in albuminuria.     

Cold and warm infusion of Ringer's acetate in healthy volunteers: the effects on haemodynamic parameters, transcapillary fluid balance, diuresis and atrial peptides

The effects of Ringer's acetate (RAc) infusion with different temperatures, 18 degrees C compared to 36 degrees C, were studied in 20 healthy volunteers. An infusion volume of 20% of the estimated extracellular volume was given over 45 min. Before and after the RAc infusion, interstitial colloid osmotic pressure and interstitial fluid hydrostatic pressure were measured on the lateral part of the thorax and in the lower leg. Blood sampling and pressure measurements were performed through a cannula placed in the left radial artery, and arterial oxygen saturation was measured by pulse oximetry. Atrial peptides ANF (99-126) and ANF (1-98) in plasma were measured as indicators of volume loading. Cold RAc infusion increased mean arterial pressure from 82 (s.d. +/- 7) to 96 (s.d. +/- 9) mmHg (10.9-12.8 kPa) at the end of the infusion with a simultaneous fall in heart rate. Warm RAc infusion gave no changes in blood pressure or heart rate. The arterial oxygen saturation during the infusion of cold RAc was higher than during warm RAc infusion. Cold infusion produced the expected haemodilution with a fall in erythrocyte volume fraction (EVF) from 0.39 (+/- 0.03) to 0.33 (+/- 0.03) and a fall in plasma colloid osmotic pressure (COPp) from 21.7 (+/- 1.1) mmHg to 15.0 (+/- 1.3) mmHg (2.9-2.0 kPa). Warm infusion induced a nearly identical haemodilution. Interstitial colloid osmotic pressure fell from 11.6 (+/- 2.3) mmHg to 8.9 (+/- 2.7) mmHg (1.5-1.2 kPa) after warm infusion while cold infusion gave no changes. The changes in interstitial fluid hydrostatic pressure were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Visual system maldevelopment disrupts extraocular muscle-specific myosin expression

We measured hepatic albumin synthesis in five volunteers (4 men and 1 woman) at 3 and 6 h after recovery from intense exercise. A primed-constant infusion of a stable isotopic tracer of phenylalanine was used to determine hepatic fractional synthetic rate (FSR) and absolute synthetic rate (ASR) of albumin from the enrichment of phenylalanine in albumin. The infusion of the stable isotope tracer began 2 h after upright exercise or upright rest. Albumin FSR and ASR were 6.39 +/- 0.48%/day and 120 +/- 9 mg.kg body wt-1.day-1, respectively, 3-6 h after recovery from exercise; the FSR and ASR on the time control study day were 5.94 +/- 0.47%/day and 104 +/- 9 mg.kg body wt-1.day-1, respectively. The 6 and 16% increases (P < 0.05) in FSR and ASR after exercise were associated with an elevated plasma albumin content at 5 and 6 h of recovery (P < 0.05), an increased total protein content throughout recovery (P < 0.05), and a negative free water clearance (P < 0.05) at 2, 3, and 6.5 h of recovery compared with baseline values; these variables were unchanged from their baselines on the time control study day. Increased albumin content and reduced free water clearance contribute to a retention of fluid within the circulation after intense exercise. The measured increase in albumin synthesis could not account for the entire increase in albumin content at 6 h of recovery from exercise. However, we estimate that if the increased activity was maintained for the next 18 h, it could account for the expected increase in albumin content at 24 h of recovery.     

Effect of glucose supplement timing on protein metabolism after resistance training

We determined the effect of the timing of glucose supplementation on fractional muscle protein synthetic rate (FSR), urinary urea excretion, and whole body and myofibrillar protein degradation after resistance exercise. Eight healthy men performed unilateral knee extensor exercise (8 sets/approximately 10 repetitions/approximately 85% of 1 single maximal repetition). They received a carbohydrate (CHO) supplement (1 g/kg) or placebo (Pl) immediately (t = 0 h) and 1 h (t = +1 h) postexercise. FSR was determined for exercised (Ex) and control (Con) limbs by incremental L-[1-13C]leucine enrichment into the vastus lateralis over approximately 10 h postexercise. Insulin was greater (P < 0.01) at 0.5, 0.75, 1.25, 1.5, 1.75, and 2 h, and glucose was greater (P < 0.05) at 0.5 and 0.75 h for CHO compared with Pl condition. FSR was 36.1% greater in the CHO/Ex leg than in the CHO/Con leg (P = not significant) and 6.3% greater in the Pl/Ex leg than in the Pl/Con leg (P = not significant). 3-Methylhistidine excretion was lower in the CHO (110.43 +/- 3.62 mumol/g creatinine) than P1 condition (120.14 +/- 5.82, P < 0.05) as was urinary urea nitrogen (8.60 +/- 0.66 vs. 12.28 +/- 1.84 g/g creatinine, P < 0.05). This suggests that CHO supplementation (1 g/kg) immediately and 1 h after resistance exercise can decrease myofibrillar protein breakdown and urinary urea excretion, resulting in a more positive body protein balance.     

