Peripheral blood flow responses to exercise after successful correction of coarctation of the aorta.

OBJECTIVES: The purpose of this study was to characterize peripheral flow kinetics in response to progressive discontinuous maximal exercise in 10 patients who underwent repair of coarctation of the aorta and 11 age-matched healthy adolescents. BACKGROUND: An impairment of leg blood flow has been suggested on the basis of exaggerated femoral muscle lactate accumulation in patients with successful repair of coarctation. Few data are available describing blood flow kinetics of the exercising leg in such patients. METHODS: Duplex ultrasound provided transcutaneous measurements of peak systolic and end-diastolic flow velocities of the femoral, humeral and renal arteries at rest and immediately after mild, moderate and maximal exercise intensities for computation of mean velocity, resistance index and femoral blood flow. RESULTS: Femoral mean velocity and femoral blood flow increased linearly with exercise intensity in both groups, but the slope of this increase was significantly lower in patients. Similarly, humeral mean velocity increased significantly less in patients than in control subjects. Femoral resistance index sharply decreased from that at rest (patients [mean +/- SE] 1.4 +/- 0.04; control subjects 1.4 +/- 0.03) to mild exercise intensity in both groups (patients 0.69 +/- 0.03; control subjects 0.72 +/- 0.03). A further decrease was observed at maximal exercise in patients (0.60 +/- 0.04, p = 0.08) but not in control subjects (0.69 +/- 0.02). CONCLUSIONS: These observations suggest that despite a greater exercise-induced femoral vasodilation, patients with successful correction of coarctation of the aorta demonstrate an impaired lower limb blood flow in response to strenuous dynamic exercise. In the absence of stenosis at rest, this alteration could result from exaggerated flow turbulence in the descending aorta distal to the site of correction because of loss of elasticity at the site of the resection of the coarcted segment.

Decreased plasma atriopeptin response to volume-overloading maneuvers and exercise after atriopulmonary anastomosis of Fontan.

Atriopulmonary anastomosis results in a chronic right atrial pressure-volume overload. Water and salt retention is a frequent clinical observation in patients after atriopulmonary anastomosis. The purpose of this study was to examine if this could be related to an inability to increase already elevated circulating atriopeptin (ANP) in response to central volume-overloading conditions. Eighteen patients (mean age 16 +/- 6 years) with an atriopulmonary anastomosis underwent routine cardiac catheterization during which a 5-minute head-down 10 degrees tilt was performed. Peripheral venous and right atrial blood samples were obtained under basal conditions, and after tilting and angiography for determination of ANP concentrations. At a different time, circulating ANP levels were measured during a maximal graded exercise protocol. Increased circulating ANP concentrations were found under basal conditions (114 +/- 10 pg/ml). Tilting and cardioangiography resulted in significant increases in mean atrial pressure (basal: 12 +/- 0.7 mm Hg; tilt: 13.4 +/- 0.63 mm Hg; after angiography: 15.8 +/- 0.8 mm Hg), but not in atrial or peripheral ANP. Compared with the expected threefold increase in plasma ANP induced by maximal exercise in healthy control subjects, only a slight (0.25-fold) increase was found in patients. These observations suggest a reduced stimulus-release response after atriopulmonary anastomosis, which could be related to a loss of atrial stretch receptor sensitivity, achievement of the limit for maximal right atrial secretion, or an alteration in right atrial compliance, or a combination.

Comparison of cardiovascular adjustments to exercise in adolescents 8 to 15 years of age after correction of tetralogy of fallot, ventricular septal defect or atrial septal defect.

