Assessment of fitness in patients with cystic fibrosis and mild lung disease

The purpose of this investigation was to examine if exercise-induced arterial oxyhemoglobin desaturation selectively observed in highly trained endurance athletes could be related to differences in the pulmonary diffusing capacity (DL) measured during exercise. The DL of 24 male endurance athletes was measured using a 3-s breath-hold carbon monoxide procedure (to give DLCO) at rest as well as during cycling at 60% and 90% of these previously determined VO2max. Oxyhemoglobin saturation (SaO2%) was monitored throughout both exercise protocols using an Ohmeda Biox II oximeter. Exercise-induced oxyhemoglobin desaturation (DS) (SaO2% < 91% at VO2max) was observed in 13 subjects [88.2 (0.6)%] but not in the other 11 nondesaturation subjects [NDS: 92.9 (0.4)%] (P < or = 0.05), although VO2max was not significantly different between the groups [DS: 4.34 (0.65) l/min vs NDS: 4.1 (0.49) l/min]. At rest, no differences in either DLCO [ml CO.mmHg-1.min-1: 41.7 (1.7) (DS) vs 41.1 (1.8) (NDS)], DLCO/VA [8.2 (0.4) (DS) vs 7.3 (0.9) (NDS)], MVV [l/min: 196.0 (10.4) (DS) vs 182.0 (9.9) (NDS)] or FEV1/FVC [86.3 (2.2) (DS) vs 82.9 (4.7) (NDS)] were found between groups (P > or = 0.05). However, VE/VO2 at VO2max was lower in the DS group [33.0 (1.1)] compared to the NDS group [36.8 (1.5)] (P < or = 0.05). Exercise DLCO (ml CO.mmHg-1.min-1) was not different between groups at either 60% VO2max [DS: 55.1 (1.4) vs NDS: 57.2 (2.1)] or at 90% VO2max [DS: 61.0 (1.8) vs NDS: 61.4 (2.9)]. A significant relationship (r = 0.698) was calculated to occur between SaO2% and VE/VO2 during maximal exercise. The present findings indicate that the exercise-induced oxyhemoglobin desaturation seen during submaximal and near-maximal exercise is not related to differences in DL, although during maximal exercise SaO2 may be limited by a relatively lower exercise ventilation.     

Gender effect on beta-endorphin response to exercise

PURPOSE: Twelve healthy men (26.4 yr) and women (26.8 yr) were compared at rest and after cycling for 25 min at 60 and 80% VO2max to determine whether gender and menstrual cycle influenced circulating beta-endorphin concentration (BE). METHODS: VO2max was determined on a cycle ergometer, and subjects completed the exercise in a randomized order. Women were tested in both the luteal (L) and follicular (F) phases of their menstrual cycle, which was confirmed by their blood estrogen levels. All tests were conducted in the morning after a 30-min rest (12-h postabsorptive). An indwelling venous catheter placed in a forearm vein enabled blood sampling at rest, 25 min of cycling, and 25 min of recovery. RESULTS: Resting BE was similar for men before both 60 and 80% intensities of exercise, 5.27 +/- 0.43 and 5.30 +/- 0.33 pmol.mL-1, respectively. BE was not significantly changed at 60% VO2max (6.54 +/- 0.33 pmol.mL-1) but significantly increased at 80% VO2max (11.90 +/- 1.98 pmol.mL-1). Women tended to have slightly lower BE during the L compared with F, but this did not reach significance (L = 4.40 +/- 0.22, F = 4.73 +/- 0.30 pmol.mL-1). Cycling at 60% VO2max did not significantly increase BE in the L (5.41 +/- 0.42 pmol.mL-1) nor the F (5.35 +/- 0.40 pmol.mL-1). Cycling at 80% VO2max increased BE to a similar extent in both the L and F phase, respectively (10.44 and 10.96). Although the BE concentrations tended to be slightly lower in women compared with men at 80% VO2max, this did not reach statistical significance. CONCLUSIONS: These data suggest that women cycling at 80% VO2max will have a similar BE response to men independent of their menstrual cycle. BE in women at rest and who exercise at lower exercise intensities may have slightly lower BE levels then men independent of the time of the women's menstrual cycle.     

