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PubMed1981

Lack of correlation between exercise capacity and indexes of resting left ventricular performance in heart failure.

Symptoms of congestive heart failure occur most commonly during exercise, but cardiac performance is usually quantitated at rest. The relation between exercise capacity and measurements of cardiac performance at rest is little known. Treadmill exercise was performed in 21 patients with heart failure due to cardiomyopathy. Exercise duration averaged 9.1 +/- 0.7 (standard error of the mean) minutes (normal value 12 or more minutes) and did not correlate with resting ejection fraction of 26.4 +/- 2.7 percent (r = -0.06). Left ventricular diastolic dimension of 6.6 +/0 0.2 cm, mean velocity of circumferential fiber shortening and ratio of preejection period to left ventricular ejection time did not correlate with treadmill time (r = -0.03). Repeat studies after treatment of heart failure also failed to show correlations between changes in exercise capacity and changes in left ventricular performance at rest. Thus, measures of left ventricular performance obtained at rest do not accurately reflect exercise tolerance and symptomatic status of patients with congestive heart failure.

Adult↗

PubMed1982

Effect of isosorbide dinitrate on submaximal exercise capacity of patients with chronic left ventricular failure.

The effect of chewable isosorbide dinitrate on submaximal bicycle exercise capacity was evaluated in a double-blind randomized study involving 13 patients with chronic heart failure. All patients had impaired maximal exercise capacity (VO2 max = 12.0 +/- 2.6 ml/kg/min) due to fatigue and dyspnea but not angina. The administration of isosorbide dinitrate lowered the resting mean blood pressure (82 +/- 9. mm Hg to 78 +/- 10 mm Hg, (p less than 0.03)) and the resulting pulmonary wedge pressure (26 +/- 5 mm Hg to 12 +/- 6 mm Hg, (p less than 0.01)). Isosorbide dinitrate acutely improved exercise duration during upright bicycle exercise at a workload fixed at 50 percent of the maximal workload (placebo): 21.8 +/- 14.1 min vs isosorbide dinitrate: 31.4 +/- 13.6 min, (p less than 0.003)) due to reduced exertional dyspnea. Administration of chewable isosorbide dinitrate acutely improved submaximal exercise tolerance in patients with chronic heart failure.

Double-Blind Method↗

PubMedDate not supplied

Short-term exercise training in patients with chronic atrial fibrillation: effects on exercise capacity, AV conduction, and quality of life.

PURPOSE: A randomized study was conducted to determine whether short-term exercise training in patients with chronic atrial fibrillation (AF) might improve exercise capacity and quality of life (QOL), and influence atrioventricular conduction. METHODS: Atrial fibrillation patients (age 64 +/- 7 years) were randomized to exercise training (n = 15) or a 2-month control period (n = 15) followed by the training program. Twenty-four training sessions consisted of aerobic exercise and muscle strengthening. A cycle ergometer test and a 15-minute resting high-frequency spectral electrocardiogram analysis were performed and a QOL questionnaire (SF-36) was completed before and after training. Because there were no changes after 2 months in the control group, pooled data for all patients are presented before and after training. RESULTS: Cumulated work at Borg scale 17 increased by 41% +/- 36%. Heart rate at rest and after 10 minutes of exercise decreased from 75 +/- 14 to 68 +/- 14 bpm and 145 +/- 19 to 137 +/- 21 bpm, respectively. HF increased from 81 +/- 17 to 91 +/- 22 milliseconds. Four of the 8 scales and 1 of the 2 summary scales of the Short-Form-36 improved. P <.05 for all results. CONCLUSIONS: Exercise capacity, heart rate variability, and QOL improved after 2 months of exercise training in patients with chronic AF. Heart rates at rest and during exercise decreased.

Aged↗

PubMed1987

The effect of oral supplementation with L-carnitine on maximum and submaximum exercise capacity.

