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.     

Skeletal muscle lactate accumulation and creatine phosphate depletion during heavy exercise in congestive heart failure. Cause of limited exercise capacity?

OBJECTIVE: To study the mechanisms of limited exercise capacity and skeletal muscle energy production in male patients with congestive heart failure. DESIGN: Muscle biopsy study. PATIENTS: Skeletal muscle metabolic response to maximal bicycle exercise was studied in 10 patients with chronic congestive heart failure (ejection fraction 0.22 +/- 0.05; peak oxygen consumption, VO2 15.1 +/- 4.9 ml.min-1.kg-1) and in nine healthy subjects (peak VO2 33.5 +/- 6.7 ml.min-1.kg-1). Activities of skeletal muscle enzymes were measured from the vastus lateralis muscle of 48 patients (ejection fraction 0.24 +/- 0.06, peak VO2 17.4 +/- 5.4 ml.min-1.kg-1) and 36 healthy subjects (peak VO2 38.3 +/- 8.4 ml.min-1.kg-1). RESULTS: Although blood lactate levels were lower in patients than in healthy subjects (2.2 +/- 0.3 vs 5.2 +/- 0.6 mmol.l-1; P < 0.001) at peak exercise (96 +/- 11 W for patients and 273 +/- 14 W for controls), skeletal muscle lactate was similarly elevated (25.6 +/- 3.2 vs 22.7 +/- 2.7 mmol.kg-1) and creatine phosphate was equally depressed (P < 0.02) to low levels (7.0 +/- 1.9 vs 6.7 +/- 0.9 mmol.kg-1). The muscle ATP decreased by 21% (P < 0.05) and 8% (P < 0.01) in the patients and controls, respectively. Activities of rate limiting enzymes of the citric acid cycle (alpha-ketoglutarate dehydrogenase) and oxidation of free fatty acids (carnitine palmitoyltransferase II) were 48% and 21% lower than in controls, but the mean phosphofructokinase activity was unchanged in congestive heart failure. CONCLUSIONS: It seems that the main limiting factor of exercise performance during heavy exercise is the same in congestive heart failure and healthy subjects, a high rate of skeletal muscle lactate accumulation and high-energy phosphate depletion. In congestive heart failure, the low activity of aerobic enzymes is likely to impair energy production and lead to lactate acidosis at low workloads.     

Young and old subjects matched for aerobic capacity have similar noradrenergic responses to exercise

Sympathetic nervous system activity as indicated by circulating norepinephrine has been demonstrated to increase with advancing chronological age both at rest and during submaximal exercise. Much of the earlier work investigating this aging phenomenon used a younger group that had a higher peak oxygen consumption (VO2) than did the older group, which made comparisons difficult. In the present study, young [n = 7, 36 +/- 1.0 (SE) yr] and old subjects (n = 8, 61 +/- 1.2 yr) were matched on peak VO2 and then exercised at approximately the same relative submaximal VO2 (75%) and power output on a cycle ergometer for 21 min. Blood samples were collected at rest and in the 7th, 14th, and last minute of a 21-min exercise bout via an indwelling catheter in an antecubital vein. The norepinephrine responses for the young and old groups, respectively, were as follows: rest, 486 +/- 111 vs. 673 +/- 108; 7 min, 1,258 +/- 255 vs. 1,185 +/- 172; 14 min, 1,639 +/- 316 vs. 1,528 +/- 288; and 21 min, 2,038 +/- 488 vs. 1,936 +/- 453 pg/ml. These responses were not significantly different between the groups at any time period. The epinephrine values for the age groups were not statistically different: rest, 115 +/- 60 vs 88 +/- 51; 7 min, 140 +/- 18 vs. 326 +/- 88; 14 min, 216 +/- 33 vs. 366 +/- 104; and 21 min, 324 +/- 100 vs. 447 +/- 113 pg/ml.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of the Asymptomatic Cardiac Ischemia Pilot and modified Asymptomatic Cardiac Ischemia Pilot versus Bruce and Cornell exercise protocols

