Erect Exercise Research Articles

Effects of exercise position on the ventilatory responses to exercise in chronic heart failure

Objective: Patients with heart failure frequently complain of orthopnoea. The objective was to assess the ventilatory response of patients with chronic heart failure during erect and supine exercise. Design: Maximal incremental exercise testing with metabolic gas exchange measurements in erect and supine positions conducted in random order. Setting: Tertiary referral centre for cardiology. Patients: Nine patients with heart failure (aged 61.9±6.1 years) and 10 age matched controls (63.8±4.6). Outcome measures: Metabolic gas exchange measurements. The slope of the relation between ventilation and carbon dioxide production. Ratings of perceived breathlessness during exercise. Results: Oxygen consumption ( V ̇ O 2 ) and ventilation were higher during erect exercise at each stage in each group. Peak V O 2 was [mean (SD)] 17.12 ml/kg/min (4.07) erect vs 12.92 (3.61) supine in the patients ( P<0.01) and 22.62 (5.03) erect-supine vs 19.16 (3.78) erect ( P<0.01) in the controls. Ratings of perceived exertion were higher in the patients at each stage, but unaffected by posture. There was no difference in the slope of the relation between ventilation and carbon dioxide production between erect and supine exercise 36.39 (6.12) erect vs 38.42 (8.89) supine for patients; 30.05 (4.52) vs 28.80 (3.96) for controls. Conclusions: In this group of patients during exercise, there was no change in the perception of breathlessness, nor the ventilatory response to carbon dioxide production with change in posture, although peak ventilation was greater in the erect position. The sensation of breathlessness may be related to the appropriateness of the ventilatory response to exertion rather than to the absolute ventilation.

978-65 Exercise Forearm Vascular Responses in Patients Studied 7 Days After Myocardial Infarction

We have reported that exercise hypotension in patients with ischaemic heart disease may be due to abnormal vasodilation, Whilst exercise hypotension is not common in post infarction patients, we hypothesised that forearm vascular responses may commonly be abnormal. We assessed the frequency of abnormal forearm vascular responses in an unselected group of patients studied 7 days post myocardial infarction and the association with exercise blood pressure (BP) responses and with baroreceptor gain. Forty consecutive consenting patients (36 male 4 female age 33–74 mean 56.2 years) were studied 7 days post myocardial infarction and were compared with 20 healthy controls (14 male 6 female age 44–69 mean 56.2 years). All subjects underwent assessment of changes in forearm vascular resistance (FVR) by venous occlusion plethysmography during semi erect exercise, BP recordings during erect treadmill exercise, and baroreceptor gain assessed by the change in RR interval per unit change in blood pressure induced by phenylephrine (standard phenylephrine ramp method). (expressed as mean ± SD): FVR increased during exercise by 41 ± 67% in patients versus 124 ± 110% in controls (p = 0,001), and fell in 12 patients. Using an increase of 15% (one standard deviation below the mean for the controls) as the cut off for normality, 15 patients exhibited abnormal exercise vascular responses. Exercise hypotension was demonstrated in 4 patients all of whom had abnormal forearm vascular responses. Baroreceptor gain was lower in patients with abnormal forearm vascular responses than those with normal forearm vascular responses (24 ± 62, msec/mmHg vs 73 ± 67 msec/mmHg, p = 0.04). Impaired forearm vasoconstriction or vasodilation during leg exercise is common in patients studied 7 days post MI, even in patients without exercise hypotension and is associated with low baroreceptor gain. Exercise hypotension may only result in patients with abnormal forearm vascular responses, if they are unable to augment cardiac output. The absence of exercise hypotension in the majority of these patients implies a vigorous cardiac output response

Atrial natriuretic peptide response to postural change and medication in familial dysautonomia

Circulating atrial natriuretic peptide (ANP) was assayed before and after postural change and exercise in 54 patients with familial dysautonomia (FD) and 20 controls. ANP levels were compared with blood pressure, heart rate, plasma catecholamines and parameters of renal function. Compared with controls supine FD subjects had elevated blood pressures, heart rates and ANP levels (39 +/- 4 pg/ml vs. 23 +/- 3 pg/ml, p < 0.01). With the erect posture and exercise in FD subjects, blood pressure fell below control values, with ANP lowered. In FD subjects, blood pressure was correlated with ANP levels when supine and when erect and with heart rate post exercise. In controls, ANP levels did not correlate with other parameters. In FD patients on metoclopramide, supine and erect blood pressure and ANP levels were higher. FD subjects treated with fludrocortisone, had elevated supine and erect noradrenaline (p < 0.05 and p = 0.06); and those on diazepam had lower erect and post exercise noradrenaline (p < 0.05), but ANP levels were similar. In conclusion, sympathetic denervation may increase FD patients' responsiveness to other regulators of cardiovascular integrity, such as ANP. In addition, circulating ANP and catecholamines in FD subjects appear to be influenced by commonly used medications, such as metoclopramide.

Mechanism of exercise hypotension in patients with ischemic heart disease. Role of neurocardiogenically mediated vasodilation.

