Persistence of arrhythmia exercise response in healthy young men

This study assesses the persistence of arrhythmia at rest or during exercise tests, or both, after a mean follow-up period of 6.7 years in 76 young men (mean age 21.5 years) without evidence of organic heart disease. The exercise test was performed using a near-maximal protocol based on progressively increasing intermittent work loads, each of 5 minutes' duration. The initial work load was 50 W. The electrocardiogram was continuously registered throughout all stages of the examination. Arrhythmia was defined as the occurrence of greater than or equal to 1 supraventricular or 1 ventricular premature beat at any stage of the examination. At the follow-up examination, the rate of persistence of arrhythmia did not differ significantly among the subgroups, irrespective of follow-up interval, type of arrhythmia, or arrhythmia patterns of response to exercise. Two-dimensional echocardiography did not show any structural abnormalities and Doppler examination did not demonstrate significant abnormal flow patterns. Our data show that almost all patients continued to present arrhythmia after the follow-up period, without any evidence of development of organic heart disease. Moreover, the arrhythmia pattern of response to exercise remained constant throughout the years. At this time, arrhythmia without underlying heart disease seems to be of a benign natural course in these young men.     

Isometric effects on treadmill exercise response in healthy young men

This study evaluated the hypothesis that the isometric stress of load carrying augments the dynamic exercise response seen on the treadmill, and estimated the magnitude of this effect on heart rate and blood pressure for several methods of carrying the same load. Thirteen healthy subjects carried 40 lb in the right hand (H), 40 lb on the back (B), 20 lb in each hand (D) and no weight (N) while walking for 3 minutes on the treadmill at a grade of 0 at 1.7 miles/ hour. A statistically significant increase in the rate of rise and peak levels of systolic blood pressure, heart rate, estimated mean blood pressure, the product of estimated mean blood pressure and heart rate and systolic blood pressure-heart rate product was shown when task H was compared with tasks B, D and N. Values for tasks D and B did not differ significantly.The effects of isometric and dynamic exercise combined were greater than those of dynamic exercise alone. An effective technique of load distribution reduced the rate of increase in blood pressure, heart rate and the peak attained during dynamic exercise, thereby suggesting a lower level of myocardial oxygen consumption for a given weight-carrying task. These results can be applied to evaluation of patients with heart disease and estimation of their exercise tolerance.     

Cardiac function and plasma catecholamines during upright exercise in healthy young subjects

Radionuclide left ventricular ejection fraction, left ventricular volume changes and plasma catecholamines were recorded in six healthy untrained male subjects at rest and during upright exercise at increasing work loads. During mild submaximal exercise mean left ventricular ejection fraction increased 10% because of end-diastolic dilation, while a further 4% increase of left ventricular ejection fraction was recorded at heavy submaximal exercise mainly due to increased end-systolic contraction. Great individual changes were recorded during maximal exercise.

Alterations in plasma catecholamines were most pronounced at the high exercise levels indicating that changes in cardiac contractility are not linearly correlated with changes in sympathetic nervous activity.

Repeat studies showed only minor variations of mean left ventricular ejection fraction and plasma catecholamines indicating an acceptable reproducibility of the measurements. Variations of both left ventricular ejection fraction and catecholamines were smaller during exercise than at rest.     

Afterload reduction by nifedipine--the acute haemodynamic response to exercise in hypertensive subjects