Two trials were conducted to investigate the effects of L-carnitine supplementation upon maximum and submaximum exercise capacity. Two groups of healthy, untrained subjects were studied in double-blind cross-over trails. Oral supplementation of 2 g per day L-carnitine was used for 2 weeks in the first trial and the same dose but for 4 weeks in the second trial. Maximum and submaximum exercise capacity were assessed during a continuous progressive cycle ergometer exercise test performed at 70 rpm. In trial 1, plasma concentrations of lactate and beta-hydroxybutyrate were measured pre- and post-exercise. In trial 2, pre- and post-exercise plasma lactate were measured. The results of treatment with L-carnitine demonstrated no significant changes in maximum oxygen uptake (VO2max) or in maximum heart rate. In trial 1, there was a small improvement in submaximal performance as evidenced by a decrease in the heart-rate response to a work-load requiring 50% of VO2max. The more extensive trial 2 did not reproduce the significant result obtained in trial 1, that is, there was no significant decrease in heart rate at any given submaximal exercise intensity, under carnitine-supplemented conditions. Plasma metabolic concentrations were unchanged following L-carnitine, in both trials. It is concluded, that in contrast to other reports, carnitine supplementation may be of little benefit to exercise performance since the observed effects were small and inconsistent.

3-Hydroxybutyric Acid↗

PubMed2005

Exercise capacity and cardiovascular adaptations to aerobic training early after stroke.

Clinicians are becoming increasingly interested in the use of aerobic training to enhance functional outcomes after stroke. Several studies have demonstrated the effectiveness of training among individuals in the chronic poststroke period. However, there is limited information on the response to training in earlier stages of recovery. The purpose of this article is to review what is known regarding the capacity of people early after stroke (<4 months) to respond to the physiological demands of exercise (exercise capacity) as well as their ability to make long-term cardiovascular adaptations to aerobic exercise. There is evidence that exercise capacity, as measured by peak oxygen consumption on maximal exercise tests, is reduced in this population. There is also evidence, albeit limited, that exercise trainability soon after stroke can be both feasible and safe, if appropriate screening and monitoring are used. Moreover, there are early indications that activity-level functions such as walking speed, mobility, and balance may be enhanced through such programs. Further research is necessary to elucidate the most appropriate timing and design of fitness programs for people early after stroke.

Activities of Daily Living↗

PubMed2002

Epidural analgesia enhances functional exercise capacity and health-related quality of life after colonic surgery: results of a randomized trial.

BACKGROUND: Multimodal analgesia programs have been shown to decrease hospital stay, but it not clear which functions are restored after surgery. The objective of this study is to evaluate the impact of epidural anesthesia and analgesia on functional exercise capacity and health-related quality of life. METHODS: Sixty-four patients undergoing elective colonic resection were randomized to either patient-controlled analgesia with morphine or thoracic epidural analgesia with bupivacaine and fentanyl (epidural group). All patients in both groups received similar perioperative care and were offered the same amount of postoperative oral nutrition and assistance with mobilization. Primary outcome was functional exercise capacity as measured by the 6-min walking test, and secondary outcome was health-related quality of life, as measured by the SF-36 health survey. These were assessed before surgery and at 3 and 6 weeks after hospital discharge. Other variables measured in hospital included pain and fatigue visual analogue scale, bowel function, time out of bed, nutritional intake, complication rate, readiness for discharge, and length of hospital stay. RESULTS: Although the 6-min walking test and the SF-36 physical health component decreased in both groups at 3 and 6 weeks after surgery, the patient-controlled analgesia group experienced a significantly greater decrease at both times (P < 0.01). Patients in the epidural group had lower postoperative pain and fatigue scores, which allowed them to mobilize to a greater extent (P < 0.05) and eat more (P < 0.05). Length of hospital stay and incidence of complications were similar in both groups, although patients in the epidural group were ready to be discharged earlier. CONCLUSIONS: The superior quality of pain relief provided by epidural analgesia had a positive impact on out-of-bed mobilization, bowel function, and intake of food, with long-lasting effects on exercise capacity and health-related quality of life.

