Influence of long‐term oxygen therapy on heart rate and QT time‐series in hypoxic patients with chronic obstructive pulmonary disease

Background: There is increasing interest in the cardiovascular pathology independently associated with chronic obstructive pulmonary disease (COPD). We examined the influence of long‐term oxygen therapy (LTOT) on heart rate (RR) and QT time‐series in COPD. Methods: Ten hypoxic stable COPD patients underwent Holter ECG monitoring for 24 h and physical activity/energy expenditure monitoring for 5 days before and after LTOT. Variability of RR and QT time‐series was quantified using standard statistics and their structural (correlation/scaling) properties were assessed using multifractal analysis. Pre‐ and post‐LTOT cardiac/activity parameters were compared to examine the influence of oxygen therapy and circadian variation. Results: PaO₂ increased (P = 0·0004) whilst PaCO₂ was unchanged (P = 0·56) following LTOT. Activity/energy expenditure estimates were also unchanged following LTOT (P = 0·64–0·99), but RR variability was increased during the morning (P < 0·05) and night (P < 0·1, trend only). Multifractality of RR and QT time‐series was not significantly changed following LTOT, although QT multifractality showed some time‐dependent fluctuations. Trends in RR and QT time‐series over 24‐h were similar pre‐ and post‐LTOT, indicating a generally normal circadian response. Conclusions: An increase in HRV following LTOT (but notably in the absence of altered activity levels) provides tentative evidence that LTOT has a direct effect on heart rate control in COPD. This beneficial influence was expressed mainly during the morning, and the relevance of this diurnal variation in response requires further investigation. It was also confirmed that both RR and (to a lesser degree) QT time‐series in COPD have a multifractal structure, and this is not affected appreciably by LTOT.     

Effects of pharmacological adrenergic and vagal modulation on fractal heart rate dynamics

Breakdown of short‐term fractal‐like behaviour of HR indicates an increased risk for adverse cardiovascular events and mortality, but the pathophysiological background for altered fractal HR dynamics is not known. Our aim was to study the effects of pharmacological modulation of autonomic function on fractal correlation properties of heart rate (HR) variability in healthy subjects. Short‐term fractal scaling exponent (α₁) along with spectral components of HR variability were analysed during the following pharmacological interventions in healthy subjects: (i) noradrenaline (NE) infusion (n=22), (ii) NE infusion after phentolamine (PHE) (n=8), (iii) combined NE + adrenaline (EPI) infusion (n=12), (iv) vagal blockade with high dose of atropine (n=10), (v) and vagal activation by low dose of atropine (n=10). Then α₁ decreased progressively during the incremental doses of NE (from 0·85 ± 0·250 to 0.55 ± 0·23, P<0·0001). NE also decreased the average HR (P<0·001) and increased the high frequency spectral power (P<0·001). Vagal blockade with atropine increased the α₁ value (from 0·82 ± 0·22 to 1·24 ± 0·41, P<0·05). Combined NE + EPI infusion and vagal activation with a low dose atropine did not result in any changes in α₁, and α‐adrenergic blockade by PHE did not completely reverse the effects of NE on α₁. Increased levels of circulating NE result in reduction of short‐term correlation properties of HR dynamics. The results suggest that coactivation of cardiac vagal outflow at the time of high levels of a circulating sympathetic transmitter explains the breakdown of fractal‐like behaviour of human HR dynamics.     

The exercise heart rate profile in master athletes compared to healthy controls

Endurance exercise protects the heart via effects on autonomic control of heart rate (HR); however, its effects on HR indices in healthy middle‐aged men are unclear. This study compared HR profiles, including resting HR, increase in HR during exercise and HR recovery after exercise, in middle‐aged athletes and controls. Fifty endurance‐trained athletes and 50 controls (all male; mean age, 48·7 ± 5·8 years) performed an incremental symptom‐limited exercise treadmill test. The electrocardiographic findings and HR profiles were evaluated. Maximal O₂ uptake (52·6 ± 7·0 versus 34·8 ± 4·5 ml kg^?1 min^?1; P<0·001) and the metabolic equivalent of task (15·4 ± 1·6 versus 12·2 ± 1·5; P<0·001) were significantly higher in athletes than in controls. Resting HR was significantly lower in athletes than in controls (62·8 ± 6·7 versus 74·0 ± 10·4 beats per minute (bpm), respectively; P<0·001). Athletes showed a greater increase in HR during exercise than controls (110·1 ± 11·0 versus 88·1 ± 15·4 bpm; P<0·001); however, there was no significant between‐group difference in HR recovery at 1 min after cessation of exercise (22·9 ± 5·6 versus 21·3 ± 6·7 bpm; P = 0·20). Additionally, athletes showed a lower incidence of premature ventricular contractions (PVCs) during exercise (0·0% versus 24·0%; P<0·001). Healthy middle‐aged men participating in regular endurance exercise showed more favourable exercise HR profiles and a lower incidence of PVCs during exercise than sedentary men. These results reflect the beneficial effect of endurance training on autonomic control of the heart.     

