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Right ventricular dysfunction and the exercise limitation of chronic obstructive pulmonary disease.

This study examined right ventricular function during exercise in patients with chronic obstructive pulmonary disease to answer the following questions: Is there a significant correlation between oxygen consumption at maximal exercise and exercise right ventricular ejection fraction? Does the right ventricular ejection fraction response to exercise correlate with exercise changes in pulmonary artery pressure, total pulmonary resistance or pulmonary vascular resistance? Which combinations of cardiac, ventilatory and blood gas variables are the best predictors of oxygen consumption at maximal exercise? Twenty-six patients with stable chronic obstructive pulmonary disease performed symptom-limited supine bicycle exercise with simultaneous hemodynamic and radionuclide ventriculographic measurements. The oxygen consumption at maximal exercise correlated with the exercise right ventricular ejection fraction (n = 21, r = 0.66; p less than 0.005), exercise stroke volume (r = 0.68; p less than 0.001), exercise cardiac output (r = 0.77; p less than 0.00005) and exercise ventilation (r = 0.85; p less than 0.00001). The change in right ventricular ejection fraction from rest to exercise correlated inversely with the change from rest to exercise in total pulmonary resistance (r = -0.51; p less than 0.05) but not with the change in mean pulmonary pressure (r = -0.37) or in pulmonary vascular resistance (r = 0.09). Multivariate analysis showed that the variables giving the highest combined correlation with oxygen consumption were ventilation and right ventricular ejection fraction (r = 0.95, adjusted r2 = 0.88). These results suggest that exercise oxygen consumption of patients with chronic obstructive pulmonary disease is related to right ventricular systolic function, exercise right ventricular dysfunction is related, in part, to abnormal exercise total pulmonary resistance, and exercise limitation in chronic obstructive pulmonary disease occurs as a result of the dynamic interaction between disordered right heart function and ventilation.

Adult↗

The effect of light, moderate and severe bicycle exercise on lymphocyte subsets, natural and lymphokine activated killer cells, lymphocyte proliferative response and interleukin 2 production.

The purpose of the present study was to evaluate the effect of acute bicycle exercise at different exercise intensities on the immune system. Six healthy volunteers exercised on a bicycle ergometer for 1 h at 25%, 50% and 75% of VO2max with an interval of 2 to 3 weeks. Blood samples were collected in the basal state, at the end of exercise and 2 h later. The absolute concentrations of all lymphocyte subsets increased during and fell after exercise at 50% and 75% of VO2max, but did not change significantly at 25% of VO2max. However, at all exercise levels, the percentage of CD3+ blood mononuclear cells decreased due to a decline in the fraction of CD4+ cells. This decline was most pronounced at 75% of VO2max. The fraction of NK cells expressing either the CD16 or the CD56 marker increased during exercise and declined to prevalues 2 h later, however the changes were most pronounced at 75% of VO2max. The natural killer (NK) cell and lymphokine activated killer (LAK) cell activities (lysis per fixed number of mononuclear cells) were increased during all exercise intensities, but were only suppressed below basal levels after exercise at 75% of VO2max. Indomethacin in vitro abolished the post-exercise suppression of NK cell activity and the proportion of CD14+ monocytes increased 2 h after exercise only at 75% of VO2max. These findings indicate that after exercise NK cell function is inhibited by prostaglandins released by monocytes. During exercise at 50% and 75% of VO2max the proliferative response of blood mononuclear cells (BMNC) following stimulation with phytohaemagglutinin A (PHA) decreased, whereas that following stimulation with interleukin-2 (IL-2) was enhanced. The IL-2 production by BMNC in vitro was markedly decreased during and after exercise at 75% of VO2max and this inhibition could be abolished by indomethacin in vitro. In conclusion, the response of the immune system to exercise depends on exercise intensity. In essence, the response is enhanced during exercise, however, after heavy exercise it is suppressed due to an increased level of prostaglandins produced by the elevated number of monocytes.

