Effects of load and type of physical training on resting and postexercise cardiac autonomic control

The aim of the study was to investigate the influence of training load and exercise mode on heart rate variability and heart rate recovery (HRR) in healthy individuals. The subjects were divided into three groups: sedentary (SED), resistance trained (RT) and aerobically trained (RT). Resting and postmaximal exercise RR intervals were recorded on supine and seated position, respectively. The HRV indices calculated in the resting position were RMSSD and LF and HF power densities. The following HRR indices were calculated throughout the 5‐minute postmaximal recovery period: semi‐logarithmic regression analysis of the first 30 s (T30); absolute difference between the peak and 60 s HR (HRR_60s); and mono‐exponential time constant of HRR (HRRτ). The RMSSD on subsequent 30‐s segments (RMSSD_30s) on recovery period was also calculated. Both RT and AT groups presented faster HRR than SED (P<0·05). The aerobic trained group was the only group that presented vagal reactivation, when analysing the RMSSD_30s. There were no correlations between the Baecke sport score and the HRV vagal‐related indices. However, it was significantly correlated with HRR. It was concluded that that the training load positively influences the HRR, but has no effect on the HRV at rest and that the type of exercise, showed a marked influence on HRV recovery.     

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.     

Autonomic nervous function at rest in aerobically trained and untrained oldermen

Therelationship between aerobictraining, vagal influence on the heart and ageing was examined by assessing aerobic fitness andresting heart rate variability in trained and untrained older men. Subjects were 11 trained cyclistsand runners (mean age=6±61·6 years) and 11 untrained, age-matchedmen (mean age=66±1·2 years). Heart rate variability testing involvedsubjects lying supine for 25 min during which subjects’ breathing was paced andmonitored (7·5 breaths min^?1). Heart rate variability was assessedthrough time series analysis (HRV_ts) of the interbeat interval. Results indicated thattrained older men (3·55±0·21 l min^?1) hadsignificantly (P<0·05) greater VO _2maxthan that of control subjects (2·35±0·15 l min^?1).Also, trained older men (52±1·8 beats min^?1) hadsignificantly (P<0·05) lower supine resting heart rate than that of controlsubjects (65±4·2 beats min^?1). HRV_ts at highfrequencies was greater for trained men (5·98±0·22) than for untrainedmen (5·23±0·32). These data suggest that regular aerobic exercise inolder men is associated with greater levels of HRV_ts at rest.     

A programme based on repeated hypoxia–hyperoxia exposure and light exercise enhances performance in athletes with overtraining syndrome: a pilot study

Overtraining syndrome (OTS) is a major concern among endurance athletes and is a leading cause in preventing them to perform for long periods. Intermittent exposure to hypoxia has been shown to be an effective way of improving performance without exercising. Aim of this pilot study was to evaluate intermittent hypoxia–hyperoxia training combined with light exercise as an intervention to facilitate athletes with OTS to restore their usual performance level. Thirty-four track and field athletes were recruited: 15 athletes with OTS volunteered to participate and undertook a conditioning programme consisting of repeated exposures to hypoxia (O₂ at 10%) and hyperoxia (O₂ at 30%) (6–8 cycles, total time 45 min–1 h), three times a week, delivered 1·5–2 h after a low-intensity exercise session (2 bouts of 30 min, running at 50% of VO_2max with 10 min rest between bouts) over 4 weeks. Nineteen healthy track and field athletes volunteered to participate as a control group and followed their usual training schedule. Measurements before and after the intervention included exercise capacity, analysis of heart rate variability and hematological parameters. In athletes with OTS, a 4-week light exercise combined with intermittent hypoxia–hyperoxia training improved exercise performance (191·9 ± 26·9 W versus 170·8 ± 44·8 W in exercise capacity test, P = 0·01). Heart rate variability analysis revealed an improved sympatho-parasympathetic index (low frequency/high frequency ratio, 8·01 ± 7·51 before and 1·45 ± 1·71 after, P = 0·007). Hematological parameters were unchanged. Our pilot study showed that intermittent hypoxia–hyperoxia training and low-intensity exercise can facilitate functional recovery among athletes with OTS in a relatively short time.     