Changes in cardiac autonomic regulation after prolonged maximal exercise

Harmful cardiac events occurs frequently after exercise. However, the cardiac autonomic regulation after vigorous exercise is not well known. This study was designed to assess heart rate (HR) variability before and after a 75 km cross‐country skiing race. HR variability was assessed by using standard statistical measures along with spectral and quantitative Poincarè plot analysis of HR variability in 10 healthy male subjects (age 36 ± 11 years). The average HR was at the same level 1 day after the race as before the race, but on the second day, HR was significantly lower (P<0·001) compared with the prerace and 1 day after values. The normalized high‐frequency (HF) spectral component of HR variability (nuHF) was lower (P<0·01) on the first day after the maximal exercise compared with the pre‐exercise values but returned to or even exceeded the prerace level on the second day (P<0·01). The changes in short‐term R‐R interval variability analysed from the Poincaré plot were similar to those observed in the HF spectral component. The normalized low‐frequency (LF) spectral component of HR variability (nuLF) was higher (P<0·01) on the first day after the exercise compared with the prerace levels and it also returned to the pre‐exercise level or even dropped below it on the second day after the race. The mean time it took the HF spectral component to return to the pre‐exercise level was 4·2 ± 4·2 h (ranging from 0 to 12 h). This recovery time correlated inversely with the maximal oxygen consumption (VO_2max) measured during the bicycle exercise test before the skiing race (r=?0·712, P<0·016). The cardiac vagal outflow is blunted for several hours after prolonged vigorous exercise. The recovery time of reduced vagal outflow depends on individual cardiorespiratory fitness and there is an accentuated rebound of altered autonomic regulation on the second day after prolonged exercise.     

A new method to quantify postexercise ST‐deviation – the ST‐deficit. A study in men at high and low‐risk for coronary heart disease

Background Quantitative heart rate adjusted exercise ST criteria like μV/beats per minute (bpm) improve the diagnostic accuracy of the exercise ECG. However, there are few quantitative HR adjusted postexercise variables available. The aim of the present exercise study was to evaluate a new such variable from computerized averaging of the postexercise ECG. Methods The presence of possible myocardial ischaemia in a population based sample of 74 elderly male hypertensives at high‐risk of coronary heart disease, and in 42 age‐matched clinically healthy males (reference group) at low‐risk was assessed by exercise ECG. All men had a normal resting ECG without signs of ischaemia. Variables studied: standard ST‐criteria, ST/HR slope ≤–2·4 μV · bpm^–1, shape of the rate‐recovery loop, the latter also with a new quantitative variable, the ST‐deficit. Results In spite of a normal resting ECG many subjects showed an abnormal ST/HR slope during exercise, 43% in the hypertension group and 26% in the reference group. An abnormal rate‐recovery loop (ST‐deficit) also contributed substantially to identify patients with possible myocardial ischaemia, 30 vs. 10%, respectively (P<0·02); cumulatively for the two HR adjusted criteria 53% vs. 29%, respectively (P<0·02). Mean ST‐deficit was significantly lower in the high‐risk group. Conclusions Effort‐related myocardial ischaemia is frequently silent in elderly high‐risk hypertensives and necessitates testing, preferably with computerized exercise ECG and heart rate adjusted ST criteria. A new quantitative variable to assess the postexercise rate‐recovery loop in the time domain, the ST‐deficit is described. This variable seems to effectively discriminate between subjects with low and high‐risk for coronary heart disease and thus provides new information. Further studies are warranted to validate this variable against myocardial perfusion scintigraphy and coronary angiography.     