Adult↗

Strenuous exercise and immunological changes: a multiple-time-point analysis of leukocyte subsets, CD4/CD8 ratio, immunoglobulin production and NK cell response.

This study was designed to examine the impact of exhaustive endurance exercise on a number of immune parameters of physically fit male subjects (VO2max 66.5 +/- 5.3 ml/min/kg) who performed treadmill exercise at 65% of their VO2max for 120 min. Serial blood samples were taken before, during and after exercise and changes in leukocyte and lymphocyte subset concentrations; immunoglobulin production in vitro; and natural killer (NK) cell response were measured. The exercise regimen was found to induce the well-known phenomenon of leukocytosis which consisted primarily of a granulocytosis and lymphocytosis. Among the lymphocyte subsets, peripheral pan T cells (CD3+) as well as helper (CD4+) and suppressor (CD8+) T cells were found to be elevated. A relatively smaller increase in CD4+ than CD8+ cells resulted in depressed CD4/CD8 ratios throughout the exercise period. After exercise, T cells declined progressively and, 2 h post-exercise, were less than 60% of their pre-exercise level. In contrast, the CD4/CD8 ratio demonstrated a progressive increase, thus representing a reversal in the pattern observed during exercise and a trend towards an elevated ratio during recovery. B cells (CD19+) were relatively unaffected by exercise, although IgM production by pokeweed mitogen-stimulated lymphocytes obtained from blood samples after 120 min of exercise was significantly depressed. NK cells were affected dramatically by exercise. Both CD16+ cell numbers and NK cytotoxicity were increased during exercise, followed by a persistent depression in the post-exercise period. The strenuous exercise induced profound effect on NK cells as evidenced by a 40% depression of the NK cell count for as long as 7 days after the cessation of exercise. Our results provide direct kinetic evidence demonstrating that exhaustive exertion alters both lymphocyte distribution pattern and effector function, suggestive of possible exercise-induced immune compromise, particularly in the post-exercise recovery period.

Adult↗

Exercise rapidly increases expression of the monocarboxylate transporters MCT1 and MCT4 in rat muscle.

We examined the effect of a single exercise session on the protein and mRNA expression of the monocarboxylate transporters MCT1 and MCT4 in rat soleus (SOL), and red (RG) and white gastrocnemius (WG) muscles. Muscle samples were obtained at rest before 2 h of treadmill exercise (21 m min(-1), 15% grade) and immediately after exercise, as well as 5, 10 and 24 h after exercise. During the 2 h exercise bout, MCT1 proteins in RG (+60%) and WG (+56%) were increased (P < 0.05). MCT1 protein was further increased thereafter, with peak increments occurring 10 h after exercise in RG (+157%), WG (+193%) and SOL (+179%) (P < 0.05). Twenty-four hours after exercise, MCT1 protein was still up-regulated in WG (+100%) and SOL (+55%) (P < 0.05), but not in RG. MCT1 mRNA was up-regulated during exercise in RG (+53%) and WG (+98%) and remained elevated until 24 h post-exercise in RG (P < 0.05), but in WG, MCT1 mRNA decreased transiently to pre-exercise levels at 5 and 10 h after exercise, before increasing again at 24 h (+150%) (P < 0.05). MCT4 protein and mRNA were not increased in WG muscle during and after exercise (P > 0.05). In contrast, during exercise, in RG (+41%) and SOL (+98%) MCT4 protein was increased (P < 0.05). Peak increases in MCT4 protein were observed 10 h after exercise in RG (+131%) and SOL (+323%) (P < 0.05). MCT4 protein was still up-regulated 24 h after exercise (RG: +106%; SOL +225%) (P < 0.05). MCT4 mRNA in RG was not increased until 10 (+132%) and 24 h after exercise (+55%) (P < 0.05). These studies have shown that MCT1 and 4 proteins are transiently up-regulated by a single bout of exercise, involving post-transcriptional and transcriptional mechanisms. Thus, MCT1 and MCT4 belong to a class of selected metabolic genes that are very rapidly up-regulated with an exercise stimulus.

Animals↗

Adaptation of the left ventricle to exercise-induced hypertrophy.

