Interactive effects of exercise intensity and recovery posture on postexercise hypotension.

Postexercise reduction in blood pressure, termed postexercise hypotension (PEH), is relevant for both acute and chronic health reasons and potentially for peripheral cardiovascular adaptations. We investigated the interactive effects of exercise intensity and recovery postures (seated, supine, and standing) on PEH. Thirteen normotensive men underwent a V̇o2max test on a cycle ergometer and five exhaustive constant load trials to determine critical power (CP) and the gas exchange threshold (GET). Subsequently, work-matched exercise trials were performed at two discrete exercise intensities (10% > CP and 10% < GET), with 1 h of recovery in each of the three postures. For both exercise intensities, standing posture resulted in a more substantial PEH (all P < 0.01). For both standing and seated recovery postures, the higher exercise intensity led to larger reductions in systolic [standing: -33 (11) vs. -21 (8) mmHg; seated: -34 (32) vs. -17 (37) mmHg, P < 0.01], diastolic [standing: -18 (7) vs. -8 (5) mmHg; seated: -10 (10) vs. -1 (4) mmHg, P < 0.01], and mean arterial pressures [-13 (8) vs. -2 (4) mmHg, P < 0.01], whereas in the supine recovery posture, the reduction in diastolic [-9 (9) vs. -4 (3) mmHg, P = 0.08) and mean arterial pressures [-7 (5) vs. -3 (4) mmHg, P = 0.06] was not consistently affected by prior exercise intensity. PEH is more pronounced during recovery from exercise performed above CP versus below GET. However, the effect of exercise intensity on PEH is largely abolished when recovery is performed in the supine posture.NEW & NOTEWORTHY The magnitude of postexercise hypotension is greater following the intensity above the critical power in a standing position.

Heated environment increases blood pressure drop and postural sway during initial orthostasis in healthy subjects.

PURPOSE: We tested the hypothesis that heat stress influences the closed-loop cardio-postural control by an increased blood pressure (BP) drop and postural sway. METHODS: Fourteen healthy individuals (eight women) performed two orthostatic tests under thermal reference (TC; ~ 24 ºC) and HOT (~ 38 ºC) conditions. The center-of-pressure (COP) displacements and the electromyography (EMG) activity of the calf muscles (medial gastrocnemius and tibialis anterior) were recorded during the initial orthostasis (ORT onset) after the supine-to-stand challenge. At the same period, BP (beat-to-beat) was continuously monitored, and supine-to-stand variations (∆%) were calculated. Sublingual temperature (Tsl) was measured as a surrogate of internal temperature. RESULTS: Tsl increased in HOT compared to TC (TC 36.5 ± 0.3 vs. HOT 36.7 ± 0.3 ºC; p < 0.01). COP distance was greater in HOT compared to TC condition (TC 596.6 ± 242.4 vs. HOT 680.2 ± 249.1 mm; p < 0.01). EMG activity of the gastrocnemius decreased in HOT compared to TC condition (TC 95.5 ± 19.8 vs. HOT 78.4 ± 22.8%mV; p = 0.02). EMG of tibialis did not change between TC and HOT (TC 83.5 ± 42.9 vs. HOT 66.1 ± 31.9% mV; p = 0.29). BP showed a greater fall in HOT compared to TC condition (∆%TC - 24.5 ± 13.2 vs. ∆%HOT - 33.2 ± 20.2%; p = 0.01). CONCLUSION: Heat stress causes a greater fall in blood pressure and a reduction in musculoskeletal pump activity during orthostatic onset. These effects could be potential mechanisms that underlie augmented postural instability under a heated environment.

Effects of posture changes on dynamic cerebral autoregulation during early pregnancy in women with obesity and/or sleep apnea.

