Cardiac autonomic function and baroreflex changes following 4 weeks of resistance versus aerobic training in individuals with pre-hypertension

Aim: Cardiac autonomic modulation and baroreflex sensitivity (BRS) are altered in individuals with hypertension. Aerobic exercise (AE) training has been shown to improve both measures, yet little is known about the effects of resistance exercise (RE). The purpose of this study was to examine the heart rate variability (HRV) and BRS following 4 weeks of resistance or aerobic training in a population with borderline high blood pressure (BP). Methods: Twenty‐nine mild hypertensives were recruited and randomly assigned to 4 weeks of RE or AE training. Before and after training, resting measures of HRV frequencies and BRS were obtained. Results: There was a significant decrease in resting systolic BP for both exercise training modes (RE 136 ± 3.0 pre‐ to 132 ± 3.4 post‐training vs. AE 142 ± 4.0 pre‐ to 137 ± 3.6 mmHg post‐training, P = 0.019). Diastolic BP decreased significantly following both exercise training modes (RE 78 ± 1.31 pre to 74 ± 1.1 post vs. AE 80 ± 1.7 pre to 77 ± 1.6 mmHg post, P = 0.002). A significant time by training mode interaction for low frequency : high frequency (HF) ratio (P = 0.017) with AE decreasing the ratio (275.21 ± 67.28 to 161.26 ± 61.49) and RE increasing this ratio (143.73 ± 65.00 to 227.83 ± 59.41). Natural log‐transformed (ln) HRV values showed a time‐by‐training mode interaction for ln HF (P = 0.05) as ln HF increased (4.7 ± 0.38 to 5.4 ± 0.35 ms²) following AE and decreased (5.98 ± 0.37 to 5.76 ± 0.42 ms²) following RE. BRS increased following aerobic training and decreased after resistance training (6.74 ± 1.2 to 7.94 ± 1.3 and 10.44 ± 1.2 to 9.1 ± 1.2 ms mmHg^?1 respectively, P = 0.021). Conclusions: Aerobic exercise improved the autonomic nervous system (increasing vagal tone, reducing sympathovagal balance while increasing BRS) while RE showed no improvements in cardiac autonomic tone and decreased BRS.     

The carotid baroreflex is reset following prolonged exercise in humans

Aim: Alterations in the carotid baroreflex (CBR) control of arterial pressure may explain the reduction in arterial pressure and left ventricular (LV) function after prolonged exercise. We examined the CBR control of heart rate (HR) and mean arterial pressure (MAP), in addition to changes in LV function, pre- to post-exercise. Methods: Seven males (age, mean ± SEM; 29 ± 4 years) completed 4 h of ergometer rowing at a workload of 10–15% below the lactate threshold. The CBR control of HR and MAP was assessed via the rapid neck-suction/pressure protocol. LV systolic function was measured by echocardiography, where ejection fraction (EF), the ratio of systolic blood pressure to end systolic volume (SBP/ESV) and stroke volume (SV) were estimated. Results: Following exercise MAP was reduced (12 ± 3%) and HR was elevated (35 ± 5%; P < 0.05). Furthermore, CBR control of MAP was relocated to the left on the stimulus–response curve (P < 0.05) demonstrating that the CBR operated around a lower arterial pressure. Concomitantly, LV systolic function was reduced, indicated by a decrease in EF (22 ± 2%), SBP/ESV (32 ± 14%) and SV (25 ± 5%, P < 0.05). The reduced EF and SBP/ESV were associated with the decreased MAP operating point (r² = 0.71 and r² = 0.47, respectively, P < 0.05). Conclusion: The CBR is reset after prolonged exercise to a lower prevailing arterial pressure. This resetting of the CBR may contribute to the reduction arterial pressure and LV function after exercise.     