Cardiac functional and structural adaptations to exercise-induced hypertrophy were studied in 68 pigs. Pigs were exercise trained on a treadmill for 10 wk. Sequential measurements were made of cardiac dimensions, [left ventricular end-diastolic diameter (EDD), changes in diameter (delta D%), wall thickness (WTh), wall thickening (WTh%), left ventricular pressure (LVP), time derivative of pressure (dP/dt), stroke volume, total body O2 consumption (VO2), blood gases, and systemic hemodynamics] at rest and during moderate and severe exercise. Postmortem studies included morphometric measurements of capillary density, arteriolar density, mitochondria, and myofibrils. All of the exercise-trained pigs showed significant increases in aerobic capacity. Maximum O2 consumption (VO2 max) increased by 37.5% in group 1 (moderate exercise training) and 34% in group 3 (heavy exercise training). Cardiac hypertrophy ranged from less than 15% in a group (n = 8) subjected to moderate exercise training to greater than 30% in a group (n = 11) subjected to heavy exercise training. Before training, exercise was characterized by a decreasing EDD during progressive exercise; this was reversed after exercise training. Stroke volume and end-diastolic volumes during exercise showed a highly significant increase after exercise training and hypertrophy. Morphometric measurements showed that mitochondria and cell membranes increased with increasing myocyte growth in all exercise groups, but there was only a partially compensated adaptation of capillary proliferation. Arteriolar number and length increased in all exercise groups. Intrinsic contractility as measured by delta D%, WTh%, or left ventricular dP/dt did not increase with exercise training and in some instances decreased. Therefore, left ventricular adaptation to strenuous exercise in the pig heart is primarily one of changes in left ventricular dimensions and a compensated hypertrophy. Exercise-induced increases in EDD and stroke volume can be accounted for by decreases in peripheral resistance and increased cardiac dimensions.

Acclimatization↗

Exercise when young provides lifelong benefits to bone structure and strength.

UNLABELLED: Short-term exercise in growing rodents provided lifelong benefits to bone structure, strength, and fatigue resistance. Consequently, exercise when young may reduce the risk for fractures later in life, and the old exercise adage of "use it or lose it" may not be entirely applicable to the skeleton. INTRODUCTION: The growing skeleton is most responsive to exercise, but low-trauma fractures predominantly occur in adults. This disparity has raised the question of whether exercised-induced skeletal changes during growth persist into adulthood where they may have antifracture benefits. This study investigated whether brief exercise during growth results in lifelong changes in bone quantity, structure, quality, and mechanical properties. MATERIALS AND METHODS: Right forearms of 5-week-old Sprague-Dawley rats were exercised 3 days/week for 7 weeks using the forearm axial compression loading model. Left forearms were internal controls and not exercised. Bone quantity (mineral content and areal density) and structure (cortical area and minimum second moment of area [I(MIN)]) were assessed before and after exercise and during detraining (restriction to home cage activity). Ulnas were removed after 92 weeks of detraining (at 2 years of age) and assessed for bone quality (mineralization) and mechanical properties (ultimate force and fatigue life). RESULTS: Exercise induced consistent bone quantity and structural adaptation. The largest effect was on I(MIN), which was 25.4% (95% CI, 15.6-35.3%) greater in exercised ulnas compared with nonexercised ulnas. Bone quantity differences did not persist with detraining, whereas all of the absolute difference in bone structure between exercised and nonexercised ulnas was maintained. After detraining, exercised ulnas had 23.7% (95% CI, 13.0-34.3%) greater ultimate force, indicating enhanced bone strength. However, exercised ulnas also had lower postyield displacement (-26.4%; 95% CI, -43.6% to -9.1%), indicating increased brittleness. This resulted from greater mineralization (0.56%; 95% CI, 0.12-1.00%), but did not influence fatigue life, which was 10-fold greater in exercised ulnas. CONCLUSIONS: These data indicate that exercise when young can have lifelong benefits on bone structure and strength, and potentially, fracture risk. They suggest that the old exercise adage of "use it or lose it" may not be entirely applicable to the skeleton and that individuals undergoing skeletal growth should be encouraged to perform impact exercise.

