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The ability to regain control of balance is vital in limiting falls and injuries. Little is known regarding how the autonomic nervous system responds during recovery from balance perturbations of different intensities. The purpose of this study was to examine the cardiovascular response following a standing balance perturbation of varying intensities, quantify cardiac baroreflex sensitivity (cBRS) during standing perturbations, and to establish the stability of the cardiac baroreflex during quiet standing before and after balance disturbances. Twenty healthy participants experienced three different perturbation intensity conditions that each included 25 brief posteriorly-directed perturbations, 8-10 s apart. Three perturbation intensity conditions (low, medium, high) were given in random order. Physiological data were collected in quiet stance for 5 min before testing (Baseline) and again after the perturbation conditions (Recovery) to examine baroreflex stability. Beat-to-beat heart rate (HR) and systolic blood pressure (SBP) analysis post-perturbation indicated an immediate acceleration of the HR for 1-2 s, with elevated SBP 4-5 s post-perturbation. Heart rate changes were greatest in the medium (p = 0.035) and high (p = 0.012) intensities compared to low, while there were no intensity-dependent changes in SBP. The cBRS was not intensity-dependent (p = 0.402) but when perturbation conditions were combined, cBRS was elevated compared to Baseline (p = 0.046). The stability of baseline cBRS was excellent (ICC = 0.896) between quiet standing conditions. In summary, HR, but not SBP or cBRS were intensity-specific during postural perturbations. This was the first study to examine cardiovascular response and cBRS to postural perturbations., (© 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Background Autonomic dysregulation represents a hallmark of coronary artery disease (CAD). Therefore, we investigated the effects of exercise-based cardiac rehabilitation (CR) on autonomic function and neuro-cardiovascular stress reactivity in CAD patients. Methods and Results Twenty-two CAD patients (4 women; 62±8 years) were studied before and following 6 months of aerobic- and resistance-training-based CR. Twenty-two similarly aged, healthy individuals (CTRL; 7 women; 62±11 years) served as controls. We measured blood pressure, muscle sympathetic nerve activity, heart rate, heart rate variability (linear and nonlinear), and cardiovagal (sequence method) and sympathetic (linear relationship between burst incidence and diastolic blood pressure) baroreflex sensitivity during supine rest. Furthermore, neuro-cardiovascular reactivity during short-duration static handgrip (20s) at 40% maximal effort was evaluated. Six months of CR lowered resting blood pressure (P<0.05), as well as muscle sympathetic nerve activity burst frequency (48±8 to 39±11 bursts/min; P<0.001) and burst incidence (81±7 to 66±17 bursts/100 heartbeats; P<0.001), to levels that matched CTRL and improved sympathetic baroreflex sensitivity in CAD patients (P<0.01). Heart rate variability (all P>0.05) and cardiovagal baroreflex sensitivity (P=0.11) were unchanged following CR, yet values were not different pre-CR from CTRL (all P>0.05). Furthermore, before CR, CAD patients displayed greater blood pressure and muscle sympathetic nerve activity reactivity to static handgrip versus CTRL (all P<0.05); yet, responses were reduced following CR (all P<0.05) to levels observed in CTRL. Conclusions Six months of exercise-based CR was associated with marked improvement in baseline autonomic function and neuro-cardiovascular stress reactivity in CAD patients, which may play a role in the reduced cardiac risk and improved survival observed in patients following exercise training.

The autonomic nervous system elicits continuous beat-by-beat homeostatic adjustments to cardiovascular control. These modifications are mediated by sensory inputs (e.g., baroreceptors, metaboreceptors, pulmonary, thermoreceptors, and chemoreceptors afferents), integration at the brainstem control centres (i.e., medulla), and efferent autonomic neural outputs (e.g., spinal, preganglionic, and postganglionic pathways). However, extensive electrical stimulation and functional imaging research show that the brain's higher cortical regions (e.g., insular cortex, medial prefrontal cortex, anterior cingulate cortex) partake in homeostatic regulation of the cardiovascular system at rest and during exercise. We now appreciate that these cortical areas form a network, namely the "cortical autonomic network" (CAN), which operate as part of a larger central autonomic network comprising 2-way communication of cortical and subcortical areas to exert autonomic influence. Interestingly, differential patterns of CAN activity and ensuing cardiovascular control are present in disease states, thereby highlighting the importance of considering the role of CAN as an integral aspect of cardiovascular regulation in health and disease. This review discusses current knowledge on human cortical autonomic activation during volitional exercise, and the role of exercise training on this activation in both health and disease.