The incidence of syncope during orthostasis increases in early human pregnancy, which may be associated with cerebral blood flow (CBF) dysregulation in the upright posture. In addition, obesity and/or sleep apnea per se may influence CBF regulation due to their detrimental impacts on cerebrovascular function. However, it is unknown whether early pregnant women with obesity and/or sleep apnea could have impaired CBF regulation in the supine position and whether this impairment would be further exacerbated in the upright posture. Dynamic cerebral autoregulation (CA) was evaluated using transfer function analysis in 33 women during early pregnancy (13 with obesity, 8 with sleep apnea, 12 with normal weight) and 15 age-matched nonpregnant women during supine rest. Pregnant women also underwent a graded head-up tilt (30° and 60° for 6 min each). We found that pregnant women with obesity or sleep apnea had a higher transfer function low-frequency gain compared with nonpregnant women in the supine position (P = 0.026 and 0.009, respectively) but not normal-weight pregnant women (P = 0.945). Conversely, the transfer function low-frequency phase in all pregnancy groups decreased during head-up tilt (P = 0.001), but the phase was not different among pregnant groups (P = 0.180). These results suggest that both obesity and sleep apnea may have a detrimental effect on dynamic CA in the supine position during early pregnancy. CBF may be more vulnerable to spontaneous blood pressure fluctuations in early pregnant women during orthostatic stress compared with supine rest due to less efficient dynamic CA, regardless of obesity and/or sleep apnea.

Orthostatic intolerance: a handicap of aging or physical deconditioning?

Despite several studies that have been investigated physical inactivity and age-related effects on orthostatic tolerance, impaired hemodynamics and postural balance responses to orthostatic stress are incorrectly attributed to aging or sedentarism alone. The isolated effects from aging and sedentarism should be investigated through comparative studies between senior athletes and age-matched controls, and physical activity assessments on aging follow-up studies. On the other hand, bed rest and space flight studies mimic accelerated physical inactivity or disuse, which is not the same physiological decline provoked by aging alone. Thus, the elementary question is: could orthostatic intolerance be attributed to aging or physical inactivity? The main purpose of this review is to provide an overview of possible mechanisms underlying orthostatic tolerance contrasting the paradigm of aging and/or physical inactivity. The key points of this review are the following: (1) to counterpoint all relevant literature on physiological aspects of orthostatic tolerance; (2) to explore the mechanistic aspects underneath the cerebrovascular, cardiorespiratory, and postural determinants of orthostatic tolerance; and (3) examine non-pharmacological interventions with the potential to counterbalance the physical inactivity and aging effects. To date, the orthostatic intolerance cannot be attributed exclusively with aging since physical inactivity plays an important role in postural balance, neurovascular and cardiorespiratory responses to orthostatic stress. These physiological determinates should be interpreted within an integrative approach of orthostatic tolerance, that considers the interdependence between physiological systems in a closed-loop model. Based on this multisystem approach, acute and chronic countermeasures may combat aging and sedentarism effects on orthostatic tolerance.

Intermittent compression of the calf muscle as a countermeasure to protect blood pressure and brain blood flow in upright posture in older adults.

PURPOSE: Orthostatic hypotension, leading to cerebral hypoperfusion, can result in postural instability and falls in older adults. We determined the efficacy of a novel, intermittent pneumatic compression system, applying pressure around the lower legs, as a countermeasure against orthostatic stress in older adults. METHODS: Data were collected from 13 adults (4 male) over 65 years of age. Non-invasive ultrasound measured middle cerebral artery blood velocity (MCAv) and finger photoplethysmography measured mean arterial blood pressure (MAP). Intermittent lower leg compression was applied in a peristaltic manner in the local diastolic phase of each cardiac cycle to optimize venous return during 1-min of seated rest and during a sit-to-stand transition to 1-min of quiet standing with compression initiated 15 s before transition. RESULTS: During seated rest, compression resulted in a 4.5 ± 6.5 mmHg increase in MAP, and 2.3 ± 2.1 cm/s increase in MCAv (p < 0.05). MAP and MCAv increased during the 15 s of applied compression before the posture transition (2.3 ± 7.2 mmHg and 2.1 ± 4.0 cm/s, respectively, p < 0.05) with main effects for both variables confirming continued benefit during the transition and quiet stand periods. CONCLUSIONS: Application of carefully timed, intermittent compression to the lower legs of older adults increased MAP and MCAv during seated rest and maintained an elevated MAP and MCAv during a transition to standing posture. Future research could assess the benefits of this technology for persons at risk for orthostatic hypotension on standing and while walking in an effort to reduce injurious, unexplained falls in older adults.

The effect of hypercapnia on regional cerebral blood flow regulation during progressive lower-body negative pressure.