Surgical correction of tetralogy of Fallot (TF) has generally been associated with a reduced maximal exercise tolerance, possibly related to the ventriculotomy inherent to the intracardiac repair procedure. This study documents the exercise hemodynamics of a group of patients operated on for TF who showed similar clinical and functional characteristics, and compares these responses to those of age-matched patients operated on for an isolated ventricular septal defect (VSD) or atrial septal defect (ASD) in an attempt to better understand the role of the ventriculotomy in the exercise limitation. Thirty patients, ages 12 to 19 years, operated on before 5 years of age for complete repair of TF (n = 13), VSD (n = 7) or ASD (n = 10) and 10 age-matched control subjects underwent a progressive maximal cycling test to determine the maximal oxygen uptake (VO2 max), and completed submaximal cycling at intensities of 33 and 66% VO2 max, respectively, to determine the cardiac output (CO2-rebreathing). No significant differences in VO2 max were observed (TF = 37.6 +/- 10; VDS = 34.0 +/- 9.2; ASD = 36.5 +/- 7; controls = 41.3 +/- 6.0 ml/kg/min). The maximal heart rate, however, remained lower in all patient groups in comparison with control subjects (p less than or equal to 0.05) (TF = 178 +/- 14; VSD = 172 +/- 17; ASD = 179 +/- 16; controls = 191 +/- 12 beats/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac output response to dynamic exercise after atrial switch repair for transposition of the great arteries.

Results from this study showed that patients who underwent successful operation for transposition of the great arteries had no appropriate increase in stroke volume in response to exercise of a nature similar to common recreational activities. The impairment, most likely due to disturbances in both venous return and ventricular systolic function, is compensated for by an increase in peripheral oxygen extraction; however, this increase may not be adequate with maturation or during prolonged exercise when cardiovascular constraints are more important.

Comparison of cardiac output determinants in response to upright and supine exercise in patients with cystic fibrosis.

This study characterizes cardiac output response to progressive submaximal upright cycling in CF patients. Thirty-one CF patients as well as 11 aged-matched CF control subjects completed cardiac output determinations (CO2-rebreathing) at rest, and at submaximal exercise corresponding to 30, 50 and 75 percent VO2max, in both upright and supine positions. The VO2max was similar in three of four groups, but lower in those with severe CF. The cardiac output generally increased with exercise intensity in both positions, except in severe CF. The change from upright to supine posture resulted in a significant increase in SI at rest and for every submaximal exercise in control subjects, but not CF patients. These observations may suggest that the abnormal cardiac output response observed in severe CF could be related to a potential limitation in ventricular diastolic reserve found in all CF patients independent of disease severity which becomes more apparent under increased ventricular preload.

Prolactinotrophic effect of endogenous and exogenous heat loads in human male adults.

Factors associated with heat-induced increase in blood prolactin (PRL) were investigated. Ten male volunteers (23.7 +/- 2.2 yr) were exposed to exogenous heating (head-out immersion) in 41 degrees C water (control 37 degrees C) for 30 min with and without face fanning and cooling. In seven of the subjects, endogenous heating was produced by a 45-min exercise in a warm environment (41 degrees C; control 10 degrees C) with and without selective face fanning. Venous blood was collected before and after each trial; blood hormones were analyzed by radioimmunologic techniques. Heat loading, whether exogenous or endogenous in origin, induced significant increases in blood PRL, beta-endorphin, and vasoactive intestinal peptide (VIP) levels. Blood thyrotropin (TSH) level decreased significantly during water immersion and more significantly with face cooling. From measurement in peripheral blood, the differential beta-endorphin, VIP, and TSH responses to selective face ventilation during exogenous and endogenous heat exposures suggest that blood PRL released in heat derives from secretory stimuli that are independent of these prolactinotropic factors.

Plasma atrial natriuretic peptide during brief upright and supine exercise in humans.