Gene therapy with bilirubin-UDP-glucuronosyltransferase in the Gunn rat model of Crigler-Najjar syndrome type 1

PURPOSE: The purpose of this study was to investigate the relationship between training-induced alterations in plasma volume (PV) and changes in fluid and electrolyte regulatory hormones during prolonged exercise. METHODS: Seven male subjects (VO2peak 49.2 +/- 2.4 mL.kg-1.min-1, X +/- SE) performed a cycling test before (C) and after (T) 6 d of training and after 6 d of detraining (DT). Training was conducted for 2 h.d-1 at 68% VO2peak at a room temperature between 26-28 degrees C. The 60-min exercise challenge included 20 min at 50%, 65%, and 75% VO2peak workloads. RESULTS: Training resulted in a calculated 13.8 +/- 1.6% PV expansion (P < 0.05) which recovered to C levels with DT (1.8 +/- 2.3%, P > 0.05). Compared with that at C, training resulted in a reduction of aldosterone (ALDO) concentration at all exercise intensities (P < 0.05) which normalized to C levels with DT. With T, epinephrine (EPI) concentrations were reduced at the highest power output only (365 +/- 51 vs 113 +/- 22 pg.mL-1; P < 0.05) and returned to C levels with DT. Arginine vasopressin (AVP) concentrations were also reduced at the highest workload only (20.2 +/- 3.2 pg.mL-1 vs 10.4 +/- 0.7 pg.mL-1; P < 0.05) and remained depressed after DT (11.8 +/- 1.3 pg.mL-1; P < 0.05). Atrial natriuretic factor (ANF) and norepinephrine (NOREPI) were not affected by T or DT. CONCLUSIONS: The results suggest that concentrations of ALDO, and to a lesser extent EPI, during exercise are related to PV levels, whereas ANF and NOREPI concentrations are not. AVP concentrations are related to other adaptive factors, the effects of which persist for a longer time course than do PV changes.     

Hypohydration effects on skeletal muscle performance and metabolism: a 31P-MRS study

The purpose of this study was to determine whether hypohydration reduces skeletal muscle endurance and whether increased H+ and Pi might contribute to performance degradation. Ten physically active volunteers (age 21-40 yr) performed supine single-leg, knee-extension exercise to exhaustion in a 1.5-T whole body magnetic resonance spectroscopy (MRS) system when euhydrated and when hypohydrated (4% body wt). 31P spectra were collected at a rate of one per second at rest, exercise, and recovery, and were grouped and averaged to represent 10-s intervals. The desired hydration level was achieved by having the subjects perform 2-3 h of exercise in a warm room (40 degrees C dry bulb, 20% relative humidity) with or without fluid replacement 3-8 h before the experiment. Time to fatigue was reduced (P < 0.05) by 15% when the subjects were hypohydrated [213 +/- 12 vs. 251 +/- 15 (SE) s]. Muscle strength was generally not affected by hypohydration. Muscle pH and Pi/beta-ATP ratio were similar during exercise and at exhaustion, regardless of hydration state. The time constants for phosphocreatine recovery were also similar between trials. In summary, moderate hypohydration reduces muscle endurance, and neither H+ nor Pi concentration appears to be related to these reductions.     