PURPOSE: Previous work indicates that dynamic cerebral blood flow (CBF) regulation is impaired during hypercapnia; however, less is known about the impact of resting hypercapnia on regional CBF regulation during hypovolemia. Furthermore, there is disparity within the literature on whether differences between anterior and posterior CBF regulation exist during physiological stressors. We hypothesized: (a) lower-body negative pressure (LBNP)-induced reductions in cerebral blood velocity (surrogate for CBF) would be more pronounced during hypercapnia, indicating impaired CBF regulation; and (b) the anterior and posterior cerebral circulations will exhibit similar responses to LBNP. METHODS: In 12 healthy participants (6 females), heart rate (electrocardiogram), mean arterial pressure (MAP; finger photoplethosmography), partial pressure of end-tidal carbon dioxide (PETCO2), middle cerebral artery blood velocity (MCAv) and posterior cerebral artery blood velocity (PCAv; transcranial Doppler ultrasound) were measured. Cerebrovascular conductance (CVC) was calculated as MCAv or PCAv indexed to MAP. Two randomized incremental LBNP protocols were conducted (- 20, - 40, - 60 and - 80 mmHg; three-minute stages), during coached normocapnia (i.e., room air), and inspired 5% hypercapnia (~ + 7 mmHg PETCO2 in normoxia). RESULTS: The main findings were: (a) static CBF regulation in the MCA and PCA was similar during normocapnic and hypercapnic LBNP trials, (b) MCA and PCA CBV and CVC responded similarly to LBNP during normocapnia, but (c) PCAv and PCA CVC were reduced to a greater extent at - 60 mmHg LBNP (P = 0.029; P < 0.001) during hypercapnia. CONCLUSION: CBF regulation during hypovolemia was preserved in hypercapnia, and regional differences in cerebrovascular control may exist during superimposed hypovolemia and hypercapnia.

Comparison of pulse contour, aortic Doppler ultrasound and bioelectrical impedance estimates of stroke volume during rapid changes in blood pressure.

NEW FINDINGS: What is the central question of this study? Pulse contour analysis of the finger arterial pressure by Windkessel modelling is commonly used to estimate stroke volume continuously. But is it valid during dynamic changes in blood pressure? What is the main finding and its importance? Second-by-second analysis revealed that pulse contour analysis underestimated stroke volume by up to 25% after standing from a squat, and 16% after standing thigh-cuff release, when compared with aortic Doppler ultrasound estimates. These results reveal that pulse contour analysis of stroke volume should be interpreted with caution during rapid changes in physiological state. ABSTRACT: Dynamic measurements of stroke volume (SV) and cardiac output provide an index of central haemodynamics during transitional states, such as postural changes and onset of exercise. The most widely used method to assess dynamic fluctuations in SV is the Modelflow method, which uses the arterial blood pressure waveform along with age- and sex-specific aortic properties to compute beat-to-beat estimates of aortic flow. Modelflow has been validated against more direct methods in steady-state conditions, but not during dynamic changes in physiological state, such as active orthostatic stress testing. In the present study, we compared the dynamic SV responses from Modelflow (SVMF ), aortic Doppler ultrasound (SVU/S ) and bioelectrical impedance analysis (SVBIA ) during two different orthostatic stress tests, a squat-to-stand (S-S) transition and a standing bilateral thigh-cuff release (TCR), in 15 adults (six females). Second-by-second analysis revealed that when compared with estimates of SV by aortic Doppler ultrasound, Modelflow underestimated SV by up to 25% from 3 to 11 s after standing from the squat position and by up to 16% from 3 to 7 s after TCR (P < 0.05). The SVMF and SVBIA were similar during the first minute of the S-S transition, but were different 3 s after TCR and at intermittent time points between 34 and 44 s (P < 0.05). These findings indicate that the physiological conditions elicited by orthostatic stress testing violate some of the inherent assumptions of Modelflow and challenge models used to interpret bioelectrical impedance responses, resulting in an underestimation in SV during rapid changes in physiological state.

Corticospinal excitability for flexor carpi radialis decreases with baroreceptor unloading during intentional co-contraction with opposing forearm muscles.