High levels of circulating angiotensin II shift the open-loop baroreflex control of splanchnic sympathetic nerve activity,heart rate and arterial pressure in anesthetized rats

Although an acute arterial pressure (AP) elevation induced by intravenous angiotensin II (ANG II) does not inhibit sympathetic nerve activity (SNA) compared to an equivalent AP elevation induced by phenylephrine, there are conflicting reports as to how circulating ANG II affects the baroreflex control of SNA. Because most studies have estimated the baroreflex function under closed-loop conditions, differences in the rate of input pressure change and the magnitude of pulsatility may have biased the estimation results. We examined the effects of intravenous ANG II (10 μg kg⁻¹ h⁻¹) on the open-loop system characteristics of the carotid sinus baroreflex in anesthetized and vagotomized rats. Carotid sinus pressure (CSP) was raised from 60 to 180 mmHg in increments of 20 mmHg every minute, and steady-state responses in systemic AP, splanchnic SNA and heart rate (HR) were analyzed using a four-parameter logistic function. ANG II significantly increased the minimum values of AP (67.6 ± 4.6 vs. 101.4 ± 10.9 mmHg, P < 0.01), SNA (33.3 ± 5.4 vs. 56.5 ± 11.5%, P < 0.05) and HR (391.1 ± 13.7 vs. 417.4 ± 11.5 beats/min, P < 0.01). ANG II, however, did not attenuate the response range for AP (56.2 ± 7.2 vs. 49.7 ± 6.2 mmHg), SNA (69.6 ± 5.7 vs. 78.9 ± 9.1%) or HR (41.7 ± 5.1 vs. 51.2 ± 3.8 beats/min). The maximum gain was not affected for AP (1.57 ± 0.28 vs. 1.20 ± 0.25), SNA (1.94 ± 0.34 vs. 2.04 ± 0.42%/mmHg) or HR (1.11 ± 0.12 vs. 1.28 ± 0.19 beats min⁻¹ mmHg⁻¹). It is concluded that high levels of circulating ANG II did not attenuate the response range of open-loop carotid sinus baroreflex control for AP, SNA or HR in anesthetized and vagotomized rats.     

Increased finger arterial blood pressure after exercise detraining in women with parental hypertension: autonomic tasks

The effects of exercise detraining on resting finger arterial blood pressure (BP), the carotid-cardiac vagal baroreflex, and BP and heart rate (HR) responses to mental arithmetic and forehead cold exposure were studied in young (19 ± 1.1 years) normotensive women with parental history of hypertension. Following 8 weeks of aerobic exercise for 25 min, 3 days week^?1 at an intensity of 60% V˙O _{2 peak}, subjects ceased training for 6–8 weeks. After detraining, V˙O _{2 peak} (mL kg^?1 min^?1) was reduced by 11.5% (41.1 ± 6.9 to 36.4 ± 4.8) coincident with an ≈ 10 %increase in submaximal exercise heart rate. Responses to the laboratory tasks were then compared. Detraining was accompanied by increases (P <0.05) in resting systolic (SBP) (113.6 ± 8.9 to 121.2 ± 9.0), diastolic (DBP) (63.0 ± 8.4 to 68.3 ± 6.8), and mean arterial (MAP) (78.7 ±8.4 to 84.2 ± 7.3) BP (mmHg). None of the above changes occurred in sedentary matched-control subjects. Systolic blood pressure was elevated during forehead cold exposure and MAP was elevated during mental arithmetic after detraining, but the rates of response and recovery for SBP, DBP and MAP were not altered by detraining. Despite higher submaximal exercise HR after detraining, HR responses to autonomic challenges, including the carotid-cardiac vagal baroreflex, were unchanged between training and detraining. Our results indicate that exercise detraining increases resting finger arterial BP in young normotensive women at risk for hypertension with no effects on the rate of response or recovery of heart rate and BP during autonomic tasks known to elicit sympathetic and carotid-cardiac vagal activities in this population. The use of auscultatory brachial artery pressures in a similar study of women diagnosed with hypertension will clarify the clinical meaning of our findings.     