The Asymptomatic Cardiac Ischemia Pilot (ACIP) and modified ACIP treadmill exercise protocols were developed to test patients with coronary artery disease and to linearly increase work load between stages. The physiologic changes that occurred with ACIP and modified ACIP were compared to those with the Bruce and Cornell protocols in 28 normal subjects and 16 men with coronary artery disease. The exercise protocols were randomly assigned over 2 days, and gas exchange data were obtained continuously with each test. In normal subjects, the peak heart rate, systolic blood pressure, peak oxygen consumption rate (VO2) and minute ventilation were similar for the 4 protocols tested, with exercise time shortest for the Bruce protocol in comparison with the ACIP, modified ACIP and Cornell protocols (10.2 +/- 3.1 vs 13.4 +/- 4.9, 13.9 +/- 4.5, and 15.0 +/- 4.2 minutes, respectively; p < 0.001). The difference between predicted and observed VO2 was smallest for the ACIP protocol (37.0 +/- 11.0 vs 35.8 +/- 13.5 ml/kg/min) and greatest for the Bruce protocol (41.1 +/- 11.8 vs 36.7 +/- 15.0 ml/kg/min) in normal subjects, as well as in patients with coronary artery disease (ACIP protocol 26.9 +/- 7.1 vs 22.5 +/- 6.7, and Bruce protocol 29.1 +/- 7 vs 22.6 +/- 5.7 ml/kg/min, respectively). The ratio of VO2 to work rate, expressed as a slope, was similar in normal subjects for the 4 protocols tested. However, in patients with coronary artery disease, the slope was 0.84 and 0.83 for the ACIP and modified ACIP protocols, respectively, versus 0.61 and 0.71 for the Bruce and Cornell protocols, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prediction of blood lactate accumulation from excess CO2 output during constant exercise

To determine the predictability of blood lactate accumulation from excess CO2 output derived from bicarbonate buffering of lactic acid during constant exercise, eight normal active volunteers were studied during three stages of constant exercise on a cycle ergometer. Three work rates consisted of 100% (stage I), 120% (stage II) and 150% (stage III) of each subject's anaerobic threshold (AT), each of which was lasted for 4 min. Excess CO2 output (Ex CO2, ml) at each stage of constant exercise was estimated form the integral of difference between total VCO2 and aerobic VCO2 (from regression line for VCO2 and VO2 at exercise intensities below the AT obtained in incremental exercise test). Ex CO2 per body mass (Ex CO2-mass-1) was increased progressively with blood lactate (La) accumulation from rest to each stage of constant exercise. Mean values (+/-SD) in the measured La accumulation (delta La,measured) and predicted La accumulation (delta La,predicted) at three stages of constant exercise were 1.82 +/- 0.83 vs 3.19 +/- 1.70 for stage 1, 5.58 +/- 3.47 vs 7.09 +/- 3.28 for stage II and 12.19 +/- 2.36 vs 12.74 +/- 1.83 mmol.l-1 for stage III, respectively. There was a significant difference between delta La,measured and delta La,predicted at stage I (p < 0.05), but no significant differences between these two variables at stage II and III. The averaged difference from delta La,predicted to delta La,measured at stage III (0.55 mmol.l-1) showed a tendency to be smaller than stage I (1.38 mmol.l-1) and II (1.50 mmol.l-1). On the other hand, delta La,predicted was found to correlate very closely with delta La,measured (r = 0.954, P < 0.001, n = 20). The results of this study suggest that the changes of La accumulation could be predicted from excess CO2 output generated in constant exercises above the AT.     