In 16 people with essential hypertension, heart rate (HR), bloodpressure (BP) and relative cardiac volumes were measured atrest and during submaximal upright exercise before and after10 mg of sublingual nifedipine using radionuclide ventriculography. In 10 patients who had had no previous therapy (BP 152/103±5/3mmHg) nifedipine produced a fall in BP of 6/12±3/3 mmHg(SEM) and a rise in HR of 15±5 bpm (P<0.001). Thiswas associated with a rise in LVEF of 0.07±0.02 (P<0.005)and in cardiac output of 44±9%, presumably as a resultof ventricular offloading. The cardiac response to exercisegiven the different starting values, was unchanged by nifedipine.Thus the HR was 101±6 bpm at rest after nifedipine andon exercise rose to 124±6 bpm (P<0.001): stroke volumewas +22±8% at rest after nifedipine and rose to +43±12%on exercise. Thus cardiac output which had increased by 44±9%after nifedipine increased by 100±10% from the initialvalue. In 6 patients pre-treated with atenolol (100 mg) and with similarresting BP (158/101±5/4 mmHg) there was a fall in BPof 32/15±3/2 mmHg after nifedipine which was greaterthan in the previously untreated group (P<0.01). In thisgroup HR increased by 8±3 bpm (P<0.05). Followingnifedipine the exercise response was similar given the differentstarting values. The combination of nifedipine and a beta adrenoceptor antagonistcan depress myocardial function and the difference between pressure–volumeratios in the two groups supports this view but there was noimportant depressant effect. We conclude that the combinationof beta blocker and nifedipine therapy is effective and safein hypertensive subjects without significant myocardial dysfunction.     

Above-normal left ventricular systolic performance during exercise in young subjects with mild hypertension

Debate continues on whether left ventricular (LV) systolic functionduring exercise is abnormal in young subjects with mild hypertensionand on whether the abnormal blood pressure (BP) trend observedin hypertensives during prolonged exercise is due to impairedLV function. LV function was measured by means of M-mode echocardiographyduring prolonged exercise in 13 physically trained, young, mildhypertensives and 12 age-matched, trained normotensives withsimilar working capacity. Systolic BPIend-systolic volume (SBPIESV) and end-systolic stress/ESVat rest were greater in the hypertensives (P<0.0001 and P–0.034),while LV filling was impaired (P–0.05). BP clianges duringthe first 20 min of exercise were similar in the two groups,but thereafter the between-group BP difference tended to declineprogressively. LV diastolic dimension was similar at rest. Duringexercise it slightly increased in the normotensives and slightlydecreased in the hypertensives (P–0.032). Exercise ejectionfraction (P–0.018), SBPIESV (P<0.0001) and stress/ESV(P–0.027) were greater in the hypertensives throughoutthe test. SBPIESV normalized for LV wall thickness (P<0.0001)and the changes in SBPIESV from rest to exercise were also greaterin the hypertensives (P–0.002). Stroke volume increasedto a lower extent in the hypertensives, but the between-groupdifference was not statistically significant. The increase inSBPIESV from rest to exercise was related to the concentricremodelling of the ventricle in the hypertensives (P<0.0001)and the subjects grouped together (P<0.0001), but not inthe normotensives. In conclusion, increased LV systolic performance is presentearly in hypertension not only at rest but also during vigorousexercise. It is partly due to concentric remodelling of theleft ventricle and partly to enhanced inotropic state.     

Changes in the electrocardiographic response to exercise in healthy women.

Changes in the P wave, QRS complex, ST segment, and T wave during and after maximal exercise were quantitatively analysed in 116 healthy women with a mean age of 39. The corrected orthogonal Frank lead electrocardiogram was continuously recorded and computer processed during bicycle ergometry. With exercise, maximal spatial P wave vectors shifted downward. The Q wave amplitude became more negative and the R wave amplitude diminished considerably in leads X and Y: the S wave amplitude decreased only slightly in these leads. The QRS vectors shifted towards right and posteriorly during exertion and a further shift in the same direction was seen in the recovery period. The ST segment amplitude 60 ms after the J point decreased with exertion and became negative at heart rates above 140 beats per minute, in particular in lead Y. ST segment depression increased with age. The T wave amplitude decreased during exercise and increased sharply in the recovery period. Though mean R wave amplitude in leads X and Y became more negative with exercise, this response was unpredictable in individual women. The exercise induced changes in QRS vectors in women resembled those described in men. Changes in the amplitude of the R wave should not be used for the diagnosis of coronary disease in women. ST segment depression was more pronounced in the inferiorly oriented lead Y than in lead X but it was unrelated to changes in the QRS vectors in these leads.     