Middle cerebral artery blood velocity depends on cardiac output during exercise with a large muscle mass

We tested the hypothesis that pharmacological reduction of the increase in cardiac output during dynamic exercise with a large muscle mass would influence the cerebral blood velocity/perfusion. We studied the relationship between changes in cerebral blood velocity (transcranial Doppler), rectus femoris blood oxygenation (near-infrared spectroscopy) and systemic blood flow (cardiac output from model flow analysis of the arterial pressure wave) as induced by dynamic exercise of large (cycling) vs. small muscle groups (rhythmic handgrip) before and after cardioselective β₁ adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.). During rhythmic handgrip, the increments in systemic haemodynamic variables as in middle cerebral artery mean blood velocity were not influenced significantly by metoprolol. In contrast, during cycling (e.g. 113 W), metoprolol reduced the increase in cardiac output (222 ± 13 vs. 260 ± 16%), heart rate (114 ± 3 vs. 135 ± 7 beats min^?1) and mean arterial pressure (103 ± 3 vs.112 ± 4 mmHg), and the increase in cerebral artery mean blood velocity also became lower (from 59 ± 3 to 66 ± 3 vs. 60 ± 2 to 72 ± 3 cm s^?1; P < 0.05). Likewise, during cycling with metoprolol, oxyhaemoglobin in the rectus femoris muscle became reduced (compared to rest; ?4.8 ± 1.8 vs. 1.2 ± 1.7 μmol L^?1, P < 0.05). Neither during rhythmic handgrip nor during cycling was the arterial carbon dioxide tension affected significantly by metoprolol. The results suggest that as for the muscle blood flow, the cerebral circulation is also affected by a reduced cardiac output during exercise with a large muscle mass.     

Role of adenosine in exercise‐induced human skeletal muscle vasodilatation

The role of adenosine in exercise‐induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline‐induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one‐legged, knee‐extensor exercise at ～48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (F_aBF) by ～20%, i.e. from 3.6 ± 0.5 to 2.9 ± 0.5 L min^?1, and leg vascular conductance (VC) from 33.4 ± 9.1 to 27.7 ± 8.5 mL min^?1 mmHg^?1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) F_aBF from 0.3 ± 0.03 L min^?1 to a 15‐fold peak elevation (P < 0.05) at 4.1 ± 0.5 L min^?1. Continuous infusion of adenosine at rest and during one‐legged exercise at ～62% of peak power output increased (P < 0.05) F_aBF dose‐dependently to level off (P = ns) at 8.3 ± 1.0 and 8.2 ± 1.4 L min^?1, respectively. One‐legged exercise alone increased (P < 0.05) F_aBF to 4.7 ± 1.7 L min^?1. Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least ～20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.     

Cerebral oxygenation decreases during exercise in humans with beta‐adrenergic blockade

Aim: Beta‐blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation. Methods: Acting as their own controls, eight healthy subjects performed a continuous incremental cycle test to exhaustion with or without administration of the non‐selective beta‐blocker propranolol. Changes in cerebral blood flow velocity were measured with transcranial Doppler ultrasound and those in cerebral oxygenation were evaluated using near‐infrared spectroscopy and the calculated cerebral mitochondrial oxygen tension derived from arterial to internal jugular venous concentration differences. Results: Arterial lactate and cardiac output increased to 15.3 ± 4.2 mm and 20.8 ± 1.5 L min^?1 respectively (mean ± SD). Frontal lobe oxygenation remained unaffected but the calculated cerebral mitochondrial oxygen tension decreased by 29 ± 7 mmHg (P < 0.05). Propranolol reduced resting heart rate (58 ± 6 vs. 69 ± 8 beats min^?1) and at exercise exhaustion, cardiac output (16.6 ± 3.6 L min^?1) and arterial lactate (9.4 ± 3.7 mm ) were attenuated with a reduction in exercise capacity from 239 ± 42 to 209 ± 31 W (all P < 0.05). Propranolol also attenuated the increase in cerebral blood flow velocity and frontal lobe oxygenation (P < 0.05) whereas the cerebral mitochondrial oxygen tension decreased to a similar degree as during control exercise (delta 28 ± 10 mmHg; P < 0.05). Conclusion: Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity.     