Concurrent activation of antagonistic muscles (co-contraction) is used for stiffening a joint, whereas its neural control under hemodynamic stress (e.g., posture change, high gravity, and hemorrhage) is unknown. Corticospinal excitability during co-contraction may be altered with baroreceptor unloading due to potential modulations in spinal and/or inhibitory pathways (e.g., disynaptic group I inhibition and GABA-mediated intracortical inhibition). The purpose of this study was to understand the effect of baroreceptor unloading on corticospinal excitability during co-contraction in humans. Motor evoked potential and cortical silent period in a wrist flexor muscle were examined using transcranial magnetic stimulation in two groups of healthy young adults. All subjects performed isometric contraction of the wrist flexors (flexion) and co-contraction of the wrist flexors and extensors (co-contraction). Spinal disynaptic inhibition was also assessed with the ratio of H-reflex responses to unconditioned and conditioned electrical stimulations of the peripheral nerves for the muscles. In one of the groups, baroreflex unloading was induced by applying lower body negative pressure. There was no significant effect of baroreflex unloading on cortical silent period or H-reflex measure of disynaptic inhibition. With baroreflex unloading, motor evoked potential area in the flexor carpi radialis was decreased during co-contraction but not during flexion. The results indicated that baroreceptor unloading decreases corticospinal excitability during co-contraction of antagonistic muscles, apparently by influencing neural pathways that were not probed with cortical silent period or spinal disynaptic inhibition.

Cardiovascular regulation: associations between exercise and head-up tilt.

It was hypothesized that faster cardiorespiratory kinetics during exercise are associated with higher orthostatic tolerance. Cardiorespiratory kinetics of 14 healthy male subjects (30 ± 4 years, 179 ± 8 cm, 79 ± 8 kg) were tested on a cycle ergometer during exercise with changing work rates of 30 and 80 W. Pulmonary oxygen uptake ( ) was measured breath-by-breath and heart rate (HR), mean arterial blood pressure (MAP), and total peripheral resistance (TPR) were measured beat-to-beat. Muscular oxygen uptake ( ) was estimated from HR and . Kinetic parameters were determined by time-series analysis, using cross-correlation functions (CCFmax(x)) between the parameter and the work rate. Cardiovascular regulations of MAP, HR, and TPR during orthostatic stress were measured beat-to-beat on a tilt seat. Changes between the minima and maxima during the 6° head-down tilt and the 90° head-up tilt positions were calculated for each parameter (Δtilt-up). correlated significantly with ΔTPRtilt-up (r = 0.790, p ≤ 0.001). CCFmax(HR) was significantly correlated with ΔHRtilt-up (r = -0.705, p = 0.002) and the amplitude in HR from 30 to 80 W (rSP = -0.574, p = 0.016). The observed correlations between cardiorespiratory regulation in response to exercise and orthostatic stress during rest might allow for a more differential analysis of the underlying mechanisms of orthostatic intolerance in, for example, patient groups.

The effects of aging on the distribution of cerebral blood flow with postural changes and mild hyperthermia.

PURPOSE: Cerebral blood flow (CBF) would be impaired with dual stresses of heat and orthostatic changes, even if those stresses are mild, in the elderly with declined cardio- and cerebrovascular functions with aging. To test the hypothesis, we compared the response of blood flow in the internal carotid artery (ICA) and vertebral artery (VA) to dual stresses of heat and orthostatic changes between the elderly and young individuals. METHODS: Nine elderly and eight young healthy men (71.3 ± 3.0 and 23.3 ± 3.1 years, mean ± SD, respectively) underwent measurements of blood flow in the ICA, VA and external carotid artery (ECA) via ultrasonography. The measurements were obtained in sitting and supine positions under normothermic (NT) and mildly hyperthermic (HT) conditions (ambient temperature 28 °C). Esophageal temperatures increased from NT (36.4 ± 0.2 °C, mean ± SE) to HT (37.4 ± 0.2 °C) with lower legs immersion in 42 °C water. RESULTS: With heat stress, ECA blood flow increased in both postures in both age groups (effect of heat, p < 0.001), whereas ICA blood flow remained unchanged. With postural changes from supine to sitting, ECA blood flow remained unchanged whereas ICA blood flow decreased (effect of posture, p = 0.027) by 18% in NT in the young and by 20% in HT in the elderly. VA blood flow remained unchanged under both heat stress and postural changes. CONCLUSIONS: The CBF is impaired under dual stresses of heat and orthostatic changes in healthy aged individuals, even if the levels of the stresses are mild.