Hemodynamic response to isometric exercise in elderly subjects

The haemodynamic responses to isometric exercise (handgrip) performed during right cardiac catheterization were tested in 9 elderly patients (1 female, 8 males) with average age of 67.8 +/- 2.3 years, without clinical and instrumental signs of cardiovascular disease. The parameters tested before and after handgrip were: heart rate (FC), systolic blood pressure (PAS), diastolic blood pressure (PAD), mean blood pressure (PAM), cardiac output (PC), cardiac index (IC), systolic index (IS), mean pulmonary pressure (PPM), end-diastolic pulmonary pressure (PPTD), systemic arterial resistance (RST), pulmonary arterial resistance (RPT), stroke volume (GS), left ventricular systolic stress index (ILS). Statistical analysis was carried out using the Student test. Stress produced a highly significant increase (p less than 0.001) of PPM (+28%) of PPTD (+ 33.1%), a modestly significant increase (p less than 0.01) of PAD (+ 15.6%), PAM (+ 18.2%), ILS (+ 24%,), RPT (+ 25%), a weakly significant increase (p less than 0.05) of PAS (+ 20%), RST (+ 15.6%). No significant variation attributable to FC, IC, IS, GS was observed. Our subjects presented a reduced tolerance to isometric exercise.     

Ventilatory efficiency during exercise in healthy subjects

When evaluating dyspnea in patients with heart or lung disease it is useful to measure the quantity of ventilation needed to eliminate metabolically produced CO2 (i.e., the ventilatory efficiency). Mathematically, the relationship between ventilation (VE) and CO2 output is determined by the arterial CO2 pressure and the physiologic dead space-tidal volume ratio. We decided to determine how age, sex, size, fitness, and the type of ergometer influenced ventilatory efficiency in normal subjects. Three methods were compared for expressing this relationship: (1) the VE versus CO2 output slope below the ventilatory compensation point, commonly used by cardiologists for estimating the severity of heart failure; (2) the VE/CO2 output ratio at the anaerobic threshold, commonly used by pulmonologists; and (3) the lowest VE/CO2 output ratio during exercise, the latter parameter not previously reported. We studied 474 healthy adults, between 17 and 78 years of age during incremental cycle and treadmill cardiopulmonary exercise tests at three test sites, correcting the total VE for the equipment dead space. The lowest VE/CO2 output ratio was insignificantly different from the ratio at the anaerobic threshold, less variable than that for the slope relationship, and unaffected by the site, ergometer, and gas exchange measurement systems. The regression equation for the lowest VE/CO2 output ratio was 27.94 + 0.108 x age + (0.97 = F, 0.0 = M) - 0.0376 x height, where age is in years and height is in centimeters. We conclude that the lowest VE/CO2 output ratio is the preferred noninvasive method to estimate ventilatory inefficiency.     

Blunted growth hormone response to maximal exercise in middle-aged versus young subjects and no effect of endurance training.

The purpose of this study was to evaluate the GH response to exercise and the effects of endurance training on this response in early middle-aged men. Seven healthy middle-aged [M; 42.0+/-2.4 (+/-SD) yr old] and five young (Y; 21.2+/-1.1 yr old) competition cyclists were investigated before and after 4 months of intensive endurance training. Subjects performed an exhaustive incremental exercise test (50 watts for 3 min) with gas exchange measurement, and blood samples for lactate, glucose, and GH determinations were drawn before exercise, at the end of the exercise, and in the recovery phase (1, 3, 5, 10, 15, 20, and 30 min). Basal insulin-like growth factor I was also determined. At exhaustion no differences were found in relative maximal heart rate or blood lactate and glucose peaks. On the contrary, the two groups had markedly different GH responses; in fact, the peak GH response to exhaustive exercise was much lower in M than in Y (8.1+/-1.3 vs. 57.1+/-15.5 microg/L; P<0.01). The training, similar in subjects of the same group, increased progressively from 182 to 300 km/week (+64.8%) in M and from 350 to 600 km/week (+71.4%) in Y. After the training, the percent increase in maximal oxygen consumption was similar in the two groups (M, +15.2%; Y, +17.5%), confirming that the efficiency of the training performed was comparable. In neither group did training have any effect on the GH peak response to exercise, confirming the blunted GH response in M compared to Y (6.7+/-1.0 vs. 61.0+/-12.9 microg/L; P<0.01). Similarly, insulin-like growth factor I concentrations were not significantly affected by training. In conclusion, active middle-aged subjects, compared with the young, showed a blunted GH response to a physiological stimulus such as exercise, indicating that the age-related decline in GH secretion appears in early middle age. This response was not modified by training in either early middle-aged or young subjects.     