Plasma protein thiols: an early marker of oxidative stress in asthma and chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) and asthma are both characterized by heterogeneous chronic airway inflammation and obstruction as well as oxidative stress (OS). However, it is unknown whether OS occurs in early disease and how to best assess its presence. Plasma OS markers (TBARS, PSH, taurine, GSH, ergothioneine and paraoxonase 1 activity) and lung function tests were measured in patients with mild stable asthma (n = 24) and mild stable COPD (n = 29) and in age‐ and sex‐matched controls. Forced expiratory volume in 1 s (FEV₁) was associated with age both in patients and control groups. By contrast, FEV₁ was positively correlated with PSH only in COPD (ρ = 0·49, P = 0·007). In multiple logistic regression analysis, lower PSH was the only OS marker independently associated with increased odds of both asthma (OR = 0·32, 95% CI 0·13–0·78, P = 0·01) and COPD (OR = 0·50, 95% CI 0·26–0·95, P = 0·03). These findings suggest that proteins ‐SH are a sensitive OS marker in early COPD and asthma.     

Heart Rate Turbulence Impairment and Ventricular Arrhythmias in Patients with Systemic Sclerosis

Background: Arrhythmias, conduction disturbances, and cardiac autonomic nervous system dysfunction are the most frequent cardiovascular complications in systemic sclerosis (scleroderma). The aim of the study was to assess heart rate turbulence (HRT) in systemic sclerosis patients and to identify the relationship between HRT and occurrence of arrhythmias. Methods: Forty‐five patients with scleroderma (aged 54.6 ± 14.7 years) and 30 healthy sex‐ and age‐matched subjects were examined. In addition to routine studies, 24‐hour Holter monitoring with assessment of HRT was performed. Results: As compared to controls, HRT was significantly impaired in systemic sclerosis patients. Abnormal HRT defined as turbulence onset (TO) ≥0.0% and/or turbulence slope (TS) ≤2.5 ms/RR (ms/RR interval) was found in 19 (42%) scleroderma patients and in no members of the control group. Serious ventricular arrhythmias Lown class IV (VA‐LownIV), for example, couplets and/or nonsustained ventricular tachycardias, were observed in 16 (36%) scleroderma patients. The median value of TS was significantly lower in systemic sclerosis patients with VA‐LownIV than in patients without VA‐LownIV (3.68 vs 7.00 ms/RR, P = 0.02). The area under curve of ROC analysis for prediction of VA‐LownIV was 0.72 (95% confidence interval [CI] 0.56–0.87) and revealed that TS <9.0 ms/RR was associated with VA‐Lown IV occurrence, with sensitivity of 93.7% and specificity of 44.8%. Univariate and multivariate analyses confirmed that lower values of TS were associated with VA‐LownIV occurrence (odds ratio 1.52, 95% CI 1.09–2.12, P = 0.01). Conclusions: Patients with systemic sclerosis are characterized by significant HRT impairment. Assessment of HRT and especially TS is useful in the identification of patients at risk for ventricular arrhythmias. (PACE 2010; 920–928)     