Predicted maximal heart rate for upper body exercise testing

Age‐predicted maximal heart rate (HR_MAX) equations are commonly used for the purpose of prescribing exercise regimens, as criteria for achieving maximal exertion and for diagnostic exercise testing. Despite the growing popularity of upper body exercise in both healthy and clinical settings, no recommendations are available for exercise modes using the smaller upper body muscle mass. The purpose of this study was to determine how well commonly used age‐adjusted prediction equations for HR_MAX estimate actual HR_MAX for upper body exercise in healthy young and older adults. A total of 30 young (age: 20 ± 2 years, height: 171·9 ± 32·8 cm, mass: 77·7 ± 12·6 kg) and 20 elderly adults (age: 66 ± 6 years, height: 162 ± 8·1 cm, mass: 65·3 ± 12·3 kg) undertook maximal incremental exercise tests on a conventional arm crank ergometer. Age‐adjusted maximal heart rate was calculated using prediction equations based on leg exercise and compared with measured HR_MAX data for the arms. Maximal HR for arm exercise was significantly overpredicted compared with age‐adjusted prediction equations in both young and older adults. Subtracting 10–20 beats min^?1 from conventional prediction equations provides a reasonable estimate of HR_MAX for upper body exercise in healthy older and younger adults.     

Influence of exercise training on heart rate variability in post-menopausal women with elevated arterial blood pressure

Low heart rate variability (HRV) has been reported to be an independent risk factor for the development of coronary heart disease in women and has recently been identified as a risk factor for cardiac sudden death and all-cause mortality. We have recently demonstrated that endurance-trained post-menopausal women demonstrate higher levels of HRV than sedentary control subjects. The purpose of the present study was to test the hypothesis that 12 weeks of regular aerobic exercise would increase HRV in sedentary post-menopausal women with elevated arterial blood pressure (BP) (i.e. either high normal BP or stage I hypertension). A secondary aim was to test the hypothesis that the increase in HRV with exercise training, if observed, would be associated with an increase in spontaneous cardiac baroreflex sensitivity (SBRS), an important physiological determinant of HRV. To accomplish these aims, we studied eight sedentary post-menopausal women (age=54·5±1·3 years) before and after 12 weeks of aerobic exercise training (3·3±0·3 days per week at 70%±2% of maximal heart rate for 43±3 min per day). Maximal oxygen uptake and body weight did not change (P>0·05) with training, but percentage fat (35·5±2·6% vs. 34·5±2·3%, P<0·05) decreased and treadmill time to exhaustion increased (9·8±0·5 vs. 11·3±0·5 min, P<0·05). Supine resting levels of heart rate, RR interval and the standard deviation of the RR interval (time domain measure of HRV) were unchanged (all P>0·05) from baseline levels after 12 weeks of aerobic training. Similarly, the high-frequency, low-frequency and total power of HRV (frequency domain measures) were also unchanged from baseline (all P>0·05). SBRS was also not different before and after aerobic exercise training (1062 vs. 1363 ms mmHg^?1 respectively, P>0·05). In contrast, systolic and diastolic BP were reduced approximately 8 and approximately 5 mmHg with training (both P<0·05) respectively. These results indicate that 12 weeks of moderate-intensity aerobic exercise training does not increase HRV or SBRS, despite producing a clinically significant reduction in BP at rest in post-menopausal women with elevated BP. Considered together with our previous findings in female master endurance athletes, these findings suggest that more intense and prolonged exercise training may be required to produce increases in HRV and SBRS in sedentary post-menopausal women.     