Procoagulatory changes induced by head-up tilt test in patients with syncope: observational study.

BACKGROUND: Orthostatic hypercoagulability is proposed as a mechanism promoting cardiovascular and thromboembolic events after awakening and during prolonged orthostasis. We evaluated early changes in coagulation biomarkers induced by tilt testing among patients investigated for suspected syncope, aiming to test the hypothesis that orthostatic challenge evokes procoagulatory changes to a different degree according to diagnosis. METHODS: One-hundred-and-seventy-eight consecutive patients (age, 51 ± 21 years; 46% men) were analysed. Blood samples were collected during supine rest and after 3 min of 70° head-up tilt test (HUT) for determination of fibrinogen, von Willebrand factor antigen (VWF:Ag) and activity (VWF:GP1bA), factor VIII (FVIII:C), lupus anticoagulant (LA1), functional APC-resistance, and activated prothrombin time (APTT) with and without activated protein C (C+/-). Analyses were stratified according to age, sex and diagnosis. RESULTS: After 3 min in the upright position, VWF:Ag (1.28 ± 0.55 vs. 1.22 ± 0.54; p < 0.001) and fibrinogen (2.84 ± 0.60 vs. 2.75 ± 0.60, p < 0.001) increased, whereas APTT/C+/- (75.1 ± 18.8 vs. 84.3 ± 19.6 s; p < 0.001, and 30.8 ± 3.7 vs. 32.1 ± 3.8 s; p < 0.001, respectively) and APC-resistance (2.42 ± 0.43 vs. 2.60 ± 0.41, p < 0.001) decreased compared with supine values. Significant changes in fibrinogen were restricted to women (p < 0.001) who also had lower LA1 during HUT (p = 0.007), indicating increased coagulability. Diagnosis vasovagal syncope was associated with less increase in VWF:Ag during HUT compared to other diagnoses (0.01 ± 0.16 vs. 0.09 ± 0.17; p = 0.004). CONCLUSIONS: Procoagulatory changes in haemostatic plasma components are observed early during orthostasis in patients with history of syncope, irrespective of syncope aetiology. These findings may contribute to the understanding of orthostatic hypercoagulability and chronobiology of cardiovascular disease.

Blunted cardiac autonomic dynamics to active standing test in postmenopausal women.

Introduction: Although both aging and menopause influence cardiovascular autonomic control, the effect of menopause per se remains unclear. The current study was undertaken to test the hypothesis that post-menopausal women (PMW) have a blunted cardiovascular autonomic adjustment to active standing compared to pre-menopausal women. Thus, we compared the heart rate variability (HRV) indexes from supine (SUP) to orthostatic (ORT) positions among young women (YW), young men (YM), older men (OM), and PMW. Methods: The participants rested for 10 min in SUP and then stood up and remained for 5 min in ORT. ECG was continuously recorded, and R-R time series of about 300 beats were analyzed using linear (spectral analysis) and non-linear (symbolic analysis) methods. The variation from SUP to ORT was calculated (Δ = ORT-SUP) for each HRV index. Results: In SUP, no difference was found for any HRV index among groups. However, Δ0V% and ΔLFn (cardiac sympathetic modulation) were reduced in PWM compared to all groups (OM, YW, and YM), while Δ2UV% and ΔHFn (cardiac vagal modulation) were reduced in PMW than the younger group (YW and YM). No differences were found among the male groups (OM and YM). Discussion: In light of our results, the cardiac autonomic dynamic response to orthostatic stress is blunted in post-menopausal women compared to younger women and older men, a finding that might be influenced not only by aging.

Diagnostic yield of head-up tilt table test in hypertrophic cardiomyopathy and unexplained syncope: the knot does not seem to be unraveling.