Intensity of Nordic Walking in young females with different peak O2 consumption

The purpose of this cross‐sectional study was to determine the physiological reaction to the different intensity Nordic Walking exercise in young females with different aerobic capacity values. Twenty‐eight 19–24‐year‐old female university students participated in the study. Their peak O₂ consumption (VO₂ peak kg^?1) and individual ventilatory threshold (IVT) were measured using a continuous incremental protocol until volitional exhaustion on treadmill. The subjects were analysed as a whole group (n = 28) and were also divided into three groups based on the measured VO₂ peak kg^?1 (Difference between groups is 1 SD) as follows: 1. >46 ml min^?1 kg^?1 (n = 8), 2. 41–46 ml min^?1 kg^?1 (n = 12) and 3. <41 ml min^?1 kg^?1 (n = 8). The second test consisted of four times 1 km Nordic Walking with increasing speed on the 200 m indoor track, performed as a continuous study (Step 1 – slow walking, Step 2 – usual speed walking, Step 3 – faster speed walking and Step 4 – maximal speed walking). During the walking test expired gas was sampled breath‐by‐breath and heart rate (HR) was recorded continuously. Ratings of perceived exertion (RPE) were asked using the Borg RPE scale separately for every 1 km of the walking test. No significant differences emerged between groups in HR of IVT (172·4 ± 10·3–176·4 ± 4·9 beats min^?1) or maximal HR (190·1 ± 7·3–191·6 ± 7·8 beats min^?1) during the treadmill test. During maximal speed walking the speed (7·4 ± 0·4–7·5 ± 0·6 km h^?1) and O₂ consumption (30·4 ± 3·9–34·0 ± 4·5 ml min^?1 kg^?1) were relatively similar between groups (P > 0·05). However, during maximal speed walking, the O₂ consumption in the second and third groups was similar with the IVT (94·9 ± 17·5% and 99·4 ± 15·5%, respectively) but in the first group it was only 75·5 ± 8·0% from IVT. Mean HR during the maximal speed walking was in the first group 151·6 ± 12·5 beats min^?1, in the second (169·7 ± 10·3 beats min^?1) and the third (173·1 ± 15·8 beats min^?1) groups it was comparable with the calculated IVT level. The Borg RPE was very low in every group (11·9 ± 2·0–14·4 ± 2·3) and the relationship with VO₂and HR was not significant during maximal speed Nordic Walking. In summary, the present study indicated that walking is an acceptable exercise for young females independent of their initial VO₂ peak level. However, females with low initial VO₂ peak can be recommended to exercise with the subjective ‘faster speed walking’. In contrast, females with high initial VO₂ peak should exercise with maximal speed.     

Effect of non-hypotensive haemorrhage on plasma catecholamine levels and cardiovascular variability in man

Background: It is well known from animal research that non‐hypotensive haemorrhage produces sympathoexcitatory responses assessable by both the rise in plasma catecholamine levels and the shift of autonomic influences on the heart to more sympathetic and less parasympathetic control. Data in humans are restricted. Methods: Heart rate variability (HRV), systolic blood pressure (FINAPRES) variability (BPV), and catecholamine plasma levels were measured before and after haemorrhage in 30 healthy blood donors and compared with those from 10 control subjects without blood loss. Spectral power of HRV and BPV in very low (0·02–0·06 Hz), low (0·07–0·14 Hz), and high (0·15–0·40 Hz) frequency bands were calculated by Fourier analysis. Catecholamine plasma levels were assayed by dual column reverse‐phased high‐performance liquid chromatography (HPLC). Results: Haemorrhage of 5·6 ± 1·2 ml kg^?1 body weight increased plasma norepinephrine levels (215 ± 92 pg ml^?1 versus 254 ± 95 pg ml^?1; P = 0·002), increased BPV in the low frequency band (Mayer waves; 1·8 ± 1·0 ln [mmHg²] versus 2·0 ± 0·9 ln [mmHg²]; P = 0·021), and decreased the vagally transmitted high frequency HRV (6·9 ± 1·1 ln [MI²] versus 6·5±1·2 ln [MI²]; P<0·0001), but did not induce significant changes in heart rate (66 ± 11 bpm versus 67 ± 11 bpm; P = 0·79) and arterial blood pressure (mean values: 84 ± 13 mmHg versus 87 ± 13 mmHg; P = 0·12). Conclusions: As suggested by plasma norepinephrine levels, systolic BPV and HRV, non‐hypotensive haemorrhage produces sympathoexcitatory responses as well as vagal withdrawal of heart rate control in humans.     

Effect of set configuration on hemodynamics and cardiac autonomic modulation after high‐intensity squat exercise

The aim of this study was to compare the effect of two different high‐intensity resistance exercise (RE) set configurations on the following: systolic blood pressure (SBP), rate pressure product (RPP), heart rate (HR) variability (HRV), and HR complexity (HRC). Ten well‐trained males performed three parallel squat sets until failure (traditional training; TT) with the four repetitions maximum load (4RM), and a rest of 3 min between sets. Thereafter, participants performed a cluster training session (CT) of equated load but with resting time distributed between each repetition. Dependent variables were recorded before, during, and after RE. Mean SBP (25·7 versus 10·9% percentage increase; P = 0·016) and RPP (112·5 versus 69·9%; P = 0·01) were significantly higher in TT. The decrease in HRV after exercise and the drop of HRC during exercise were similar in CT and TT. Change of standard deviation of normal RR intervals after TT correlated with change in SBP (r = 0·803; P = 0·009) while the change of Sample Entropy during exercise correlated with the increment of RPP during CT (ρ = ?0·667; P = 0·05). This study suggests that set configuration influences acute cardiovascular responses during RE. When intensity, volume and work‐to‐rest ratio are equated, CT is less demanding in terms of SBP and RPP. A greater hemodynamic response during exercise would be associated with a faster parasympathetic recovery.     