Chronotropic incompetence response to exercise in congestive heart failure,relationship with the cardiac autonomic status

In chronic congestive heart failure (CHF), attenuated heart rate response to exercise, a manifestation of chronotropic incompetence (CI), contributes to limiting exercise capacity. The present study was thus conducted to evaluate the respective role of chronic attenuation of cardiac vagal tone associated with depressed baroreflex sensitivity or affected cardiac sympathetic responsiveness in CHF patients with CI. Spontaneous cardiac baroreflex sensitivity (BRS) assessed by sequence method and spectral‐ and time‐domain analysis of heart rate variability (HRV) were analysed in 21 chronic CHF patients. All patients performed a symptom‐limited exercise test with measurement of gas exchange. Chronic incompetence which was defined as failure to achieve ≥80% of the heart rate reserve (%HRR) given by (HR_peak – HR_rest)/(predictive maximal heart rate – HR_rest) was observed in 14 (66%) patients. There was no significant difference in age, heart rate, peak oxygen uptake or left ventricular ejection fraction between the patients with and without CI. Although there was no significant difference in BRS, low frequency power of HRV in normalized units (LFnu) and SDNN were significantly lower in CI patients. Percentage of HRR correlated significantly with LFnu on 15 min (r=0·64, P<0·005) and, with LFnu on 24 h (r=0·52, P<0·01), SDNN (r=0·48, P=0·03) and SDANN (r=0·48, P=0·03), but not BRS (r=0·04, P=NS). Autonomic nervous system derangement is a complex process in CHF. The role of basal depressed cardiac sympathetic tone seems to contribute more closely than depressed baroreflex sensitivity to the impaired heart rate response to exercise frequently observed in CHF patients.     

The influence of water ingestion on postexercise hypotension and standing haemodynamics

In young healthy adults, postexercise hypotension (PEH) occurs after a single bout of dynamic exercise due to peripheral vasodilation. Gravitational stress may further aggravate the magnitude of PEH, thus predisposing to orthostatic intolerance. As water drinking activates sympathetic vasoconstriction, it might offset PEH via enhanced α‐adrenergic vascular responsiveness. We hypothesized that water ingestion before exercise would decrease the magnitude of PEH and improve the haemodynamic reaction to active standing postmaximal exercise. In a randomized fashion, 17 healthy adults (nine men; eight women, 21·2 ± 1·6 years) ingested 50 and 500 ml of water before completing resting, cycle ergometer and recovery protocols on two separate days. After exercise, measurements [arterial blood pressure (BP), heart rate and spectral heart rate variability (HRV)] were taken in the seated position followed by 5 min of active standing. Compared to that seen post‐50 ml of water, the 500 ml volume elicited an overall increase in BP (P < 0·05). Nevertheless, the magnitude of PEH was not different after either volume of water. There was an overall bradycardic effect of water, and this was accompanied by increased high‐frequency power (P < 0·05). Finally, no BP, heart rate or HRV differences were found between conditions in response to active standing. These data suggest that, despite being well preserved after maximal exercise, the water pressor response does not affect the magnitude of PEH. They also indicate that drinking 500 ml of water does not impact the BP, heart rate or HRV response to 5 min of active standing during recovery postmaximal exercise.     

The influence of whole body vibration on the central and peripheral cardiovascular system

The purpose of this study was to investigate the physiological changes of the cardiovascular system in response to whole body vibration during quiet standing and identify whether there is a greater influence on the central or peripheral cardiovascular system. Twenty healthy participants (12 male and 8 female) were assessed over two separate testing sessions for changes in peripheral skin temperature, peripheral venous function, blood flow velocity in the dorsalis pedis artery, blood pressure and heart rate during quiet standing with 40 Hz 1·9 mm synchronous vibration. Vibration exposure totalled 5 min in 1 min increments with 5 min recovery during each testing session. There were no significant changes in heart rate, blood pressure or peripheral skin temperature. Significant results were obtained for blood flow velocity with increases from 0·5 + 0·2 cm·s^?1 at baseline to 1 + 0·2 cm·s^?1 during vibration, returning to baseline levels during the recovery period. Due to the absence of changes in heart rate, blood pressure or lower leg and foot temperature, the change in blood flow velocity can be attributed to changes in peripheral vascular function. The results suggest a high level of sensitivity of the peripheral vascular system to vibration exposure; therefore, further studies should be completed to ascertain the physiological mechanisms underlying the effects of vibration on the peripheral vascular system.     