BACKGROUND: Conflicting results have been published considering the diagnostic performance of head-up tilt test (HUTT) in patients with hypertrophic cardiomyopathy (HCM). We aimed to conduct a meta-analysis to evaluate the diagnostic value of HUTT in the evaluation of unexplained syncope in patients with HCM. METHODS: We performed a structured systematic database search using the following keywords: hypertrophic cardiomyopathy, syncope, unexplained syncope, head-up tilt test, tilt table test, tilt testing, orthostatic stress, autonomic function, autonomic response. Studies in which the HUTT was used to define autonomic dysfunction in patients with syncope at baseline or without syncope were included in the final analysis. RESULTS: A total of 252 HCM patients from 6 studies (159 patients without a history of syncope and 93 with a history of syncope, respectively) were evaluated. HUTT was positive in 50 (19.84%) of 252 patients (in 21 of 93 patients (22.58%) with a history of syncope and in 29 of 159 patients (18.24%) without a history of syncope, respectively). The pooled total sensitivity and specificity of the HUTT for detecting syncope were 22.1% (14.8-35.1%) and 83.6% (73.2-91.6%), respectively. The summary receiver operator curve showed that HUTT had an only modest discriminative ability for syncope with an area under the curve value of 0.565 (0.246-0.794). CONCLUSION: Although HUTT has significant limitations in diagnosis of unexplained syncope in patients with HCM, it may still be used to determine hypotensive susceptibility. Other autonomic tests can be used in diagnostic workflow in this population.

Cardiovascular responses to leg-press exercises during head-down tilt.

Introduction: Physical exercise and gravitational load affect the activity of the cardiovascular system. How these factors interact with one another is still poorly understood. Here we investigate how the cardiovascular system responds to leg-press exercise during head-down tilt, a posture that reduces orthostatic stress, limits gravitational pooling, and increases central blood volume. Methods: Seventeen healthy participants performed leg-press exercise during head-down tilt at different combinations of resistive force, contraction frequency, and exercise duration (30 and 60 s), leading to different exercise power. Systolic (sBP), diastolic (dBP), mean arterial pressure (MAP), pulse pressure (PP) and heart rate (HR) were measured continuously. Cardiovascular responses were evaluated by comparing the values of these signals during exercise recovery to baseline. Mixed models were used to evaluate the effect of exercise power and of individual exercise parameter on the cardiovascular responses. Results: Immediately after the exercise, we observed a clear undershoot in sBP (Δ = -7.78 ± 1.19 mmHg), dBP (Δ = -10.37 ± 0.84 mmHg), and MAP (Δ = -8.85 ± 0.85 mmHg), an overshoot in PP (Δ = 7.93 ± 1.13 mmHg), and elevated values of HR (Δ = 33.5 ± 0.94 bpm) compared to baseline (p < 0.0001). However, all parameters returned to similar baseline values 2 min following the exercise (p > 0.05). The responses of dBP, MAP and HR were significantly modulated by exercise power (correlation coefficients: rdBP = -0.34, rMAP = -0.25, rHR = 0.52, p < 0.001). All signals' responses were modulated by contraction frequency (p < 0.05), increasing the undershoot in sBP (Δ = -1.87 ± 0.98 mmHg), dBP (Δ = -4.85 ± 1.01 and Δ = -3.45 ± 0.98 mmHg for low and high resistive force respectively) and MAP (Δ = -3.31 ± 0.75 mmHg), and increasing the overshoot in PP (Δ = 2.57 ± 1.06 mmHg) as well as the value of HR (Δ = 16.8 ± 2.04 and Δ = 10.8 ± 2.01 bpm for low and high resistive force respectively). Resistive force affected only dBP (Δ = -4.96 ± 1.41 mmHg, p < 0.0001), MAP (Δ = -2.97 ± 1.07 mmHg, p < 0.05) and HR (Δ = 6.81 ± 2.81 bpm, p < 0.0001; Δ = 15.72 ± 2.86 bpm, p < 0.0001; Δ = 15.72 ± 2.86 bpm, p < 0.05, depending on the values of resistive force and contraction frequency), and exercise duration affected only HR (Δ = 9.64 ± 2.01 bpm, p < 0.0001). Conclusion: Leg exercises caused only immediate cardiovascular responses, potentially due to facilitated venous return by the head-down tilt position. The modulation of dBP, MAP and HR responses by exercise power and that of all signals by contraction frequency may help optimizing exercise prescription in conditions of limited orthostatic stress.

Spontaneous fluctuation indices of the cardiovagal baroreflex accurately measure the baroreflex sensitivity at the operating point during upright tilt.