Probabilistic reasoning in the law. Part 2: Assessment of probabilities and explanation of the value of trace evidence other than DNA

The purpose of this study was to investigate the recovery of muscle force generating capacity (FGC) of the lower limbs following a session of cycle exercise (CE). Fourteen male cyclists (mean +/- SD age 25 +/- 4 yrs and VO2max 65.8 +/- 5 ml x kg(-1)min(-1)) performed tests assessing lower limb muscle FGC at rest (pre-test), as well as 6 and 24 hrs following CE performed on a mechanically-braked cycle ergometer. The CE consisted of 30 min at a workload corresponding to the lactate (Dmax) threshold (+/-15 W), and four 60 s rides at 120% VO2max with one min rest between each ride. At the completion of the CE a 6 or 24 hr recovery period was initiated, after which, each subject's muscle FGC was measured. The analysis of lower limb muscle FGC included, (1) 6 s all-out cycle test; (2) a maximal isokinetic leg extension at 60, 120 and 180 degrees x s(-1); and (3) a maximal concentric squat jump. Statistical analysis showed that compared to pre-test levels, a significant reduction in both isokinetic peak torque at 60 degrees x s(-1) and isoinertial maximum force occurred after 6 hrs of recovery. Although not significant, reductions also occurred at 6 hrs of recovery in isokinetic peak torque at 120 and 180 degrees x s(-1), as well as maximum rate of force development (RFD) during the squat jumps. No significant differences were observed between isokinetic peak torque, maximum force or RFD pre-test and following the 24 hr recovery period, indicating these tests had returned to normal by this time. No significant differences were found between peak power (PP) during the 6 s cycle test, pre-test and following either 6 or 24 hrs of recovery. These findings confirm earlier research that maximal voluntary strength is reduced for at least 6 hours following exhaustive dynamic exercise. The reduction in muscle FGC should be considered when resistance training is scheduled after endurance exercise.     

Can the ventilatory equivalent for carbon dioxide predict the severity of functional impairment in patients with cardiac insufficiency?

OBJECTIVE: To evaluate whether the changes in the ventilatory equivalent for carbon dioxide (VE/VCO2), during the early stages of cardiopulmonary exercise testing, can predict maximal oxygen consumption (VO2max) in patients with chronic heart failure. METHODS: We studied 38 patients (30 males, mean age 56 +/- 11 years) with chronic heart failure. All patients performed maximal symptom limited, treadmill exercise test with breath-by-breath respiratory gas analysis. They were divided in two groups according to their maximal oxygen consumption (group I-VO2max above 14 ml/kg/min and group II-VO2max below 14 ml/kg/min). In both groups, we analysed VE/VCO2 at rest, at the anaerobic threshold (AT) and at peak exercise, and the percentage of VE/VCO2 reduction from rest to AT. RESULTS: Eleven patients had a VO2max below 14 ml/kg/min (group II). At rest VE/VCO2 = 53 +/- 13 in group II versus 47 +/- 10 in group I (p = 0.048), at the AT VE/VCO2 = 46 +/- 12 in group II versus 36 +/- 7 in group I (p = 0.001) and at peak exercise VE/VCO2 = 46.2 +/- 13 in group II versus 36.2 +/- 6 in group I (p = 0.0002). There was a 24% reduction in the VE/VCO2, from rest to AT in group I, compared to a 16% reduction in group II (p = 0.004). A reduction in the VE/VCO2 from rest to AT less than 16% predicted a VO2max below 14 ml/kg/min with a sensitivity of 60% and a specificity of 93%. CONCLUSIONS: Patients with severe functional impairment have higher values of VE/VCO2 in all exercise stages. A reduction of VE/VCO2 from rest to anaerobic threshold of less than 16% is a high specific predictor of a VO2max below 14 ml/kg/min.     

Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise

To evaluate the extent to which decreased plasma free fatty acid (FFA) concentration contributes to the relatively low rates of fat oxidation during high-intensity exercise, we studied FFA metabolism in six endurance-trained cyclists during 20-30 min of exercise [85% of maximal O2 uptake (VO2max)]. They were studied on two occasions: once during a control trial when plasma FFA concentration is normally low and again when plasma FFA concentration was maintained between 1 and 2 mM by intravenous infusion of lipid (Intralipid) and heparin. During the 20-30 min of exercise, fat and carbohydrate oxidation were measured by indirect calorimetry, and the rates of appearance (Ra) of plasma FFA and glucose were determined by the constant infusion of [6,6-2H2]glucose and [2H2]palmitate. Lipid-heparin infusion did not influence the Ra or rate of disappearance of glucose. During exercise in the control trial, Ra FFA failed to increase above resting levels (11.0 +/- 1.2 and 12.4 +/- 1.7 mumol.kg-1.min-1 for rest and exercise, respectively) and plasma FFA concentration dropped from a resting value of 0.53 +/- 0.08 to 0.29 +/- 0.02 mM. The restoration of plasma FFA concentration resulted in a 27% increase in total fat oxidation (26.7 +/- 2.6 vs. 34.0 +/- 4.4 mumol.kg-1.min-1, P < 0.05) with a concomitant reduction in carbohydrate oxidation, apparently due to a 15% (P < 0.05) reduction in muscle glycogen utilization. However, the elevation of plasma FFA concentration during exercise at 85% VO2max only partially restored fat oxidation compared with the levels observed during exercise at 65% VO2max. These findings indicate that fat oxidation is normally impaired during exercise at 85% VO2max because of the failure of FFA mobilization to increase above resting levels, but this explains only part of the decline in fat oxidation when exercise intensity is increased from 65 to 85% VO2max.     

Effect of graded exercise on esophageal motility and gastroesophageal reflux in nontrained subjects

The effects of graded exercise on esophageal motility and gastroesophageal reflux were evaluated in nine nontrained subjects, using a catheter with three strain-gauge transducers connected to a solid-state datalogger and an ambulatory intraesophageal pH monitor. Subjects exercised on a stationary bike at 45%, 60%, 75%, and 90% of peak O2 uptake (VO2 max). Durations of exercise sessions and rest periods varied among subjects. Studies were performed after an overnight fast and subjects received only intravenous infusion of 5% glucose solution during the study. Plasma concentrations of gastrin, motilin, glucagon, pancreatic polypeptide (PP), and vasoactive intestinal peptide (VIP) were determined at rest and before and after each exercise session. The duration, amplitude, and frequency of esophageal contractions declined with increasing exercise intensity, and the differences were significant (P < or = 0.05) for all three variables at 90% VO2 max. The number of gastroesophageal reflux episodes and the duration of esophageal acid exposure were significantly (P < or = 0.05) increased during exercise at 90% VO2 max. Plasma regulatory peptide concentrations showed no significant changes between rest and the various exercise sessions. Thus, exercise has profound effects on esophageal contractions and gastroesophageal reflux, which are intensity dependent. These effects were not mediated by the hormones measured. The results were similar to those observed in highly trained athletes, suggesting that the effects of exercise on esophageal function are similar in trained and nontrained subjects performing at similar percentages of VO2 max, even though the absolute levels of exercise achieved in each group are different.     

Metabolic profile of high intensity intermittent exercises

To evaluate the magnitude of the stress on the aerobic and the anaerobic energy release systems during high intensity bicycle training, two commonly used protocols (IE1 and IE2) were examined during bicycling. IE1 consisted of one set of 6-7 bouts of 20-s exercise at an intensity of approximately 170% of the subject's maximal oxygen uptake (VO2max) with a 10-s rest between each bout. IE2 involved one set of 4-5 bouts of 30-s exercise at an intensity of approximately 200% of the subject's VO2max and a 2-min rest between each bout. The accumulated oxygen deficit of IE1 (69 +/- 8 ml.kg-1, mean +/- SD) was significantly higher than that of IE2 (46 +/- 12 ml.kg-1, N = 9, p < 0.01). The accumulated oxygen deficit of IE1 was not significantly different from the maximal accumulated oxygen deficit (the anaerobic capacity) of the subjects (69 +/- 10 ml.kg-1), whereas the corresponding value for IE2 was less than the subjects' maximal accumulated oxygen deficit (P < 0.01). The peak oxygen uptake during the last 10 s of the IE1 (55 +/- 6 ml.kg-1.min-1) was not significantly less than the VO2max of the subjects (57 +/- 6 ml.kg-1.min-1). The peak oxygen uptake during the last 10 s of IE2 (47 +/- 8 ml.kg-1.min-1) was lower than the VO2max (P < 0.01). In conclusion, this study showed that intermittent exercise defined by the IE1 protocol may tax both the anaerobic and aerobic energy releasing systems almost maximally.     