The factors associated with the exercise-induced increase in plasma atrial natriuretic peptide (ANP) have not been clearly established. Thus the purpose of the study was to further document the stimulus for the exercise-induced release of ANP and to examine the role of ANP in the control of hydromineral balance during exercise. Eight healthy male volunteers (25.1 +/- 4.5 yr) were submitted to a graded cycling exercise in both the upright and supine positions. Venous blood was sampled at rest and at the end of each 5-min work load at 40, 60, and 80% maximal oxygen uptake (Vo2max), at maximal exercise, and during recovery through an indwelling catheter for the determination of plasma vasopressin, aldosterone, catecholamines, plasma renin activity, and ANP concentrations. Results indicate a significant increase in ANP (pg/ml) from rest to maximal exercise in the upright position [rest, 21.9 +/- 10.2; 40%, 24.7 +/- 12.6; 60%, 32.4 +/- 17*; 80%, 47.8 +/- 27.7*; 100% Vo2max, 65.9 +/- 34.5* (*P less than or equal to 0.05)]. Supine concentrations were significantly higher than upright at 40 (37.9 +/- 15.2), 60 (54.0 +/- 18.8), and 80% Vo2max (68.9 +/- 16.6). Plasma ANP during maximal exercise was similar in both positions. Plasma vasopressin, aldosterone, renin activity, and catecholamines increased with increasing exercise intensity in both positions, although lower values were systematically observed in the supine position. The association of higher plasma ANP and blunted plasma vasopressin, plasma renin activity, and norepinephrine concentrations during supine exercise suggests that ANP may exert modulatory effects on the control of the hydromineral hormonal system during exercise.

Plasma atriopeptin response to prolonged cycling in humans.

The exercise-induced increase in plasma atriopeptin (ANP) has been related to exercise intensity. The independent effect of duration on the ANP response to dynamic exercise remains incompletely documented. The purpose of this study was to describe the time course of plasma ANP concentration during a 90-min cycling exercise protocol and to examine this in light of concurrent variations in plasma arginine vasopressin (AVP), aldosterone (ALD), and catecholamine (norepinephrine and epinephrine) concentrations as well as plasma renin activity (PRA). Seven male and four female healthy college students (23 +/- 2 yr) completed a prolonged exercise protocol on a cycle ergometer at an intensity of 67% of maximal O2 uptake. Venous blood was sampled through an indwelling catheter at rest, after 15, 30, 45, 60, and 90 min of exercise, and after 30 min of passive upright recovery. Results (means +/- SE) indicate an increase in ANP from rest (22 +/- 2.6 pg/ml) at 15 min of exercise (45.3 +/- 7.4 pg/ml) with a further increase at 30 min (59.4 +/- 9.8 pg/ml) and a leveling-off thereafter until completion of the exercise protocol (51.7 +/- 10.7 pg/ml). In plasma ALD and PRA, a significant increase was found from rest (ALD, 21.4 +/- 6.4 ng/dl), PRA, 2.5 +/- 0.5 ng.ml-1.h-1 after 30 min of cycling, which continued to increase until completion of the exercise (ALD 46.6 +/- 8.7 ng/dl, PRA 9.5 +/- 0.9 ng.ml-1.h-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Early onset of pulmonary gas exchange disturbance during progressive exercise in healthy active men.

Some recent studies of competitive athletes have shown exercise-induced hypoxemia to begin in submaximal exercise. We examined the role of ventilatory factors in the submaximal exercise gas exchange disturbance (GED) of healthy men involved in regular work-related exercise but not in competitive activities. From the 38 national mountain rescue workers evaluated (36 +/- 1 yr), 14 were classified as GED and were compared with 14 subjects matched for age, height, weight, and maximal oxygen uptake (VO2 max; 3.61 +/- 0.12 l/min) and showing a normal response (N). Mean arterial PO2 was already lower than N (P = 0.05) at 40% VO2 max and continued to fall until VO2 max (GED: 80.2 +/- 1.6 vs. N: 91.7 +/- 1.3 Torr). A parallel upward shift in the alveolar-arterial oxygen difference vs. %VO2 max relationship was observed in GED compared with N from the onset throughout the incremental protocol. At submaximal intensities, ideal alveolar PO2, tidal volume, respiratory frequency, and dead space-to-tidal volume ratio were identical between groups. As per the higher arterial PCO2 of GED at VO2 max, subjects with an exaggerated submaximal alveolar-arterial oxygen difference also showed a relative maximal hypoventilation. Results thus suggest the existence of a common denominator that contributes to the GED of submaximal exercise and affects the maximal ventilatory response.

Fluid-regulating and sympathoadrenal hormonal responses to peak exercise following cardiac transplantation.