Twenty‐four hour variation in heart rate variability indices derived from fractional differintegration

Assuming that RR time‐series behave as a fractionally differintegrated Gaussian process, García‐González et al. (2003) recently proposed new indices for quantifying variability and structure in RR data. One of these was the ‘fractional noise quantifier’ (fnQ), measuring the departure of an RR time‐series from a monofractal structure (i.e. a measure of its multifractality). Sixty‐nine participants (aged = 34·5 ± 12·4 years, body mass index (BMI) = 23·9 ± 2·9 kg m^?2, maximal oxygen uptake rate (O_2peak) = 42·4 ± 10·9 ml min^?1 kg^?1, 39 males) provided continuous beat‐to‐beat ECG recordings for a 24‐h period. Fractional differintegration was used to quantify fnQ, and heart rate variability was calculated in the time domain. All variables were evaluated during consecutive 1‐h periods and also during four 6‐h blocks corresponding to morning, afternoon, evening and night periods. Apart from RR, circadian trends in all variables were independent of gender (P = 0·11–0·59). Apart from fnQ, all variables exhibited circadian variation (0·0005<P<0·012). Although fnQ was statistically uniform during the 24‐h period, it showed a trend towards elevated values during evening and night. The main finding of this study was that fnQ was elevated by around 10% during the evening and night, although this was not statistically significant. This suggests that the structure of RR time‐series in healthy individuals is most strongly ‘multifractal’ during evening and night periods. fnQ appears to be a plausible surrogate measure of multifractality in RR time‐series.     

Standardized submaximal exercise testing in never smokers: a normative study

In a population survey on the south‐western coast of Norway, 373 never smokers aged 18–73 years (230 women) without respiratory symptoms performed a standardized, progressive, incremental submaximal bicycle exercise test. All individuals were able to do an exercise involving oxygen uptake of 1·0 l min^–1, 80% of the subjects reached 1·5 l min^–1 and 50% of the subjects reached 2·0 l min^–1. The respiratory frequency (RF), ventilation (VE) and heart rate (HR) for a given oxygen uptake were all higher in women than in men. Significant predictors of failure to reach oxygen uptake of 1·5 and 2·0 l min^–1 were sex, age, body height and weight. Prediction equations are given for respiratory frequency, heart rate and ventilation for an oxygen uptake of 1·0 l min^–1 in women and 1·5 l min^–1 in men; and body height is a strong predictor for all dependent variables. A multiple linear regression analysis in women showed that age was a significant predictor of respiratory frequency (P<0·05), ventilation (P<0·001) and heart rate (P<0·001), while in men age was a significant predictor only of ventilation (P<0·001) during the bicycle exercise protocol.     

正常人和急性心肌梗死患者心率震荡斜率的昼夜变化及与心率的相关性

目的观察正常人和急性心肌梗死（AMI）患者心率震荡（HRT）的昼夜变化规律,探讨不同人群心率与震荡斜率（TS）的相关性。方法选择100例AMI患者,平均年龄（60.87±13.72）岁,男66例,女34例;82例正常对照者,平均年龄（59.23±13.31）岁,男54例,女28例。两组均进行24h动态心电图检查,定量测定一昼夜中每小时的平均心率（HR）与TS的均值,采用圆形分布统计分析方法,计算两组TS值在昼夜分布中的高峰时点及集中时段。结果（1）正常对照组TS值在24h分布上有明显的集中趋势,高峰时点为04：34（P〈0.05）,集中时段为21：25～11：41;AMI组TS值在24h分布上无明显集中趋势（P〉0.05）。（2）正常对照组HR与TS呈负相关关系（r=-0.771,P〈0.01）;AMI组HR与TS不存在直线相关关系（r=-0.312,P〉0.05）。结论正常人TS值有昼夜节律性,明显受HR的影响。作为心脏的一个基本生物节律,其主要受自主神经的调控。而AMI患者的这种生物节律性消失,可能与自主神经功能紊乱有关。     