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.     

Autonomic neuropathy precedes cardiovascular dysfunction in rats with diabetes

Background Our team previously demonstrated arterial stiffening and cardiac hypertrophy in type 2 diabetic rats at 8 but not 4 weeks after being administered streptozotocin (STZ) and nicotinamide (NA). The present study focused on investigating the effects of type 2 diabetes on cardiac autonomic nerve function in the STZ‐ and NA‐treated animals, using modern spectral estimation technique. Design An autoregressive process was performed to each detrended signal of heart rate and systolic blood pressure measured in the 4‐ and 8‐week STZ‐NA rats with anaesthesia. The power of low‐frequency and high‐frequency oscillations was automatically quantified with each spectral peak by computing the residuals. The closed‐loop baroreflex gain was estimated using the square root of the ratio between heart rate and systolic blood pressure powers in the low‐frequency band. Results Compared with the age‐matched controls, both the 4‐ and 8‐week STZ‐NA diabetic rats had significantly decreased low‐frequency oscillations of heart rate but not systolic blood pressure variability, showing a decline in baroreflex gain (0·451 ± 0·060 and 0·484 ± 0·056 vs. 1·196 ± 0·064 ms mmHg^?1, P < 0·05). On the other hand, the low frequency–high frequency power ratio of the heart period was also diminished in the two diabetic groups, indicating a shift in sympatho‐vagal balance of the heart control (0·472 ± 0·109 and 0·504 ± 0·090 vs. 1·857 ± 0·336, P < 0·05). Conclusions The cardiac autonomic dysfunction in the absence of any significant changes in vascular dynamics, 4 but not 8 weeks after induction of type 2 diabetes, suggests that the diabetic autonomic neuropathy may precede arterial stiffening and cardiac hypertrophy in the STZ‐ and NA‐treated rats.     

The impact of short duration,high intensity exercise on cardiac troponin release

The aim of this study was to assess the appearance of cardiac troponins (cTnI and/or cTnT) after a short bout (30 s) of ‘all‐out’ intense exercise and to determine the stability of any exercise‐related cTnI release in response to repeated bouts of high intensity exercise separated by 7 days recovery. Eighteen apparently healthy, physically active, male university students completed two all‐out 30 s cycle sprint, separated by 7 days. cTnI, blood lactate and catecholamine concentrations were measured before, immediately after and 24 h after each bout. Cycle performance, heart rate and blood pressure responses to exercise were also recorded. Cycle performance was modestly elevated in the second trial [6·5% increase in peak power output (PPO)]; there was no difference in the cardiovascular, lactate or catecholamine response to the two cycle trials. cTnI was not significantly elevated from baseline through recovery (Trial 1: 0·06 ± 0·04 ng ml^?1, 0·05 ± 0·04 ng ml^?1, 0·03 ± 0·02 ng ml^?1; Trial 2: 0·02 ± 0·04 ng ml^?1, 0·04 ± 0·03 ng ml^?1, 0·05 ± 0·06 ng ml^?1) in either trial. Very small within subject changes were not significantly correlated between the two trials (r = 0·06; P>0·05). Subsequently, short duration, high intensity exercise does not elicit a clinically relevant response in cTnI and any small alterations likely reflect the underlying biological variability of cTnI measurement within the participants.     

