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Effect of isotonic exercise training on left ventricular volume during upright exercise.

To determine the changes in left ventricular volume and their time course during exercise we studied 30 runners. Left ventricular end-diastolic and end-systolic volumes were measured from biapical two-dimensional echocardiograms recorded during graded upright bicycle exercise. The validity of this echocardiographic technique was assessed by comparing measurements at rest and exercise with results obtained by gated equilibrium radionuclide angiography in 10 patients with coronary artery disease. Although the absolute volume measurements were lower by echocardiography, ejection fraction was not significantly different and the directional changes in volume during exercise were comparable. In the runners, resting left ventricular end-diastolic volume measurements by echocardiography correlated with their maximum bicycle exercise endurance times (r = .80). Left ventricular end-diastolic volume, stroke volume, and ejection fraction increased during exercise with the most marked changes occurring in the first half of exercise. Systolic blood pressure/end-systolic volume (SBP/ESV) also increased during exercise, but the largest change occurred during the second half of exercise. Left ventricular volumes were larger in the 12 competitive marathon runners (maximum exercise duration greater than or equal to 27 min) as compared with the 18 noncompetitive runners (exercise duration less than or equal to 23 min): resting end-diastolic volume 130 +/- 29 (SD) ml vs 87 +/- 20 ml (p less than .001), respectively. During exercise the competitive runners exhibited a larger increase in end-diastolic volume and the noncompetitive athletes showed a greater increase in SBP/ESV. Therefore, highly trained competitive marathon runners make greater use of the less energy-consuming Frank-Starling mechanism to accomplish high levels of isotonic exercise performance as compared with less well-trained runners.

Blood Pressure↗

Role of exercise echocardiography as a predictor of coronary artery disease. Detection of exercise-induced asynergy by M-mode echocardiography.

Left ventricular asynergy has been shown to occur commonly in patients with coronary artery disease (CAD) and to be induced or exaggerated by exercise. The purpose of this study is to report on a method to detect asynergy and estimate its severity by M-mode echocardiographic analysis of left ventricular wall motion at rest and during supine ergometric exercise. Sixteen patients with CAD underwent graded supine ergometric exercise until anginal pain occurred or apparent ischemic changes were noted on ECG. This study was done using the following criteria: 1) Asynergy at rest was defined as occurring when the amplitudes of the interventricular septum and/or the posterior left ventricular wall were below normal values at rest. 2) Asynergy during exercise was defined as occurring when one or both of the two amplitudes were more than 2 mm below the values at rest (severe) or were unchanged in spite of sufficient exercise load (mild). The results were as follows: 1) In the normal subjects, the septal and posterior wall amplitudes increased during exercise (ranging from 7 mm to 9 mm for the septum, and from 13 mm to 16 for the posterior wall). In patients with CAD, asynergy at rest was demonstrated in only 3 cases (19%), whereas septal and/or posterior wall asynergy during exercise was noted in 75% of cases. 2) The location of exercise-induced asynergy detected by echocardiography showed a good correlation with that of coronary artery lesions (greater than or equal to 75% stenosis) recognized by angiography. 3) Significant differences were observed between changes in left ventricular dimensions in patients with CAD and those of normals during exercise. In the normal subjects, left ventricular end-systolic dimension (ESD) decreased without significant change in end-diastolic dimension (EDD) during exercise. On the other hand, both ESD and EDD increased during exercise in patients with CAD. Although echocardiographic analysis of left ventricular wall motion during exercise has some limitations, this study suggests that asynergy induced or exaggerated by ergometric exercise can be successfully detected by M-mode echocardiography.

Adult↗

Symptoms, exercise capacity and exercise hemodynamics: interrelationships and their role in quantification of the valvular lesion.