Myocardial velocities measured during adenosine, dobutamine and supine bicycle exercise: a tissue Doppler study in healthy volunteers

Background: Dobutamine stress echocardiography (DSE) quantified by tissue Doppler (TVI) have improved the diagnostic capacity of the procedure. Quantification of other stress modalities, e.g. adenosine stress echo (ASE) and exercise stress echocardiography (ESE) are necessary for assessing any pathophysiological differences in different forms of stress. Methods: Ten healthy individuals underwent ASE, DSE, and ESE during a span of 2–5 days. Left ventricular (LV) apical images at rest and peak stress (max) were postprocessed using TVI on a GE System FiVe equipment. ECG‐derived QRS duration (QRSD, ms), heart rate (HR, bpm), TVI‐estimated basal systolic velocities (S2V, cm s^?1), ejection time (S2T, ms) and strain (S, %) were computed off‐line and compared. Longitudinal displacement imaging, tissue tracking, was also made. Results: Data for ASE, DSE and ESE during peak stress were (HR: 84 ± 12***, 142 ± 19, 137 ± 27; P<0·001) (QRSD: 92 ± 18**, 74 ± 13, 79 ± 9; P<0·05), (S2T: 307 ± 34***, 175 ± 53, 192 ± 25; P<0·001) and (S%: 26·0 ± 3·0, 21·2 ± 7·3, 22·1 ± 5·1; P = n.s.) respectively. Velocity response, registered in the LV septum at max, was lowest during ASE (7·4 ± 1·4) highest during DSE (13·0 ± 2·7; P<0·001 versus ASE) and somewhat intermediate during ESE (11·3 ± 3·5; P<0·001 versus ASE). In contrast, strain and displacement did not differ. Conclusion: ASE evokes significantly less LV systolic response compared with both DSE and ESE. Increased velocity (P<0·05 versus rest) and strain (P>0·05) response at a much lower HR indicates that adenosine has minor effects on contraction presumably secondary to vasodilatation. Powerful chronotropic response to DSE and ESE is probably prerequisite for strong velocity response at the expense of strain and displacement. TVI‐assisted stress echocardiography thereby shows different LV systolic response in healthy individuals, depending on stress modality.     

Cardiovascular functioning during the menstrual cycle

Variations in cardiovascular functioning during the ‘normal’ menstrual cycle have been little researched. Resting‐blood pressures, resting‐heart rate, rate‐pressure product (RPP) and a derived index of fitness (Schneider Index) were monitored throughout natural, hormonally defined menstrual cycles. Volunteers were 26 women (20–48 years) who had regular (25–35 days) cycles. Their blood pressures and heart rate (at rest and according to Schneider’s protocol) were measured at the same time daily (Monday–Friday) for 5 weeks. Daily, early morning‐urine samples were assayed for sex hormones enabling accurate definition of cycle phase for each woman. Resting systolic‐blood pressure was significantly higher in the ovulatory phase (P<0·05) than in the follicular or luteal phases, but resting‐diastolic pressures did not differ significantly between phases. Resting‐heart rate was significantly higher in both ovulatory (P<0·01) and luteal (P<0·01) phases than in the menstrual and follicular phases. The Schneider Index was higher during the follicular phase than during the ovulatory (P<0·005) or luteal (P<0·01) phases, the RPP was higher during the ovulatory phase than during the bleeding (P<0·05) and follicular (P<0·005) phases. These findings provide a pattern of menstrual cycle‐related variation in cardiovascular functioning that can be related to established actions of the ovarian steroids.     

