Lower limb vascular conductance and resting popliteal blood flow during head‐up and head‐down postural challenges

This study hypothesized that central and local reflex mechanisms affecting vascular conductance (VC) through the popliteal artery compensated for the reduction in muscle perfusion pressure (MPP) to maintain popliteal blood flow (PBF) during head‐down tilt (35? HDT), but not in head‐up tilt (45? HUT). Resting measurements were made on 15 healthy men in prone position to facilitate the access to the popliteal artery, on two separate days in random order during horizontal (HOR), HDT or HUT. In each body position, the body was supported, and the ankles were maintained in relaxed state so that there was no muscle tension, as with normal standing. Popliteal blood flow velocity and popliteal arterial diameter were measured by ultrasound, and PBF was calculated. MPP was corrected to mid‐calf from measured finger cuff pressure, and VC was estimated by dividing PBF by MPP. The MPP in HDT (48 ± 2 mmHg) was ~100mmHg less than in HUT (145 ± 2 mmHg). PBF was similar between HOR (51 ± 18 ml min^?1) and HDT (47 ± 13 ml min^?1), but was lower in HUT (30 ± 9 ml min^?1). VC was different between HDT (1·0 ± 0·3 ml min^?1 mmHg^?1), HOR (0·6 ± 0·2 ml min^?1 mmHg^?1) and HUT (0·2 ± 0·1 ml min^?1 mmHg^?1). In conclusion, the interactions of central and local regulatory mechanisms resulted in a disproportionate reduction of VC during HUT lowering PBF even though MPP was higher, while in HDT, increased VC contributed to maintain PBF at the same level as the HOR control condition.     

Relationship between arterial baroreflex sensitivity and exercise capacity in patients with acute myocardial infarction

To investigate the relationship between arterial baroreflex sensitivity (BRS) and exercise capacity, we examined arterial BRS and its relation to exercise capacity during upright bicycle exercise in 40 uncomplicated patients with acute myocardial infarction. Arterial BRS was measured 3 weeks (20 ± 5 days) after acute myocardial infarction and assessed by calculating the regression line relating phenylephrine‐induced increases in systolic blood pressure to the attendant changes in the R–R interval. All patients underwent graded symptom‐limited bicycle exercise with direct measurements of hemodynamic and metabolic measurements. In all patients, the average arterial BRS was 5·6 ± 2·6 ms mmHg^?1. There were no significant correlations between arterial BRS and hemodynamic measurements at rest. However, arterial BRS was negatively related to systemic vascular resistance at peak exercise (r = ?0·60, P = 0·0001) and percent change increase in systemic vascular resistance from rest to peak exercise (r = ?0·45, P = 0·003), whereas arterial BRS was positively related to cardiac output (r = ?0·48, P = 0·002) and stroke volume at peak exercise (r = 0·42, P = 0·007), and percent change increase in cardiac output (r = ?0·55, P = 0·0002) and stroke volume from rest to peak exercise (r = 0·41, P = 0·008). Furthermore, arterial BRS had modest but significant correlations with peak oxygen consumption (r = ?0·48, P = 0·002) and exercise duration (r = 0·35, P = 0·029), indicating that patients with better arterial BRS have better exercise capacity in patients with acute myocardial infarction. These results suggest that arterial BRS was linked to central and peripheral hemodynamic responses to exercise and hence, contributed to exercise capacity after acute myocardial infraction.     

Effects of intense exercise training on endothelium-dependent exercise-induced vasodilatation