Exercise-induced hypotension in patients with coronary artery disease (CAD) has been considered to be due to an inability to achieve an adequate increase in cardiac output to match the demands of exercise. We investigated 10 consecutive patients (9 men and 1 woman; age, 38 to 71 years; mean, 52 years) with angiographically documented CAD and exercise-induced hypotension (EIH) (BPPeak < BPRest). Ten approximately age- and sex-matched patients with documented CAD and normal exercise blood pressure response (NBP) served as control subjects. Nine patients with EIH and all 10 control subjects underwent forearm plethysmography and radionuclide ventriculography (RNV) during semierect cycle exercise. Forearm vascular resistance (FVR) fell by 35 +/- 21% in exercise-induced hypotension patients versus an increase of 78 +/- 65% in patients with an NBP response (P < .0001). Left ventricular ejection fraction increased by 5.1 +/- 7.5% in the group with EIH versus a fall of 4.1 +/- 6.2% in the control group (P = .004). Cardiac output at peak exercise (RNV) increased by 2.2 +/- 0.89-fold in the group with EIH versus 1.49 +/- 0.47-fold in the control group (P = .04). The tenth patient in the group with EIH underwent invasive hemodynamic evaluation during erect exercise. Systolic blood pressure fell (136/80Rest to 50/40Peak) and cardiac output (Fick) tripled, whereas calculated systemic vascular resistance decreased by a factor of 10. Successful angioplasty to an isolated circumflex lesion resulted in resolution of symptoms and abnormal hemodynamic responses during exercise. Abnormal vasodilation associated with a normal or even increased rather than decreased cardiac output response appears to be an important mechanism underlying EIH in some patients with CAD. In the present study, this appears to have been the dominant mechanism in 8 and contributory in 2 of the consecutive patients studied.

Abnormal vascular responses to supine exercise in hypertrophic cardiomyopathy.

Exercise hypotension has been documented in hypertrophic cardiomyopathy. It is not the result of an inability to augment cardiac output but instead relates to an inappropriate and exaggerated decrease in systemic vascular resistance at high work loads. To enable us to examine the behavior of the peripheral vasculature during exercise, 103 consecutive patients underwent maximal symptom-limited supine bicycle exercise with measurement of forearm blood flow. A minimum reduction of 12% from the basal value was defined as a normal response based on the study of 25 normal controls. In the patients, two patterns of forearm blood flow were observed. Sixty-four patients had an appropriate reduction in forearm blood flow of 40 +/- 16% from resting flow. In 39 patients, the forearm blood flow either failed to decrease or increased with exercise by 45 +/- 105% of the resting value. Patients with an abnormal forearm vasodilator response were younger (31 +/- 13 versus 46 +/- 14 years), and more of them had a family history of hypertrophic cardiomyopathy and sudden death than did those with a normal vasoconstrictor response (16 of 39 versus eight of 64). Left ventricular end-diastolic cavity dimensions were smaller in those with an abnormal forearm blood flow response, but other clinical, echocardiographic, and arrhythmic variables were similar. To assess the relation of abnormal peripheral vascular responses to erect exercise blood pressure response, patients underwent treadmill exercise testing with careful monitoring of systolic blood pressure response. Thirty-eight patients had significant exercise hypotension with failure of the systolic blood pressure to increase during progressive exercise (n = 6) or an abrupt decrease in systolic blood pressure (20-60 mm Hg) from the peak value (n = 32); 65 patients had a normal exercise blood pressure response, but 18 of these patients had an oscillation in systolic blood pressure of 10 mm Hg or more early in the recovery phase. Thirty-one of 39 patients with an abnormal forearm blood flow response demonstrated exercise hypotension during the erect exercise testing, and the remaining eight patients had a normal exercise blood pressure response; however, five of these eight had abnormal oscillations in blood pressure during recovery (r = 0.61, p less than 0.001). The relation of abnormal peripheral vascular responses to exercise hypotension confirms the observation of hemodynamic instability in patients with hypertrophic cardiomyopathy. The finding of abnormal vascular responses in patients known to be at increased risk (young age and a family history of hypertrophic cardiomyopathy and sudden death) suggests that hemodynamic mechanisms may be important in the occurrence of sudden death in hypertrophic cardiomyopathy.

The response of the nasal airway to exercise.

Exercise causes a fall in nasal resistance that may be due to sympathetic vasoconstriction in the nasal mucosa. Other factors potentially involved in the exercise effect on nasal resistance are: increased alae nasi muscle activity, passive redistribution of blood to exercising muscle and away from the nasal mucosa, increased nasal air flow, and hyperventilation. In order to determine the importance of these factors, 6 healthy adults had nasal pressure/flow data collected at rest and after bicycle exercise at 100 to 160 W. Erect exercise with nose breathing, erect exercise with mouth breathing, voluntary isocapnic hyperventilation at the minute volumes achieved during exercise, and supine exercise were performed. The alae nasi muscles were voluntarily activated during pressure/flow measurements. The pressure/flow data were displayed on a logarithmic plot; parallel rightward shifts of this plot indicate falls in nasal resistance mediated by enlargement of the air passage. The position of the plot was defined by the flow rate at which the slope of the logarithmic plot steepens abruptly (Vtr). Erect exercise with nose breathing caused a fall in nasal resistance in all 6 subjects (mean change in Vtr, +14.4 L/min). Exercise mouth breathing and supine exercise caused similar falls in nasal resistance in all subjects (mean change of Vtr, +14.1 and +14.2 L/min, respectively). Voluntary isocapnic hyperventilation had no effect on nasal pressure/flow properties in any subject (mean change in Vtr, -1.3 L/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Increased myocardial ischemia during supine compared to erect exercise demonstrated by thallium-201 myocardial perfusion imaging