Effect of fluid ingestion on muscle metabolism during prolonged exercise

Five trained men were studied during 2 h of cycling exercise at 67% peak oxygen uptake at 20-22 degrees C to examine the effect of fluid ingestion on muscle metabolism. On one occasion, the subjects completed this exercise without fluid ingestion (NF) while on the other they ingested a volume of distilled deionized water that prevented loss of body mass (FR). No differences in oxygen uptake during exercise were observed between the two trials. Heart rate was lower (P < 0.01) throughout exercise when fluid was ingested, and rectal temperature after 2 h of exercise was lower (38.0 +/- 0.2 and 38.6 +/- 0.2 degrees C for FR and NF, respectively; P < 0.01), as was muscle (vastus lateralis) temperature (38.5 +/- 0.4 and 39.1 +/- 0.5 degrees C for FR and NF, respectively; P < 0.05). Resting muscle ATP, creatine phosphate, creatine, glycogen, and lactate levels were similar in the two trials, as were the postexercise ATP, creatine phosphate, and creatine levels. In contrast, muscle glycogen was higher (P < 0.05) and muscle lactate was lower (P < 0.05) after 2 h of exercise in FR compared with NF. Net muscle glycogen utilization during exercise was reduced by 16% when fluid was ingested (318 +/- 46 and 380 +/- 53 mmol/kg dry weight for FR and NF, respectively; P < 0.05). These results indicate that fluid ingestion reduces muscle glycogen use during prolonged exercise, which may account, in part, for the improved performance previously observed with fluid ingestion.     

Effects of a single bout of exercise on glucose effectiveness

The effects of a single bout of exercise on glucose effectiveness (SG) and insulin sensitivity (SI) in 22 sedentary subjects were estimated with a minimal model approach. The intravenous glucose tolerance test (IVGTT) was performed 1) 11 h after an exercise bout on a cycle ergometer at the lactate threshold level (mild exercise) for 60 min, 2) 11 h after an exercise bout at the 4 mM lactate level (hard exercise) for 36 +/- 1 min, 3) 11 h after an exhaustive-exercise bout (exhaustive exercise) for 96 +/- 7 min, or 4) without any prior exercise (control). Only the exhaustive exercise increased the glucose disappearance constant (2.69 +/- 0.28 vs. 2.05 +/- 0.13%/min; P < 0.05) and SI (15.0 +/- 2.0 vs. 10.3 +/- 0.9 x 10(-5) min/pM: P < 0.05) in comparison with the control condition. The SG and SG at zero insulin (GEZI) were not affected by any exercise condition. However, a marked individual difference in GEZI emerged after the exhaustive exercise and could be divided into two subgroups: one decreased in GEZI (0.014 +/- 0.001 vs. 0.007 +/- 0.001 min-1) and the other increased in GEZI (0.014 +/- 0.001 vs. 0.021 +/- 0.003 min-1). The former subgroup was accompanied by elevated levels of plasma creatine kinase (100 +/- 16 vs. 598 +/- 315 IU/l; P < 0.05) and myoglobin (Mb; 46 +/- 4 vs. 126 +/- 47 ng/ml; P < 0.05), whereas the latter subgroup showed no significant change in creatinine kinase (99 +/- 10 vs. 128 +/- 9 IU/l; P > 0.05) and Mb (50 +/- 7 vs. 51 +/- 4 ng/ml; P > 0.05). In both subgroups, SI was similarly increased after the exhaustive exercise. These results thus suggest that a single bout of exercise that results in muscle damage or changes in muscle permeability, as reflected in the increased creatine kinase and Mb levels, decreases GEZI, whereas exhaustive exercise without such alterations increases GEZI.     

Fluid and electrolyte hormonal responses to exercise and acute plasma volume expansion

To investigate the effect of acute graded increases in plasma volume (PV) on fluid and regulatory hormone levels, eight untrained men (peak aerobic power 45.2 +/- 2.2 ml.kg-1.min-1) performed prolonged cycle exercise (46 +/- 4% maximal aerobic power on three occasions, namely, with no PV expansion (Con) and after 14% (Low) and 21% (High) expansions, respectively. The exercise plasma levels of aldosterone (Aldo), arginine vasopressin (AVP), and atrial natriuretic peptide (ANP) were all altered by acute PV increases. A pronounced blunting (P < 0.05) of the Aldo response during exercise was observed, the magnitude of which was directly related to the amount of hypervolemia (Con < Low < High). At 120 min of exercise, Aldo concentrations were 660 +/- 71, 490 +/- 85, and 365 +/- 78 pg/ml for Con, Low, and High conditions, respectively. In contrast, the lower AVP and the higher ANP observed during exercise appeared to be due to the effect of PV expansion on resting concentrations. Because osmolality did not vary among conditions, the results indicate that PV represents an important primary stimulus in the response of Aldo to exercise. The lower exercise blood concentrations of both epinephrine and norepinephrine observed with PV expansion would suggest that a lower sympathetic drive may be implicated at least in the lower Aldo responses.     