Differences in duration of Huntington's disease based on age at onset

OBJECTIVE: The accurate determination of limitations in physical activity is important in evaluating patients with heart failure and in assessing the efficacy of treatment. However, the conventional measures used to evaluate hemodynamics, functional class, and exercise capacity all have limitations. Our objective was to develop a simple method (The Master-Borg test) for evaluating the physical activity of patients with chronic heart failure using self-evaluation of the sensation of dyspnea at a constant workload. METHODS: Patients with NYHA class I (N = 20), class II (N = 20), and class III (N = 20) chronic heart failure performed a symptom-limited treadmill exercise test to determine peak VO2 and anaerobic threshold (AT). Patients subsequently performed Master's two-step test for 90 s and maximal dyspnea was self-rated using the visual analog Borg scale (the Master-Borg test). RESULTS: The mean workload in the Master-Borg test was 15.2+/-1.6 mL x min(-1) x kg(-1). A significant correlation was found between the Master-Borg score and peak VO2 (r = 0.87) or AT (r = 0.84). The reproducibility of the Master-Borg tests was represented by a correlation coefficient of 0.93. CONCLUSION: Although simple and inexpensive, the Master-Borg test accurately represents ordinary activity levels, relates the sensation of dyspnea to peak exercise tolerance, and can be completed by most patients with heart failure. Master-Borg scores correlated with peak VO2 and AT, and can differentiate among NYHA classes I, II, and III. The Master-Borg test appears to be clinically useful for evaluating the value of physical activity and exercise capacity of patients with chronic heart failure.     

Effect of exercise intensity on glucose and insulin metabolism in obese individuals and obese NIDDM patients

OBJECTIVE: The primary purpose of this study was to evaluate the acute effect of exercise of differing intensity on plasma glucose and insulin responses to an oral glucose challenge. RESEARCH DESIGN AND METHODS: Six obese men and six obese men with NIDDM of similar age, weight, percentage body fat, and VO2peak participated in the study. Each subject underwent two 7-day exercise programs in a counterbalanced order at 2-week intervals. During each 7-day exercise period, the subjects cycled every day at a power output corresponding to 50% VO2peak for 70 min or 70% VO2peak for 50 min. Muscle glycogen utilization was estimated during exercise on day 7 using a [3H]glucose infusion technique in conjunction with indirect calorimetry. During the day before and after each 7-day exercise period, a 3-h oral glucose tolerance test (OGTT) was administered after a 12-h overnight fast. RESULTS: The average caloric expenditure did not differ between exercise at 50 and 70% VO2peak in both obese and obese NIDDM subjects. However, the carbohydrate oxidation was higher (P < 0.05) during exercise at 70 than 50% VO2peak in obese subjects (77 +/- 5 vs. 68 +/- 6 g) and obese NIDDM subjects (70 +/- 4 vs. 58 +/- 6 g). Muscle glycogen utilization was also higher (P < 0.05) during exercise at 70 than 50% VO2peak in obese subjects (59 +/- 9 vs. 30 +/- 7 g) and in obese NIDDM subjects (48 +/- 5 vs. 24 +/- 5 g). In obese subjects, plasma glucose response area during the OGTT did not change after 7 days of exercise at either 50 or 70% VO2peak. Plasma insulin response area during the OGTT also did not change after 7 days of exercise at 50% VO2peak. However, plasma insulin response area was reduced (P < 0.05) after 7 days of exercise at 70% VO2peak (9,644 +/- 1,783 vs 7,538 +/- 1,522 microU.ml-1.180 min-1). In obese NIDDM subjects, both plasma glucose and insulin response areas during the OGTT did not decrease after 7 days of exercise at either 50 or 70% VO2peak. CONCLUSIONS: It is concluded that the exercise-induced improvement in insulin sensitivity is influenced by exercise intensity in obese individuals. The improved insulin sensitivity after 7 days of exercise at 70% VO2peak in obese individuals may be related to greater muscle glycogen utilization during exercise. The lack of improvement in glucose tolerance and insulin sensitivity after 7 days of exercise at either 50 or 70% VO2peak in obese NIDDM patients may be due to the fact that the NIDDM patients selected in the present study were relatively hypoinsulinemic.     