Short-term variability of exhaled nitric oxide in young male patients with mild asthma and in healthy subjects

BACKGROUND: Exhaled nitric oxide (NOexp) is an indicator of eosinophilic airways inflammation. This study evaluated short-term variability of NOexp in 13 healthy subjects (19-41 years, eight males) and in 31 patients with asthmatic respiratory symptoms (19-21 years, all male) to obtain data for assessment of short-term changes of NOexp in clinical situations. METHODS: Mild asthma was confirmed in 10 patients (Group = asthma). Twenty-one patients with asthmatic respiratory symptoms did not fulfill the functional criteria of asthma (Group = respiratory symptoms). The procedure to determine NOexp followed the European Respiratory Society (ERS) guidelines; the mean expiratory flow used during sampling was 0.09-0.12 l/s. NOexp for each subject was determined as the mean of at least three successive measurements at the baseline, followed by determinations at 10 min, 6 h and 24 h after the baseline. RESULTS: At the baseline, the mean (SD) value of NOexp was 6.6 (2.3) parts per billion (ppb) in the healthy controls, and significantly higher both in patients with respiratory symptoms (14.6 (11) ppb, P = 0.0076) and in those with asthma (34.2 (43) ppb, P < 0.001). Intraclass correlation coefficient of NOexp measured at baseline and after an interval of 10 min was 0.959 in healthy subjects, 0.986 in patients with respiratory symptoms and 0.936 in asthma patients, respectively. Short-term variability in terms of coefficient of variation (CoV) of repeated measurements of NOexp at 10 min, 6 hand 24 h was 5.1, 10.8 and 11.7% in healthy subjects, 71, 16.4 and 22.2% in patients with respiratory symptoms and 13.5, 19.4 and 26.4% in asthma patients, respectively. CONCLUSIONS: Reproducibility of NOexp using standardized methods was good both in healthy subjects and in asthmatic patients. However, in asthmatics the short-term variation of NOexp was over two times as high as in healthy subjects. The level of NOexp was elevated, except in asthma, also in patients with asthmatic respiratory symptoms who did not fulfill the functional criteria of asthma.     

Effects of caffeine on blood pressure response during exercise in normotensive healthy young men

The possible combined effects of caffeine and exercise on blood pressure (BP) regulation were examined in 34 healthy, normotensive (BP less than 135/85 mm Hg) young men (mean age 27 +/- 3 years) in a placebo-controlled, double-blind crossover design. Each subject performed submaximal and symptom-limited maximal supine bicycle exercise 1 hour apart after ingestion of placebo or caffeine (3.3 mg/kg). Heart rate, BP, cardiac output and peripheral vascular resistance were compared for placebo and caffeine days. Postdrug baseline showed that caffeine increased systolic and diastolic BP and peripheral vascular resistance (p less than 0.001 for each) and decreased heart rate (p less than 0.01) but did not change stroke volume or cardiac output. BP and vascular resistance effects of caffeine remained during submaximal exercise resulting in an additive increase in BP while negative chronotropic effects of caffeine disappeared. At maximal exercise substantially more subjects (15 on caffeine vs 7 on placebo, p less than 0.02) had systolic BP greater than or equal to 230 mm Hg and/or greater than or equal to 100 mm Hg for diastolic BP. Plasma norepinephrine levels were not significantly different across days, but epinephrine was higher at maximal exercise and cortisol was increased post-drug and throughout maximal exercise on caffeine days. Data indicate that caffeine increases BP additively during submaximal exercise and may cause excessive BP responses at maximal exercise for some individuals. The pressor effects of caffeine appear to be due to increasing vascular resistance rather than cardiac output.     