Ventilatory and lactate threshold determinations in healthy normals and cardiac patients: methodological problems

In healthy normal individuals (n = 69), coronary patients with myocardial ischaemia (n = 27) and patients with chronic heart failure (CHF, n = 33), four widely applied methods to determine ventilatory threshold (VT) were analysed: V-slope, ventilatory equivalent for O2 (EqO2), gas exchange ratio (R) and end-tidal partial pressure of oxygen. Lactate threshold [LAT, log lactate vs log oxygen uptake (VO2)] was also determined. Analysis focused on rate of success of threshold determination, comparability of threshold methods, reproducibility and interobserver variability. Cycle ergometry protocols with ramp-like mode and graded steady-state mode used in exercise testing were considered separately. In healthy normal individuals and coronary patients with myocardial ischaemia, at least three VT could be determined during ramp-like mode and two VT during graded steady-state mode, 82% of the time. For CHF patients, the rate of successful determination of VT was lower. Compared to LAT, VO2 at VT was significantly higher using R and EqO2 methods of VT determination in healthy normal subjects (P < 0.01), and significantly higher when using all four methods in coronary patients (P < 0.01 or P < 0.05, respectively). No difference was observed between VO2 at VT and LAT in CHF patients. In healthy normal individuals, day-to-day reproducibility of VT and LAT was high (error of a single determination from duplicate determinations was between 3.9% and 6.2% corresponding to a VO2 of 52.2 and 89.2 ml.min-1). Interobserver variability was low (error between 0.3% and 5% corresponding to a VO2 of 9.8 and 68 ml.min-1). In CHF patients, interobserver variability was moderately greater (error between 4.6% and 8.2%, corresponding to a VO2 of 35.1 and 62.4 ml.min-1). To optimize threshold determination, standardized procedures are suggested.     

Smaller lungs in women affect exercise hyperpnea

We subjected 29 healthy young women (age: 27 +/- 1 yr) with a wide range of fitness levels [maximal oxygen uptake (VO2 max): 57 +/- 6 ml . kg-1 . min-1; 35-70 ml . kg-1 . min-1] to a progressive treadmill running test. Our subjects had significantly smaller lung volumes and lower maximal expiratory flow rates, irrespective of fitness level, compared with predicted values for age- and height-matched men. The higher maximal workload in highly fit (VO2 max > 57 ml . kg-1 . min-1, n = 14) vs. less-fit (VO2 max < 56 ml . kg-1 . min-1, n = 15) women caused a higher maximal ventilation (VE) with increased tidal volume (VT) and breathing frequency (fb) at comparable maximal VT/vital capacity (VC). More expiratory flow limitation (EFL; 22 +/- 4% of VT) was also observed during heavy exercise in highly fit vs. less-fit women, causing higher end-expiratory and end-inspiratory lung volumes and greater usage of their maximum available ventilatory reserves. HeO2 (79% He-21% O2) vs. room air exercise trials were compared (with screens added to equalize external apparatus resistance). HeO2 increased maximal expiratory flow rates (20-38%) throughout the range of VC, which significantly reduced EFL during heavy exercise. When EFL was reduced with HeO2, VT, fb, and VE (+16 +/- 2 l/min) were significantly increased during maximal exercise. However, in the absence of EFL (during room air exercise), HeO2 had no effect on VE. We conclude that smaller lung volumes and maximal flow rates for women in general, and especially highly fit women, caused increased prevalence of EFL during heavy exercise, a relative hyperinflation, an increased reliance on fb, and a greater encroachment on the ventilatory "reserve." Consequently, VT and VE are mechanically constrained during maximal exercise in many fit women because the demand for high expiratory flow rates encroaches on the airways' maximum flow-volume envelope.     