The effects of changing intracellular pH on calcium and potassium currents in smooth muscle cells from the guinea-pig ureter

Effect of weight training exercise and treadmill exercise on postexercise oxygen consumption. Med. Sci. Sports Exerc., Vol. 30, No. 4, pp. 518-522, 1998. To compare the effect of weight training (WT) and treadmill (TM) exercise on postexercise oxygen consumption (VO2), 15 males (mean +/- SD) age = 22.7 +/- 1.6 yr; height = 175.0 +/- 6.2 cm; mass = 82.0 +/- 14.3 kg) performed a 27-min bout of WT and a 27-min bout of TM exercise at matched rates of VO2. WT consisted of performing two circuits of eight exercises at 60% of each subject's one repetition maximum with a work/rest ratio of 45 s/60 s. Approximately 5 d after WT each subject walked or jogged on the TM at a pace that elicited an average VO2 matched with his mean value during WT. VO2 was measured continuously during exercise and the first 30 min into recovery and at 60 and 90 min into recovery. VO2 during WT (1.58 L.min-1) and TM exercise (1.55 L.min-1) were not significantly (P > 0.05) different; thus the two activities were matched for VO2. Total oxygen consumption during the first 30 min of recovery was significantly higher (P < 0.05) as a result of WT (19.0 L) compared with that during TM exercise (12.7 L). However, VO2 values at 60 (0.32 vs 0.29 L.min-1), and 90 min (0.33 vs 0.30 L.min-1) were not significantly different (P > 0.05) between WT and TM exercise, respectively. The results suggest that, during the first 30 min following exercise. WT elicits a greater elevated postexercise VO2 than TM exercise when the two activities are performed at matched VO2 and equal durations. Therefore, total energy expenditure as a consequence of WT will be underestimated if based on exercise VO2 only.     

Thermoregulatory effects of caffeine ingestion during submaximal exercise in men

BACKGROUND: The exclusive effect of caffeine ingestion on exercise thermoregulation is unclear; data indicate that caffeine may have a positive effect, a negative effect, or no effect. METHODS: Rectal (TRE) and mean skin (TSK) temperatures, skin heat conductance (HSK), and sweat rate (MSW) were measured during 30 min of rest and subsequent 70 min of submaximal cycle-ergometer exercise (67% VO2PEAK) in 11 aerobically conditioned men (mean +/- SD 29 +/- 6 yr, 49 +/- 6 mL x min(-1) x kg(-1) VO2PEAK) under two conditions: a caffeine (10 mg x kg(-1) ingestion (CI) session and a noncaffeine ingestion (NCI) control session. RESULTS: There were no significant differences in physiological or thermoregulatory parameters during exercise: X (+/-SE) end exercise levels for the NCI and CI sessions, respectively, were VO2 = 2.50 +/- 0.09 vs. 2.55 +/- 0.09 L x min(-1); heart rate = 145 +/- 7 vs. 145 +/- 5 bpm; HSK = 30 +/- 3 vs. 28 +/- 3 kcal x m(-2) x h(-1) x degrees C(-1); MSW = 393 +/- 35 vs. 378 +/- 36 g x m(-2) x h(-1); and TRE = 38.3 +/- 0.2 vs. 38.4 +/- 0.1 degrees C. Control TSK was lower than that for CI by 0.4 to 0.5 degrees C at rest and during exercise. CONCLUSION: Ingestion of a high level (10 mg x kg(-1) of caffeine has no effect on skin heat conductance, sweating, or the rate of increase and final level of rectal temperature during moderate, submaximal leg exercise.     

Skeletal muscle function and its relation to exercise tolerance in chronic heart failure