Hypervolemia in men from fluid ingestion at rest and during exercise

BACKGROUND: Plasma osmolality (Osm) is important for controlling and maintaining plasma volume (PV) and body water. The effect of oral rehydration fluids for ameliorating dehydration is well-established; but optimal composition and Osm of fluids for hyperhydrating normally hydrated subjects is less clear. METHODS: Six treatments were used without and with oral fluids of varying ionic and constituent concentrations for hyperhydrating six previously euhydrated men (30 +/- SD 8 yr, 76.84 +/- 16.19 kg, 73 +/- 12 ml.kg-1 PV, 40 +/- 10 ml.min-1.kg-1 peak VO2) sitting at rest for 90 min (VO2 = 0.39 +/- SE 0.02 L.min-1) and during subsequent 70 min of submaximal exercise (VO2 = 2.08 +/- SE 0.33 L.min-1, 70 +/- 7% peak VO2). The hypothesis was that the fluid composition is more important than plasma Osm for increasing PV in euhydrated subjects at rest and maintaining it during exercise. Drink formulation compositions, given at 10 ml.kg-1 body wt, (mean = 768 ml), for the sitting period were: Performance 1 (P1; 55 mEq Na+, 365 mOsm.kg H2O-1), P2 (97 mEq Na+, 791 mOsm.kg-1), P2G (113 mEq Na+, 4% glycerol, 1382 mOsm.kg-1), AstroAde (AA; 164 mEq Na+, 253 mOsm.kg-1), and 01 and 02 (no drinking). The exercise drink (10 ml.kg-1, 768 ml) was P1 for all treatments except 02 (no drinking); thus, drink designations were: P1/P1, P2/P1, P2G/P1, AA/P1, 0/P1, and 0/0. RESULTS: PV at rest increased (p < 0.05) by 4.7% with P1 and by 7.9% with AA. Percent change in PV during exercise was +1% to +3% (NS) with AA/P1; -6% to 0% (NS) with P1/P1, P2/P1, P2G/P1, and 0/P1; and -8% to -5% (p < 0.05) with 0/0. AA, with the lowest Osm of 253 mOsm.kg-1, increased PV at rest (as did P1) and maintained it during exercise, whereas the other drinks with lower Na+ and higher Osm of 365-1382 mOsm.kg-1 did not. CONCLUSION: Drink composition appears to be more important than its Osm for increasing PV at rest and for maintaining it during exercise in previously euhydrated subjects.     

Muscle quality. II. Effects Of strength training in 65- to 75-yr-old men and women

To determine the effects of strength training (ST) on muscle quality (MQ, strength/muscle volume of the trained muscle group), 12 healthy older men (69 +/- 3 yr, range 65-75 yr) and 11 healthy older women (68 +/- 3 yr, range 65-73 yr) were studied before and after a unilateral leg ST program. After a warm-up set, four sets of heavy-resistance knee extensor ST exercise were performed 3 days/wk for 9 wk on the Keiser K-300 leg extension machine. The men exhibited greater absolute increases in the knee extension one-repetition maximum (1-RM) strength test (75 +/- 2 and 94 +/- 3 kg before and after training, respectively) and in quadriceps muscle volume measured by magnetic resonance imaging (1,753 +/- 44 and 1, 955 +/- 43 cm3) than the women (42 +/- 2 and 55 +/- 3 kg for the 1-RM test and 1,125 +/- 53 vs. 1,261 +/- 65 cm3 for quadriceps muscle volume before and after training, respectively, in women; both P < 0.05). However, percent increases were similar for men and women in the 1-RM test (27 and 29% for men and women, respectively), muscle volume (12% for both), and MQ (14 and 16% for men and women, respectively). Significant increases in MQ were observed in both groups in the trained leg (both P < 0.05) and in the 1-RM test for the untrained leg (both P < 0.05), but no significant differences were observed between groups, suggesting neuromuscular adaptations in both gender groups. Thus, although older men appear to have a greater capacity for absolute strength and muscle mass gains than older women in response to ST, the relative contribution of neuromuscular and hypertrophic factors to the increase in strength appears to be similar between genders.     