Dysregulation of autonomic control often develops with advancing age, favoring a chronic state of heightened sympathetic outflow with parasympathetic withdrawal. However, the mechanisms of this age-related autonomic impairment are not known. This study tested the hypothesis that inter-individual differences in autonomic outflow across the adult age-span are related to cerebral cortex thickness. A total of 55 healthy, active individuals participated in this study (21-73years; 18 female). Physical fitness was treated as a possible covariate (VO 2peak : 26-81mL/kg/min). Cardiovagal baroreflex sensitivity, heart rate variability, and muscle sympathetic nerve activity (MSNA) were assessed during a laboratory session. T1-weighted images acquired at 3T facilitated measures of cortical thickness (Brain Voyager 2.8.4). A priori cortical regions of interest included the medial prefrontal cortex (MPFC) and insula cortex. Cortical thickness at the MPFC correlated strongly with markers of autonomic outflow including heart rate variability (ln-high frequency power (slope: -16, r 2 =0.65), SDNN (slope: 22, r 2 =0.22), total power (slope: 2872, r 2 =0.24)), and MSNA variables (burst frequency (slope: 1, r 2 =0.16), burst incidence (slope: -26, r 2 =0.62) and total MSNA (slope: -847, r 2 =0.56)). Further associations with burst incidence were observed within the left insula (p<0.05). Importantly, the strength of the relationship between autonomic variables and cortical thickness was determined by age, and was not altered following adjustments for cardiorespiratory fitness. The current results implicate cortical atrophy in the frontal lobe as a contributor to both the sympathetic and parasympathetic changes that occur with age., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Experimental models of physical inactivity associated with a sedentary lifestyle or extreme forms of inactivity with bed rest or spaceflight affect the balance between parasympathetic and sympathetic nervous system regulation of the cardiovascular system. Deconditioning effects are rapidly seen in the regulation of heart rate to compensate for physical modifications in blood volume and cardiac function. Reflex regulation of cardiovascular control during exercise by metaboreflex and baroreflex is altered by bed rest and spaceflight. These models of extreme inactivity provide a reference to guide physical activity requirements for optimal cardiovascular health., (Copyright © 2014 Elsevier B.V. All rights reserved.)

This brief review discusses the current state of knowledge regarding the cortical circuitry associated with autonomic cardiovascular responses to volitional exercise in conscious humans. Studies to date have emphasized the autonomic nervous system adjustments that occur through top-down central command features as well as bottom-up signals arising from skeletal muscle. While in its infancy, the pattern of cortical circuitry associated with exercise seem to depend on the nature of the exercise but with common patterns arising in the insula cortex, dorsal anterior cingulate cortex, medial prefrontal cortex, and hippocampus., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Beginning with clinical evidence of fatal cardiac arrhythmias in response to severe stress, in epileptic patients, and following stroke, the role of the cerebral cortex in autonomic control of the cardiovascular system has gained both academic and clinical interest. Studies in anesthetized rodents have exposed the role of several forebrain regions involved in cardiovascular control. The introduction of functional neuroimaging techniques has enabled investigations into the conscious human brain to illuminate the temporal and spatial activation patterns of cortical regions that are involved with cardiovascular control through the autonomic nervous system. This symposia report emphasizes the research performed by the authors to understand the functional organization of the human forebrain in cardiovascular control during physical stressors of baroreceptor unloading and handgrip exercise. The studies have exposed important associations between activation patterns of the insula cortex, dorsal anterior cingulate, and the medial prefrontal cortex and cardiovascular adjustments to physical stressors. Furthermore, these studies provide functional anatomic evidence that sensory signals arising from baroreceptors and skeletal muscle are represented within the insula cortex and the medial prefrontal cortex, in addition to the sensory cortex. Thus, the cortical pathways subserving reflex cardiovascular control integrate viscerosensory inputs with outgoing traffic that modulates the autonomic nervous system., (Copyright © 2012 Wiley Periodicals, Inc.)