Orthotopic heart transplantation results in cardiac denervation that can disrupt the normal regulation of hydromineral balance. This study compared the exercise-induced variations in plasma osmolality; atrial natriuretic peptide (ANP), arginine vasopressin (AVP), norepinephrine (NE), epinephrine (E), and dopamine (DA) concentrations; and plasma renin activity (PRA) of six cardiac transplant recipients (HTX) and six healthy age-matched controls (C) submitted to graded upright maximal cycling. Venous blood samples were obtained at rest, at submaximal (70% O2 uptake) and peak exercise, and after 10 and 30 min of sitting recovery. Peak O2 uptake was not different between groups despite lower maximal heart rate in HTX (136 +/- 6 vs. 183 +/- 9 beats/min). Baseline plasma ANP and PRA were higher in HTX (203 +/- 55 pg/ml and 29.9 +/- 7.4 ng.ml-1 x h-1) than in C (71 +/- 17 pg/ml and 5.4 +/- 0.96 ng.ml-1 x h-1); AVP was lower in HTX than in C (1.1 +/- 0.3 vs. 3.2 +/- 0.8 pg/ml; P < 0.05); and circulating E, NE, and DA were not different between groups. Exercise resulted in more marked increases in HTX than in C for ANP (300 vs. 100%), AVP (2,000 vs. 300%), NE (860 vs. 500%), and DA (611 vs. 187%) but not for PRA and a higher E response in C than in HTX (455 vs. 1,258%). These observations confirm that the potential for ANP release to central volume loading is independent of intact cardiac innervation. The exaggerated AVP response in HTX could, however, reflect the absence of inhibitory influences consecutive to denervation.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise after surgical repair of congenital cardiac lesions.

Congenital heart defects arise in approximately 1% of all live births, independent of ethnic and geographical considerations. With the development of new surgical procedures and current technologies a large number of these heart lesions can be surgically corrected in infancy. In the majority of cases patients evaluated some 10 to 20 years after surgery are asymptomatic and can lead a normal life. Despite their satisfactory clinical outcome patients may, nevertheless, show an abnormal pattern of physiological responses when submitted to dynamic exercise. This paper reviews the scientific literature concerning the exercise capabilities and the cardiorespiratory adjustments to exercise in patients surgically corrected for 4 of the most common congenital heart lesions: isolated atrial septal defect, isolated ventricular septal defects, pulmonary stenosis and tetralogy of Fallot. The maximal exercise tolerance of postoperative congenital heart defect patients may usually be related to: (a) the age of the patients at the time of surgery; (b) the severity of the lesions remaining after surgery; and (c) the age of the patients at the time of investigation. Although normal maximal exercise capabilities may be found in a good number of patients operated for either of the 4 lesions considered, this does not imply normal exercise haemodynamics. A general observation made in these 4 groups of patients is that of a subnormal exercise cardiac output which may or may not be fully compensated by an increase in peripheral oxygen extraction. The limitation in exercising cardiac output may, in turn, be attributed to either a subnormal stroke volume or a limitation in the chronotropic response to exercise or a combination of both factors. Residual pulmonary stenosis, increased pulmonary vascular resistance, increased myocardial stiffness are all factors that may contribute to the cardiac output limitation. A thorough explanation of underlying causes for the abnormal haemodynamic response to exercise, however, still remains to be provided.

Exercise-induced cardiac hypertrophy. Fact or fallacy?