Animals↗

Glycogen reduction in non-exercising muscle depends on blood lactate concentration.

The purpose of this study was to determine for the first time by repeated non-invasive 13C-NMR spectrometry whether blood lactate concentration affects glycogen reduction in non-exercising muscle during prolonged (6 h) physical exercise in healthy adult males. Such an effect would indirectly show that glycogenolysis independent of nervous activation occurs in non-exercising muscle. After an overnight fast, 12 subjects performed alternating one-leg cycle exercise and arm cranking exercise at an average work load of 106 (SD 26) W [63 (9)% maximum oxygen consumption for one-leg exercise] and 69 (13) W [61 (10)% maximum oxygen consumption for arm cranking exercise], respectively. During the 6-h exercise test, glycogen concentration of the non-exercising calf muscle decreased by 17 (7)% while the glycogen concentration in the exercising calf muscle decreased by 45 (8)%. In a resting control group (n=6), the glycogen concentration did not decrease significantly. The higher the exercise intensity and therefore blood lactate concentration, the smaller was the glycogen reduction in the non-exercising calf muscles. We conclude that during prolonged physical exercise glycogenolysis in non-exercising human muscles decreases as exercise intensity increase contrary to exercising muscles. This observation might be an indirect evidence for a non-exercise induced glycogenolysis in inactive muscles.

Adult↗

Physiologic changes with maximal exercise in asymptomatic valvular aortic stenosis assessed by Doppler echocardiography.

OBJECTIVES: We hypothesized that the physiologic response to exercise in valvular aortic stenosis could be measured by Doppler echocardiography. BACKGROUND: Data on exercise hemodynamics in patients with aortic stenosis are limited, yet Doppler echocardiography provides accurate, noninvasive measures of stenosis severity. METHODS: In 28 asymptomatic subjects with aortic stenosis maximal treadmill exercise testing was performed with Doppler recordings of left ventricular outflow tract and aortic jet velocities immediately before and after exercise. Maximal and mean volume flow rate (Qmax and Qmean), stroke volume, cardiac output, maximal and mean aortic jet velocity (Vmax, Vmean), mean pressure gradient (delta P) and continuity equation aortic valve area were calculated at rest and after exercise. The actual change from rest to exercise in Qmax and Vmax was compared with the predicted relation between these variables for a given orifice area. Subjects were classified into two groups: Group I (rest-exercise Vmax/Qmax slope > 0, n = 19) and Group II (slope < or = 0, n = 9). RESULTS: Mean exercise duration was 6.7 +/- 4.3 min. With exercise, Vmax increased from 3.99 +/- 0.93 to 4.61 +/- 1.12 m/s (p < 0.0001) and mean delta P increased from 39 +/- 20 to 52 +/- 26 mm Hg (p < 0.0001). Qmax rose with exercise (422 +/- 117 to 523 +/- 209 ml/s, p < 0.0001), but the systolic ejection period decreased (0.33 +/- 0.04 to 0.24 +/- 0.04, p < 0.0001), so that stroke volume decreased slightly (98 +/- 29 to 89 +/- 32 ml, p = 0.01). The increase in cardiac output with exercise (6.5 +/- 1.7 to 10.2 +/- 4.4 liters/min, p < 0.0001) was mediated by increased heart rate (71 +/- 17 to 147 +/- 28 beats/min, p < 0.0001). There was no significant change in the mean aortic valve area with exercise (1.17 +/- 0.45 to 1.28 +/- 0.65, p = 0.06). Compared with Group I patients, patients with a rest-exercise slope < or = 0 (Group II) tended to be older (69 +/- 12 vs. 58 +/- 19 years, p = 0.07) and had a trend toward a shorter exercise duration (5.3 +/- 2.9 vs. 7.3 +/- 4.9 min, p = 0.20). There was no difference between groups for heart rate at rest, blood pressure, stroke volume, cardiac output, Vmax, mean delta P or aortic valve area. With exercise, Group II subjects had a lower cardiac output (7.4 +/- 2.4 vs. 11.5 +/- 4.6 liters/min, p = 0.005) and a smaller percent increase in Vmax (3 +/- 9% vs. 22 +/- 14%, p < 0.0001). CONCLUSIONS: Doppler echocardiography allows assessment of physiologic changes with exercise in adults with asymptomatic aortic stenosis. A majority of subjects show a rest-exercise response that closely parallels the predicted relation between Vmax and Qmax for a given orifice area. The potential utility of this approach for elucidating the relation between hemodynamic severity and clinical symptoms deserves further study.