To compare the symptoms with the objectively-determined exercise capacity, the symptoms as well as the exercise capacity with the exercise hemodynamics and the symptoms, exercise capacity and exercise hemodynamics with the severity of the valvular lesion, in 154 patients with aortic regurgitation, mitral regurgitation, aortic stenosis or mitral stenosis, the symptoms were classified according to the New York Heart Association and the exercise capacity was determined by means of bicycle ergometry with simultaneous measurement of heart rate, blood pressure, pulmonary artery pressure, cardiac output and the left ventricular ejection fraction. Among the parameters studied, no relationships could be established; to a certain degree, the exercise hemodynamics correlated with the severity of the valvular lesion in that a markedly pathologic response was associated with the presence of a high-grade valvular lesion. Since the symptoms were not indicative of the exercise capacity, nor the symptoms or the exercise capacity of either the exercise hemodynamics, the exercise ejection fraction or the severity of the valvular lesion, the symptoms and the exercise capacity should be evaluated on the basis of the exercise hemodynamics before they are taken into consideration for meaningful decision-making processes such as establishment of the indication for surgery.

Adolescent↗

Patients with high baseline exercise capacity benefit from cardiac rehabilitation and exercise training programs.

Despite the well-proven benefits of cardiac rehabilitation and exercise training, no data are available on the benefits of this therapy in patients with preserved baseline exercise capacity. Therefore we assessed data before and after phase II cardiac rehabilitation and exercise programs at two large teaching institutions to determine the benefits in 163 patients with high baseline exercise capacity (> or = 6 estimated [mean 8.8 +/- 2.4] metabolic equivalents [METs]) compared with 125 patients with low baseline functional capacity (< 6 estimated [mean 4.6 +/- 0.8] METs). After cardiac rehabilitation and exercise training, patients with high baseline exercise capacity had significant improvements in triglyceride (-10%; p < 0.05), high-density lipoprotein cholesterol (+7%; p < 0.001), and low-density lipoprotein cholesterol (-4%; p = 0.09) levels; low-density lipoprotein/high-density lipoprotein ratio (-10%; p < 0.01); body mass index (-1.5%; (p < 0.001); percent body fat (-6%; p < 0.0001); and exercise capacity (+22%; p < 0.0001). Patients with high baseline exercise capacity had less relative improvement in exercise capacity (p < 0.0001) after cardiac rehabilitation but had greater relative improvement in low-density lipoprotein cholesterol level (p < 0.05) and low-density lipoprotein/high-density lipoprotein ratio (p < 0.05) than did patients with low baseline exercise capacity. These data demonstrate the benefits of cardiac rehabilitation and exercise training in patients with preserved exercise capacity and support routine referral of these patients to these programs after major cardiac events.

Adult↗

Attenuation of exercise-induced ST depression during combined isometric and dynamic exercise in coronary artery disease.

ST-segment depression was measured during submaximal dynamic (treadmill) and combined isometric-dynamic (isodynamic) exercise at comparable rate-pressure products in 11 patients (mean age 63 years) with stable coronary artery disease who were participating in an exercise training program. Each patient completed 3 separate trials. Trial 1 (baseline) was a submaximal treadmill exercise test to determine the threshold heart rate-systolic blood pressure (rate-pressure product) for ST-segment depression (greater than or equal to 1.0 mm). During trials 2 and 3, patients performed (in random order) dynamic treadmill exercise and isodynamic exercise (treadmill walking 1.5 to 2.0 mph carrying 15 to 25 kg) until threshold rate-pressure product was achieved. During trial 1, each patient showed significant ST depression (mean 1.7 mm) at target rate-pressure product (mean 18,200). Subsequent dynamic exercise trials 2 and 3 showed similar mean ST depression (1.5 mm) and rate-pressure product (18,000). During isodynamic exercise trials 2 and 3, subjects showed only minimal ST depression (mean 0.4 mm) at a rate-pressure product similar to dynamic exercise (mean 18,590). Heart rates were significantly lower (-10/min) and systolic (+20 mm Hg) and diastolic (+25 mm Hg) pressure was higher during isodynamic exercise (p less than 0.05). The rate-pressure product is not a valid index of ST response during isodynamic exercise in stable exercise-trained cardiac patients. Attenuation of ST depression during isodynamic exercise may be attributed to a combination of increased diastolic perfusion pressure, decreased heart rate and possibly to reductions in venous return and ventricular diastolic wall tension due to increased intrathoracic and abdominal pressure.

Aged↗

GH secretion in acute exercise may result in post-exercise lipolysis.