Adult↗

PubMed1997

Improvement in lower limb vasodilatory reserve and exercise capacity in patients with chronic heart failure due to valvular heart disease.

AIMS: Reduced skeletal muscle blood flow during exercise is an important factor contributing to exercise intolerance in patients with chronic heart failure. Reactive hyperaemic blood flow is the maximum flow response necessary to protect tissue against ischaemia and hypoperfusion. We examined the vasodilatory response of the lower limb to ascertain whether response was increased with the improvement in exercise capacity observed after intracardiac surgery in patients with chronic heart failure due to valvular heart disease. METHODS AND RESULTS: Calf blood flow in 23 patients was measured by venous occlusion plethysmography at rest and after a 5 min period of femoral occlusion. Immediately after this evaluation, peak oxygen uptake and anaerobic threshold were assessed by a symptom-limited cardiopulmonary exercise test using a bicycle ergometer. Both baseline calf blood flow and peak calf blood flow during reactive hyperaemia were significantly increased after surgery (baseline calf blood flow; from 2.6 +/- 0.2 to 3.8 +/- 0.4 ml.min-1 per 100 ml calf volume, P < 0.05: peak calf blood flow; from 17.5 +/- 1.3 to 25.4 +/- 2.6 ml.min-1 per 100 ml calf volume, P < 0.01). There was a significant correlation between changes in peak calf blood flow and improvement in exercise capacity (peak oxygen uptake; r = 0.42, P < 0.05; anaerobic threshold; r = 0.68, P < 0.0010). CONCLUSION: These results indicate that exercise tolerance is improved with increased lower limb vasodilatory capacity after recovery from chronic heart failure.

Aged↗

PubMed2003

Reduced exercise capacity in untreated adults with primary growth hormone resistance (Laron syndrome).

OBJECTIVE: Primary IGF-I deficiency (Laron syndrome, LS) may decrease exercise capacity as a result of a lack of an IGF-I effect on heart, peripheral muscle or lung structure and/or function. METHODS: Eight patients (six females) who had never received treatment with IGF-I, with mean age of 36 +/- 10 (SD) years (range 21-48), weight 47 +/- 9 kg (31-61), height 126 +/- 12 cm (112-140) and body mass index of 29 +/- 4 kg/m2 (24-34), and 12 age-matched controls, underwent lung function tests and incremental cycling to the limit of tolerance (CPX, MedGraphics). Predicted values for the patients were derived from adult equations based on height. RESULTS: In LS patients, lung function was near normal; vital capacity was 84 +/- 11% of expected (66-103). Peak exercise O2-uptake and the anaerobic threshold were reduced, 57 +/- 20% of predicted and 33 +/- 9% of predicted peak (P = 0.005 vs. controls), despite normal mean exercise breathing reserve. All parameters were normal in the controls. CONCLUSION: Exercise capacity in untreated adults with LS is significantly reduced. The limitation for most patients was not ventilatory but resulted either from low cardiac output and/or from dysfunction of the peripheral muscles. However, the relative contribution of each of these elements and/or the role of poor fitness needs further study.

Adult↗

PubMed1998

Acute and chronic effects of propionyl-L-carnitine on the hemodynamics, exercise capacity, and hormones in patients with congestive heart failure.