Antenatal steroids, condition at birth and respiratory morbidity and mortality in very preterm infants

The study purpose was to compare the effect of exercise training on serum lipid and apolipoprotein concentrations and the activities of intravascular enzymes related to lipid transport in previously untrained eumenorrheic, premenopausal (PRM) women (n = 21; mean age, 36 +/- 3 years) and estrogen-free postmenopausal (POM) women (n = 16; mean age, 68 +/- 8 years). Subjects trained at a progressive intensity and duration (50% to 75% maximal O2 consumption [VO2max], 200 to 300 kcal/session) 4 d/wk for 12 weeks. Before and after training, VO2max, body weight, relative body fat, and fasting blood samples were obtained following 2 weeks on a standardized diet designed to maintain body weight and during the early follicular stage for the PRM group. Blood samples were analyzed for serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), the cholesterol content of the HDL3 subfraction, apolipoprotein (apo)A-I and apoB, lipoprotein(a), and the activity of lecithin:cholesterol acyltransferase (LCAT). Total and hepatic triglyceride lipase activity (HTGLA) were determined from plasma samples obtained after heparin administration. The cholesterol content of the low-density lipoprotein (LDL) and HDL2 subfractions and endothelial-bound lipoprotein lipase activity (LPLA) were calculated. A two (group) x two (time) multivariate ANOVA (MANOVA), with repeated measures for time indicated that the exercise-induced changes in physiological measurements, serum lipid or apolipoprotein concentrations, or enzyme activities did not differ between groups. Serum concentrations of TC, LDL-C, and HDL3 cholesterol, TG, and apo A-I and apoB were higher in POM women compared with the PRM group (P < .05 for all). For the combined groups, body weight and relative body fat did not change with training, but VO2max increased an average of 18.5% (P < .05). LPLA, HTGLA, and LCAT activity were unaltered with exercise training. Except for a small but significant decrease in HDL-C (-5.5%) and an elevation in apoB (4.3%; P < .05 for both), the concentrations of serum lipids and apolipoproteins did not change over the training period. We conclude that in previously untrained women, menopausal status does not influence the exercise training response of serum lipids or apolipoproteins or activities of intravascular enzymes related to lipid transport.     

Glutathone and glutathione ethyl ester supplementation of mice alter glutathione homeostasis during exercise

The present study examined the effect of glutathione (GSH) and glutathione ethyl ester (GSH-E) supplementation on GSH homeostasis and exercise-induced oxidative stress. Male Swiss-Webster mice were randomly divided into 4 groups: starved for 24 h and injected with GSH or GSH-E (6 mmol/kg body wt, i.p.) 1 h before exercise, starved for 24 h and injected with saline (S); and having free access to food and injected with saline (C). Half of each group of mice was killed either after an acute bout of exhaustive swimming (E) or after rest (R). Plasma GSH concentration was 100-160% (P < 0.05) higher in GSH mice vs. C or S mice at rest, whereas GSH-E injection had no effect. Plasma GSH was not affected by exercise in C or S mice, but was 44 and 34% lower (P < 0.05) in E vs. R mice with GSH or GSH-E injection, respectively. S, GSH- and GSH-E-treated mice had significantly lower liver GSH concentration and the GSH:glutathione disulfide (GSSG) ratio than C mice. Hepatic and renal GSH and the GSH:GSSG ratio were significantly lower in E vs. R mice in all groups. GSH-E-treated mice had a significantly smaller exercise-induced decrease in GSH vs. C, S, and GSH-treated mice and no difference in the GSH:GSSG ratio in the kidney. Activities of gamma-glutamylcysteine synthetase and gamma-glutamyltranspeptidase in the liver and kidney were not affected by either GSH treatment or exercise. GSH concentration and the GSH:GSSG ratio in quadriceps muscle were not different among C, S and GSH-treated mice, but significantly lower in GSH-E-treated mice (P < 0.05). Hepatic malondialdehyde (MDA) content was greater in exercised mice in all but GSH-E-treated groups. GSH and GSH-E increased MDA levels in the kidney of E vs. R mice, but attenuated exercise-induced lipid peroxidation in muscle. Swim endurance time was approximately 2 h longer in GSH (351 +/- 22 min) and GSH-E (348 +/- 27) than S mice (237 +/- 17). We conclude that 1) acute GSH and GSH-E supplementation at the given doses does not increase tissue GSH content or redox status; 2) both GSH and GSH-E improve endurance performance and prevent muscle lipid peroxidation during prolonged exercise; and 3) while both compounds may impose a metabolic and oxidative stress to the kidney, this side effect is smaller with GSH-E supplementation.     