Somatosensory afferents are represented within the cortical autonomic network (CAN). However, the representation of somatosensory afferents, and the consequent cardiovascular effects, may be modified by levels of baroreceptor input. Thus, we examined the cortical regions involved with processing somatosensory inputs during baroreceptor unloading. Neuroimaging sessions (functional magnetic resonance imaging [fMRI]) recorded brain activity during 30 mmHg lower-body negative pressure (LBNP) alone and combined with somatosensory stimulation (LBNP+SS) of the forearm (n = 14). Somatosensory processing was also assessed during increased sympathetic outflow via end-expiratory apnea. Heart rate (HR), blood pressure (BP), cardiac output (Q), and muscle sympathetic nerve activity (MSNA) were recorded during the same protocols in a separate laboratory session. SS alone had no effect on any cardiovascular or MSNA variable at rest. Measures of HR, BP, and Q during LBNP were not different compared with LBNP+SS. The rise in MSNA burst frequency was attenuated during LBNP+SS versus LBNP alone (8 vs. 12 bursts/min, respectively, P < 0.05). SS did not affect the change in MSNA during apnea. Activations within the insula and dorsal anterior cingulate cortex (ACC) observed during LBNP were not seen during LBNP+SS. Anterior insula and ACC activations occurring during apnea were not modified by SS. Thus, the absence of insular and dorsal ACC activity during LBNP+SS along with an attenuation of MSNA burst frequency suggest sympathoinhibitory effects of sensory stimulation during decreased baroreceptor input by a mechanism that includes conjoint insula-dorsal ACC regulation. These findings reveal that the level of baroreceptor input influences the forebrain organization of somatosensory afferents.

Regions of the cortical autonomic network (CAN) are activated during muscle contraction. However, it is not known to what extent CAN activation patterns reflect muscle sensory inputs, top-down signals from the motor cortex, and/or motor drive to cardiovascular structures. The present study explored the functional representation of somatosensory afferent input within the CAN with an a priori interest in the insula and ventral medial prefrontal cortex (vMPFC) (n=12). Heart rate (HR) and functional MRI data were acquired during 1) 30s periods of electrical stimulation of the wrist flexors at sub-motor (SUB; Type I,II afferents) and 2) motor thresholds (MOT; Type I,II,III afferents), 3) volitional wrist flexion at 5% maximal voluntary contraction (MVC) to match the MOT tension (VOL5%), and 4) volitional handgrip at 35% MVC to elicit tachycardia (VOL35%). Compared with rest, HR did not change during SUB, MOT, or VOL5% but increased during VOL35% (p<0.001). High frequency HR variability was 29.42±18.87 ms(2) (mean±S.D.) at rest and 39.85±27.60 ms(2) during SUB (p=0.06). High frequency HR variability was decreased during VOL35% compared to rest (p≤0.005). SUB increased activity in the bilateral posterior insula, vMPFC, subgenual anterior cingulate cortex (ACC), mid-cingulate cortex (MCC), and posterior cingulate cortex. MOT increased activity in the left posterior insula and MCC. During VOL5%, activity increased in the right anterior-mid insula. VOL35% was associated with activity in the bilateral insula as well as vMPFC and subgenual ACC deactivation. These data suggest that the left posterior insula processes sensory input from muscle during passive conditions and specifically that Type I and/or II muscle afferent stimulation during SUB impacts the vMPFC and/or subgenual ACC, regions believed to be involved in brain default mode and parasympathetic activity., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Sleep apnoea, with repeated periods of hypoxia, results in cardiovascular morbidity and concomitant autonomic dysregulation. Trained apnoea divers also perform prolonged apnoeas accompanied by large lung volumes, large reductions in cardiac output and severe hypoxia and hypercapnia. We tested the hypothesis that apnoea training would be associated with decreased cardiovagal and sympathetic baroreflex gains and reduced respiratory modulation of muscle sympathetic nerve activity (MSNA; microneurography). Six trained divers and six controls were studied at rest and during asphyxic rebreathing. Despite an elevated resting heart rate (70+/-14 vs. 56+/-10 bpm; p=0.038), divers had a similar cardiovagal baroreflex gain (-1.22+/-0.47 beats/mmHg) as controls (-1.29+/-0.61; NS). Similarly, though MSNA burst frequency was slightly higher in divers at rest (16+/-4 bursts/min vs. 10+/-5 bursts/min, p=0.03) there was no difference in baseline burst incidence, sympathetic baroreflex gain (-3.8+/-2.1%/mmHg vs. -4.7+/-1.7%/mmHg) or respiratory modulation of MSNA between groups. Resting total peripheral resistance (11.9+/-2.6 vs. 12.3+/-2.2 mmHg/L/min) and pulse wave velocity (5.82+/-0.55 vs. 6.10+/-0.51 m/s) also were similar between divers and controls, respectively. Further, the sympathetic response to asphyxic rebreathing was not different between controls and divers (-1.70+/-1.07 vs. -1.74+/-0.84 a.u./% desaturation). Thus, these data suggest that, unlike patients with sleep apnoea, apnoea training in otherwise healthy individuals does not produce detectable autonomic dysregulation or maladaption., (Copyright 2010 Elsevier B.V. All rights reserved.)