After a century of research reports, the notion of exercise-induced cardiac hypertrophy is still an expected adaptation to regular exercise training. Experimental evidence reported both in animals and in humans over the past 3 decades suggests, however, that this conclusion may not be totally warranted. Data from 20 years of echocardiographic investigations of athletes and nonathletes indicate that differences in cardiac dimensions are not very large. Cross-sectional comparisons of over 1000 athletes and roughly 800 control individuals indicate an average difference of 1.6 mm in left ventricular (LV) wall thickness and of 5.3 mm in end-diastolic diameter. Differences reported after training programmes lasting 4 to 52 weeks are even smaller, with average increases of 0.3 mm in LV wall thickness and only 2.1mm in end-diastolic diameter. This article reviews data from animal and human studies concerning cardiac morphology and exercise training to show that the traditional interpretation of the literature has failed to take into account several methodological considerations or factors that may act as confounders in the interpretation of data. Results from animal studies indicate that the observation of cardiac hypertrophy is equivocal at best. In many reports the reported changes in heart size are not significant, and in instances where significant changes are reported these may be seen to be confounded by a number of factors. For example, in rats the reported training-induced hypertrophy may be related to gender differences in the responsiveness of cardiac dimensions or body and/or organ growth rather than to true heart hypertrophy. Furthermore, the interpretation of results from training studies in rats has often been based on the assumption that the metabolic, haemodynamic and thermoregulatory requirements of swimming and running exercise in rats are similar, which may in fact not be the case. In addition, the use of the heart weight/body weight ratio as an index of cardiac hypertrophy, although widespread in animal studies, is open to criticism owing to failure to control for concurrent changes in body weight. Several methodological considerations and factors confounding the outcome of exercise training in humans have also been omitted when interpreting echocardiographic cross-sectional and longitudinal findings. For example, in adult echocardiography the practical resolution of the echocardiographic technique amounts to roughly 2.2mm. It follows, therefore, that unless differences of changes in cardiac dimensions exceed the limit of resolution they are meaningless although statistically significant.(ABSTRACT TRUNCATED AT 400 WORDS)

Plasma norepinephrine, epinephrine, and dopamine beta-hydroxylase activity during exercise in man.

Many experimental studies have utilized the activity of dopamine-beta-hydroxylase (DBH) as an index of sympathetic activity, since this enzyme is not submitted to uptake mechanisms or to enzymatic metabolism as are the circulating catecholamines norepinephrine (NE) and epinephrine (E). However, large discrepancies have been found between the results of these studies. The hypothesis which is examined in this study is that these discrepancies might arise from the different intensities in the stimuli utilized. In order to examine this possibility, plasma DBH activity was measured in seven subjects at rest and in three different conditions known to increase sympathetic activity to varying degrees, i.e., during hand-grip, standing, and supra-maximal bicycle exercise. Plasma NE and E concentrations were also measured during these stimuli. The results of this study show that DBH activity increases above resting levels only during supramaximal dynamic exercise, while plasma NE and E concentrations increase during each experimental condition. Furthermore, the increases in NE and E are related to each other and are also related to heart rate when all experimental conditions are considered. On the contrary, the variations in plasma DBH (expressed as a percentage of the resting value) are not related to other sympathetic indices or to heart rate. Since NE and E vary little from subject to subject at rest and increase discretely in response to the various stimuli, these plasma catecholamine concentrations therefore appear to represent the most accurate indices of sympathetic activity.

New statistical method for detection and quantification of respiratory sinus arrhythmia.

A statistical method with the advantages of 1) enabling graphical representation of within-respiratory cycle heart rate variations, 2) detecting the presence of respiratory sinus arrhythmia (RSA) in a moving window, and 3) providing breath-by-breath RSA amplitude and phase obtained from the fitting of a sinusoid to the instantaneous relative heart rate is presented.

[Cardiac output evaluation during exercise in children treated with atrial surgery for transposition of great vessels]. / Evaluation du débit cardiaque à l'exercice chez des enfants traités par chirurgie atriale d'une transposition des gros vaisseaux.

The long-term physiopathological consequences of atrial surgery (Senning or Mustard procedures) for transposition of the great vessels with respect to exercise capacity are not well known. We measured the cardiac index by the technique of CO2 rebreathing at two submaximal levels of exercise corresponding to a stable oxygen consumption of 20 (E20) and 30 (E30) ml/min/kg in 7 patients successfully operated for transposition of the great vessels and in 7 control children paired for age, gender and body surface area. Despite an identical chronotropic response to exercise in the two groups, the increase in cardiac index was not as great in the children operated for transposition (from 6.86 +/- 0.51 to 7.71 +/- 0.78 l/min/m2) as in the control population (from 7.71 +/- 0.78 to 10.2 +/- 0.51 l/min/m2; p < 0.02). The stroke volume index was therefore significantly lower in the transposition group at both levels of exercise (52 +/- 3.2 vs 63 +/- 4.1 ml/m2; p < 0.04 at E20; and 46.4 +/- 4.3 vs 66 +/- 5.1 ml/m2 at E30). The main cause of this reduction of the stroke volume index is probably a lack of adaptation of right ventricular systolic function on exercise but it is not possible to exclude diastolic dysfunction due to reduce compliance secondary to the intraatrial patch. The conditions of preload are in fact instrumental in increasing stroke volume index at submaximal exercise levels.