Muscle glycogen accumulation after endurance exercise in trained and untrained individuals

Muscle glycogen accumulation was determined in six trained cyclists (Trn) and six untrained subjects (UT) at 6 and either 48 or 72 h after 2 h of cycling exercise at approximately 75% peak O2 uptake (VO2 peak), which terminated with five 1-min sprints. Subjects ate 10 g carbohydrate . kg-1 . day-1 for 48-72 h postexercise. Muscle glycogen accumulation averaged 71 +/- 9 (SE) mmol/kg (Trn) and 31 +/- 9 mmol/kg (UT) during the first 6 h postexercise (P < 0.01) and 79 +/- 22 mmol/kg (Trn) and 60 +/- 9 mmol/kg (UT) between 6 and 48 or 72 h postexercise (not significant). Muscle glycogen concentration was 164 +/- 21 mmol/kg (Trn) and 99 +/- 16 mmol/kg (UT) 48-72 h postexercise (P < 0.05). Muscle GLUT-4 content immediately postexercise was threefold higher in Trn than in UT (P < 0.05) and correlated with glycogen accumulation rates (r = 0.66, P < 0.05). Glycogen synthase in the active I form was 2.5 +/- 0.5, 3.3 +/- 0.5, and 1.0 +/- 0.3 micromol . g-1 . min-1 in Trn at 0, 6, and 48 or 72 h postexercise, respectively; corresponding values were 1.2 +/- 0.3, 2.7 +/- 0.5, and 1.6 +/- 0.3 micromol . g-1 . min-1 in UT (P < 0.05 at 0 h). Plasma insulin and plasma C-peptide area under the curve were lower in Trn than in UT over the first 6 h postexercise (P < 0.05). Plasma creatine kinase concentrations were 125 +/- 25 IU/l (Trn) and 91 +/- 9 IU/l (UT) preexercise and 112 +/- 14 IU/l (Trn) and 144 +/- 22 IU/l (UT; P < 0.05 vs. preexercise) at 48-72 h postexercise (normal: 30-200 IU/l). We conclude that endurance exercise training results in an increased ability to accumulate muscle glycogen after exercise.     

Skeletal muscle function at low work level as a model for daily activities in patients with chronic heart failure

AIM: Metabolic exercise abnormalities have been reported in chronic heart failure patients. This study sought to evaluate whether these abnormalities affected daily activity. METHODS AND RESULTS: In 16 patients with moderate-to-severe chronic heart failure and in eight controls we measured femoral flow (thermodilution) and metabolism (glucose, lactate, free fatty acids, blood gas values) at rest and during a constant load of 20 W, which may mimic a daily activity. At rest, chronic heart failure patients had a leg flow similar to controls, but showed a higher leg oxygen consumption (4.6 +/- 0.6 vs 2.6 +/- 0.4 ml.min-1; P < 0.05), a higher arteriovenous oxygen difference (7.2 +/- 0.5 vs 5.4 +/- 0.7 ml.dl-1; P < 0.05), and a lower femoral vein pH (7.37 +/- 5.03 vs 7.42 +/- 0.01; P = 0.01). At 20 W, chronic heart failure patients had a leg flow similar to controls, but showed increased lactate release (from resting 11.7 +/- 33 to 142 +/- 125 micrograms.min-1 P < 0.0001 vs controls, from resting 5.7 +/- 15.4 to 50 +/- 149 micrograms.min-1 ns), higher arterial concentration of free fatty acids (781 +/- 69 vs 481 +/- 85 mumol.l-1; P < 0.01), lower femoral vein HCO3 (24.1 +/- 2.6 vs 26.3 +/- 1.7 mmol.l-1; P < 0.05) and base excess (-2.3 +/- 2.3 vs -0.24 +/- 1.7 mmol.l-1; P = 0.01). CONCLUSION: In chronic heart failure patients, the important cellular metabolic alterations already present at rest partially affect daily activities, owing to a further decrease in the efficiency of muscle metabolic processes, and may preclude tolerance of heavier activities. Such alterations appear, at least in part, independent of peripheral haemodynamic responses to exercise.     