OBJECTIVES: This study sought to define the relation between muscle function and bulk in chronic heart failure (HF) and to explore the association between muscle function and bulk and exercise capacity. BACKGROUND: Skeletal muscle abnormalities have been postulated as determinants of exercise capacity in chronic HF. Previously, muscle function in chronic HF has been evaluated in relatively small numbers of patients and with variable results, with little account being taken of the effects of muscle wasting. METHODS: One hundred male patients with chronic HF and 31 healthy male control subjects were studied. They were matched for age (59.0 +/- 1.0 vs. 58.7 +/- 1.7 years [mean +/- SEM]) and body mass index (26.6 +/- 0.4 vs. 26.3 +/- 0.7 kg/m2). We assessed maximal treadmill oxygen consumption (VO2), quadriceps maximal isometric strength, fatigue (20-min protocol, expressed in baseline maximal strength) and computed tomographic cross-sectional area (CSA) at midthigh. RESULTS: Peak VO2 was lower in patients (18.0 +/- 0.6 vs. 33.3 +/- 1.4 ml/min per kg, p < 0.0001), although both groups achieved a similar respiratory exchange ratio at peak exercise (1.15 +/- 0.01 vs. 1.19 +/- 0.03, p = 0.13). Quadriceps (582 vs. 652 cm2, p < 0.05) and total leg muscle CSA (1,153 vs. 1,304 cm2, p < 0.005) were lower in patients with chronic HF. Patients were weaker than control subjects (357 +/- 12 vs. 434 +/- 18 N, p < 0.005) and also exhibited greater fatigue at 20 min (79.1% vs. 92.1% of baseline value, p < 0.0001). After correcting strength for quadriceps CSA, significant differences persisted (5.9 +/- 0.2 vs. 7.0 +/- 0.3 N/cm2, p < 0.005), indicating reduced strength per unit muscle. In patients, but not control subjects, muscle CSA significantly correlated with peak absolute VO2 (R = 0.66, p < 0.0001) and is an independent predictor of peak absolute VO2. CONCLUSIONS: Patients with chronic HF have reduced quadriceps maximal isometric strength. This weakness occurs as a result of both quantitative and qualitative abnormalities of the muscle. With increasing exercise limitation there is increasing muscle weakness. This progressive weakness occurs predominantly as a result of loss of quadriceps bulk. In patients, this muscular atrophy becomes a major determinant of exercise capacity.     

Comparison of gas exchange and hemodynamic variables during 2 types of exercise tests. Cycle-ergometry and the ergometric table

The development of stress echocardiography on an ergometric table has increased the number of stress tests in the decubitus position, whereas most of the information currently available concerns stress tests in the sitting position or on the treadmill. In order to study the influence of this position of stress testing, the authors compared the results obtained in a series of 15 patients without cardiac disease (Group I) and another series of 15 coronary patients (Group II) undergoing the two types of stress testing, in the vertical position on a bicycle ergometer and in the lateral decubitus position on the ergometric table. Effort tolerance on the bicycle ergometer was significantly greater in terms of work load (202 +/- 35 vs 180 +/- 36 watts (p < 0.001) in the controls, and 120 +/- 32 vs 106 +/- 22 watts (p < 0.05) in the coronary group), of duration of effort (19 +/- 3 vs 16 +/- 3 minutes (p < 0.001) in the controls and 10 +/- 3 vs 8 +/- 2 minutes (p < 0.05) in the coronary patients), of heart rate (190 +/- 10 vs 172 +/- 21 beats/min (p < 0.005) in controls and 118 +/- 19 vs 111 +/- 14 beats/min (p < 0.05) in the coronary patients). On the other hand, blood pressure and O2 saturation tended to be greater during exercise in the decubitus position: SBP 200 +/- 23 vs 196 +/- 27 mmHg (NS) in the controls and 158 +/- 21 vs 166 +/- 23 mmHg (NS) in the coronary patients; DBP 97 +/- 10 vs 102 +/- 27 mmHg (NS) in the controls and 85 +/- 6 vs 90 +/- 10 mmHg (NS) in the coronary patients; O2 sat 96.8 +/- 1 vs 97.6 +/- 0.8% (p < 0.05) in the coronary patients. The anaerobic threshold and peak VO2 were much higher during exercise in the sitting position: oxygen consumption at the threshold 14.8 +/- 3.8 vs 12.6 +/- 2.3 ml.kg-1.min-1 (p < 0.01), peak VO2 22.2 +/- 5.9 vs 18.8 +/- 4.7 ml.kg-1.min-1 (p < 0.01) in the coronary patients. The results of this study show that the cardiovascular stimulation obtained in the decubitus position is not identical to that obtained by traditional exercise stress testing, particularly in coronary patients.     