Carnitine is an important cofactor in the intermediary metabolism of the heart, and carnitine deficiency is associated with congestive heart failure. We therefore studied the effects of acute (IV bolus, 30 mg/kg body weight) and chronic administration (1.5 mg/d for 1 month) of propionyl-L-carnitine on hemodynamics, hormone levels, ventricular function, exercise capacity, and peak oxygen consumption in 30 patients with chronic congestive heart failure (NYHA II-III, mean EF 29.5 +/- 7%) in a phase II, parallel, single-blind, randomized, and placebo-controlled study. Acute administration of propionyl-L-carnitine caused a significant reduction in pulmonary artery and pulmonary wedge pressures at both day 1 (P < 0.001) and day 30 (P < 0.05) of the study but no other hemodynamics changes. Hormone levels did not change following acute administration of the drug. Chronic administration of propionyl-L-carnitine increased peak oxygen consumption by 45% (from 16.0 +/- 3 to 23.5 +/- 2 mL/kg/min, P +/- 0.001), exercise time by 21% (from 8.1 +/- 0.5 to 9.8 +/- 0.4 minutes, P < 0.01), and peak exercise heart rate by 12% (P < 0.01). These changes were concomitant with a reduction of pulmonary artery pressure. In the treated group, there was a slight, but significant (P < 0.01), reduction in left ventricular dimensions. Hemodynamics and hormones measured after 1 month of oral therapy remained unchanged, except for a fall in pulmonary artery pressures, with a nonsignificant trend towards a fall in filling pressures and plasma norepinephrine. The chronic changes in the propionyl-L-carnitine group were seen at 15 days of treatment, and no further changes in these parameters were seen at 1 month. We conclude that propionyl-L-carnitine increases exercise capacity and reduces ventricular size in patients with congestive heart failure. The drug has no significant effects on hemodynamics or neurohormone levels. The use of a single-blind design reduces the impact of the positive finding on exercise capacity.

Adult↗

PubMed1986

Exercise capacity and spontaneous heart rhythm after transvenous fulguration of atrioventricular conduction.

Twenty nine patients who had had refractory supraventricular tachycardia were studied 4-36 (mean 16) months after transvenous fulguration of the atrioventricular junction. Twenty two had complete atrioventricular block, five partial atrioventricular block, and two had atrioventricular conduction via an accessory atrioventricular pathway. Though all patients were free of palpitation after the procedure, exertional dyspnoea had developed in 13 and in two patients pre-existing dyspnoea had worsened. During ventricular demand pacing, exercise time was reduced to 43% of the predicted value for their age and sex. The 16 patients with rate responsive pacemakers demonstrated a significantly better but still impaired exercise capacity during "physiological" pacing as compared with their performance during constant rate pacing. In patients with complete atrioventricular block there was an increase in spontaneous ventricular rate during exercise in seven patients and in response to the Valsalva manoeuvre in eight patients. This suggests that the intrinsic ventricular pacemaker is influenced by autonomic nervous system activity in some patients. It is concluded that though transvenous fulguration is successful in controlling tachycardia it may reduce exercise capacity. Most patients remain in complete atrioventricular block after the procedure and, in contrast with the practice as described in early reports, would benefit from "physiological" pacing--though even with this mode exercise capacity is likely to be abnormal.

Adult↗

PubMed2002

Predictors of change in exercise capacity after comprehensive COPD inpatient rehabilitation.

BACKGROUND: In order to evaluate the factors associated with change in exercise capacity after comprehensive inpatient Pulmonary Rehabilitation (IPR) we studied 132 consecutive adults with Chronic Obstructive Pulmonary Disease (COPD) recovering from an acute exacerbation. MATERIAL/METHODS: Lung function, arterial blood gases, and respiratory muscle strength were measured at baseline. Perceived breathlessness (B), 6-minute walk distance (6MWD), dyspnea at rest and post-exertion (D), hospital anxiety and depression (HAD), and health-related quality of life were assessed before (T0) and after (T1) IPR. The patients were divided into two groups depending on the change in 6MWD: Improvers (IM at least +54 meters after IPR, n=81) or Non-Improvers (NIM, less than 54 meters or no change, n=51). RESULTS: At T1 61% of the patients showed improvement as here defined. The IM group showed lower 6MWD and higher B and resting-D at T0 than NIM (p<0.05). A stepwise multiple regression analysis was performed using 6MWD change as the dependent variable. and anthropometric and physiological measures at T0 as the independent variables. This regression model explained 26% of the 6MWD-change; 6MWD and PaO2 significantly contributed to this model. CONCLUSIONS: In COPD patients recovering from an acute exacerbation, the predicted change in exercise capacity using anthropometric, demographic, clinical, and physiological variables after 2 weeks of comprehensive IPR is likely to be low. The baseline level of exercise performance and arterial oxygenation show the most consistent correlation with change in walking ability in these patients.