To determine whether intense exercise training affects exercise-induced vasodilatation, six subjects underwent 4 weeks of handgrip training at 70% of maximal voluntary contraction. Exercise forearm vascular conductance (FVC) responses to an endothelium-dependent vasodilator (acetylcholine, ACH; 15, 30, 60 μg min^?1) and an endothelium-independent vasodilator (sodium nitroprusside, SNP; 1·6, 3·2, 6·4 μg min^?1) and FVC after 10 min of forearm ischaemia were determined before and after training. Training elicited significant (P<0·001) increases in grip strength (43·4 ± 2·3 vs. 64·1 ± 3·5 kg, before vs. after, mean ± SEM), forearm circumference (26·7 ± 0·4 vs. 27·9 ± 0·4 cm) and maximal FVC (0·4630 ± 0·0387 vs. 0.6258 ± 0·0389 units, P<0·05). Resting FVC did not change significantly with training (0·0723 ± 0·0162 vs. 0.0985 ± 0·0171 units, P>0·4), but exercise FVC increased (0·1330 ± 0·0190 vs. 0.2534 ± 0·0387 units, P<0·05). Before and after the training, ACH increased exercise FVC above the control (no drug) exercise FVC, whereas SNP did not. Training increased (P<0·05) the exercise FVC responses to ACH (0·3344 ± 0·1208 vs. 0.4303 ± 0·0858 units, before vs. after training, 60 μg min^?1) and SNP (0·2066 ± 0·0849 vs. 0.3172 ± 0·0628 units, 6·4 μg min^?1). However, these increases were due to the increase in control (no drug) exercise FVC, as the drug-associated increase in exercise FVC above control did not differ between trials (P>0·6). These results suggest that exercise FVC is increased by both exercise training and stimulating the release of endothelium-dependent vasodilators. However, training does not affect the vascular response to these vasodilators.     

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.     

Reproducibility of peak oxygen consumption and the impact of test variability on classification of individual training responses in young recreationally active adults

This study investigated whether VO₂peak is reproducible across repeated tests before (PRE) and after (POST) training, and whether variability across tests impacts how individual responses are classified following 3 weeks of aerobic exercise training (cycle ergometry). Data from 45 young healthy adults (age: 20·1 ± 0·9 years; VO₂peak, 42·0 ± 6·7 ml·min^?1) from two previously published studies were utilized in the current analysis. Non‐responders were classified as individuals who failed to demonstrate an increase or decrease in VO₂peak that was greater than 2·0 times the typical error of measurement (107 ml·min^?1) away from zero, while responders and adverse responders were above and below this cut‐off, respectively. VO₂peak tests at PRE (three total) and POST (three total) were highly reproducible (PRE and POST average and single measures ICCs: range 0·938–0·992), with low coefficients of variation (PRE:4·9 ± 3·1%, POST: 4·8 ± 2·7%). However, a potential learning effect was observed in the VO₂peak tests prior to training, as the initial pretraining test was significantly lower than the third (p = 0·010, PRE 1: 2 946 ± 924 ml·min^?1, PRE 3: 3 042 ± 919 ml·min^?1). This resulted in fewer individuals classified as adverse responders for Test 3 compared to any combination of tests that included Test 1, suggesting that a single ramp test at baseline may not be sufficient to accurately classify the VO₂peak response in young recreationally active individuals. Thus, it is our recommendation that the initial VO₂peak test be used as a familiarization visit and not included for analysis.     

The influence of a fast ramp rate on peak cardiopulmonary parameters during arm crank ergometry

The influence of a very fast ramp rate on cardiopulmonary variables at ventilatory threshold and peak exercise during a maximal arm crank exercise test has not been extensively studied. Considering that short arm crank tests could be sufficient to achieve maximal oxygen consumption (VO₂), it would be of practical interest to explore this possibility. Thus, this study aimed to analyse the influence of a fast ramp rate (20 W min^?1) on the cardiopulmonary responses of healthy individuals during a maximal arm crank ergometry test. Seventeen healthy individuals performed maximal cardiopulmonary exercise tests (Ultima CardiO2; Medical Graphics Corporation, St Louis, USA) in arm ergometer (Angio, LODE, Groningen, The Netherlands) following two protocols in random order: fast protocol (increment: 2 w/6 s) and slow protocol (increment: 1 w/6 s). The fast protocol was repeated 60–90 days after the 1st test to evaluate protocol reproducibility. Both protocols elicited the same peak VO₂ (fast: 23·51 ± 6·00 versus slow: 23·28 ± 7·77 ml kg^?1 min^?1; P = 0·12) but peak power load in the fast ramp protocol was higher than the one in the slow ramp protocol (119 ± 43 versus. 102 ± 39 W, P < 0·001). There was no other difference in ventilatory threshold and peak exercise variables when 1st and 2nd fast protocols were compared. Fast protocol seems to be useful when healthy young individuals perform arm cardiopulmonary exercise test. The usefulness of this protocol in other populations remains to be evaluated.     