Kinetics of oxygen uptake at the onset of exercise in boys and men

The objective of this study was to compare the O2 uptake (VO2) kinetics at the onset of heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cycling task to determine peak VO2 (VO2 peak). On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice by cycling at 50% VO2 peak for 3.5 min, once by cycling at 100% VO2 peak for 2 min, and once by cycling at 130% VO2 peak for 75 s. O2 deficit was not significantly different between boys and men (respectively, 50% VO2 peak task: 6.6 +/- 11.1 vs. 5.5 +/- 7.3 ml . min-1 . kg-1; 100% VO2 peak task: 28.5 +/- 8.1 vs. 31.8 +/- 6.3 ml . min-1 . kg-1; and 130% VO2 peak task: 30.1 +/- 5.7 vs. 35.8 +/- 5.3 ml . min-1 . kg-1). To assess the kinetics, phase I was excluded from analysis. Phase II VO2 kinetics could be described in all cases by a monoexponential function. ANOVA revealed no differences in time constants between boys and men (respectively, 50% VO2 peak task: 22. 8 +/- 5.1 vs. 26.4 +/- 4.1 s; 100% VO2 peak task: 28.0 +/- 6.0 vs. 28.1 +/- 4.4 s; and 130% VO2 peak task: 19.8 +/- 4.1 vs. 20.7 +/- 5. 7 s). In conclusion, O2 deficit and fast-component VO2 on-transients are similar in boys and men, even at high exercise intensities, which is in contrast to the findings of other studies employing simpler methods of analysis. The previous interpretation that children rely less on nonoxidative energy pathways at the onset of heavy exercise is not supported by our findings.     

The content of electrolytes (Na, K, Ca, Mg) in vertebrate otoliths and otoconia

IVOX (intravenous oxygenator and CO2 removal device) augments venous gas exchange in patients with severe respiratory failure. Controlled hypoventilation with permissive hypercapnia reduces airway pressures during mechanical ventilation and augments CO2 exchange through the IVOX. To quantify the additive effects of gradual permissive hypercapnia and IVOX on gas exchange and reduction of airway pressures, 13 adult sheep underwent tracheostomy and severe smoke inhalation injury. Seven were mechanically ventilated alone (control), and six had mechanical ventilation, systemic anticoagulation, and implantation of IVOX (size 7 with 0.21-m2 surface area) (IVOX group). Both groups were anesthetized and paralyzed for 24 hr. In the IVOX group, minute ventilation was decreased in a stepwise fashion to produce a gradual increase in PaCO2, from 30 to 95 mm Hg, over 12 hr, and then sustained for an additional 12 hr. Sodium bicarbonate was given intravenously as necessary to keep arterial pH above 7.25. There were no significant differences in mean arterial pressure, cardiac output, or pulmonary artery pressure between the two groups. In the IVOX/permissive hypercapnia group, IVOX CO2 removal increased as a linear function of PaCO2 (y = 0.87x + 8.99, R2 = 0.80). IVOX CO2 removal was only 40 ml/min at normocapnia (40 mm Hg) but increased to 91 ml/min when PaCO2 was 95 mm Hg. Both peak inspiratory pressure and minute ventilation of the IVOX/permissive hypercapnia group were significantly lower than the control group, 30 +/- 4 mm Hg vs 51 +/- 3 mm Hg and 3.9 +/- 0.3 liters vs 8.4 +/- 0.5 liters (P < 0.05) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Kinetics of the homogeneous exchange of alpha-lactalbumin adsorbed on titanium oxide surface