Adult↗

Intense response of heart rate with pronounced suppression of high-frequency power of heart rate variability to early morning exercise with high-intensity load.

Autonomic nerve activity shows circadian variation. Therefore, we put forward the hypothesis that the responses of heart rate (HR) and high-frequency (HF) power of HR variability to exercise would be different between early morning and daytime exercise. We performed ergometer constant load exercise tests [50 watts (low), 100 watts (high load)] in the early morning and during the day in 6 healthy volunteers. The HR response was fitted to an exponential hyperbolic sine function: HR= alpha*e(-beta*t) *sinh(omega*t)+gamma. In this equation, the beta/omega ratio was inversely correlated with the intensity of the HR response. HF power was determined using a recently developed algorithm with high time-resolution power. There were no significant differences in HR, HF power or systolic blood pressure (BP) pressure before exercise between early morning and daytime exercise with either the 50 or 100 watt loads. During exercise, there were no significant differences in maximal HR or maximal systolic BP between early morning and daytime exercise with either 50 or 100 watt loads. For high-load exercise, the beta/omega ratio was significantly lower in early morning exercise (mean +/- SD, 0.945 +/- 0.02) than in daytime exercise (0.987 +/- 0.03). Similarly, for 100 watt exercise, HF power of HR variability was significantly lower in early morning exercise (0.94 +/- 0.52 msec/Hz 1/2) than in daytime exercise (1.26 +/- 0.74 msec/Hz 1/2). In conclusion, the present study demonstrated that a lower beta/omega ratio in the HR response was associated with lower HF power of HR variability in early morning high-load exercise compared to that in daytime exercise, indicating that the heart rate responded more intensely to early morning exercise than to daytime exercise with a high load due, at least partly, to pronounced suppression of parasympathetic nerve activity.

Adult↗

Establishment of a predictive model of serum glucose changes under different exercise intensities and durations among patients with type 2 diabetes mellitus.

Regular exercise is regarded as one of necessary elements in treating diabetes mellitus (DM). The purpose of this study was to investigate the influence of different exercise intensities and durations on serum glucose changes after exercise in type 2 DM patients and to establish a predictive model of changes in serum glucose under different exercise intensities and durations. Thirty-seven type 2 DM patients were recruited from four teaching hospitals. A total of 12 exercise sessions were scheduled according to the results of a graded treadmill exercise test. The 12 exercise sessions were designed on the basis of different exercise intensities (40%, 60%, and 80% maximal workload) and exercise durations (10, 20, 30, and 40 min). Serum glucose level was measured before and after exercise. The findings indicate that the main effect of exercise intensity and duration was significant, but there was no interaction effect. All four variables, including exercise intensity, exercise duration, pre-exercise serum glucose levels, and gender, explained 37% of the variance in serum glucose changes after exercise. In conclusion, a dose-response relationship between exercise amount and serum glucose changes was demonstrated. This is helpful for health professionals to teach type 2 DM patients how to predict serum glucose response in different exercise situations.

Adult↗

Exercise training in patients with heart failure. A randomized, controlled trial.