Reference values for short‐term resting‐state heart rate variability in healthy adults: Results from the Brazilian Longitudinal Study of Adult Health—ELSA‐Brasil study

Heart rate variability (HRV) is a psychophysiological phenomenon with broad implications, providing an accessible index of vagal function, underpinning psychological constructs, including the capacity for social engagement and emotion regulation, and may predict future morbidity and mortality. However, the lack of reference values for short‐term HRV indices for participants of both sexes across the age spectrum is a limiting factor. This was the objective of the present study. Resting electrocardiographic records were obtained from 13,214 participants (both sexes, 35–74 years), and HRV indices in time and frequency domains (mean ± SD) were determined from 5‐min records. Results were based on a subsample of 2,874 nonmedicated, healthy participants stratified by sex across 10‐year age groupings. Men showed lower heart rate (HR, 64 ± 8 bpm vs. 68 ± 8 bpm, p < .05) and normalized high frequency (HF; 39.4 ± 18.0 normalized units [n.u.] vs. 50.4 ± 18.5 n.u., p < .05) than women, and higher N‐N variance (2,214 ± 1,890 ms² vs. 1,883 ± 1,635 ms², p < .05), standard deviation of all N‐N intervals (SDNN; 43.7 ± 17.3 ms vs. 40.3 ± 15.8 ms, p < .05) and LF/HF (2.30 ± 2.68 vs. 1.33 ± 1.82, p < .05). HR and HF (n.u.) were also higher in younger than older women. LF/HF was lower in women than men. Percentile curves showed almost all HRV indices decreasing with aging. The availability of short‐term, resting‐state HRV reference values in a large sample of healthy and nonmedicated participants from 35–74 years will provide a valuable tool for researchers, clinicians, and those in the quantified‐self community.     

Attenuated relationship between cardiac output and oxygen uptake during high-intensity exercise

Aim: Recent findings have challenged the belief that the cardiac output (CO) and oxygen consumption (VO₂) relationship is linear from rest to maximal exercise. The purpose of this study was to determine the CO and stroke volume (SV) response to a range of exercise intensities, 40–100% of VO_2max, during cycling. Methods: Ten well‐trained cyclists performed a series of discontinuous exercise bouts to determine the CO and SV vs. VO₂ responses. Results: The rate of increase in CO, relative to VO₂, during exercise from 40 to 70% of VO_2max was 4.4 ± 1.4 L L^?1. During exercise at 70–100% of VO_2max, the rate of increase in CO was reduced to 2.1 ± 0.9 L L^?1 (P = 0.01). Stroke volume during exercise at 80–100% of VO_2max was reduced by 7% when compared to exercise at 50–70% of VO_2max (134 ± 5 vs. 143 ± 5 mL per beat, P = 0.02). Whole body arterial‐venous O₂ difference increased significantly as intensity increased. Conclusion: The observation that the rate of increase in CO is reduced as exercise intensity increases suggests that cardiovascular performance displays signs of compromised function before maximal VO₂ is reached.     

Middle cerebral artery blood velocity during exercise with β‐1 adrenergic and unilateral stellate ganglion blockade in humans

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V_mean) is attenuated during cycling with β‐1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocain; 8 mL; n=8) affects the attenuated exercise – MCA V_mean following cardio‐selective β‐1 adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V_mean were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V_mean increased to the same extent (11.4 ± 1.9 vs. 11.1 ± 1.9 cm s^?1). With the pharmacological intervention the exercise CO (10 ± 1 vs. 12 ± 1 L min^?1; n=5), HR (115 ± 4 vs. 134 ± 4 beats min^?1) and ΔMCA V_mean (8.7 ± 2.2 vs. 11.4 ± 1.9 cm s^?1) were reduced, and MAP was increased (100 ± 5 vs. 86 ± 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the β‐1 blockade induced attenuation in ΔMCA V_mean (10.2 ± 2.5 cm s^?1). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.     

Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans

Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3-L4. This caused cutaneous sensory anaesthesia below T8-T9 and complete paralysis of the legs. Cycling was performed for 22.7 ± 2.7 min (mean, SE) (fatigue) and oxygen uptake (Vo₂) increased to 1.90 ± 0.13 1 min^-1. Compared with voluntary exercise at the same Vo₂, increases in heart rate (HR) (135 ± 7 vs. 130 ± 9 beats min^-1) and cardiac output (16.9 ± 1.1 vs. 17.3 ± 0.9 1 min^-1) were similar, and ventilation (54 ± 5 vs. 45 ± 4 1 min^-1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 ± 4 (rest) to 119 ± 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 ± 3 (rest) to 95 ± 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.     

Wavelet-Based System Identification of Short-Term Dynamic Characteristics of Arterial Baroreflex

The assessment of arterial baroreflex function in cardiovascular diseases requires quantitative evaluation of dynamic and static baroreflex properties because of the frequent modulation of baroreflex properties with unstable hemodynamics. The purpose of this study was to identify the dynamic baroreflex properties from transient changes of step pressure inputs with background noise during a short-duration baroreflex test in anesthetized rabbits with isolated carotid sinuses, using a modified wavelet-based time-frequency analysis. The proposed analysis was able to identify the transfer function of baroreflex as well as static properties from the transient input-output responses under normal [gain at 0.04 Hz from carotid sinus pressure (CSP) to arterial pressure (n = 8); 0.29 ± 0.05 at low (40–60 mmHg), 1.28 ± 0.12 at middle (80–100 mmHg), and 0.38 ± 0.07 at high (120–140 mmHg) CSP changes] and pathophysiological [gain in control vs. phenylbiguanide (n = 8); 0.32 ± 0.07 vs. 0.39 ± 0.09 at low, 1.39 ± 0.15 vs. 0.59 ± 0.09 (p < 0.01) at middle, and 0.35 ± 0.04 vs. 0.15 ± 0.02 (p < 0.01) at high CSP changes] conditions. Subsequently, we tested the proposed wavelet-based method under closed-loop baroreflex responses; the simulation study indicates that it may be applicable to clinical situations for accurate assessment of dynamic baroreflex function. In conclusion, the dynamic baroreflex property to various pressure inputs could be simultaneously extracted from the step responses with background noise.     

Long-lasting coronary vasoconstrictor effects and myocardial uptake of endothelin-1 in humans

The effect of intravenous administration of the endothelium-derived vasoconstrictor peptide endothelin-1 (ET-1 0.2, 1 and 8 pmol kg^?1 min^?1) on coronary blood flow in relation to plasma ET-1 as well as blood lactate and glucose levels were investigated in six healthy volunteers. Coronary sinus blood flow was measured by thermodilution. Administration of ET-1 elevated arterial plasma ET 35-fold, dose-dependently increased mean arterial blood pressure from 95±5 mmHg to 110±6 mmHg (P<0.01) and reduced heart rate from 64±4 beats min^?1 to 58±4 beats min^?1 (P<0.05) at 8 pmol kg^?1 min^?1. Coronary sinus blood flow was reduced maximally by 23±4% (P<0.01) and coronary vascular resistance increased by 48±11% (P<0.01). Coronary sinus oxygen saturation decreased from 35±1% to 22±2% at 2 min after the infusion (P<0.01). A coronary constrictor response was observed at a 4-fold elevation in plasma ET. The reduction in coronary sinus blood flow lasted 20 min and coronary sinus oxygen saturation was still reduced 60 min after the infusion. Myocardial oxygen uptake or arterial oxygen saturation were not affected by ET-1. Myocardial lactate net uptake decreased by 40% whereas glucose uptake was unaffected. At the highest infusion rate there was a net removal of plasma ET by 24±3% over the myocardium (P<0.05). The results show that ET-1 induces long-lasting reduction in coronary sinus blood flow via a direct coronary vasoconstrictor effect in healthy humans observable at a 4-fold elevation in plasma ET-1. Furthermore, there is a net removal of circulating ET-1 by the myocardium.     