Fatigue and rapid hamstring/quadriceps force capacity in professional soccer players

The aim of this study was to investigate the effect of fatigue induced by an exhaustive laboratory‐based soccer‐specific exercise on different hamstrings/quadriceps (H:Q) ratios of soccer players. Twenty‐two male professional soccer players (23·1 ± 3·4 year) performed maximal eccentric (ecc) and concentric (con) contractions for knee extensors (KE) and flexors (KF) at 60° s^?1 and 180° s^?1 to assess conventional (H_con:Q_con) and functional (H_ecc:Q_con) ratios. Additionally, they performed maximal voluntary isometric contraction for KE and KF, from which the maximal muscle strength, rate of force development (RFD) and RFD H:Q strength ratio (RFDH:Q) were extracted. Thereafter, subjects were performed an exhaustive laboratory‐based soccer‐specific exercise and a posttest similar to the pretest. There was significant reduction in H_con:Q_con (0·60 ± 0·06 versus 0·58 ± 0·06, P<0·05) and in H_ecc:Q_con (1·29 ± 0·2 versus 1·16 ± 0·2, P<0·01) after the soccer‐specific exercise. However, no significant difference between Pre and Post exercise conditions was found for RFDH:Q at 0–50 (0·53 ± 0·23 versus 0·57 ± 0·24, P>0·05) and 0–100 ms (0·53 ± 0·17 versus 0·55 ± 0·17, P>0·05). In conclusion, H:Q strength ratios based on peak force values are more affected by fatigue than RFDH:Q obtained during early contraction phase. Thus, fatigue induced by soccer‐specific intermittent protocol seems not reduce the potential for knee joint stabilization during the initial phase of voluntary muscle contraction.     

Suppression of heart rate variability after supramaximal exertion

Wingate test is short anaerobic exercise, performed with maximal power, whereas aerobic exercise at 85% maximal heart rate (HR(max)) may be performed for long period. Sustained HR elevations and changes in autonomic activity indices have been observed after latter kind of exercise. Several studies reported reduction in mean interval between consecutive R peaks in ECG (RRI) 1 h after Wingate test; however, underlying changes in autonomic activity remain elusive. In eight young males, RRI and heart rate variability (HRV) were measured daily over two 5-day trials. Subjects exercised on third day of each trial, measurements were taken 1 h after (i) two consecutive 30-s bouts of Wingate tests or (ii) after a 30-min exercise at 85% HR(max), with subjects in supine rest and breathing either spontaneously or at controlled rates of 6 and 15 breaths / min. RRI was significantly shorter after Wingate and submaximal exercise, reduction of high- and low-frequency components of HRV attained reliability only after Wingate tests. This pattern remained preserved for three modes of breathing: spontaneous, 6 and 15 breaths /min. After 24 and 48 h, no exercise effects were traceable. We hypothesize that (i) anaerobic exertion is followed by sustained inhibition of vagal activity, (ii) parasympathetic system plays dominant role in mediating suppression of high- and low-HRV frequency components during postexercise recovery, (iii) degree of alteration of autonomic activity caused by anaerobic and strenuous aerobic exercise may be similar and (iv) normalization of vagal activity precedes normalization of sympathetic cardiac nerves activity during final stage of postexercise recovery.     

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.     

Acute resistance exercise using free weights on aortic wave reflection characteristics

Aortic wave reflection characteristics such as the augmentation index (AIx), wasted left ventricular pressure energy (ΔE_w) and aortic haemodynamics, such as aortic systolic blood pressure (ASBP), strongly predict cardiovascular events. The effects of acute resistance exercise (ARE) using free‐weight exercises on these characteristics are unknown. Therefore, we sought to determine the effects of acute free‐weight resistance exercise on aortic wave reflection characteristics and aortic haemodynamics in resistance‐trained individuals. Fifteen young, healthy resistance‐trained (9 ± 3 years) individuals performed two randomized sessions consisting of an acute bout of free‐weight resistance exercise (ARE) or a quiet control (CON). The ARE consisted of three sets of 10 repetitions at 75% one repetition maximum for squat, bench press and deadlift. In CON, the participants rested in the supine position for 30 min. Measurements were made at baseline before sessions and 10 min after sessions. A two‐way ANOVA was used to compare the effects of condition across time. There were no significant interactions for aortic or brachial blood pressures. Compared to rest, there were significant increases in augmentation pressure (rest: 5·7 ± 3·0 mmHg; recovery: 10·4 ± 5·7 mmHg, P = 0·002), AIx (rest: 116·8 ± 4·2%; recovery: 123·2 ± 8·4%, P = 0·002), AIx normalized at 75 bpm (rest: 5·2 ± 7·6%; recovery: 27·3 ± 13·2%, P<0·0001), ΔE_w (rest: 1215 ± 674 dynes s cm^?2; recovery: 2096 ± 1182 dynes s cm^?2, P = 0·008), and there was a significant decrease in transit time of the reflected wave (rest: 150·7 ± 5·8 ms; recovery 145·5 ± 5·6 ms, P<0·001) during recovery from ARE compared to CON. These data suggest that ARE using free‐weight exercises may have no effect on aortic and brachial blood pressure but may significantly alter aortic wave reflection characteristics.     