OBJECTIVE: To assess the benefit of exercise training in patients with heart failure caused by left ventricular systolic dysfunction and to further describe the physiologic changes associated with exercise training in these patients. DESIGN: Randomized, controlled trial. SETTING: Urban outpatient clinic. PATIENTS: 40 men with compensated heart failure who were receiving standard medical therapy were randomly assigned to an exercise-training group or to a control group that did not exercise. Fifteen of the 21 patients assigned to exercise training and 14 of the 19 patients assigned to the control group completed the study. INTERVENTION: Patients assigned to exercise training participated in a program of three exercise sessions per week for 24 weeks. MEASUREMENTS: Symptom-limited exercise tests with gas exchange analysis done just before randomization, at week 12, and at week 24. RESULTS: At week 24, the following changes (mean +/- SE) were seen in patients in the exercise group and patients in the control group, respectively; exercise duration, 2.8 +/- 0.6 minutes and 0.5 +/- 0.5 minutes; peak oxygen consumption (VO2), 231 +/- 54 L/min and 58 +/- 38 L/min; peak ventilation, 12 +/- 3 L/min and -4 +/- 3 L/min; peak heart rate, 10 +/- 4 beats/min and -2 +/- 4 beats/min; and peak power output, 20 +/- 6 W and 2 +/- 5 W. Differences between the increases occurring in the exercise group and the changes occurring in the control group were significant (P < 0.05). Among patients in the exercise group, 85% of the increase in peak VO2 occurred by week 12, and 46% of the increase in peak VO2 was caused by the increase in peak heart rate. CONCLUSION: Exercise training does not appear to be contraindicated in patients with compensated heart failure. Exercise training improved exercise tolerance, as measured by increases in peak VO2, exercise duration, and power output. This improved exercise tolerance was caused in part by an increase in peak heart rate.

Adult↗

Kinetics of oxygen uptake during decremental ramp exercise.

BACKGROUND: The purpose of the present study was to examine the kinetics of oxygen uptake (VO2) during decremental ramp exercises after incremental ramp exercise above the anaerobic threshold. METHODS: Triangle exercise consisting of incremental and decremental exercises, and trapezoid exercise in which a constant load was inserted between incremental and decremental exercises were carried out. RESULTS: Blood lactate (La) increased in incremental phases during triangle and trapezoid exercises, and showed a further increase at constant work during trapezoid exercise. It significantly decreased during decremental exercise. Initial VO2 level during decremental exercise was significantly higher in trapezoid exercise than in triangle exercise. The VO2 level then exponentially decreased and later showed a linear decrease during both exercises. These VO2 kinetics were expressed by an approximate equation. The time constant expressing the exponential manner was about one minute on average in both exercises. The slope of the linearly decreasing phase of VO2 was significantly related to La at 100 watts during the decremental exercise. CONCLUSIONS: VO2 kinetics during decremental exercise after incremental exercise above the anaerobic threshold consists of at least three components: initial level, exponentially decreasing phase, and linearly decreasing phase.

Adult↗

Influence of water content of inspired air during and after exercise on induced bronchoconstriction.

This study looked at the influence of inspired air water content on exercise-induced bronchospasm (EIB). On separate days, 12 mild asthmatics (4M, 8F), aged 18-39 yrs (mean: 27 yrs), performed four six minute steady-state exercises on ergometer at 80% of their maximum workload. Exercises were randomized to the following inspired air conditions: dry air (0% relative humidity (RH] during exercise followed by dry (DD) or humid air (100% RH) (DH) after exercise, humid air during exercise followed by dry (HD) or humid air (HH). Room temperature was kept constant (22 +/- 1 degree C) at all visits. Forced expiratory volume in one second (FEV1) was measured before and every 5 min for 25 min after exercise. Ventilation (VE) was not significantly different whether the exercise was done under dry or humid air. There was a residual bronchodilatation at the end of exercises performed in humid air, while at this time FEV1 was already lower than baseline when exercise was done in dry air conditions. The maximal fall in FEV1(%) following exercise was significantly greater after those performed in dry air: DD (29 +/- 5.6%) and DH (30 +/- 5.8%) than in humid air: HD (12 +/- 4.9%) and HH (20 +/- 4.9%) (p less than 0.05). The time-course of recovery from bronchoconstriction was significantly improved when inhaling dry air after exercise. However, the difference found in the maximal % fall in FEV1 after exercise when recovery was in dry compared to humid air did not achieve statistical significance. In conclusion, EIB is influenced by the changes in water content during and after exercise. Bronchoconstriction following exercise is minimal if exercise is done in humid air and recovery in dry air, and maximal if the exercise is performed in dry air and recovery in humid air.