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.     

Effects of walking with blood flow restriction on limb venous compliance in elderly subjects

Venous compliance declines with age and improves with chronic endurance exercise. KAATSU, an exercise combined with blood flow restriction (BFR), is a unique training method for promoting muscle hypertrophy and strength gains by using low‐intensity resistance exercises or walking. This method also induces pooling of venous blood in the legs. Therefore, we hypothesized that slow walking with BFR may affect limb venous compliance and examined the influence of 6 weeks of walking with BFR on venous compliance in older women. Sixteen women aged 59–78 years were partially randomized into either a slow walking with BFR group (n = 9, BFR walk group) or a non‐exercising control group (n = 7, control group). The BFR walk group performed 20‐min treadmill slow walking (67 m min^?1), 5 days per week for 6 weeks. Before (pre) and after (post) those 6 weeks, venous properties were assessed using strain gauge venous occlusion plethysmography. After 6 weeks, leg venous compliance increased significantly in the BFR walk group (pre: 0·0518 ± 0·0084, post: 0·0619 ± 0·0150 ml 100 ml^?1 mmHg^?1, P<0·05), and maximal venous outflow (MVO) at 80 mmHg also increased significantly after the BFR walk group trained for 6 weeks (pre: 55·3 ± 15·6, post: 67·1 ± 18·9 ml 100 ml^?1 min^?1, P<0·01), but no significant differences were observed in venous compliance and MVO in the control group. In addition, there was no significant change in arm compliance in the BFR walk group. In conclusion, this study provides the first evidence that 6 weeks of walking exercise with BFR may improve limb venous compliance in untrained elder female subjects.     

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.     

Determination and possible application of the aerobic gas exchange threshold in aerobically untrained paraplegic subjects based on stimulated cycle ergometry

Purpose. To accurately characterise cardiopulmonary baseline performance in aerobically untrained paraplegic subjects by means of an incremental exercise test (IET) and to derive possible training recommendations based on these measurements.

Methods. Twelve motor complete paraplegic subjects with no previous experience in stimulated leg-cycling participated in the study. Exercise testing was performed on a recumbent FES-tricycle by means of a work rate and cadence controlled IET until maximal work rate was reached. Heart rate (HR) and respiratory parameters were recorded continuously.

Results. Peak oxygen uptake was 671 ± 192 mL min^?1 (mean ± standard deviation), peak HR 90 ± 12 beats min^?1, net peak power 8.4 ± 3.3 W and peak minute ventilation 23.6 ± 7.5 L min^?1. Aerobic gas exchange threshold (GET) was found to be 51% ± 10% of peak oxygen uptake and corresponded to 41% ± 13% of peak power.

Conclusions. A cadence and work rate controlled exercise test allows the determination of cardiopulmonary parameters during stimulated cycle ergometry even in aerobically untrained paraplegic subjects. The precise determination of GET allows an appropriate exercise intensity to be prescribed and thus provides a suitable method for exercise intensity calculation in the spinal cord injured population in the future.     

The relationship between exercise‐induced muscle fatigue,arterial blood flow and muscle perfusion after 56 days local muscle unloading

In the light of the dynamic nature of habitual plantar flexor activity, we utilized an incremental isokinetic exercise test (IIET) to assess the work‐related power deficit (WoRPD) as a measure for exercise‐induced muscle fatigue before and after prolonged calf muscle unloading and in relation to arterial blood flow and muscle perfusion. Eleven male subjects (31 ± 6 years) wore the HEPHAISTOS unloading orthosis unilaterally for 56 days. It allows habitual ambulation while greatly reducing plantar flexor activity and torque production. Endpoint measurements encompassed arterial blood flow, measured in the femoral artery using Doppler ultrasound, oxygenation of the soleus muscle assessed by near‐infrared spectroscopy, lactate concentrations determined in capillary blood and muscle activity using soleus muscle surface electromyography. Furthermore, soleus muscle biopsies were taken to investigate morphological muscle changes. After the intervention, maximal isokinetic torque was reduced by 23·4 ± 8·2% (P<0·001) and soleus fibre size was reduced by 8·5 ± 13% (P = 0·016). However, WoRPD remained unaffected as indicated by an unchanged loss of relative plantar flexor power between pre‐ and postexperiments (P = 0·88). Blood flow, tissue oxygenation, lactate concentrations and EMG median frequency kinematics during the exercise test were comparable before and after the intervention, whereas the increase of RMS in response to IIET was less following the intervention (P = 0·03). In conclusion, following submaximal isokinetic muscle work exercise‐induced muscle fatigue is unaffected after prolonged local muscle unloading. The observation that arterial blood flow was maintained may underlie the unchanged fatigability.     