Exercise is a potent stimulator of growth hormone (GH) secretion. We hypothesised that after a short bout of intense exercise GH may increase lipolysis during recovery. In 7 moderately trained young male subjects (21.8 +/- 0.5 years) and 7 moderately trained older male subjects (56.0 +/- 1.0 years) [(2)H(5)] glycerol was infused for 370min to measure glycerol production rate (R(a)), a measure of lipolysis. At 130 min subjects exercised on a cycle ergonometer for 20 min at 70% V(O2 max), followed by rest for 220 min. On a separate occasion the study was repeated in the young subjects with a 1h GH infusion (4microgkg(-1)h(-1)) at 130 min instead of exercise. In response to exercise, catecholamines (p < 0.02) and glycerol R(a) (p < 0.01) increased, peaking during exercise. GH concentration increased in response to exercise (p < 0.01), peaking after exercise (150-160 min) in both groups with no significant difference in peak response between groups. A post-exercise rise in glycerol R(a) was demonstrated in both groups peaking at 265-295 min in the older group (p < 0.002, peak vs. basal) and continuing to rise until 370 min in the young group (p < 0.01, peak vs. basal). The timing and magnitude of this was reproduced with the GH infusion. There was a significant correlation between the peak GH response to exercise and the post-exercise rise in glycerol R(a) measured as area under the curve (r=0.57, p < 0.04). In conclusion, this study provides evidence that the GH response to acute exercise may increase lipolysis during recovery.

Adult↗

Exercise capacity and mortality among men referred for exercise testing.

BACKGROUND: Exercise capacity is known to be an important prognostic factor in patients with cardiovascular disease, but it is uncertain whether it predicts mortality equally well among healthy persons. There is also uncertainty regarding the predictive power of exercise capacity relative to other clinical and exercise-test variables. METHODS: We studied a total of 6213 consecutive men referred for treadmill exercise testing for clinical reasons during a mean (+/-SD) of 6.2+/-3.7 years of follow-up. Subjects were classified into two groups: 3679 had an abnormal exercise-test result or a history of cardiovascular disease, or both, and 2534 had a normal exercise-test result and no history of cardiovascular disease. Overall mortality was the end point. RESULTS: There were a total of 1256 deaths during the follow-up period, resulting in an average annual mortality of 2.6 percent. Men who died were older than those who survived and had a lower maximal heart rate, lower maximal systolic and diastolic blood pressure, and lower exercise capacity. After adjustment for age, the peak exercise capacity measured in metabolic equivalents (MET) was the strongest predictor of the risk of death among both normal subjects and those with cardiovascular disease. Absolute peak exercise capacity was a stronger predictor of the risk of death than the percentage of the age-predicted value achieved, and there was no interaction between the use or nonuse of beta-blockade and the predictive power of exercise capacity. Each 1-MET increase in exercise capacity conferred a 12 percent improvement in survival. CONCLUSIONS: Exercise capacity is a more powerful predictor of mortality among men than other established risk factors for cardiovascular disease.

Adrenergic beta-Antagonists↗

The effects of 15 min and 30 min of exercise on affective responses both during and after exercise.

Although much research has examined the relationship between exercise and affect, few studies have considered the effects of exercise bouts of different durations and few researchers have questioned the longer term effects that might be associated with acute exercise. The aim of this study was to compare the effects of the standard health recommended exercise duration of 30 min with a shorter (15 min) bout of exercise upon individuals' affect scores both during and after exercise. Twenty-three (mean age 22.4 years) physically active participants engaged in two counterbalanced cycle ergometer exercise conditions for 15 min (short bout) and 30 min (moderate bout). The participants completed the Subjective Exercise Experience Scale before, during, 5 min, 30 mins, 1 h and 2 h after both exercise conditions. A series of 2 x 6 within-participant repeated-measures analyses of variance for positive well-being (P <0.01), psychological distress (P <0.01) and fatigue (P <0.01) scores revealed significant time main effects, with improved scores over time. No significant differences were noted between the 15-min and 30-min exercise bouts. These results indicate that positive affective responses are experienced by exercisers after relatively short bouts of acute exercise and these effects can still be evident some time later.

Adult↗

Effect of ticlopidine on exercise-induced platelet aggregation and exercise tolerance time in patients with ischemic heart disease.