Echocardiography and the Athlete's Heart.

In brief: Echocardiographic studies permit direct, accurate measurements of the ventricular wall thickness and cavity diameter. The authors review several of these studies, which show that elite athletes' left ventricles are larger than those of sedentary persons. Left ventricular wall thickness is greater in athletes excelling in sports involving static exercise, whereas those in endurance sports have larger ventricular cavities. These differences in cardiac dimensions may be the result of genetic makeup, prolonged and strenuous training, or a combination of both. Studies of short-term training showed only minor or no changes in left ventricular morphology, although significant improvements in performance and aerobic capacity were reported.

Breathing patterns during eccentric exercise.

Eccentric (ECC) work is interesting for rehabilitation purposes because it is more efficient than concentric (CON). This study assessed respiratory patterns and electromyographic activity (EMG) during ECC and CON cycling, both at similar power outputs and VO2 in eight healthy male subjects. Measurements include ventilation (VE), tidal volume (Vt), breathing frequency (Fb), arterial blood gases, and vastus lateralis (VL) and biceps brachii (BB) EMG. At the same mechanical power, VO2 and VE were fivefold lower in ECC as was VL EMG while BB EMG, Vd/Vt, PaO2 and PaCO2, were not different between modalities. At the same VO2, there was no difference in VE but Vt was lower and Fb higher in ECC. VL EMG was not different between modalities while BB EMG was higher in ECC. The latter observation suggests that ECC cycling may result in arm bracing and restricted chest expansion. Since hyperpnea is a known trigger of exaggerated dynamic hyperinflation, the prescription of ECC cycling for patient rehabilitation requires further assessment.

[Clinical exercise testing and the Fick equation: strategic thinking for optimizing diagnosis]. / Adaptation du transport cardiocirculatoire à l'exercice.

This article examines the expected exercise-induced changes in the components of the oxygen transport system as described by the Fick equation with a view to enable a critical analysis of a standard incremental exercise test to identify normal and abnormal patterns of responses and generate hypotheses as to potential physiological and/or pathophysiological causes. The text reviews basic physiological principals and provides useful reminders of standard equations that serve to integrate circulatory, respiratory and skeletal muscle functions. More specifically, the article provides a conceptual and quantitative framework linking the exercise-induced increase in whole body oxygen uptake to central circulatory and peripheral circulatory factors with the view to establish the normalcy of response. Thus, the article reviews the exercise response to cardiac output determinants and provides qualitative and quantitative perspective bases for making assumptions on the peripheral circulatory factors and oxygen use. Finally, the article demonstrates the usefulness of exercise testing as an effective integrative physiological approach to develop clinical reasoning or verify pathophysiological outcomes.

Efficiency of movement in health and chronic disease.

Mechanical efficiency of movement expresses the efficacy of skeletal muscles to transform biochemical energy into "external work" or movement. In young healthy humans, the mechanical efficiency and/or the work economy of various locomotor activities such as cycling, up-hill walking or running, stair climbing or swimming varies from 5 - 9% for swimming to 20-25% for cycling ergometry or stair climbing. There are five potential steps at which an extra demand or "wasting" of energy may occur in supplying energy to the contracting muscle: a) the resting metabolism b) the cost of ventilation b) the percentage of moles of ATP produced per mole of atomic oxygen processed through the mitochondria c) the percentage of molecular ATP used by myofibrils for tension production and d) the cost of multi-segment movement coordination towards a locomotor displacement. This article presents the little evidence available on the efficiency of movement in patients with chronic diseases such as COPD and discusses the mechanisms through which chronic disease may contribute to a potential "exaggerated energy demand" or "energy wastage".