Effect of physical training on exercise-induced hyperkalemia in chronic heart failure. Relation with ventilation and catecholamines

BACKGROUND: The exercise-induced rise in arterial potassium concentration ([K+]a) may contribute to exercise hyperpnea and could play a role in exertional fatigue. This study was designed to determine whether the exercise-induced rise in [K+]a is altered in patients with chronic heart failure (CHF) and whether physical training affects K+ homeostasis. METHODS AND RESULTS: We evaluated 10 subjects with CHF (ejection fraction, 23 +/- 3.9%) and 10 subjects with normal left ventricular function (NLVF) who had undergone previous coronary artery graft surgery (ejection fraction, 63 +/- 8.6%). Subjects performed an incremental cycle ergometer exercise test before and after a physical training or detraining program. Changes in [K+]a and ventilation (VE) during exercise were closely related in both groups. Subjects with CHF did less absolute work and had reduced maximal oxygen consumption (VO2max) compared with subjects with NLVF (P < .01). Exercise-induced rises in [K+]a, VE, norepinephrine, lactate, and heart rate were greater at matched absolute work rates in subjects with CHF than in subjects with NLVF (P < .01). However, when the rise in [K+]a was plotted against percentage of VO2max to match for relative submaximal effort, there were no differences between the two groups. Physical training resulted in reduced exercise-induced hyperkalemia at matched submaximal work rates in both groups (P < .01) despite no associated change in the concentration of arterial catecholamines. At maximal exercise when trained, peak increases in [K+]a were unaltered, but peak concentrations of catecholamines were raised (P < .05). The decrease in VE at submaximal work rates after training was not significant with this incremental exercise protocol, but both groups had an increased peak VE when trained (P < .01). CONCLUSIONS: Exercise-induced rises in [K+]a, catecholamines, and VE are greater at submaximal work rates in subjects with CHF than in subjects with NLVF. Physical training reduces the exercise-induced rise in [K+]a but does not significantly decrease VE during submaximal exercise with this incremental cycle ergometry protocol. The reduction in exercise-induced hyperkalemia after training is not the result of altered concentrations of arterial catecholamines. The pathophysiological significance of the increased exercise-induced hyperkalemia in CHF and the mechanisms of improved K+ homeostasis with training have yet to be established.     

Recovery from a 1-minute bout of fatiguing exercise: characteristics, reliability, and responsiveness

BACKGROUND AND PURPOSE: The purposes of this study were (1) to describe the characteristics of recovery of peak torque after a 1-minute bout of isokinetic exercise of the quadriceps femoris muscle, (2) to determine the short-term reliability of the recovery of peak torque, and (3) to determine whether the recovery of peak torque more closely associates with maximal endurance exercise capacity than does the decline in peak torque at the end of the fatigue test. SUBJECTS: Thirty-three nondisabled subjects, ranging in age from 23 to 34 years (X = 27, SD = 3.4), participated in the reliability portion (phase 1) of the study. A different group of 21 nondisabled subjects, ranging in age from 21 to 47 years (X = 27.5, SD = 5.2), participated in the correlational portion (phase 2) of the study. METHODS: The short-term reliability of percentage of decline in peak torque and recovery of peak torque was assessed in phase 1. Each subject performed two quadriceps femoris muscle fatigue tests (test-retest) on an isokinetic dynamometer. In phase 2, each subject performed a single fatigue test and a test of maximal oxygen uptake (VO2max) to examine the relationships between VO2max and percentage of decline in peak torque at the end of the fatigue test and recovery of peak torque. RESULTS: Intraclass correlation coefficient values at every 30-second interval during recovery were acceptable (ICC = .67-.87), indicating recovery of peak torque is a consistent measure of quadriceps femoris muscle performance. A high negative correlation (r = -.84) was found between the percentage of decline at 30 seconds of recovery and VO2max, but a lower negative correlation (r = -.48) was found between the percentage of decline in torque at the end of the fatigue test and VO2max. CONCLUSION AND DISCUSSION: These results suggest recovery of peak torque is a reliable measure of muscle performance and closely associates with maximal aerobic exercise capacity.     