Platelet aggregation is one of the most important mechanisms for acute myocardial infarction during exercise. We sought to evaluate the effect of ticlopidine (TP) on platelet aggregation (PA) during exercise in patients with ischemic heart disease (IHD). We studied 38 patients with IHD, 26 patients with effort angina pectoris, and 12 patients with a previous myocardial infarction. In protocol I, subjects were divided into two groups. Drugs altering platelet aggregation were withheld 2-4 weeks before the study in 25 patients (control group). TP (200 mg/day) was administered for 7 days in 13 patients (ticlopidine group). A symptom-limited modified Bruce protocol treadmill exercise test was performed. PA was measured at rest and after exercise by using optical densitometry induced by adenosine diphosphate (ADP). PA ratio (percentage of maximum) was compared. In protocol II, in 12 patients, treadmill exercise test and PA measurement were performed with and without TP. PA significantly increased after exercise in control (from 51.7+/-23.3% to 64.4+/-27.7%, p < 0.01) and ticlopidine (from 31.9+/-10.5% to 42.0+/-20.4%, p < .01) groups; however, its grade was lower in the ticlopidine group than in the control group. After exercise, PA was lower in the ticlopidine group than in control group (42.0+/-20.4% vs. 64.4+/-27.7%; p < 0.01). In the same patients, PA was lower with TP than without TP after exercise. Treadmill exercise-tolerance time was greater in the ticlopidine group than in the control group, but not statistically significant (762.3+/-139.2 vs. 711.6+/-169.6 s; NS). Exercise-tolerance time was significantly greater with TP than without TP in same patient (791.7+/-98.9 vs. 733.3+/-152.8 s; p < .05). TP suppressed the increase of PA during exercise and increased the exercise-tolerance time in patients with IHD.

Adenosine Diphosphate↗

Effects of infusion of L-arginine on exercise-induced myocardial ischemic ST-segment changes and capacity to exercise of patients with stable angina pectoris.

BACKGROUND: Results of recent studies show that intracoronary administration of L-arginine, the precursor of nitric oxide, restores endothelial function in subjects with coronary risk factors and minimal coronary artery lesions. However, few investigators have examined the clinical feasibility of using L-arginine for treatment of myocardial ischemia due to coronary artery disease. OBJECTIVE: To examine the effect of supplementary L-arginine on exercise-induced myocardial ischemia and capacity to exercise of patients with stable effort angina pectoris. METHODS: Twelve patients confirmed to have a single epicardial coronary artery stenosis underwent two treadmill exercise tests after infusion of 10% L-arginine solution or placebo (5% dextrose) according to a randomized single-blind crossover design on two days separated by an interval of less than 1 week. Respiratory gas exchange kinetics were measured and myocardial ischemia was estimated by electrocardiography before and during exercise. RESULTS: Infusion of L-arginine did not alter exercise-induced changes in heart rate and blood pressure, and objective parameters of capacity to exercise. Exercise-induced maximum ST-segment depression (by 2.1 +/- 0.9 mm; with L-arginine; by 1.9 +/- 0.9 mm with placebo, NS) and onset of 1 mm ST-segment depression after exercise (after 261 +/- 131 s with L-arginine; after 247 +/- 136 s with placebo, NS) also remained unchanged. However, ST-segment depression was restored to baseline after exercise significantly more quickly after infusion of L-arginine than it did with placebo (after 331 +/- 167 s with L-arginine; after 400 +/- 165 s with placebo: P < 0.01). CONCLUSION: Intravenous administration of L-arginine did not alter capacity to exercise or the threshold for exercise-induced myocardial ischemia. However, it did reduce the time taken for recovery after ST-segment depression, suggesting that an earlier resolution of exercise-induced myocardial ischemia occurred.

Aged↗

Exercise: Part II. Translating the exercise prescription.