Increased systolic blood pressure after mild cold and rewarming: relation to cold-induced thermogenesis and age

Aim: Higher winter mortality in elderly has been associated with augmented systolic blood pressure (SBP) response and with impaired defense of core temperature. Here we investigated whether the augmented SBP upon mild cold exposure remains after a rewarming period, and whether SBP changes are linked to thermoregulation. Therefore, we tested the following hypotheses: cold‐induced increase in SBP (1) remains augmented after rewarming in elderly compared to young adults (2) is related to non‐shivering thermogenesis (NST) upon mild cold (3) is related to vasoconstriction upon mild cold. Methods: Blood pressure, energy expenditure (EE), skin and core temperature, skin perfusion (abdomen, forearm, both sides of hand) and % body fat were measured in 12 young adults (Y) and 12 elderly (E). Supine subjects were exposed to a thermoneutral baseline 0.5 h (T_air = 30.1 °C), 1 h mild cold (T_air = 20.7 °C), 1 h rewarming (T_air = 34.8 °C) and 1 h baseline (T_air = 30.5 °C). Results: Upon mild cold only the young adults showed significant NST (Y: +2.5 ± 0.6 W m^?2, P < 0.05). No significant age effects in vasoconstriction were observed. After rewarming per cent change in SBP (%ΔSBP) remained significantly increased in both age groups and was augmented in elderly (Y: +5.0% ± 1.2% vs. E: +14.7% ± 3.1%, P < 0.05). Regression analysis revealed that %ΔSBP significantly related to ΔEE upon mild cold (P < 0.01, r² = 0.35) and in elderly also to %body fat (P < 0.02, r² = 0.57). Conclusion: Individual changes in SBP after rewarming correlate negatively to NST. Elderly did not show NST, which explains the greater SBP increase in this group. In elderly a relatively large %body fat protected against the adverse effects of mild cold.     

Does limb angular motion raise limb arterial pressure?

Aim: Mechanical factors such as the muscle pump have been proposed to augment flow by several mechanisms. The potential for limb angular motion to augment local perfusion pressure (pressure = ½ρr²ω², where ρ is the fluid density, r the radius and ω the angular velocity) has been overlooked. We sought to test the hypothesis that limb angular motion augments limb arterial pressure. Methods: Nine human subjects performed horizontal shoulder flexion (～±90° at 0.75 Hz for 30 s). We measured finger arterial pressure (photoplethysmography) in the moving (Trial 1) and non‐moving arm (Trial 2) in separate trials along with the pressure (strain gauge) generated at the fingers within a length of water‐filled tubing mounted on the moving arm in both trials. Results: Arm swinging raised (P < 0.05) the mean pressure measured in the tubing by 11 ± 2 and 14 ± 2 mmHg (Trials 1 and 2 respectively). In response to exercise, the rise in mean finger arterial pressure in the swinging limb (18 ± 3 mmHg, Trial 1) exceeded (P < 0.05) the rise in the resting limb (8 ± 2 mmHg, Trial 2) by an amount similar to the 11 mmHg rise in pressure generated in the tubing in Trial 1. Conclusions: We conclude that the swinging of a limb creates centrifugal force (a biomechanical centrifuge) which imparts additional pressure to the arteries, but not the veins owing to the venous valves, which further widens the arterial–venous pressure difference.     