BACKGROUND: We prospectively evaluated the potential of the 6-minute walk test compared with peak VO2 in predicting outcome of patients with New York Heart Association (NYHA) class II or III heart failure. METHODS AND RESULTS: Patients with a history of heart failure caused by systolic dysfunction were included. The combined final outcome (death or hospitalization for heart failure) was used as the judgment criterion. One hundred twenty-one patients (age 59+/-11 years; left ventricular ejection fraction 29.6%+/-13%) were included and followed for 1.53+/-0.98 years. Patients were separated into two groups according to outcome: group 1 (G1, 74 patients), without events, and group 2 (G2, 47 patients), who reached the combined end point. Peak VO2 was clearly different between G1 and G2 (18.5+/-4 vs. 13.9+/-4 ml/kg/min, p=0.0001) but not the distance walked (448+/-92 vs 410+/-126 m; p=0.084, not significant). Survival analysis showed that unlike peak VO2, the distance covered was barely distinguishable between the groups (p < 0.08). However, receiver operating characteristic curves revealed that the best performances for the 6-minute walk test were obtained for subjects walking < or =300 m. These patients had a worse prognosis than those walking farther (p=0.013). In this subset of patients, there was a significant correlation between distance covered and peak VO2 (r=0.65, p=0.011). Thus it appears that the more severely affected patients have a daily activity level relatively close to their maximal exercise capacity. Nevertheless, the 300 m threshold suggested by this study needs to be validated in an independent population. CONCLUSIONS: A distance walked in 6 minutes < or =300 m can predict outcome. Moreover, in these cases there is a significant correlation between the 6-minute walk test and peak VO2 demonstrating the potential of this simple procedure as a first-line screening test for this subset of patients.     

Post-exercise changes in blood pressure, heart rate and rate pressure product at different exercise intensities in normotensive humans

To evaluate the effect of exercise intensity on post-exercise cardiovascular responses, 12 young normotensive subjects performed in a randomized order three cycle ergometer exercise bouts of 45 min at 30, 50 and 80% of VO2peak, and 12 subjects rested for 45 min in a non-exercise control trial. Blood pressure (BP) and heart rate (HR) were measured for 20 min prior to exercise (baseline) and at intervals of 5 to 30 (R5-30), 35 to 60 (R35-60) and 65 to 90 (R65-90) min after exercise. Systolic, mean, and diastolic BP after exercise were significantly lower than baseline, and there was no difference between the three exercise intensities. After exercise at 30% of VO2peak, HR was significantly decreased at R35-60 and R65-90. In contrast, after exercise at 50 and 80% of VO2peak, HR was significantly increased at R5-30 and R35-60, respectively. Exercise at 30% of VO2peak significantly decreased rate pressure (RP) product (RP = HR x systolic BP) during the entire recovery period (baseline = 7930 +/- 314 vs R5-30 = 7150 +/- 326, R35-60 = 6794 +/- 349, and R65-90 = 6628 +/- 311, P < 0.05), while exercise at 50% of VO2peak caused no change, and exercise at 80% of VO2peak produced a significant increase at R5-30 (7468 +/- 267 vs 9818 +/- 366, P < 0.05) and no change at R35-60 or R65-90. Cardiovascular responses were not altered during the control trial. In conclusion, varying exercise intensity from 30 to 80% of VO2peak in young normotensive humans did not influence the magnitude of post-exercise hypotension. However, in contrast to exercise at 50 and 80% of VO2peak, exercise at 30% of VO2peak decreased post-exercise HR and RP.     

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.     

Oxidation of exogenous [13C]galactose and [13C]glucose during exercise

The present study examined the oxidation of exogenous galactose or glucose during prolonged submaximal cycling exercise. Eight highly trained volunteers exercised on two occasions on a cycle ergometer at 65% of maximal workload for 120 min, followed by a 60-min rest period and a second exercise bout of 30 min at 60% maximal workload. At random, subjects ingested a 8% galactose solution to which an [1-13C]galactose tracer was added or a 8% glucose solution to which an [U-13C]glucose tracer was added. Drinks were provided at the end of the warm-up period (8 ml/kg) and every 15 min (2 ml/kg) during the first 120 min of the test. Blood and breath samples were collected every 30 and 15 min, respectively, during the test. The exogenous carbohydrate (CHO) oxidation was calculated from the 13CO2/12CO2 ratio and CO2 production of the expired air. Peak exogenous CHO oxidation during exercise for galactose and glucose was 0.41 +/- 0.03 and 0.85 +/- 0.04 g/min, respectively. Total CHO and fat oxidation were not significantly different between the treatments. Forty-six percent of the ingested glucose was oxidized, whereas only 21% of the ingested galactose was oxidized. As a consequence, more endogenous CHO was utilized with galactose than with glucose (124.4 +/- 6.7 and 100.1 +/- 3.6 g, respectively). These results indicate that the oxidation rate of orally ingested galactose is maximally approximately 50% of the oxidation rate of a comparable amount of orally ingested glucose during 120 min of exercise.     