Circulatory response to single circuit weight and walking training sessions of similar energy cost in middle‐aged overweight females

The aim of this study was to compare circulatory responses to circuit weight (CWT) and aerobic walking training sessions of similar energy cost in middle‐aged overweight females. Thirty‐three middle‐aged pre‐menopausal females participated in the experiment. They were divided into overweight (n=18, 36·2 ± 6·3 years, 166·3 ± 8·0 cm, 83·5 ± 9·7 kg, BMI 30·2 ± 3·1 kg m^–2) and non‐overweight control (n=15, 34·1 ± 6·3 years, 165·0 ± 5·6 cm, 61·6 ± 5·0 kg, BMI 22·7 ± 1·5 kg m^–2) groups. Individual physical working capacity (PWC) was measured using the cycle ergometer test (calculated at the level of predicted HR_max (205 – ½ age). A CWT session consisted of leg extension, bench press, sit‐ups and leg press exercises. The subjects performed four circuits at the maximal possible speed, using a work‐to‐rest ratio of 60 s. Blood pressure (BP) was measured during every rest period between the exercises, and the heart rate (HR) was recorded continuously during the whole CWT programme. During the walking training session, the subjects walked as fast as possible on the indoor track. The total energy cost of the walking training session was the same as during the CWT session, approximately 270 kcal, and was controlled by a CALTRAC accelerometer. HR and BP were measured every 5 min during the walking training session. The PWC index was significantly (P<0·05) higher in the overweight group in comparison with the control females (215·4 ± 76·1 and 187·9 ± 42·4 W, respectively). The resting BP was normal in both groups (<140/90 mmHg). HR was between 120 and 140 beats min^–1 during CWT and walking sessions. There were no differences in BP during both training sessions in overweight and control subjects. It was concluded that both CWT and walking training sessions were acceptable forms of physical activity to increase cardiovascular fitness in middle‐aged overweight and normal body weight females.     

Leg uptake of calcitonin gene‐related peptide during exercise in spinal cord injured humans

Exercise‐induced increases in cardiac output (CO) and oxygen uptake (VO₂) are tightly coupled, as also in absence of central motor activity and neural feedback from skeletal muscle. Neuromodulators of vascular tone and cardiac function – such as calcitonin gene related peptide (CGRP) – may be of importance. Spinal cord injured individuals (six tetraplegic and four paraplegic) performed electrically induced cycling (FES) with their paralyzed lower limbs for 29 ± 2 min to fatigue. Voluntary cycling performed both at VO₂ similar to FES and at maximal exercise in six healthy subjects served as control. In healthy subjects, CGRP in plasma increased only during maximal exercise (33·8 ± 3·1 pmol l^?1 (rest) to 39·5 ± 4·3 (14%, P<0·05)) with a mean extraction over the working leg of 10% (P<0·05). Spinal cord injured individuals had more pronounced increase in plasma CGRP (33·2 ± 3·8 to 46·9 ± 3·6 pmol l^?1, P<0·05), and paraplegic and tetraplegic individuals increased in average by 23% and 52%, respectively, with a 10% leg extraction in both groups (P<0·05). The exercise induced increase in leg blood flow was 10–12 fold in both spinal cord injured and controls at similar VO₂ (P<0·05), whereas CO increased more in the controls than in spinal man. Heart rate (HR) increased more in paraplegic subjects (67 ± 7 to 132 ± 15 bpm) compared with controls and tetraplegics (P<0·05). Mean arterial pressure (MAP) was unchanged during submaximal exercise and increased during maximal exercise in healthy subjects, but decreased during the last 15 min of exercise in the tetraplegics. It is concluded that plasma CGRP increases during exercise, and that it is taken up by contracting skeletal muscle. The study did not allow for a demonstration of the origin of the CGRP, but its release does not require activation of motor centres. Finally, the more marked increase in plasma CGRP and the decrease in blood pressure during exercise in tetraplegic humans may indicate a role of CGRP in regulation of vascular tone during exercise.     

Haemodynamic effects of patent foramen ovale and atrial septal defect closure: a comparison during percutaneous shunt closure

