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The muscle metaboreflex effect on pulmonary ventilation (V̇E) regulation is more apparent during rhythmic exercise than rest, possibly because this reflex interacts with other mechanisms regulating V̇E during voluntary contractions, such as central command. Therefore, we tested whether one part of central command, the descending component of motor execution (i.e., descending motor drive), and the muscle metaboreflex interact synergistically to regulate V̇E. Thirteen healthy adults (9 men) completed four experiments in random order under isocapnia. The muscle metaboreflex was activated by rhythmic handgrip exercise at 60% maximal voluntary contraction (MVC) force with the dominant hand. Then, the muscle metaboreflex remained active during a 4-min recovery period via postexercise circulatory occlusion (PECO), or it was inactivated, maintaining free blood flow to the dominant upper limb. During the last 2 min of the handgrip exercise recovery, participants either performed rhythmic voluntary plantar flexion with the dominant leg at 30% MVC torque to generate descending motor drive or the dominant leg's calf muscles were involuntarily activated by electrical stimulation at a similar torque level (i.e., without descending motor drive). V̇E increased to a similar level during handgrip exercise in all conditions (≈22 L/min, P = 0.364). PECO maintained V̇E elevated above recovery with free blood flow (≈17 L/min vs. ≈13 L/min, P = 0.009). However, voluntary and involuntary plantar flexion with or without PECO evoked similar V̇E responses (Δ ≈ 4 L/min, P = 0.311). Therefore, an interaction between descending motor drive and muscle metaboreflex is not ubiquitous for V̇E regulation during rhythmic exercise. NEW & NOTEWORTHY: Voluntary (i.e., with descending motor drive) and involuntary (i.e., no descending motor drive) plantar flexion elicited similar ventilatory responses when postexercise circulatory occlusion was or was not used in an upper limb. These results indicate that the descending motor drive component of the central command and the muscle metaboreflex do not interact to regulate pulmonary ventilation during rhythmic exercise, which suggests that a supposed interaction between central command-muscle metaboreflex is more complex than previously thought. [ABSTRACT FROM AUTHOR]

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]

Key points While the hypothalamic orexinergic nervous system is established as having a pivotal role in the long‐term regulation of various organismic functions, including wakefulness, metabolism and hypertensive states, whether this system contributes to the rapid autonomic cardiovascular regulation during physical activity remains elusive. This study aimed to elucidate the role of the orexinergic nervous system in transmitting volitional motor signals, i.e. central command, to drive somatomotor and sympathetic cardiovascular responses. We first found that this system is activated by voluntary locomotor exercise as evidenced by an increased expression of Fos, a marker of neural activation, in the orexinergic neurons of Sprague–Dawley rats engaged in spontaneous wheel running. Next, using transgenic Orexin‐Cre rats for optogenetic manipulation of orexinergic neurons, we found that optogenetic excitation of orexinergic neurons caused sympathoexcitation on a subsecond timescale under anaesthesia. In freely moving conscious rats, this excitatory stimulation rapidly elicited exploration‐like behaviours, predominantly locomotor activity, along with pressor and tachycardiac responses. Meanwhile, optogenetic inhibition of orexinergic neurons during spontaneous wheel running immediately suppressed locomotor activities and blood pressure elevation without affecting basal cardiovascular homeostasis. Taken together, these findings demonstrate the essential role of the orexinergic nervous system in the central circuitry that transmits central command signals for locomotor exercise. This study not only offers insights into the brain circuit mechanisms precisely regulating autonomic cardiovascular systems during voluntary exercise but also likely contributes to our understanding of brain mechanisms underlying abnormal cardiovascular adjustments to exercise in pathological conditions, such as hypertension. The hypothalamic orexinergic nervous system plays various roles in the long‐term regulation of autonomic and endocrine functions, as well as motivated behaviours. We present a novel, rapid role of the orexinergic nervous system, revealing its significance as a crucial substrate in the brain circuit mechanisms that coordinate somatomotor and autonomic cardiovascular controls for locomotor exercise. Our data demonstrate that orexinergic neurons relay volitional motor signals, playing a necessary and sufficient role in the autonomic cardiovascular regulation required for locomotor exercise in rats. The findings contribute to our understanding of how the brain precisely regulates autonomic cardiovascular systems during voluntary exercise, providing insights into the central neural mechanisms that enhance physical performance moment‐by‐moment during exercise. [ABSTRACT FROM AUTHOR]