Exercise comes in many forms and uses different substrates (fuels) for adenosine triphosphate (energy) production. The greater the intensity of exercise, the greater the relative contribution of carbohydrate as a fuel source. However, as intensity exceeds the anaerobic threshold, anaerobic glycolysis is inhibited, forcing a decrease in exercise intensity. Proper manipulation of the exercise prescription components can create the desired health and fitness benefits, provide a high level of carbohydrate utilization, and control exercise risks while maintaining exercise intensity at aerobic levels. The calculation of target heart rate zones and proper monitoring of exercise heart rates allows for greater compliance to exercise prescriptions. Individual responses to various exercise intensities and modalities require regular assessments. Monitoring blood glucose levels before and after exercise assists in prescribing exercise duration and exercise times in relation to the medication and dietary regimen.

Blood Glucose Self-Monitoring↗

Exercise-induced flow limitation, dynamic hyperinflation and exercise capacity in patients with bronchial asthma.

It is known that, in stable asthmatics at rest, tidal expiratory flow limitation (EFL) and dynamic hyperinflation (DH) are seldom present. This study investigated whether stable asthmatics develop tidal EFL and DH during exercise with concurrent limitation of maximal exercise work rate (WRmax). A total of 20 asthmatics in a stable condition and aged 32+/-13 yrs (mean+/-SD) with a forced expiratory volume in one second (FEV1) of 101+/-21% of the predicted value were studied. Only three patients exhibited an FEV1 below the normal limits. On a first visit, patients performed a symptom-limited incremental (20 W.min(-1)) bicycle exercise test. On the second visit, the occurrence of EFL (using the negative expiratory pressure technique) and DH (via reduction in inspiratory capacity) were assessed at rest and when cycling at 33, 66 and 90% of their predetermined WRmax. FEV1 was measured to detect exercise-induced asthma, 5 and 15 min after stopping exercise at 90% WRmax. Only one patient showed EFL at rest, whereas 13 showed EFL and DH during exercise. In these 13 asthmatics, exercise capacity was significantly reduced (WRmax 75+/-9% pred) compared to the seven non-EFL patients (WRmax 95+/-13% pred). Moreover, a significant correlation of WRmax (% pred) to the change in inspiratory capacity (percentage of resting value) from rest to 90% WRmax was found. Tidal EFL during exercise was not associated with exercise-induced asthma, which was detected in only three patients. In conclusion, tidal expiratory flow limitation and dynamic hyperinflation during exercise are common in stable asthmatics with normal spirometric results and without exercise-induced asthma, and may contribute to reduction in exercise capacity.

Adult↗

Is rest or exercise hypertension a cause of a false-positive exercise test?

STUDY OBJECTIVES: To determine if a history of hypertension or an exaggerated rise in exercise systolic BP is associated with a false-positive exercise ECG. DESIGN, SETTING, AND PATIENTS: Retrospective analysis of the associations between exercise-induced ST-segment depression and a history of hypertension, exercise systolic BP, and several other clinical and exercise test variables. Among 20,097 patients referred for exercise tomographic thallium imaging in a nuclear cardiology laboratory at a tertiary care center, 1,873 patients met inclusion criteria for this study, which included no history of myocardial infarction or coronary artery revascularization, a normal resting ECG, and normal exercise thallium images. RESULTS: False-positive ST-segment depression occurred in 20% of the population. A history of hypertension was actually associated with a lower likelihood of ST-segment depression (odds ratio, 0.70; 95% confidence interval [CI], 0.55 to 0.89; p = 0. 004). A higher peak exercise systolic BP was associated with a higher likelihood of ST-segment depression (odds ratio, 1.08 for each 10-mm Hg increase in systolic BP; 95% CI, 1.03 to 1.14; p < 0. 001). However, the association between peak exercise systolic BP and ST-segment depression was so weak that this measurement could not be predictive in the individual patient (R(2) = 0.2%). For every 20-mm Hg increase in peak exercise systolic BP, the percentage of patients with ST-segment depression increased by only 3%. CONCLUSIONS: In patients with normal resting ECGs, we conclude the following: (1) a history of hypertension is not a cause of a false-positive exercise test, and (2) higher exercise systolic BP is a significant but weak predictor of ST-segment depression.

Blood Pressure↗

Changes in blood levels of eosinophil cationic protein and tryptase after exercise challenge in adolescents with exercise-induced asthma.