Upregulation of the brain renin-angiotensin system in rats with chronic renal failure

Aim: We investigated how the brain renin–angiotensin system is involved in regulation of the sympathetic activity and arterial pressure in rats with chronic renal failure. Methods: Systolic arterial pressure, heart rate and diurnal urinary noradrenaline excretion were measured for 12 weeks in spontaneously hypertensive rats (SHR) with or without subtotal nephrectomy. Expression of mRNAs related to the brain renin–angiotensin system was measured using polymerase chain reaction. Effects of a 6‐day intracerebroventricular infusion of a type 1 angiotensin II receptor antagonist (candesartan) or bilateral dorsal rhizotomy on these variables were also investigated. Results: Systolic arterial pressure and urinary excretion of noradrenaline were consistently higher in subtotally nephrectomized SHR than in sham‐operated SHR (262 ± 5 vs. 220 ± 3 mmHg, P < 0.001; 2.71 ± 0.22 vs. 1.69 ±0.19 ng g^?1 body weight day^?1, P < 0.001). Expression of renin, angiotensin‐converting enzyme and type 1 angiotensin II receptor mRNAs in the hypothalamus and lower brainstem was greater in subtotally nephrectomized SHR than in sham‐operated SHR. Continuous intracerebroventricular infusion of candesartan attenuated hypertension and the increase in urinary noradrenaline excretion in subtotally nephrectomized SHR. Dorsal rhizotomy decreased arterial pressure, urinary excretion of noradrenaline and expression of renin–angiotensin system‐related mRNAs in brains of subtotally nephrectomized SHR. Conclusion: The brain renin–angiotensin system in subtotally nephrectomized SHR appears to be activated via afferent nerves from the remnant kidney, resulting in sympathetic overactivity and hypertension in this chronic renal failure model.     

Reduced arterial O2 saturation during supine exercise in highly trained cyclists

Performance of intense dynamic exercise in highly trained athletes is associated with a reduced arterial haemoglobin saturation for O₂ (SaO ₂) and lower arterial PO ₂ (PaO ₂). We hypothesized that compared with upright exercise, supine exercise would be accompanied by a smaller reduction in SaO ₂ because of a lower maximal O₂ uptake (VPO _2max) and/or a more even ventilation–perfusion distribution. Eight elite bicyclists completed progressive cycle ergometry to exhaustion in both positions with concomitant determinations of ventilatory data, arterial blood gases and pH. During upright cycling VPO _2max averaged 75±1.6 mL O₂ min^-1 kg^-1 (±SEM) and it was 10.6±1.7% lower during supine cycling (P<0.001). Also the maximal pulmonary and alveolar ventilation were lower during supine cycling (by 15±2% and 21±3%, respectively; P< 0.001) which related to a 0.8±0.1 L lower tidal volume (P<0.001). In all subjects and independent of work posture PaO ₂ and SaO ₂ decreased from rest to exhaustion (from 99±3 to 82±2 Torr and 98.1±0.2 to 95.2±0.4%, respectively; P<0.001); alveolar–arterial PO ₂ difference increased from 6±2 to 37±3 Torr in both body positions. At exhaustion arterial PCO ₂ was lower in upright than in supine (33.4±0.6 vs. 35.9±0.9 Torr; P<0.01), suggesting a greater relative hyperventilation in upright. Arterial pH was similar in upright and supine at rest (both 7.41±0.01) and at exhaustion (7.31±0.01 vs. 7.32±0.01, respectively). We conclude that despite a lower VPO _2max and supposedly an improved ventilation–perfusion distribution, altering body position from upright to supine does not influence arterial O₂ desaturation during intense exercise.     