Adolescent↗

Exercise training in chronic obstructive pulmonary disease.

Exercise limitation is a common and disturbing manifestation of COPD. The exercise intolerance is often caused by multiple interrelated anatomic and physiologic disturbances. Importantly, exercise tolerance can be improved despite the presence of fixed structural abnormalities in the lung. Exercise training, undertaken alone or in the context of comprehensive PR, improves exercise endurance and, to a lesser degree, the maximal tolerated workload of patients with COPD. Pulmonary rehabilitation also improves dyspnea and QOL. Exercise training and PR should be considered for all patients lacking contraindications who experience exercise intolerance despite optimal medical therapy. Lower-extremity training should be included routinely in the exercise prescription. The choice of type and intensity of training should be based primarily on the patient's individual baseline functional status, symptoms, needs, and long-term goals. When tolerated, high-intensity (continuous or interval) training may lead to greater improvements in aerobic fitness than low-intensity training but is not absolutely necessary to achieve gains in exercise endurance. Upper-extremity training should be undertaken when possible. Ventilatory muscle training should be considered for patients who continue to experience exercise limitation and breathlessness despite medical therapy and general exercise reconditioning. Exercise tolerance may improve following exercise training because of gains in aerobic fitness or peripheral muscle strength; enhanced mechanical skill and efficiency of exercise; improvements in respiratory muscle function, breathing pattern, or lung hyperinflation; as well as reduction in anxiety, fear, and dyspnea associated with exercise. Gains made in exercise tolerance can last up to 2 years following a limited duration (6-12 week) rehabilitation program.

Breathing Exercises↗

Relation between left ventricular diastolic function and exercise tolerance in patients with left ventricular dysfunction.

Previous studies show no correlation between resting systolic left ventricular performance assessed as the ejection fraction and exercise tolerance. This study examined the relation between left ventricular diastolic performance and exercise tolerance in 63 patients with left ventricular dysfunction (ejection fraction less than 50%) due to known or suspected coronary artery disease. The 51 men and 12 women, aged 54 +/- 8 years (mean +/- standard deviation), underwent symptom-limited upright exercise testing on a bicycle ergometer. The exercise end-points were angina (n:5), dyspnea (n:16), and fatigue (n:42). The patients were divided into three groups: group 1 (n:28) with normal exercise tolerance (9.5 +/- 2.4 minutes), group 2 (n:18) with mild exercise intolerance (5.8 +/- 0.5 minutes), and group 3 (n:17) had severe exercise intolerance (3.7 +/- 0.9 minutes). The three groups did not differ in age, ejection fraction, end-diastolic volume, exercise end-point, exercise heart rate, and left ventricular peak filling rate at rest. The exercise peak filling rate was, however, significantly higher in group 1 (p = 0.03). Stepwise multivariate discriminant analysis of important variables identified the exercise peak filling rate as the only predictor of exercise tolerance (F = 6.0). Thus, variation in exercise peak filling rate may in part explain the variability of exercise tolerance in patients with left ventricular dysfunction; patients with preserved exercise capacity have higher exercise peak filling rate than those with exercise intolerance.

Adult↗

Chronobiological effects on exercise performance and selected physiological responses.