Considerable effort has been put into animal studies establishing the sites in the brain that are responsible for control of the autonomic nervous system. These studies relied on an electrophysiological or neurochemical response to the activation of peripheral autonomic receptors or chemical or electrical stimulation of central sites. A large number of excellent reviews summarize the results of these studies. More recently, functional imaging has been used to not only confirm the electrophysiological and anatomical studies in animals, but has allowed a more complete understanding of how the brain responds as a whole for effecting autonomic control. The earliest studies to examine forebrain control during functional imaging utilized tests that involved active participation of the subjects and included maximal inspiration, Valsalva manoeuvre, isometric handgrip and cold compress application. There were a few issues that arose from these studies. First, they involved areas of the brain that included active decision making, they were more prone to inducing movement artefact, and some of these tests could activate noxious regions in the brain in addition to autonomic sites. In fact, this dual modality activation represented a more severe complication for investigators determining nociceptive sites in the brain, since virtually all of their stimuli had concomitant autonomic responses. More recent investigations attempted to resolve these issues with more selective passive and active stimuli. In spite of the very different approaches taken to visceral activation in functional imaging studies, a consistent picture of the key areas involved in autonomic control has emerged.

In general, cardiac regulation is dominated by the sympathetic and parasympathetic nervous systems in men and women, respectively. Our recent study had revealed sex differences in the forebrain network associated with sympathoexcitatory response to baroreceptor unloading. The present study further examined the sex differences in forebrain modulation of cardiovagal response at the onset of isometric exercise. Forebrain activity in healthy men (n = 8) and women (n = 9) was measured using functional magnetic resonance imaging during 5 and 35% maximal voluntary contraction handgrip exercise. Heart rate (HR), mean arterial pressure (MAP), and muscle sympathetic nerve activity (MSNA) were collected in a separate recording session. During the exercise, HR and MAP increased progressively, while MSNA was suppressed (P < 0.05). Relative to men, women demonstrated smaller HR (8 +/- 2 vs. 18 +/- 3 beats/min) and MAP (3 +/- 2 vs. 11 +/- 2 mmHg) responses to the 35% maximal voluntary contraction trials (P < 0.05). Although a similar forebrain network was activated in both groups, the smaller cardiovascular response in women was reflected in a weaker insular cortex activation. Nevertheless, men did not show a stronger deactivation at the ventral medial prefrontal cortex, which has been associated with modulating cardiovagal activity. In contrast, the smaller cardiovascular response in women related to their stronger suppression of the dorsal anterior cingulate cortex activity, which has been associated with sympathetic control of the heart. Our findings revealed sex differences in both the physiological and forebrain responses to isometric exercise.

The purpose of the present study was to determine the cortical structures involved with integrated baroreceptor-mediated modulation of autonomic cardiovascular function in conscious humans independent of changes in arterial blood pressure. We assessed the brain regions associated with lower body negative pressure (LBNP)-induced baroreflex control using functional magnetic resonance imaging with blood oxygen level-dependent (BOLD) contrast in eight healthy male volunteer subjects. The levels of LBNP administered were 5, 15 and 35 mmHg. Heart rate (HR; representing the cardiovascular response) and LBNP (representing the baroreceptor activation level) were simultaneously monitored during the scanning period. In addition, estimated central venous pressure (CVP), arterial blood pressure (ABP) and muscle sympathetic nerve activity were recorded on a separate session. Random effects analyses (SPM2) were used to evaluate significant (P < 0.05) BOLD signal changes that correlated separately with both LBNP and HR (15- and 35-mmHg versus 5-mmHg LBNP). Compared to baseline, steady-state LBNP at 15 and 35 mmHg decreased CVP (from 7 +/- 1 to 5 +/- 1 and 4 +/- 1 mmHg, respectively) and increased MSNA (from 12 +/- 1 to 23 +/- 3 and 36 +/- 4 bursts min(-1), respectively, both P < 0.05 versus baseline). Furthermore, steady-state LBNP elevated HR from 54 +/- 2 beats min(-1) at baseline to 64 +/- 2 beats min(-1) at 35-mmHg suction. Both mean arterial and pulse pressure were not different between rest and any level of LBNP. Cortical regions demonstrating increased activity that correlated with higher HR and greater LBNP included the right superior posterior insula, frontoparietal cortex and the left cerebellum. Conversely, using the identical statistical paradigm, bilateral anterior insular cortices, the right anterior cingulate, orbitofrontal cortex, amygdala, midbrain and mediodorsal nucleus of the thalamus showed decreased neural activation. These data corroborate previous investigations highlighting the involved roles of the insula, anterior cingulate cortex and amygdala in central autonomic cardiovascular control. In addition, we have provided the first evidence for the identification of the cortical network involved specifically with baroreflex-mediated autonomic cardiovascular function in conscious humans.