Determination of baroreflex gain using auto-regressive moving-average analysis during spontaneous breathing

The heart rate component of the arterial baroreflex gain (BRG) was determined with auto-regressive moving-average (ARMA) analysis during each of spontaneous (SB) and random breathing (RB) protocols. Ten healthy subjects completed each breathing pattern on two different days in each of two different body positions, supine (SUP) and head-up tilt (HUT). The R–R interval, systolic arterial pressure (SAP) and instantaneous lung volume were recorded continuously. BRG was estimated from the ARMA impulse response relationship of R–R interval to SAP and from the spontaneous sequence method. The results indicated that both the ARMA and spontaneous sequence methods were reproducible (r=0·76 and r=0·85, respectively). As expected, BRG was significantly less in the HUT compared to SUP position for both ARMA (mean ± SEM; 3·5 ± 0·3 versus 11·2 ± 1·4 ms mmHg^–1; P<0·01) and spontaneous sequence analysis (10·3 ± 0·8 versus 31·5 ± 2·3 ms mmHg^–1; P<0·001). However, no significant difference was found between BRG during RB and SB protocols for either ARMA (7·9 ± 1·4 versus 6·7 ± 0·8 ms mmHg^–1; P=0·27) or spontaneous sequence methods (21·8 ± 2·7 versus 20·0 ± 2·1 ms mmHg^–1; P=0·24). BRG was correlated during RB and SB protocols (r=0·80; P<0·0001). ARMA and spontaneous BRG estimates were correlated (r=0·79; P<0·0001), with spontaneous sequence values being consistently larger (P<0·0001). In conclusion, we have shown that ARMA-derived BRG values are reproducible and that they can be determined during SB conditions, making the ARMA method appropriate for use in a wider range of patients.     

Abnormal vascular reactivity at rest and exercise in obese boys

Background Obese children exhibit vascular disorders at rest depending on their pubertal status, degree of obesity, and level of insulin resistance. However, data regarding their vascular function during exercise remain scarce. The aims of the present study were to evaluate vascular morphology and function at rest, and lower limb blood flow during exercise, in prepubertal boys with mild‐to‐moderate obesity and in lean controls. Materials and methods Twelve moderately obese prepubertal boys [Body Mass Index (BMI: 23·9 ± 2·6 kg m^?2)] and thirteen controls (BMI:17·4 ± 1·8 kg m^?2), matched for age (mean age: 11·6 ± 0·6 years) were recruited. We measured carotid intima‐media thickness (IMT) and wall compliance and incremental elastic modulus, resting brachial flow‐mediated dilation (FMD) and nitrate‐dependent dilation (NDD), lower limb blood flow during local knee‐extensor incremental and maximal exercise, body fat content (DEXA), blood pressure, blood lipids, insulin and glucose. Results Compared to lean controls, obese boys had greater IMT (0·47 ± 0·06 vs. 0·42 ± 0·03 mm, P < 0·05) but lower FMD (4·6 ± 2·8 vs. 8·8 ± 3·2%, P < 0·01) in spite of similar maximal shear rate, without NDD differences. Lower limb blood flow (mL min^?1·100 g^?1) increased significantly from rest to maximal exercise in both groups, although obese children reached lower values than lean counterparts whatever the exercise intensity. Conclusions Mild‐to‐moderate obesity in prepubertal boys without insulin resistance is associated with impaired endothelial function and blunted muscle perfusion response to local dynamic exercise without alteration of vascular smooth muscle reactivity.     

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.     