BACKGROUND: Exercise-induced asthma (EIA) is increasingly encountered among school children in Kuwait. Available evidence has shown that inflammatory mediators may be involved in the pathogenesis of EIA. Studies on release of inflammatory mediators have been carried out in adult patients with asthma in Kuwait, but no study on EIA involving children has taken place in this region. OBJECTIVE: To investigate changes in the concentration of some of the mediators involved in EIA in adolescent school children, using exercise challenge. DESIGN: Prospective, case control study. SETTING: Respiratory and Cardiology units Mubarak Hospital, Kuwait, between January and June 2001. SUBJECTS: Nine EIA and 14 non-EIA and 10 normal control subjects, designated as groups one, two and three aged between 13 and 17 years, who were non-smokers, were enrolled for the study. MAIN OUTCOME MEASURES: Blood eosinophils (EOS), eosinophil cationic protein (ECP) and tryptase were estimated pre-exercise, 5 and 30 minutes after exercise. Spirometry was measured at the same period. RESULTS: In group one, ECP and tryptase levels fell after exercise, but significant difference in the levels were obtained only in tryptase between pre-exercise and 30 minutes after exercise (4.1 microg/L Vs 3.8 microg/L) P <0.05, while the difference for ECP was not significant (P=0.09). In group two, both tryptase (6.0 microg/L Vs 5.7 microg/L) P < 0.05, and ECP (21.8 microg/L Vs 12.1 microg/L) P<0.01, fell after exercise. However, in group three, no appreciable difference was observed between pre and post exercise. Correlation between tryptase and EOS (r=0.770; P<0.05) and between tryptase and ECP (r=0.850; p<0.05) was observed pre-exercise and after exercise in groups one and two. CONCLUSION: A fall in the level of the mediators was observed after exercise challenge, but the relevance of this finding in the pathogenesis of EIA remains unclear. Further studies are required to verify this finding.

Adolescent↗

Supervised exercise therapy versus non-supervised exercise therapy for intermittent claudication.

BACKGROUND: Although exercise therapy is considered to be of significant benefit to people with leg pain (intermittent claudication), almost half of those affected do not undertake any exercise therapy. OBJECTIVES: To evaluate the effects of supervised versus non-supervised exercise therapy on the maximal walking time or distance for people with intermittent claudication. SEARCH STRATEGY: The Cochrane Peripheral Vascular Diseases Group searched their Specialized Register (last searched November 2005) and the Cochrane Central Register of Controlled Trials (CENTRAL) database in The Cochrane Library (last searched Issue 4, 2005). In addition, we handsearched the reference lists of relevant articles for additional trials. There was no restriction on language of publication. SELECTION CRITERIA: Randomized and controlled clinical trials comparing supervised exercise programs with non-supervised exercise programs for people with intermittent claudication. DATA COLLECTION AND ANALYSIS: Two authors (BB and EMW) independently selected trials and extracted data. One author (BB) assessed trial quality and this was confirmed by a second author (MP). For all continuous outcomes we extracted the number of participants, the mean differences, and the standard deviation. If data were available, the standardized mean difference was calculated using a fixed-effect model. MAIN RESULTS: We identified twenty-seven trials, of which 19 had to be excluded because the control group received no exercise therapy at all. The remaining eight trials involved a total of 319 male and female participants with intermittent claudication. The follow up ranged from 12 weeks to 12 months. In general, the supervised exercise regimens consisted of three exercise sessions per week. All trials used a treadmill walking test as one of the outcome measures. The overall quality of the included trials was good, though the trials were all small with respect to the number of participants, ranging from 20 to 59. Supervised exercise therapy showed statistically significant and clinically relevant differences in improvement of maximal treadmill walking distance compared with non-supervised exercise therapy regimens, with an overall effect size of 0.58 (95% confidence interval 0.31 to 0.85) at three months. This translates to a difference of approximately 150 meters increase in walking distance in favor of the supervised group. AUTHORS' CONCLUSIONS: Supervised exercise therapy is suggested to have clinically relevant benefits compared with non-supervised regimens, which is the main prescribed exercise therapy for people with intermittent claudication. However, the clinical relevance has not been demonstrated definitely and will require additional studies with a focus on the improvements in quality of life.

Directly Observed Therapy↗