Aged↗

PubMed1989

Relation of exercise capacity to resting arterial oxygen transport in left ventricular dysfunction.

To determine the relation between arterial oxygen delivery and exercise capacity, 38 men with mild to severe chronic left ventricular (LV) dysfunction (New York Heart Association functional class II or III) were studied. All diagnostic cardiac catheterizations were performed 1 week before the exercise tests and the mean LV ejection fraction was 0.30 +/- 0.07. All patients performed graded treadmill exercise tests according to the Sheffield protocol. The relation between supine resting hemodynamic measurements did not correlate with exercise duration. Only resting cardiac output (r = 0.54, p less than 0.01) and systemic vascular resistance (r = -0.51, p less than 0.05) correlated weakly with exercise duration. However, arterial oxygen transport was highly related to exercise duration (r = 0.76, p less than 0.001) and peak oxygen consumption (r = 0.71, p less than 0.001). Thus, knowledge of calculated arterial oxygen transport can predict exercise capacity in patients with chronic LV dysfunction.

Adult↗

PubMed1983

Failure of dobutamine to increase exercise capacity despite hemodynamic improvement in severe chronic heart failure.

The acute hemodynamic and metabolic effects of dobutamine administered during exercise were studied in 8 patients with severe chronic heart failure. Exercise was performed on an upright bicycle ergometer using a graded protocol. During exercise performed without administration of dobutamine, exhaustion occurred after 4.5 +/- 1.2 minutes of exercise. The cardiac index increased from 1.61 +/- 0.25 to 2.67 +/- 0.59 liters/min/m2 (p less than 0.001), the arteriovenous oxygen difference from 7.8 +/- 1.7 to 12.5 +/- 2.4 ml/100 ml (p less than 0.001), and oxygen uptake from 7.9 +/- 3.0 to 41.2 +/- 15.7 mg/100 ml (p less than 0.001). During exercise performed with the administration of dobutamine, the cardiac index was significantly greater than during the control state, 3.23 +/- 0.78 versus 2.67 +/- 0.59 liters/min/m2 (p less than 0.001), while the arteriovenous oxygen difference was significantly lower, 11.2 +/- 2.1 vs 12.5 +/- 2.4 ml/100 ml (p less than 0.01). The arterial lactate level was not significantly changed, 45.3 +/- 17.6 versus 41.2 +/- 15.7 mg/100 ml. Although the dobutamine level tended to increase maximal oxygen uptake compared with the control period of exercise, 9.1 +/- 1.2 versus 8.5 +/- 1.4 ml/kg/min (p less than 0.05), it did not significantly increase exercise capacity, 4.8 +/- 1.5 versus 4.5 +/- 1.2 min. Thus administration of dobutamine in patients with severe chronic heart failure increased the cardiac index during maximal exercise but failed to increase exercise capacity. Since arteriovenous oxygen difference is reduced, dobutamine probably increases blood flow to the nonexercising tissues and not to the actively metabolizing muscles.

Cardiac Output↗

PubMed1998

Relative efficacy of medical therapy and revascularization for improving exercise capacity in patients with chronic left ventricular dysfunction.