Arterial and venous plasma catecholamines during submaximal steady-state exercise

Arterial and venous plasma catecholamine responses to 15 min of cycling at 60% of maximal oxygen uptake were examined 11 times during exercise and recovery in nine young men. Intra-arterial blood pressure, heart rate and oxygen uptake were recorded continuously. All variables increased significantly during the initial 4 min, after which oxygen uptake, diastolic blood pressure and arterial plasma adrenaline showed no further increase. Heart rate and plasma noradrenaline, however, continued to increase, although significantly more slowly, and were closely correlated (r = 0·81, 95% CI 0·71–0·87), as were systolic blood pressure and heart rate (r = 0·78, 95% CI 0·71–0·87). Venous plasma adrenaline showed a steady increase during the whole exercise period and thus a different response pattern from arterial plasma adrenaline. In conclusion, arterial plasma catecholamines respond to steady-state exercise by a two-phase pattern paralleling the changes in arterial blood pressure and heart rate. Venous sampling does not reveal this association.     

Ventilation and Heart Rate Response During Exercise in Normals: Relevance for Rate Variable Pacing

The observation of a close relationship of heart rate to oxygen uptake (HH-VO₂) and heart rate to minute ventilation (HR-VE)has been shown to be of particular value in rate variable pacing. However, the impact of anaerobic threshold (AT)for the HH-VO₂ and HH-VE slope has been studied Jess. Twenty-three male and 16 female subjects, mean age 52 ± 7 years, were selected in whom complete heart catherization and extensive noninvasive sludies excluded major cardiopulmonary disease. Semisupine bicycle exercise testing with analysis of respiratory gas exchange was performed using a ramping work rate protocol with work increments of 20 watts/min. At the respiratory AT, determined by the V slope method, oxygen uptake (VO₂-AT)was 15.2 ± 3.0 mL/kg in males versus 13.8 ± 2.3 mL/kg in females and heart rate (HR-AT)was 109 ± 18 beats/min versus 119 ± 20 beats/min, respectively. Heart rate was highly correlated (r ±0.9)to VO₂ and minute ventilation (VE). A linear regression for HR-VO₂, however, was found only in 16/39 and for HR-VE in 11/39 subjects. Assuming the AT as the breakpoint of two linear curves, it could be demonstrated that compared to low exercise HR appeared to increase at maximal exercise more in relation to VO₂ but less in relation to VE; in men the individual slopes for HR-VO₂ were 2.6 ± 0.7 below but 3.2 ± 1.0 above AT (P < 0.05) and the slopes for HH-VE were 1.6 ± 0.5 below but 1.0 ± 0,4 above AT (P < 0.05). Similarly, in women the individual slopes for HR-VO₂ were 3.7 ± 1.4 below but 4.3 ± 1.4 above AT (P < 0.05)and the slopes for HR-VE were 2.1 ± 0.9 below but 1.3 ± 0.4 above AT (P < 0.05). The differences between male and female subjects were significant. The nonlinear behavior of the HB-VO₂ and HR-VE relation from rest to maximal exercise should have a particular impact in respiratory controlied pacing systems.