Increased myocardial ischemia during supine compared to erect exercise demonstrated by thallium-201 myocardial perfusion imaging

Comparison of supine and erect bicycle exercise electrocardiography in coronary heart disease: Accentuation of exercise-induced ischemic ST depression by supine posture

Exercise-induced electrocardiographic ST depression was compared during supine and erect graded bicycle exercise in 43 patients with chest pain but no prior myocardial infarct; all had ≥1 mm of ST depression during either erect or supine exercise; 16 had multivessel, 24 had 1-vessel and 3 had no coronary artery disease. Supine exercise used 4 minutes/stage and erect exercise used either 4 minutes or 3 minutes/stage with identical graded work loads for both postures. Chest pain occurred in 31 patients during erect and in 29 during supine exercise. ST depression was ≥1 mm in 28 patients during erect exercise and in all 43 during supine exercise (p <0.001); mean maximal ST depression was 1.3 ± 0.2 mm during erect and 2.6 ± 0.2 mm during supine exercise (p <0.001). Maximal work load was higher during erect than supine exercise (745 ± 32 versus 678 ± 32 kpm/min; p <0.001). The accentuation of ST depression by supine posture was not attributable to the changes in heart rate, rate-pressure product or mean blood pressure during supine versus erect exercise. In the 10 patients who had 2 erect bicycle tests using work load durations of 3 and 4 minutes, the maximal ST depression was not significantly different (erect 3 minutes 1.3 ± 0.5 mm and erect 4 minutes 1.4 ± 0.4 mm). In 7 patients who also had a maximal treadmill exercise test, the maximal ST depression was significantly greater during supine exercise (2.3 ± 0.4 mm) than during either an erect bicycle test (0.6 ± 0.4 mm) or treadmill exercise (0.7 ± 0.4 mm) (p <0.05). Supine posture should be considered as an important potentiator of exercise-induced myocardial ischemia whem comparing indicators such as electrocardiography, radionuclide ventriculography and thallium-201 myocardial perfusion imaging during exercise.

Independent effects of heart rate and exercise on left ventricular wall movement measured by reflected ultrasound

Movement of the posterior wall of the left ventricle was assessed using an ultrasound technique in 11 normal subjects at rest and immediately after maximal erect exercise. Maximal posterior wall velocity was measured as the maximal slope of the wall movement from the end-diastolic position to the end-systolic position, and posterior wall excursion was measured as the maximal amplitude of movement anteriorly. Maximum posterior wall velocity increased from a mean of 37 mm/sec at rest to 96 mm/sec after exercise ( P < 0.001), and posterior wall excursion increased from 4.00 mm at rest to 6.8 mm after exercise ( P < 0.001). The effect of heart rate alone on posterior wall movement was evaluated using the technique of atrial pacing. Increasing the heart rate in 6 patients resulted in a reduction in both posterior wall velocity and excursion. At identical heart rates in 5 patients there was a significant increase in both posterior wall velocity and excursion during exercise compared to atrial pacing. It is suggested that changes in posterior wall movement reflect alterations in left ventricular function independent of heart rate, and that these changes can be measured by reflected ultrasound.

Mechanism of prolongation of the R-R interval with electrical stimulation of the carotid sinus nerves in man.

To elucidate the mechanism by which stimulation of the carotid sinus nerves prolongs the R-R interval, the effects of activating an implanted carotid sinus nerve stimulator were studied in eight patients at varying levels of background autonomic activity and with varying types of efferent autonomic blockade. Beta-receptor blockade was induced with intravenous propranolol, 0.20 mg/kg, and parasympathetic blockade with intravenous atropine, 0.04 mg/kg. In the supine position, average prolongation of the R-R interval due to stimulation of the carotid sinus nerves was 269 ± 56 msec prior to autonomic blocking drugs, 442 ± 214 msec after propranolol (NS), and 44 ± 13 msec after propranolol and atropine ( P &lt; 0.025). Comparable changes were produced in the standing position. With moderate treadmill exercise, stimulation of the carotid sinus nerves prolonged the R-R interval by only 40 ± 30 msec prior to blocking drugs, 62 ± 19 msec after propranolol, and 40 ± 30 msec after propranolol and atropine. It is concluded that the prolongation of the R-R interval produced by stimulation of the carotid sinus nerves is secondary to augmented parasympathetic activity, and the attenuation of this response during erect exercise appears to be due to a centrally mediated reduction in the responsiveness of the parasympathetic nervous system to baroreceptor stimuli.

Effects of I.C.I. 50172 in man during erect exercise.

Effects of I.C.I. 50172 in man during erect exercise.