Spontaneous fluctuation indices of cardiovagal baroreflex have been suggested to be inaccurate measures of baroreflex function during orthostatic stress compared with alternate open-loop methods (e.g. neck pressure/suction, modified Oxford method). We therefore tested the hypothesis that spontaneous fluctuation measurements accurately reflect local baroreflex gain (slope) at the operating point measured by the modified Oxford method, and that apparent differences between these two techniques during orthostasis can be explained by a resetting of the baroreflex function curve. We computed the sigmoidal baroreflex function curves supine and during 70° tilt in 12 young, healthy individuals. With the use of the modified Oxford method, slopes (gains) of supine and upright curves were computed at their maxima (Gmax) and operating points. These were compared with measurements of spontaneous indices in both positions. Supine spontaneous analyses of operating point slope were similar to calculated Gmax of the modified Oxford curve. In contrast, upright operating point was distant from the centering point of the reset curve and fell on the nonlinear portion of the curve. Whereas spontaneous fluctuation measurements were commensurate with the calculated slope of the upright modified Oxford curve at the operating point, they were significantly lower than Gmax. In conclusion, spontaneous measurements of cardiovagal baroreflex function accurately estimate the slope near operating points in both supine and upright position.

Relationship between aerobic endurance training and dynamic cerebral blood flow regulation in humans.

The incidence of orthostatic intolerance is elevated in endurance-trained individuals. We sought to test the hypothesis that aerobic endurance training is associated with an attenuated control of the cerebral vasculature. Endurance trained (ET, n = 13) and age-matched untrained (UT, n = 11) individuals (peak O2 consumption, mean ± SEM; 63 ± 1 vs 42 ± 1 mL/min/kg, P < 0.05) were examined while supine and seated upright. Dynamic cerebral autoregulation (CA) was assessed by calculation of the rate of regulation (RoR) from the arterial blood pressure (ABP) and middle cerebral artery (MCA) mean blood velocity (V mean ) responses to a bilateral thigh cuff release, which evoked a transient hypotension. Cerebral oxygenation (oxyhemoglobin; HbO2 ) was determined with near-infrared spectroscopy. When seated upright, cuff release evoked a greater decrease in ABP (P < 0.001), MCA V mean (P = 0.096) and HbO2 (P < 0.001) in ET compared with UT. However, RoR was similar in ET and UT individuals while seated upright (to 0.193 ± 0.039 vs 0.129 ± 0.029/s, P > 0.05), and there was no significant difference in the relative change in RoR from the supine to upright positions (ΔRoR: -65 ± 7 and -69 ± 7%, for ET and UT, respectively). These findings suggest that aerobic endurance training is not associated with an attenuation in dynamic CA.

Autonomic nervous system and postural control regulation during orthostatic test as putative markers of physical resilience among community-dwelling older adults.

INTRODUCTION: We examined whether autonomic nervous system (ANS) and postural control regulation during orthostatic test reflect physical resilience by studying their associations with maximal walking speed and mortality. METHODS: The participants were community-dwelling Finnish men (n = 303) and women (n = 386) aged 75, 80, and 85 years at baseline. Systolic and diastolic blood pressure (BP), heart rate, heart rate variability (HRV), respiratory rate, and postural sway were obtained using a digital sphygmomanometer, a single-channel ECG, and thigh- and chest-worn accelerometers. Linear and Cox regression models were used to estimate the associations of the physiological indices with maximal 10-m walking speed and 5-year mortality separately for sexes. RESULTS: Better maintenance of BP under orthostatic stress was associated with faster walking speed in women and lower mortality hazard in men. Greater HRV in terms of low frequency power and lower respiration rate in supine position and smaller orthostatic changes in these were associated with faster walking speed especially in women. Less postural sway after standing up was associated with faster walking speed in women (-0.057, SE 0.022, p = 0.011) and more postural sway with increased mortality hazard in men (HR 1.71, 95 % CI 1.20-2.43) even after controlling for BP responses. CONCLUSIONS: In addition to ANS regulation at rest and under stress, adaptation of postural control system to orthostasis may be used in quantifying older adults' physical resilience. Wearable sensors capturing stimulus-response patterns and natural fluctuations of body functions may provide opportunities to monitor and incorporate different subsystems' resilience also in free-living conditions.