Complex ventricular arrhythmia in apparently healthy young subjects

The aim of this study of 20 young subjects (28 +/- 10.6 years) with no apparent cardiac disease on clinical examination and chest X-ray was to determine the origin of complex ventricular arrhythmias: monomorphic or polymorphic ventricular extrasystoles, isolated or in valves (average 18 158 +/- 12 388 per 24 hours) and/or ventricular tachycardia (5 cases, sustained in 3). These arrhythmias were aggravated (N = 6), disappeared (N = 8) or remained unchanged (N = 5) during exercise. The inter-critical ECG showed ST changes in 5 cases. The extrasystoles had a left bundle branch block configuration in 14 cases and a right bundle branch block configuration in 9 cases. Nine patients were Grade 2 (45%) and 11 patients Grade 4B of Lown's classification. Complementary investigations (echocardiography), radionuclide investigations, right and left heart catheterisation, selective right and left ventriculography and coronary angiography) showed a high incidence of arrhythmogenic right ventricular dysplasia (N - 14) associated with left ventricular abnormalities in 13 cases: hypofixation of Thallium (N = 14) associated with left ventricular abnormalities in 13 cases: hypofixation of Thallium (N = 11), abnormal global left ventricular function (N = 13) with decreased ejection fractions in half the cases, left ventricular dilatation in a third of cases (average and diastolic volume: 109.8 ml/m2), mean velocity of circumferential fibre shortening decreased in 86% of cases (average 0.88 cir/sec), angiographic abnormalities of segmental left ventricular wall motion in 36% of cases; 2 clinically silent cases of mitral valve prolapse were associated with these left ventricular changes; these cases represent forms of arrhythmogenic cardiac disease localised to the right ventricle or involving both ventricles which should be searched for routinely in young patients with apparently normal hearts but with idiopathic and severe ventricular arrhythmias. The diagnosis can only be established by angiography. In other cases, isolated left ventricular abnormalities are detected: two cases of hypertrophic non obstructive cardiomyopathy including one apical form, a condition which may be suspected from analysis of the surface ECG and careful 2D echocardiographic study; phonomechanography may be normal; one idiopathic left ventricular aneurysm which was only diagnosed at ventriculography; one dilated cardiomyopathy affecting the left ventricle. In our series, none of the patients had coronary artery disease and two patients even had no abnormality of any of these investigations.(ABSTRACT TRUNCATED AT 400 WORDS)     

Changes in the electrocardiographic response to exercise in healthy women

Changes in the P wave, QRS complex, ST segment, and T wave during and after maximal exercise were quantitatively analysed in 116 healthy women with a mean age of 39. The corrected orthogonal Frank lead electrocardiogram was continuously recorded and computer processed during bicycle ergometry. With exercise, maximal spatial P wave vectors shifted downward. The Q wave amplitude became more negative and the R wave amplitude diminished considerably in leads X and Y: the S wave amplitude decreased only slightly in these leads. The QRS vectors shifted towards right and posteriorly during exertion and a further shift in the same direction was seen in the recovery period. The ST segment amplitude 60 ms after the J point decreased with exertion and became negative at heart rates above 140 beats per minute, in particular in lead Y. ST segment depression increased with age. The T wave amplitude decreased during exercise and increased sharply in the recovery period. Though mean R wave amplitude in leads X and Y became more negative with exercise, this response was unpredictable in individual women. The exercise induced changes in QRS vectors in women resembled those described in men. Changes in the amplitude of the R wave should not be used for the diagnosis of coronary disease in women. ST segment depression was more pronounced in the inferiorly oriented lead Y than in lead X but it was unrelated to changes in the QRS vectors in these leads.