BACKGROUND: In patients with left ventricular dysfunction one of the aims of therapy may be to improve functional capacity. This study compared the improvement of functional capacity in response to medical therapy with that caused by revascularization. METHODS: Fifty-two patients with severe left ventricular dysfunction were divided into groups with ischemic cardiomyopathy undergoing revascularization (group A, n = 20) or incremental medical treatment (group B, n = 16) and a control group receiving maximal medical therapy at the start of the study (group C, n = 16). All patients underwent a baseline metabolic exercise test with evaluation of peak oxygen consumption and derived exercise capacity in metabolic equivalents (METS) with standard electrocardiographic and hemodynamic monitoring. Therapy was then optimized in the medical treatment group, whereas the revascularization group underwent coronary bypass grafting. All patients subsequently underwent follow-up metabolic exercise testing. RESULTS: In groups A, B, and C resting left ventricular ejection fractions were comparable (26%+/-5%, 25%+/-7%, and 23%+/-8%, respectively), as were results of initial metabolic exercise tests (4.7+/-0.9 METS, 4.7+/-1.4 METS, and 5.2+/-1.4 METS). At follow-up group A improved exercise capacity from 4.7 to 5.6 METS (p = 0.01). Groups B (4.7 to 5.0 METS) and C (5.2 to 5.6 METS) had no significant improvement. The mean respiratory exchange ratio improved significantly in group A (1.14 to 1.20, p = 0.02), as did left ventricular ejection fraction (26% to 31%, p = 0.02). However, neither parameter changed significantly in groups B or C. CONCLUSIONS: In patients with severe left ventricular dysfunction improvements of exercise capacity are more marked after coronary revascularization than may be obtained after maximization of medical therapy.

Adult↗

PubMed1995

Good exercise capacity at hospital discharge predicts recovery of baroreflex sensitivity after myocardial infarction.

Myocardial infarction results in depressed baroreflex sensitivity, which has been shown to be associated with increased risk of ventricular arrhythmias and sudden death. We measured baroreflex sensitivity in 37 patients with acute myocardial infarction before hospital discharge and 3 months after the infarction to find out whether the baroreflex sensitivity recovers during that period. In addition, baroreflex sensitivity was assessed in 15 healthy controls. Baroreflex sensitivity was assessed from the regression line relating the change in R-R interval to the change in systolic blood pressure following an intravenous bolus injection of phenylephrine. There was a wide inter-individual variation in the change of baroreflex sensitivity (delta baroreflex sensitivity) in infarction patients, but the average baroreflex sensitivity showed no significant change during the 3-month follow-up (10.2 + 5.6 to 11.8 +/- 7.5 ms.mmHg-1, ns) and remained lower than the baroreflex sensitivity of the controls (16.4 +/- 9.7 ms.mmHg-1, P < 0.05). delta Baroreflex sensitivity correlated significantly with exercise capacity measured before hospital discharge. When the patients were divided into tertiles according to the delta baroreflex sensitivity (-3.3 +/- 1.5 ms.mmHg-1 in the lowest tertile, 1.0 +/- 1.0 ms.mmHg-1 in the middle tertile and 7.5 +/- 4.0 ms.mmHg-1 in the highest tertile) the exercise capacity was found to increase from the lowest to the highest tertile (exercise time 357 +/- 115 s, 418 +/- 126 s and 461 +/- 141 s, respectively; P < 0.05 lowest vs highest tertile). Patients with a low exercise tolerance (exercise time < 360 s) showed a significantly smaller delta baroreflex sensitivity than patients with a good exercise tolerance (exercise time > or = 480 s) (-0.5 +/- 4.4 vs 5.3 +/- 5.4 ms.mmHg-1, P < 0.05), respectively. delta Baroreflex sensitivity was not related to the location or type of infarction, thrombolytic therapy, presence of angina pectoris or left ventricular function at the time of discharge. In conclusion, exercise capacity assessed before hospital discharge seems to be a predictor of baroreflex sensitivity recovery in patients with a recent myocardial infarction.

Aged↗

PubMed1992

Hemodynamic changes due to afterload reduction as a predictor of exercise capacity in patients with dilated cardiomyopathy.