Early in the twentieth century, Walter B. Cannon (1871–1945) introduced his overarching hypothesis of "homeostasis" (Cannon 1932)—the ability to sustain physiological values within a narrow range necessary for life during periods of stress. Physical exercise represents a stress in which motor, respiratory and cardiovascular systems must be integrated across a range of metabolic stress to match oxygen delivery to oxygen need at the cellular level, together with appropriate thermoregulatory control, blood pressure adjustments and energy provision. Of these, blood pressure regulation is a complex but controlled variable, being the function of cardiac output and vascular resistance (or conductance). Key in understanding blood pressure control during exercise is the coordinating role of the autonomic nervous system. A long history outlines the development of these concepts and how they are integrated within the exercise context. This review focuses on the renaissance observations and thinking generated in the first three decades of the twentieth century that opened the doorway to new concepts of inquiry in cardiovascular regulation during exercise. The concepts addressed here include the following: (1) exercise and blood pressure, (2) central command, (3) neurovascular transduction with emphasis on the sympathetic nerve activity and the vascular end organ response, and (4) tonic neurovascular integration. [ABSTRACT FROM AUTHOR]

Aims: Patients with sympathetic excess are those most likely to benefit from novel interventions targeting the autonomic nervous system. To inform such personalized therapy, we identified determinants of augmented muscle sympathetic nerve activity (MSNA) in heart failure, versus healthy controls. Methods and results: We compared data acquired in 177 conventionally‐treated, stable non‐diabetic patients in sinus rhythm, aged 18–79 years (149 males; 28 females; left ventricular ejection fraction [LVEF] 25 ± 11% [mean ± standard deviation]; range 5–60%), and, concurrently, under similar conditions, in 658 healthy, normotensive volunteers (398 males; aged 18–81 years). In heart failure, MSNA ranged between 7 and 90 bursts·min−1, proportionate to heart rate (p < 0.0001) and body mass index (BMI) (p = 0.03), but was unrelated to age, blood pressure, or drug therapy. Mean MSNA, adjusted for age, sex, BMI, and heart rate, was greater in heart failure (+14.2 bursts·min−1; 95% confidence interval [CI] 12.1–16.3; p < 0.0001), but lower in women (−5.0 bursts·min−1; 95% CI 3.4–6.6; p < 0.0001). With spline modeling, LVEF accounted for 9.8% of MSNA variance; MSNA related inversely to LVEF below an inflection point of ∼21% (p < 0.006), but not above. Burst incidence was greater in ischaemic than dilated cardiomyopathy (p = 0.01), and patients with sleep apnoea (p = 0.03). Burst frequency correlated inversely with stroke volume (p < 0.001), cardiac output (p < 0.001), and peak oxygen consumption (p = 0.002), and directly with norepinephrine (p < 0.0001) and peripheral resistance (p < 0.001). Conclusion: Burst frequency and incidence exceeded normative values in only ∼53% and ∼33% of patients. Such diversity encourages selective deployment of sympatho‐modulatory therapies. Clinical characteristics can highlight individuals who may benefit from future personalized interventions targeting pathological sympathetic activation. [ABSTRACT FROM AUTHOR]

Physiological homeostasis depends upon adequate integration and responsiveness of sensory information with the autonomic nervous system to affect rapid and effective adjustments in end organ control. Dysregulation of the autonomic nervous system leads to cardiovascular disability with consequences as severe as sudden death. The neural pathways involved in reflexive autonomic control are dependent upon brainstem nuclei but these receive modulatory inputs from higher centers in the midbrain and cortex. Neuroimaging technologies have allowed closer study of the cortical circuitry related to autonomic cardiovascular adjustments to many stressors in awake humans and have exposed many forebrain sites that associate strongly with cardiovascular arousal during stress including the medial prefrontal cortex, insula cortex, anterior cingulate, amygdala and hippocampus. Using a comparative approach, this review will consider the cortical autonomic circuitry in rodents and primates with a major emphasis on more recent neuroimaging studies in awake humans. A challenge with neuroimaging studies is their interpretation in view of multiple sensory, perceptual, emotive and/or reflexive components of autonomic responses. This review will focus on those responses related to non-volitional baroreflex control of blood pressure and also on the coordinated responses to non-fatiguing, non-painful volitional exercise with particular emphasis on the medial prefrontal cortex and the insula cortex. [ABSTRACT FROM AUTHOR]