Fine localization of low and high calcium dependent ATPase activities in the rat sciatic nerve

It has been suggested that ubiquinone improves exercise performance and antioxidant capacity. We studied the effects of ubiquinone supplementation (120 mg.day-1 for 6 weeks) on aerobic capacity and lipid peroxidation during exercise in 11 young (aged 22-38 years) and 8 older (aged 60-74 years), trained men. The cross-over study was double-blind and placebo-controlled. Serum ubiquinone concentration increased after supplementation (P < 0.0001 for treatment) in both age groups. The maximal oxygen uptake (VO2max) was measured using a direct incremental ergometer test. In the young subjects, the VO2max after placebo and ubiquinone treatment was 58.5 (95% confidence interval: 53.0-64.0) and 59.0 ml.min-1.kg-1 (52.2-66.8), respectively. The corresponding results in the older subjects were: 37.2 (31.7-42.7) and 33.7 ml.min-1.kg-1 (26.2-41.7) (P < 0.0001 for age group, P > 0.05 for treatment). In a prolonged test (60-min submaximal, then incremental load until exhaustion) time to exhaustion was longer after the placebo [young men: 85.7 (82.4-89.0), older men: 82.9 min (75.8-89.9)] than after ubiquinone [young men: 82.1 (78.5-85.8), older men: 77.2 min (70.1-83.7); P = 0.0003 for treatment]. Neither ubiquinone supplementation nor exercise affected serum malondialdehyde concentration. Oral ubiquinone was ineffective as an ergogenic aid in both the young and older, trained men.     

Decline in maximal oxygen uptake on work performance in rats during the developmental phase

Development-related changes in maximal oxygen uptake (VO2max) and work performance were examined in young sedentary rats 4-11 weeks after birth during exercise. The running speed to elicit VO2max increased from 4 to 8 weeks of age, whereas the exercise VO2max declined progressively. Therefore, the work performance during the developmental phase, when rapid growth occurs, seems to be little related to the decline in the relative VO2 max.     

Assessment of lipid peroxidation in rats of different body weight by determining expired ethane

Expired ethane is regarded as an indicator of reactive oxygen species induced lipid peroxidation. We investigated whether Wistar rats of different body weights (BW: 78 +/- 6, 121 +/- 12 and 347 +/- 30 g) and hence different metabolic rates per unit weight, expire different amounts of ethane. We found that expired ethane (pmol/100 g BW/min) decreases with increasing BW (8.6 +/- 1.8, 6.3 +/- 1.5 and 2.8 +/- 0.6, respectively). These values aas well as a recently published average value of 1.0 pmol ethane/100 g BW/min for healthy humans (average BW: 78 kg) indicate a positive relationship between lipid peroxidation and metabolic rate.     

X-SCID B cell responses to interleukin-4 and interleukin-13 are mediated by a receptor complex that includes the interleukin-4 receptor alpha chain (p140) but not the gamma c chain

We previously reported that patients with mild to moderate airflow limitation have a lower exercise capacity than age-matched controls with normal lung function, but the mechanism of this reduction remains unclear (1). Although the reduced exercise capacity appeared consistent with deconditioning, the patients had altered breathing mechanics during exercise, which raised the possibility that the reduced exercise capacity and the altered breathing mechanics may have been causally related. Reversal of reduced exercise capacity by an adequate exercise training program is generally accepted as evidence of deconditioning as the cause of the reduced exercise capacity. We studied 11 asymptomatic volunteer subjects (58 +/- 8 yr of age [mean +/- SD]) selected to have a range of lung function (FEV1 from 61 to 114% predicted, with a mean of 90 +/- 18% predicted). Only one subject had an FEV1 of less than 70% predicted. Gas exchange and lung mechanics were measured during both steady-state and maximal exercise before and after training for 30 min/d on 3 d/wk for 10 wk, beginning at the steady-state workload previously determined to be the maximum steady-state exercise level that subjects could sustain for 30 min without exceeding 90% of their observed maximal heart rate (HR). The training workload was increased if the subject's HR decreased during the training period. After 10 wk, subjects performed another steady-state exercise test at the initial pretraining level, and another maximal exercise test. HR decreased significantly between the first and second steady-state exercise tests (p < 0.05), and maximal oxygen uptake (VO2max) and ventilation increased significantly (p < 0.05) during the incremental test, indicating a training effect. However, the training effect did not occur in all subjects. Relationships between exercise parameters and lung function were examined by regression against FEV1 expressed as percent predicted. There was a significant positive correlation between VO2max percent predicted and FEV1 percent predicted (p < 0.02), and a negative correlation between FEV1 and end-expiratory lung volume (EELV) at maximal exercise (p < 0.03). There was no significant correlation between FEV1 and maximal HR achieved during exercise; moreover, all subjects achieved a maximal HR in excess of 80% predicted, suggesting a cardiovascular limitation to exercise. These data do not support the hypothesis that the lower initial VO2max in the subjects with a reduced FEV1 was due to deconditioning. Although increased EELV at maximal exercise, reduced VO2max and a reduced VO2max response with training are all statistically associated with a reduced FEV1, there is no direct evidence of causality.     