Standardized intermittent static exercise increases peritendinous blood flow in human leg

Alteration in tendinous and peritendinous blood flow during and after exercise is suggested to contribute to the development of Achilles tendon injury and inflammation. In the present study a method for evaluating the influence of standardized workload on peritendinous flow is presented. The radioactive isotope xenon-133 was injected just ventrally to the Achilles tendon 5 cm proximal to the tendon's insertion on the calcaneus. The disappearance of ¹³³Xe was used to determine blood flow during intermittent static exercise of the calf muscle (1·5 s exercise/1·5 s rest) for 30 min at a workload equivalent to individual body weight (1 BW) in six healthy volunteers around both Achilles tendons (n = 12). During intermittent static exercise, blood flow was increased from 1·8 ± 0·3 ml 100 g tissue^?1 min^?1 (mean value and SEM) (rest) to 6·1 ± 1·3 ml 100 g tissue^?1 min^?1 (exercise) (P<0·05). The exercise induced an average increase in blood flow (3·4-fold) equivalent to results previously obtained during regular dynamic heel raises (P>0·05). It is concluded that the method is well suited to study the influence of standardized workload on the physiology and pathophysiology of the tissue around the Achilles tendon in humans.     

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.     

The effect of a very low-calorie diet-induced weight loss on the severity of obstructive sleep apnoea and autonomic nervous function in obese patients with obstructive sleep apnoea syndrome

The aim of this study was to examine the effect of a very low-calorie diet (VLCD)-induced weight loss on the severity of obstructive sleep apnoea (OSA), blood pressure and cardiac autonomic regulation in obese patients with obstructive sleep apnoea syndrome (OSAS). A total of 15 overweight patients (14 men and one woman, body weight 114 ± 20 kg, age 52 ± 9 years, range 39–67 years) with OSAS were studied prospectively. They were advised to follow a 2·51–3·35 MJ (600–800 kcal) diet daily for a 3-month period. In the beginning of the study, the patients underwent nocturnal sleep studies, autonomic function tests and 24-h electrocardiograph (ECG) recording. In addition, 15 age-matched, normal-weight subjects were studied. They underwent the Valsalva test, the deep-breathing test and assessment of heart rate variability at rest. The sleep studies and autonomic function tests were repeated after the weight loss period. There was a significant reduction in weight (114 ± 20 kg to 105 ± 21 kg, P<0·001), the weight loss being 9·2 ± 4·0 kg (range 2·3–19·5 kg). This was associated with a significant improvement in the oxygen desaturation index (ODI4) during sleep (31 ± 20–19 ±18, P<0·001). Before the weight loss the OSAS patients had significantly higher blood pressure (150 ± 18 vs. 134 ± 20, P<0·05, for systolic blood pressure, 98 ± 10 vs. 85 ± 13, P<0·05, for diastolic blood pressure) and heart rate (67 ± 10 beats min^?1 vs. 60 ± 13, P<0·05) at rest than the control group. They had also lower baroreflex sensitivity (4·7 ± 2·8 ms mmHg^?1 vs. 10·8 ± 7·1 ms mmHg^?1, P<0·01). During the weight reduction, the blood pressure declined significantly, and the baroreflex sensitivity increased by 49%. In conclusion, our experience shows that weight loss with VLCD is an effective treatment for OSAS. Weight loss improved significantly sleep apnoea and had favourable effects on blood pressure and baroreflex sensitivity that may have prognostic implications.     

Acute hormonal responses following different velocities of eccentric exercise

The aim of this study was to compare the acute hormonal responses following two different eccentric exercise velocities. Seventeen healthy, untrained, young women were randomly placed into two groups to perform five sets of six maximal isokinetic eccentric actions at slow (30° s^?1) and fast (210° s^?1) velocities with 60‐s rest between sets. Growth hormone, cortisol, free and total testosterone were assessed by blood samples collected at baseline, immediately postexercise, 5, 15 and 30 min following eccentric exercise. Changes in hormonal responses over time were compared between groups, using a mixed model followed by a Tukey's post hoc test. The main findings of the present study were that the slow group showed higher growth hormone values immediately (5·08 ± 2·85 ng ml^?1, P = 0·011), 5 (5·54 ± 3·01 ng ml^?1, P = 0·004) and 15 min (4·30 ± 2·87 ng ml^?1, P = 0·021) posteccentric exercise compared with the fast group (1·39 ± 2·41 ng ml^?1, 1·34 ± 1·97 ng ml^?1 and 1·24 ± 1·87 ng ml^?1, respectively), and other hormonal responses were not different between groups (P>0·05). In conclusion, slow eccentric exercise velocity enhances more the growth hormone(GH) response than fast eccentric exercise velocity without cortisol and testosterone increases.     