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

We compared the integrated cardiovascular and autonomic responses to hypercapnia and hypoxia to test the hypothesis that these stimuli differentially affect muscle sympathetic nerve activity (MSNA) discharge patterns and cardiovagal and sympathetic baroreflex function in a manner related to ventilatory chemoreflex sensitivity. Six males and six females underwent 5 mm of hypoxia (end-tidal Po2 = 45 Torr) and 5 mm of hypercapnia (end-tidal Pco2 = + 8 Ton from baseline), causing similar ventilatory responses. A downward right shift in cardiovagal set point was observed during both conditions, which was strongly related to the change in inspiratory time (Ti) from baseline to hypercapnia (r² = 0.67, P = 0.007) and hypoxia (r² = 0.79, P < 0.001). Cardiovagal baroreflex gain was decreased during hypoxia (20.1 ± 6.9 vs. 8.9 ± 5.1 ms/mmHg, P < 0.001) but not hypercapnia (26.7 ± 12.7 vs. 23.0 ± 9.1 ms/mmHg). Both hypoxia and hypercapnia increased MSNA burst amplitude, whereas hypoxia, but not hypercapnia, also increased in MSNA burst frequency (21 ± 9 vs. 28 ± 7 bursts/mm, P = 0.03) and total MSNA (4.56 ± 3.07 vs. 7.37 ± 3.26 mV/mm, P = 0.002). However, neither hypercapnia nor hypoxia affected sympathetic burst probability or baroreflex gain. Hypoxia also caused a greater reduction in total peripheral resistance (P = 0.04), a greater increase in heart rate (P = 0.002), and a trend for a greater cardiac output response (P = 0.06) compared with hypercapnia. Nonetheless, central venous pressure remained unchanged during either condition. These results suggest that hypercapnia and hypoxia exert differential effects on cardiovagal, but not sympathetic, baroreflex gain and set point in a manner not related to ventilatory chemoreflex sensitivity. Furthermore, the data suggest that the individual's respiratory pattern to hypoxia or hypercapnia, as reflected in the inspiratory time, was a strong determinant of cardiovagal baroreflex set-point rather than the total ventilatory chemoreflex gain per Se. [ABSTRACT FROM AUTHOR]

Abstract: The purpose of this study was to assess the power and the frequency of low-frequency (LF; 0.04–<0.15Hz) oscillations in systolic blood pressure (SBP) and R–R interval (RRi) across the continuum of risk of cardiovascular disease, including age. A potential confound in such determinations is low spontaneous breathing frequency in some individuals. We measured beat-to-beat SBP, RRi and respiration in healthy YOUNG (33±3years) and OLDER subjects (62±5years) and older patients with hypertension (HT, 61±5years), coronary artery disease without (CAD, 62±5years) and with type 2 diabetes (CAD+DM, 62±4years, n =28 for all groups) during spontaneous breathing at supine rest. Power (PowerLF) and median frequency (MedLF) of LF oscillations were calculated by power spectral analysis after removing respiratory effects by least-mean-square adaptive filtering. OLDER had higher PowerLF-SBP (5.5±3.0 vs. 3.4±2.5mmHg2, p =0.002) and lower PowerLF-RRi than YOUNG (339±460 vs. 575±422ms2, p =0.001) whereas neither variable differed between OLDER and patient groups. MedLF-SBP (0.072±0.009 vs. 0.080±0.011Hz, p =0.005) and MedLF-RRi (0.072±0.010 vs. 0.079±0.013Hz, p =0.027) were lower in OLDER compared with YOUNG. Compared with OLDER, MedLF-RRi was lower in CAD (0.065±0.006Hz, p =0.015) and CAD +DM (0.066±0.008Hz, p =0.012); whereas CAD+DM had also lower MedLF-SBP (0.065±0.006Hz, p =0.012). No differences were observed between OLDER and HT and between CAD and CAD+DM in these variables. We concluded that age is major determinant of the power of LF oscillations in SBP and RRi at rest, whereas the median frequency of these oscillations is altered also by coronary artery disease. [Copyright &y& Elsevier]