Effect of epinephrine on muscle glycogenolysis during exercise in trained men

To test the hypothesis that an elevation in circulating epinephrine increases intramuscular glycogen utilization, six endurance-trained men performed two 40-min cycling trials at 71 +/- 2% of peak oxygen uptake in 20-22 degrees C conditions. On the first occasion, subjects were infused with saline throughout exercise (Con). One week later, after determination of plasma epinephrine levels in Con, subjects performed the second trial (Epi) with an epinephrine infusion, which resulted in a twofold higher (P < 0.01) plasma epinephrine concentration in Epi compared with Con. Although oxygen uptake was not different when the two trials were compared, respiratory exchange ratio was higher throughout exercise in Epi compared with Con (0.93 +/- 0.01 vs. 0.89 +/- 0.01; P < 0.05). Muscle glycogen concentration was not different when the trials were compared preexercise, but the postexercise value was lower (P < 0.01) in Epi compared with Con. Thus net muscle glycogen utilization was greater during exercise with epinephrine infusion (224 +/- 37 vs. 303 +/- 30 mmol/kg for Con and Epi, respectively; P < 0.01). In addition, both muscle and plasma lactate and plasma glucose concentrations were higher (P < 0.05) in Epi compared with Con. These data indicate that intramuscular glycogen utilization, glycolysis, and carbohydrate oxidation are augmented by elevated epinephrine during submaximal exercise in trained men.     

Risk factors for chronic graft-versus-host disease after bone marrow transplantation: a retrospective single centre analysis

We retrospectively compared the changes in serum albumin concentration and colloid osmotic pressure between survivors and nonsurvivors of prolonged (> or = 7 days) critical illness over a 2-year period from 1 July 1995. All patients had serum albumin measured daily, and colloid osmotic pressure measured 5 days a week, throughout their ICU admission. They received crystalloid and colloid infusions as well as parenteral or enteral feeding. Infusions of albumin were not used to treat hypoalbuminaemia. One hundred and forty-five patients were included, 66 nonsurvivors and 79 survivors. Nonsurvivors were significantly older than survivors [mean (95% CI): 58 (3.8) and 49 (4.1) years, respectively] and had a greater risk of death [mean (95% CI): 0.44 (0.06) and 0.28 (0.05); p < 0.05]. There was no significant difference in gender, APACHE II score [mean (95% CI): 22 (2.7) (nonsurvivors); 18 (2.3) (survivors)] or length of stay [median (interquartile range): 14 (9-27) days (nonsurvivors); 15 (9-26) days (survivors)]. There was no difference between the two groups in the absolute minimum serum albumin concentrations reached, the time to reach that minimum or the minimum in the first 7 days. However, nonsurvivors had a significantly lower mean serum albumin concentration: [mean (95% CI): 15.7 (5.1) g.l-1 compared with 18.3 (4.6) g.l-1 in survivors; p < 0.05]. They also had a lower recovery mean (the weighted mean after the minimum value): [mean (95% CI): 13.3 (5.1) g.l-1 (nonsurvivors) and 18.6 (5.3) g.l-1 (survivors); p < 0.01]. Analysis of colloid osmotic pressure results showed no difference between the groups in mean, minimum or recovery mean. Regression analysis of mean colloid osmotic pressure and albumin revealed that albumin only contributed 17% of the colloid osmotic pressure in these patients. The similar decrease in albumin in nonsurvivors and survivors may reflect the acute inflammatory response and/or haemodilution. However, survivors showed an ability to increase serum albumin concentrations, possibly owing to resumption of synthesis. The colloid osmotic pressure varied little between or within either group of patients, possibly because of the use of artificial colloids. There was no relationship between death and colloid osmotic pressure.     

Cerebral processing of words and the development of chronic pain

Decreased glutamine availability is proposed as a mechanism for changes in immune function with intense exhaustive exercise. Less is known about the immunomodulatory effects of regular nonexhaustive exercise. To determine the effects of low intensity regular exercise and dietary glutamine supplementation on plasma glutamine concentrations, lymphocyte metabolism, and immune function, male (278 +/- 5 g) and female (182 +/- 1 g) Sprague-Dawley Buffalo rats were fed nutritionally complete casein-based semi-purified diets +/- 2% w/w glutamine. Rats were trained (21 d), as confirmed by higher (P < 0.05) succinate dehydrogenase activity in soleus muscle, to swim 2 or 4 h.d-1 or remained sedentary. Exercise lowered plasma concentrations of tryptophan, glutamate, methionine, alanine, threonine, aspartate, asparagine, and ornithine and increased the lysine concentration (P < 0.05). Neither diet nor exercise altered plasma glutamine concentrations, lymphocyte phenotypes in spleen, or the in vitro rates of splenocyte energy metabolism (production of glucose and glutamine metabolites or ATP concentrations in the incubation media). Compared with nonsupplemented rats, splenic cytolytic activity (lysis of 51Cr labeled YAC-1 cells) was reduced (P < 0.05) in the glutamine-supplemented exercising group. Under these conditions, glutamine supplementation does not appear to provide any added benefit to the exercise-trained animal.     