Objectives: We investigated the haemodynamic effect of percutaneous closure of an intra‐atrial shunt, using non‐invasive finger pressure measurements. Background: Percutaneous closure of both patent foramen ovale (PFO) and atrial septal defect (ASD) is widely practised. Currently no data are available on short‐term haemodynamic changes induced by closure. Methods: Twenty‐five consecutive patients (mean age 49 ± 17 years, 10 men) who underwent a percutaneous closure of a PFO (n = 15) or ASD (n = 10) were included in this study. During the procedure blood pressure and heart rate (HR) were monitored continuously with a Finometer^®. Changes in systolic, mean, and diastolic pressure, stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were computed from the pressure registrations using Modelflow^® methodology. Results: Baseline characteristics were similar for the PFO and ASD patients. After PFO closure none of the haemodynamic parameters changed significantly. After ASD closure the systolic, mean, and diastolic pressures increased 7·1 ± 5·4 (P = 0·003), 3·8 ± 3·5 (P = 0·007) and 2·0 ± 3·0 mmHg (P = ns) respectively. HR decreased 5·1 ± 5·3 beats per minute (P = 0·01). SV, CO and TPR increased 8·5 ± 6·4 ml (13·5%; P = 0·002), 0·21 ± 0·45 l min^?1 (5·6%; P = ns) and 0·02 ± 0·14 dynes (4·1%; P = ns) respectively. The changes in SV differ between the PFO and ASD patients (P = 0·009). Conclusions: Using non‐invasive finger pressure measurements, we found that SV, mean and systolic blood pressure increased immediately after percutaneous closure of an ASD in adults, whereas the percutaneous PFO closure had no effect on haemodynamic characteristics.     

Cardiac sympathetic activity is associated with inflammation and neurohumoral activation in patients with idiopathic dilated cardiomyopathy

Background: Idiopathic dilated cardiomyopathy (IDC) is characterized by sympathetic nervous overactivity, inflammation and neurohumoral activation; however, their interrelationships are poorly understood. Methods and results: We studied 99 patients with IDC (age 54 ± 1 years, left ventricular ejection fraction (EF) 40 ± 1%, maximum oxygen uptake (VO₂max) 20 ± 1 ml kg^?1 min^?2, mean ± SEM) by using ¹²³I‐metaiodobenzylguanidine (MIBG) imaging. MIBG washout and MIBG heart/mediastinum (H/M)‐ratio at 4 h postinjection were calculated. In addition, the plasma levels of interleukin (IL)‐6 and N‐terminal B‐type natriuretic peptide (NT‐proBNP) were measured. MIBG washout and MIBG H/M ratio had a significant correlation with IL‐6 (r = 0·42, P<0·001 and r = ?0·31, P<0·01) and NT‐proBNP (r = 0·48, P<0·001 and r = ?0·40, P<0·001). During a median follow‐up of 4·1 years, 20 patients (20%) had an adverse cardiac event (death, heart transplantation or application of biventricular pacemaker or implantable cardioverter–defibrillator). In these patients, MIBG washout was higher (53 ± 4 versus 40 ± 2%, P = 0·01) and H/M ratio lower (1·38 ± 0·04 versus 1·51 ± 0·02, P = 0·01) than in patients without an event. Conclusions: In dilated cardiomyopathy, myocardial sympathetic innervation and activity are related to inflammation and neurohumoral activation. These relationships are at least partly independent of left ventricular function and exercise capacity.     

Temporal age‐related changes in spectral,fractal and complexity characteristics of heart rate variability

Cross‐sectional studies have suggested that heart rate (HR) variability, analysed using traditional time and frequency domain methods, is related to ageing, but no longitudinal studies have estimated the age dependence of HR fluctuation. This study evaluated temporal age‐related changes in 12‐h measures of HR variability among 109 patients with coronary artery disease (CAD), who underwent repeat Holter recordings at 32‐month intervals. Time and frequency domain measures, along with fractal and complexity measures of HR variability, were determined at the baseline and after 32 months. Changes in HR dynamics were compared with various laboratory variables, exercise data and angiographic progression of CAD. Traditional time and frequency domain measures of HR variability did not change significantly during the follow‐up, but the power‐law scaling slope decreased from ?1·29 ± 0·20 to ?1·36 ± 0·23 (P<0·01) and the short‐term fractal exponent (α₁) of HR dynamics from 1·29 ± 0·14–1·22 ± 0·18 (P<0·001). The approximate entropy value also decreased from 1·00 ± 0·19 to 0·95 ± 0·18 (P<0·05). The changes in HR behaviour were not related to demographic data, laboratory values or angiographic progression of CAD. Only a weak correlation was observed between the change in the power‐law slope and the baseline glucose value (P<0·05). This longitudinal study shows that the fractal characteristics of HR dynamics and the complexity properties of R‐R intervals undergo rapid changes along with ageing, and that fractal and complexity analysis techniques are more sensitive than traditional analysis methods in documenting temporal age‐related changes in HR behaviour.