Previous studies investigating the impact of circadian rhythms on physiological variables during exercise have yielded conflicting results. The purpose of the present investigation was to examine maximal aerobic exercise performance, as well as the physiological and psychophysiological responses to exercise, at four different intervals (0800 hours, 1200 hours, 1600 hours, and 2000 hours) within the segment of the 24-h day in which strenuous physical activity is typically performed. Ten physically fit, but untrained, male university students served as subjects. The results revealed that exercise performance was unaffected by chronobiological effects. Similarly, oxygen uptake, minute ventilation and heart rate showed no time of day influences under pre-, submaximal, and maximal exercise conditions. Ratings of perceived exertion were unaffected by time of day effects during submaximal and maximal exercise. In contrast, rectal temperature exhibited a significant chronobiological rhythm under all three conditions. Under pre- and submaximal exercise conditions, significant time of day effects were noted for respiratory exchange ratio, while a significant rhythmicity of blood pressure was evident during maximal exercise. However, none of these physiological variables exhibited significant differential responses (percent change from pre-exercise values) to the exercise stimulus at any of the four time points selected for study. Conversely, resting plasma lactate levels and lactate responses to maximal exercise were found to be significantly sensitive to chronobiological influences. Absolute post-exercise plasma norepinephrine values, and norepinephrine responses to exercise (percent change from pre-exercise values), also fluctuated significantly among the time points studied. In summary, these data suggest that aerobic exercise performance does not vary during the time frame within which exercise is normally conducted, despite the fact that some important physiological responses to exercise do fluctuate within that time period.

Adult↗

Exercise and side effects among 749 patients during and after treatment for cancer: a University of Rochester Cancer Center Community Clinical Oncology Program Study.

GOALS: Despite advances in cancer treatment and symptom management, many patients experience side effects from cancer treatments that cause suffering and impair quality of life (QOL). Exercise is a method for enhancing QOL among cancer patients that shows promise in reducing side effects. However, patient participation in exercise is not well defined. We report on exercise participation during and within 6 months after chemotherapy and radiation therapy, the association of exercise with treatment side effects, and the communication between physicians and patients about exercise in a large (N = 749) nationwide sample of cancer patients. PATIENTS AND METHODS: Participants completed measures that included questions concerning exercise during and after treatment, treatment side effects, and communication with physicians regarding exercise. Questionnaires were administered 2 weeks and 6 months after completion of therapy. RESULTS: Almost half of the 749 participating patients reported exercising while undergoing chemotherapy and/or radiation, and more than half reported exercising during the 6 months after treatment. Exercise was associated with less severe side effects during and after treatment (p < or = 0.050). More than 30% of patients reporting exercise did not discuss exercise with a physician; however, those who did were more likely to talk with their oncologist than with their primary care provider. CONCLUSIONS: Cancer patients report exercising and appear amenable to attempting exercise during and within 6 months after treatment. Research is needed to assess (1) the frequency, intensity, duration, and mode of exercise; (2) randomized controlled trials with exercise and its influence on treatments and side effects; and (3) physician-patient communication regarding exercise during cancer treatment.

Academic Medical Centers↗

Silent versus symptomatic myocardial ischemia during exercise testing: a comparison with coronary angiographic findings.

Two-hundred-and-eighty individuals with anginal complaints, without prior myocardial infarction and with a positive exercise stress test were divided into a group (n = 67) with exercise-induced silent myocardial ischemia and another group (n = 213) with exercise-induced angina pectoris. Both underwent coronary angiography and were compared with each other with respect to various exercise and angiographic parameters. Patients with exercise-induced silent ischemia attained a longer mean exercise duration (P less than 0.001), a higher peak exercise heart rate (P less than 0.0001) and a higher peak exercise rate pressure product (P less than 0.001) than patients with exercise-induced angina pectoris. In the latter group, more patients showed exercise-induced ST-segment depression greater than 2 mm (P less than 0.05). The group of patients with silent ischemia encompassed more individuals with normal coronary arteries (P less than 0.0001). More patients with exercise-induced angina pectoris had three-vessel disease (P less than 0.0001). The exclusion of patients with normal coronary arteries (23% in those with silent ischemia group and 6% in those with exercise-induced angina had no influence on the level of significance for peak heart rate, mean exercise duration and exercise duration greater than 10 min. Thus, in this population, exercise-induced silent myocardial ischemia is associated with better exercise performance and less extensive coronary arterial pathology than in exercise-induced angina pectoris.

Adult↗