Effects of nonesterified fatty acids on glucose metabolism after glucose ingestion

Impaired suppression of plasma nonesterified fatty acids (NEFAs) after glucose ingestion may contribute to glucose intolerance, but the mechanisms are unclear. Evidence that insulin inhibits hepatic glucose output (HGO), in part by suppressing plasma NEFA levels, suggests that impaired suppression of plasma NEFA after glucose ingestion would impair HGO suppression and increase the systemic delivery of glucose. To test this hypothesis, we studied glucose kinetics (constant intravenous [3-3H]glucose [0.4 microCi/min], oral [1-14C]glucose [100 microCi]), whole-body substrate oxidation, and leg glucose uptake in eight normal subjects (age, 39 +/- 9 years [mean +/- SD]; BMI, 24 +/- 2 kg/m2) in response to 75 g oral glucose on two occasions. In one study, plasma NEFAs were prevented from falling by infusion of 20% Liposyn (45 ml/h) and heparin (750 U/h). Plasma glucose rose more rapidly during lipid infusion (P < 0.05), and mean levels tended to be higher after 120 min (6.45 +/- 0.41 vs. 5.81 +/- 0.25 SE, 0.1 < P < 0.05, NS); peak glucose levels were similar. Total glucose appearance (Ra) was higher during lipid infusion due to a higher HGO (28.4 +/- 1.0 vs. 21.2 +/- 1.5 g over 4 h, P < 0.005). Total glucose disposal (Rd) was also higher (88 +/- 2 vs. 81 +/- 3 g in 4 h, P < 0.05). Plasma insulin rose more rapidly after glucose ingestion with lipid infusion, and leg glucose uptake was 33% higher (P < 0.05) during the 1st hour. During lipid infusion, subjects oxidized less glucose (47 +/- 3 vs. 55 +/- 2 g, P < 0.05) and more fat (7.1 +/- 0.8 vs. 3.9 +/- 0.9 g, P < 0.02). In summary, 1) impaired suppression of NEFAs after oral glucose impairs insulin's ability to suppress HGO, and 2) in normal subjects the greater insulin response compensates for the increased systemic glucose delivery by increasing peripheral glucose Rd.     

A report on the composition of mercurials used in traditional medicines in Oman

The purposes of this study were 1) to investigate glucose tolerance and insulin action immediately after exercise and 2) to determine how long the improved glucose homeostatic mechanisms observed 12-16 h after exercise persist. Nine (seven men, two women) moderately trained middle-aged (51 +/- 3 yr) subjects performed 45 min of exercise at 73 +/- 2% of peak O2 uptake for 5 days, followed by 7 days of inactivity. Oral glucose tolerance tests (OGTT; 75 g) were performed immediately postexercise (IPE; approximately 30 min) after the final exercise bout and 1, 3, 5, and 7 days after exercise. The incremental area under the plasma glucose curve was markedly higher IPE (355 +/- 82 mM.min) compared with those on days 1 (136 +/- 57 mM.min; P < 0.05) and 3 (173 +/- 62 mM.min; P < 0.05). The glucose area was significantly higher on days 5 (213 +/- 80 mM.min) and 7 (225 +/- 84 mM.min) compared with those on days 1 and 3 (P < 0.05). The incremental insulin area IPE (3,729 +/- 1,104 microU.ml-1.min) was 43% higher compared with that on day 1 (2,603 +/- 635 microU.ml-1.min; P < 0.05) and 66% higher compared with that on day 3 (2,240 +/- 517 microU.ml-1.min; P < 0.05). The insulin area increased to 3,616 +/- 617 microU.ml-1.min after 5 days of inactivity (P < 0.05). An additional 48 h of inactivity did not result in any further increase in the plasma insulin response.(ABSTRACT TRUNCATED AT 250 WORDS)