Arterial wave dynamics preservation upon orthostatic stress: a modelling perspective.

Pressure-flow travelling waves are a key topic for understanding arterial haemodynamics. However, wave transmission and reflection processes induced by body posture changes have not been thoroughly explored yet. Current in vivo research has shown that the amount of wave reflection detected at a central level (ascending aorta, aortic arch) decreases during tilting to the upright position, despite the widely proved stiffening of the cardiovascular system. It is known that the arterial system is optimized when in the supine position, i.e. propagation of direct waves is enabled and reflected waves are trapped, protecting the heart; however, it is not known whether this is preserved with postural changes. To shed light on these aspects, we propose a multi-scale modelling approach to inquire into posture-induced arterial wave dynamics elicited by simulated head-up tilting. In spite of remarkable adaptation of the human vasculature following posture changes, our analysis shows that, upon tilting from supine to upright: (i) vessel lumens at arterial bifurcations remain well matched in the forward direction, (ii) wave reflection at central level is reduced due to the backward propagation of weakened pressure waves produced by cerebral autoregulation, and (iii) backward wave trapping is preserved.

Cardiovascular autonomic regulation in fighter pilots: Lessons from active standing tests.

Fighter pilots (FP) are exposed to flight accelerations and stressful situations that defy cardiovascular control during and after flight. FP presents a smaller adjustment in sympatho-vagal balance during tilt test after flight compared to baseline, suggesting a huge impact of flight on autonomic modulation to the heart. We undertake to test the hypothesis that FP will have a smaller vagal reentrance and lower sympathetic withdrawal during the recovery at the supine position after a prolonged active standing test that mimics flight hemodynamic demands. Twenty-one military personnel (20-34 years old), composed of 9 FP and 12 non-pilots (NP) matched by age, V̉O2max and body mass index were enroled in the experimental protocol. R-R intervals were continuously recorded in the supine position for 15 min (SUPbaseline ), during the prolonged active standing test (45 min) windowed in six 5 min time frames (from ORT1 to ORT6), and a recovery period in the supine position for 15 min (SUPrecovery ). Heart rate variability was performed by spectral analysis to obtain the normalized low (LFn) and high (HFn) frequency components. The variation (Δ) from baseline (Δ = ORT6 - SUPbaseline ) and from recovery (Δ = SUPrecovery -ORT6) periods were calculated. FP had a smaller ΔLFn (sympathetic mediated) and ΔHFn (vagal meditated) during recovery after active standing as compared to NP. Both groups showed similar changes in ΔLFn and ΔHFn during orthostatic stress compared to baseline, with no differences over time. Therefore, FP show a smaller vagal reentrance and a lower sympathetic reduction during recovery at supine following active standing compared to NP.

Orthostasis Is Impaired Due to Fatiguing Intensive Acute Concentric Exercise Succeeded by Isometric Weight-Loaded Wall-Sit in Delayed-Onset Muscle Soreness: A Pilot Study.

The aim of the study was to investigate any indication of diminished orthostatic tolerance as a result of fatiguing intensive acute concentric exercise with a successive isometric wall-sit followed by an orthostatic stress test, with a special focus on any distinguishable alterations due to a delayed-onset muscle soreness effect. The exercise protocol was carried out among nineteen (10 female, 9 male) junior swimmers from the Hungarian National Swim Team. All athletes showed a positive orthostatic stress test right after our exercise protocol. The diastolic blood pressure was significantly lower due to the delayed-onset muscle soreness effect in the standing position after the supine position of the orthostatic stress test, in contrast to the athletes who did not experience delayed-onset muscle soreness. Furthermore, the heart rate was dysregulated in athletes with a delayed-onset muscle soreness effect when they assumed a supine position after the sustained standing position during the orthostatic stress test, in contrast to the athletes without delayed-onset muscle soreness. Interesting to note is that, in three subjects, the sustained standing position decreased the heart rate below the level of the initial supine position and six athletes experienced dizziness in the standing position, and all of these athletes were from the group that experienced delayed-onset muscle soreness. Accordingly, this study, for the first time, demonstrated that delayed-onset muscle soreness impairs orthostasis after unaccustomed fatiguing intensive acute concentric exercise with a successive isometric weight-loaded wall-sit; however, validation of this association should be investigated in a larger sample size.