Sixteen patients with dilated cardiomyopathy were examined hemodynamically in order to clarify the relationship between the exercise capacity and the effects of afterload reduction at rest using supine graded bicycle exercise testing before and after sublingual administration of 10 mg nifedipine. 1) The integration of work loads was weakly correlated with the stroke index (r = 0.64), heart rate (r = -0.58) and plasma norepinephrine concentration at rest (r = 0.49), but not with the left ventricular ejection fraction, cardiac index, pulmonary arterial diastolic pressure or the mean arterial pressure at rest. 2) Changes in stroke index and heart rate after administration of nifedipine correlated well with the integration of work loads (r = -0.84, r = 0.81, respectively). Thus, in patients with dilated cardiomyopathy changes in stroke volume and heart rate due to afterload reduction at rest were better predictors of exercise capacity than the baseline left ventricular hemodynamic parameters.

Adult↗

PubMed2005

Myocardial and vascular dysfunction and exercise capacity in the metabolic syndrome.

The metabolic syndrome (MS) is associated with cardiovascular risk exceeding that expected from atherosclerotic risk factors, but the mechanism of this association is unclear. We sought to determine the effects of the MS on myocardial and vascular function and cardiorespiratory fitness in 393 subjects with significant risk factors but no cardiovascular disease and negative stress echocardiographic findings. Myocardial function was assessed by global strain rate, strain, and regional systolic velocity (s(m)) and diastolic velocity (e(m)) using tissue Doppler imaging. Arterial compliance was assessed using the pulse pressure method, involving simultaneous radial applanation tonometry and echocardiographic measurement of stroke volume. Exercise capacity was measured by expired gas analysis. Significant and incremental variations in left ventricular systolic (s(m), global strain, and strain rate) and diastolic (e(m)) function were found according to the number of components of MS (p <0.001). MS contributed to reduced systolic and diastolic function even in those without left ventricular hypertrophy (p <0.01). A similar dose-response association was present between the number of components of the MS and exercise capacity (p <0.001) and arterial compliance. The global strain rate and e(m) were independent predictors of exercise capacity. In conclusion, subclinical left ventricular dysfunction corresponded to the degree of metabolic burden, and these myocardial changes were associated with reduced cardiorespiratory fitness. Subjects with MS who also have subclinical myocardial abnormalities and reduced cardiorespiratory fitness may have a higher risk of cardiovascular disease events and heart failure.

Blood Pressure↗

PubMed1994

Moderate carnitine depletion and long-chain fatty acid oxidation, exercise capacity, and nitrogen balance in the rat.

Carnitine plays a central role in lipid metabolism by transporting long-chain fatty acids into the mitochondria for beta-oxidation. Reduction of carnitine concentration does not automatically imply that functional carnitine deficiency exists with direct consequences on energy metabolism. In our experimental model, we reduced tissue concentrations of carnitine to levels that are comparable to those in patients with various metabolic disorders with secondary carnitine deficiency and did a study on the in vivo effects of moderate carnitine depletion on palmitate oxidation, exercise capacity, and nitrogen balance. Thirty rats were divided into a carnitine-depleted group (group I) and pair-fed controls (group II). Carnitine depletion resulting in a 48% reduction of tissue carnitine concentrations was induced by feeding ad libitum a carnitine-free oral diet consisting of parenteral nutrition solutions. Palmitate oxidation was measured by collecting expired 14CO2 after an intraperitoneal injection of [1-14C]palmitate, and exercise capacity was determined by having the rats swim to exhaustion. Despite the 48% depletion of carnitine in serum, muscle, and liver, there were no differences in cumulative palmitate oxidation in 3 h (group I, 40 +/- 7%; group II, 37 +/- 9% of injected activity), swimming time to exhaustion (group I, 8.1 +/- 2.8 h; group II, 7.7 +/- 3.6 h), or nitrogen balance (group I, 1.1 +/- 0.5 g of nitrogen/kg/d; group II, 1.2 +/- 0.5 g of nitrogen/kg/d). We conclude that carnitine depletion of 48% has no effect on palmitate oxidation, exercise capacity, or nitrogen balance in the rats studied.

Animals↗