Effects of aerobic exercise training and yoga on the baroreflex in healthy elderly persons

It is unclear whether the age-associated reduction in baroreflex sensitivity is modifiable by exercise training. The effects of aerobic exercise training and yoga, a non-aerobic control intervention, on the baroreflex of elderly persons was determined. Baroreflex sensitivity was quantified by the α-index, at high frequency (HF; 0.15–0.35 Hz, reflecting parasympathetic activity) and mid-frequency (MF; 0.05–0.15 Hz, reflecting sympathetic activity as well), derived from spectral and cross-spectral analysis of spontaneous fluctuations in heart rate and blood pressure. Twenty-six (10 women) sedentary, healthy, normotensive elderly (mean 68 years, range 62–81 years) subjects were studied. Fourteen (4 women) of the sedentary elderly subjects completed 6 weeks of aerobic training, while the other 12 (6 women) subjects completed 6 weeks of yoga. Heart rate decreased following yoga (69 ± 8 vs. 61 ± 7 min^?1, P < 0.05) but not aerobic training (66 ± 8 vs. 63 ± 9 min^?1, P = 0.29). VO₂ max increased by 11% following yoga (P < 0.01) and by 24% following aerobic training (P < 0.01). No significant change in α_MF (6.5 ± 3.5 vs. 6.2 ± 3.0 ms mmHg^?1, P = 0.69) or α_HF (8.5 ± 4.7 vs. 8.9 ± 3.5 ms mmHg^?1, P = 0.65) occurred after aerobic training. Following yoga, α_HF (8.0 ± 3.6 vs. 11.5 ± 5.2 ms mmHg^?1, P < 0.01) but not α_MF (6.5 ± 3.0 vs. 7.6 ± 2.8 ms mmHg^?1, P = 0.29) increased. Short-duration aerobic training does not modify the α-index at α_MF or α_HF in healthy normotensive elderly subjects. α_HF but not α_MF increased following yoga, suggesting that these parameters are measuring distinct aspects of the baroreflex that are separately modifiable.     

Vasoactive neuroendocrine responses associated with tolerance to lower body negative pressure in humans

The purpose of this investigation was to test the hypothesis that peripheral vasoconstriction and orthostatic tolerance are associated with increased circulating plasma concentrations of noradrenaline, vasopressin and renin–angiotensin. Sixteen men were categorized as having high (HT, n=9) or low (LT, n=7) tolerance to lower body negative pressure (LBNP) based on whether the endpoint of their pre‐syncopal‐limited LBNP (peak LBNP) exposure exceeded ?60 mmHg. The two groups were matched for age, height, weight, leg volume, blood volume and maximal oxygen uptake, as well as baseline blood volume and plasma concentrations of vasoactive hormones. Peak LBNP induced similar reductions in mean arterial pressure in both groups. The reduction in legarterial pulse volume (measured by impedance rheography), an index of peripheral vascular constriction, from baseline to peak LBNP was greater (P<0·05) in the HT group (?0·041 ± 0·005 ml 100 ml^?1) compared to the reduction in the LT group (?0·025 ± 0·003 ml 100 ml^?1). Greater peak LBNP in the HT group was associated with higher (P<0·05) average elevations in plasma concentrations of vasopressin (pVP, Δ=+7·2 ± 2·0 pg ml^?1) and plasma renin–angiotensin (PRA, Δ=+2·9 ± 1·3 ng Ang II ml^?1 h^?1) compared to average elevations of pVP (+2·2 ± 1·0 pg ml^?1) and PRA (+0·1 ± 0·1 ng Ang II ml^?1 h^?1) in the LT group. Plasma noradrenaline concentrations were increased (P<0·05) from baseline to peak LBNP in both HT and LT groups, with no statistically distinguishable difference between groups. These data suggest that the renin–angiotensin and vasopressin systems may contribute to sustaining arterial pressure and orthostatic tolerance by their vasoconstrictive actions.