Changes in maximum oxygen uptake during prolonged training, overtraining, and detraining in horses

Thirteen standardbred horses were trained as follows: phase 1 (endurance training, 7 wk), phase 2 (high-intensity training, 9 wk), phase 3 (overload training, 18 wk), and phase 4 (detraining, 12 wk). In phase 3, the horses were divided into two groups: overload training (OLT) and control (C). The OLT group exercised at greater intensities, frequencies, and durations than group C. Overtraining occurred after 31 wk of training and was defined as a significant decrease in treadmill run time in response to a standardized exercise test. In the OLT group, there was a significant decrease in body weight (P < 0.05). From pretraining values of 117 +/- 2 (SE) ml.kg-1.min-1, maximal O2 uptake (VO2max) increased by 15% at the end of phase 1, and when signs of overtraining were first seen in the OLT group, VO2max was 29% higher (151 +/- 2 ml.kg-1.min-1 in both C and OLT groups) than pretraining values. There was no significant reduction in VO2max until after 6 wk detraining when VO2max was 137 +/- 2 ml.kg-1.min-1. By 12 wk detraining, mean VO2max was 134 +/- 2 ml.kg-1.min-1, still 15% above pretraining values. When overtraining developed, VO2max was not different between C and OLT groups, but maximal values for CO2 production (147 vs. 159 ml.kg-1.min-1) and respiratory exchange ratio (1.04 vs. 1.11) were lower in the OLT group. Overtraining was not associated with a decrease in VO2max and, after prolonged training, decreases in VO2max occurred slowly during detraining.     

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.     

Correction of urinary calcium levels for urine osmotic pressure]

This study was performed to clarify the relationship between isocapnic buffering and maximal aerobic capacity (VO2max) in athletes. A group of 15 trained athletes aged 21.1 (SD 2.6) years was studied. Incremental treadmill exercise was performed using a modified version of Bruce's protocol for determination of the anaerobic threshold (AT) and the respiratory compensation point (RC). Ventilatory and gas exchange responses were measured with an aeromonitor and expressed per unit of body mass. Heart rate and ratings of perceived exertion were recorded continuously during exercise. The mean VO2max, oxygen uptake (VO2) at AT and RC were 58.2 (SD 5.8) ml x kg(-1) x min(-1), 28.0 (SD 3.3) ml x kg(-1) x min(-1) and 52.4 (SD 6.7) ml x kg(-1) x min(-1), respectively. The mean values of AT and RC, expressed as percentages of VO2max, were 48.3 (SD 4.2)% and 90.0 (SD 5.2)%, respectively. The mean range of isocapnic buffering defined as VO2 between AT and RC was 24.4 (SD 4.5) ml x kg(-1) x min(-1), and the mean range of hypocapnic hyperventilation (HHV) defined as VO2 between RC and the end of exercise was 5.8 (SD 3.0) ml x kg(-1) x min(-1). The VO2max per unit mass was significantly correlated with AT (r = 0.683, P < 0.01). In addition, VO2max/mass was closely correlated with both the range of isocapnic buffering (r = 0.803, P < 0.001) and RC (r = 0.878, P < 0.001). However, no correlation was found between VO2max per unit mass and the range of HHV (r = 0.011, NS.). These findings would suggest that the prominence of isocapnic buffering, in addition to the anaerobic threshold, may have been related to VO2max of the athletes. The precise mechanisms underlying this proposed relationship remain to be elucidated.