Effects of exercise on fluid exchange and body composition in man during 14-day bed rest

To determine the cause of the body weight loss during bed rest (BR), fluid balance and anthropometric measurements were taken from seven men (19-21 yr) during three 2-wk BR periods which were separated by 3-wk ambulatory recovery periods. Caloric intake was 3,073 +/- 155 (SD) kcal/day. During two of the three BR periods they performed supine isotonic exercise at 68% of VO2max on the ergometer for 1 h/day; or supine isometric exercise at 21% of maximal leg extension force for 1 min followed by a 1-min rest for 1 h/day. No prescribed exercise was given during the other BR period. During BR, body weight decreased slightly with no exercise (-0.43 kg, NS), but decreased significantly (P less than 0.05) by -0.91 kg with isometric and by -1.77 kg with isotonic exercise. About one-third of the weight reduction with isotonic exercise was due to fat loss (-0.69 kg) and, the remainder, to loss of lean body mass (-0.98 kg). It is concluded that the reduction in body weight during bed rest has two major components: First, a loss of lean body mass caused by assumption of the horizontal body position that is independent of the metabolic rate. Second, a loss of body fat content that is proportional to the metabolic rate.     

Energy requirements of middle-aged men are modifiable by physical activity

BACKGROUND: Energy requirements for weight maintenance decrease with age. Often, this decline is not proportionately matched by reduced energy intake, resulting in weight gain. OBJECTIVE: We hypothesized that energy requirements for total daily weight maintenance in healthy, sedentary, middle-aged men would increase after regular aerobic exercise or aerobic exercise plus weight loss to levels comparable with those in middle-aged athletes. DESIGN: Weight-maintenance energy requirements were determined during weight stability (+/- 0.25 kg) in 14 lean, sedentary (LS) men; 18 obese, sedentary (OS) men; and 10 male athletes of comparable ages (x +/- SEM: 58 +/- 1 y). Studies were done at baseline and after 6 mo of aerobic exercise (LS men) or aerobic exercise plus weight loss (OS men) or 3 mo of deconditioning (athletes). RESULTS: The interventions raised maximal oxygen uptake (VO2max) by 15% in the LS men and by 13% in the OS men and decreased it by 14% in athletes (all P < 0.01), eliminating the differences among groups at baseline. Body fat was reduced significantly in LS and OS men; fat-free mass decreased in OS men. Average daily energy requirements increased by 8% in LS men and by 5% in OS men (both P < 0.01) to levels comparable with the baseline requirements of athletes and correlated with VO2max (r2 = 0.22, P < 0.0001) and fat-free mass (r2 = 0.05, P < 0.02) across the range of VO2max achieved by all subjects. CONCLUSIONS: Under free-living conditions, aerobic exercise eliminated the difference in weight-maintenance energy requirements between middle-aged sedentary and athletic men, suggesting that energy requirements of healthy, middle-aged men are modifiable by regular physical activity.     

Pivalic acid-induced carnitine deficiency and physical exercise in humans

To study the effect of carnitine depletion on physical working capacity, healthy subjects were administered pivaloyl-conjugated antibiotics for 54 days. The mean carnitine concentration in serum decreased from 35.0 to 3.5 mmicromol/L, and in muscle from 10 to 4.3 micromol/g noncollagen protein (NCP). Exercise tests were performed before and after 54 days' administration of the drug. At submaximal exercise, there was a slight increase in the concentration of 3-hydroxybutyrate in serum, presumably caused by decreased fatty acid oxidation in the liver. There was also a decreased consumption of muscle glycogen, indicating decreased glycolysis in the skeletal muscle. The muscle presumably had enough energy available, since there was no significant decrease in the concentration of adenosine triphosphate (ATP) and creatine phosphate during exercise. The work at maximal oxygen uptake (VO2max) and the maximal heart rate were reduced. Since VO2max is considered dependent on heart function, carnitine depletion seemed to affect cardiac function.