Expiratory muscle fatigue impairs exercise performance

High-intensity, exhaustive exercise may lead to inspiratory as well as expiratory muscle fatigue (EMF). Induction of inspiratory muscle fatigue (IMF) before exercise has been shown to impair subsequent exercise performance. The purpose of the present study was to determine whether induction of EMF also affects subsequent exercise performance. Twelve healthy young men performed five 12-min running tests on a 400-m track on separate days: a preliminary trial, two trials after induction of EMF, and two trials without prior muscle fatigue. Tests with and without prior EMF were performed in an alternate order, randomly starting with either type. EMF was defined as a ≥20% drop in maximal expiratory mouth pressure achieved during expiratory resistive breathing against 50% maximal expiratory mouth pressure. The average distance covered in 12 min was significantly smaller during exercise with prior EMF compared to control exercise (2872 ± 256 vs. 2957 ± 325 m; P = 0.002). Running speed was consistently lower (0.13 m s⁻¹) throughout the entire 12 min of exercise with prior EMF. A significant correlation was observed between the level of EMF (decrement in maximal expiratory mouth pressure after resistive breathing) and the reduction in running distance (r ² = 0.528, P = 0.007). Perceived respiratory exertion was higher during the first 800 m and heart rate was lower throughout the entire test of running with prior EMF compared to control exercise (5.3 ± 1.6 vs. 4.5 ± 1.7 points, P = 0.002; 173 ± 10 vs. 178 ± 7 beats min⁻¹, P = 0.005). We conclude that EMF impairs exercise performance as previously reported for IMF.     

Maintained cerebrovascular function during post-exercise hypotension

The post-exercise period is associated with hypotension, and an increased risk of syncope attributed to decreases in venous return and/or vascular resistance. Increased local and systemic vasodilators, sympatholysis, and attenuated baroreflex sensitivity following exercise are also manifest. Although resting cerebral blood flow is maintained, cerebrovascular regulation to acute decreases in blood pressure has not been characterized following exercise. We therefore aimed to assess cerebrovascular regulation during transient bouts of hypotension, before and after 40 min of aerobic exercise at 60 % of estimated maximum oxygen consumption. Beat to beat blood pressure (Finometer), heart rate (ECG), and blood velocity in the middle cerebral artery (MCAv; transcranial Doppler ultrasound) were assessed in ten healthy young humans. The MCAv-mean arterial pressure relationship during a pharmacologically (i.v. sodium nitroprusside) induced transient hypotension was assessed before and at 10, 30, and 60 min following exercise. Despite a significant reduction in mean arterial pressure at 10 min post-exercise (?10 ± 6.9 mmHg; P < 0.05) and end-tidal PCO₂ (10 min post: ?2.9 ± 2.6 mmHg; 30 min post: ?3.9 ± 3.5 mmHg; 60 min post: ?2.7 ± 2.0 mmHg; all P < 0.05), neither resting MCAv nor the cerebrovascular response to hypotension differed between pre- and post-exercise periods (P > 0.05). These data indicate that cerebrovascular regulation remains intact following a moderate bout of aerobic exercise.     

Dynamic cerebral autoregulation assessment using chaotic analysis in diabetic autonomic neuropathy

Cerebral autoregulation (CA) was assessed by chaotic analysis based on mean arterial blood pressure (MABP) and mean cerebral blood flow velocity (MCBFV) in 19 diabetics with autonomic neuropathy (AN) and 11 age-matched normal subjects. MABP in diabetics dropped significantly in response to tilting (91.6 ± 14.9 vs. 74.1 ± 13.4 mmHg, P < 0.05). Valsalva ratio of heart rate was reduced in diabetics compared to normal (1.1 ± 0.1 vs. 1.5 ± 0.2, P < 0.05). It indicated AN affects the vasomotor tone of peripheral vessels and baroreflex. Nonlinear results showed higher correlation dimension values of MABP and MCBFV in diabetics compared to normal, especially MABP (3.7 ± 2.3 vs. 2.0 ± 0.8, P < 0.05). It indicated CA is more complicated in diabetics. The lower Lyapunov exponent and the higher Kolmogorov entropy values in diabetics indicated less predictable behavior and higher chaotic degree. This study suggests impaired autoregulation would be more chaotic and less predictable.