Peripheral hypercapnic chemosensitivity (PHC) is the ventilatory response to hypercapnia and is enhanced with acute whole body exercise. However, little is known about the mechanism(s) responsible for the exercise-related increase in PHC and if progressive exercise leads to further augmentation. We hypothesized that unloaded cycle exercise (0 W) would increase PHC but progressively increasing the intensity would not further augment the response. Twenty healthy subjects completed two testing days. Day 1 was a maximal exercise test on a cycle ergometer to determine peak power output (Wmax). Day 2 consisted of six 12-min stages: 1) rest on chair, 2) rest on bike, 3) 0 W unloaded cycling, 4) 25% Wmax, 5) 50% Wmax, and 6) ~70% Wmax with ~10 min of rest between each exercise stage. In each stage, PHC was assessed via two breaths of 10% CO2 (~21% O2) repeated five times with ~45 s between each to ensure end-tidal CO2 (PETCO2) and ventilation returned to baseline. Prestimulus PETCO2 was not different between rest and unloaded cycling (P = 0.478). There was a significant increase in PHC between seated rest and 25% Wmax (0.71 ± 0.37 vs. 1.03 ± 0.52 L·mmHg-1·min-1, respectively, P = 0.0006) and between seated rest and unloaded cycling (0.71 ± 0.37 vs. 1.04 ± 0.4 L·mmHg-1·min-1, respectively, P = 0.0017). There was no effect of exercise intensity on PHC (1.03 ± 0.52 vs. 0.95 ± 0.58 vs. 1.01 ± 0.65 L·mmHg-1·min-1 for 25, 50, and 70% Wmax, P = 0.44). The increased PHC response from seated rest to unloaded and 25% Wmax, but no effect of exercise intensity suggests a possible feedforward/feedback mechanism causing increased PHC sensitivity through the act of cycling. [ABSTRACT FROM AUTHOR]

Background: Repetitive experiences of certain stresses evoke feedforward cardiovascular responses via central command (CC)--central signals from the higher brain. However, it is unclear whether the anticipatory cardiovascular responses before pain stimulation occur after repetitive pain experiences and how nitrous oxide/oxygen inhalation (N2O), a sedative widely used in dentistry, affects the responses. We tested the hypothesis that the repetitive cold pressor test (CPT) alters the anticipatory cardiovascular responses, which are attenuated by N2O. Materials and methods: Beat-to-beat systolic (SBP) and diastolic blood pressure (DBP), heart rate (HR), and finger arterial stiffness (β-stiffness) were measured during the 5-min rest, 30-s countdown (CD) before CPT, 2-min CPT, and 3-min recovery (CPT[1st]) in 15 young adults [age, 28 ± 4 years]. The same protocols were repeated randomly with the second CPT (CPT + CC) or placebo test (PLCB + CC). Results: SBP and DBP increased from baseline in CPT[1st] and CPT + CC under room air (RA) and 40 % N2O, while SBP was lower under N2O than under RA in CPT[1st]. HR in CPT[1st] was lower under N2O than under RA. The change (Δ) in HR was smaller during CPT[1st] than during CPT + CC under N2O, and a similar trend was observed under RA. ΔSBP by CD was lower under N2O than under RA in CPT[1st] but not in CPT + CC. HR increased with CD in CPT + CC but not in CPT[1st] under both RA and N2O. β-stiffness increased by CD regardless of the pain experience, while it was lower under N2O. Conclusion: Repetitive pain experiences induce a feedforward HR increase. 40 % N2O decreases vascular stiffness, which may attenuate the anticipatory pressor response only when the feedforward HR increase does not exist.

Patients with heart failure with reduced (HFrEF) and preserved ejection fraction (HFpEF) exhibit severe exercise intolerance that may be due, in part, to inappropriate cardiovascular and hemodynamic adjustments to exercise. Several neural mechanisms and locally released vasoactive substances work in concert through complex interactions to ensure proper adjustments to meet the metabolic demands of the contracting skeletal muscle. Specifically, accumulating evidence suggests that disease-related alterations in neural mechanisms (e.g., central command, exercise pressor reflex, arterial baroreflex, and cardiopulmonary baroreflex) contribute to heightened sympathetic activation and impaired ability to attenuate sympathetic vasoconstrictor responsiveness that may contribute to reduced skeletal muscle blood flow and severe exercise intolerance in patients with HFrEF. In contrast, little is known regarding these important aspects of physiology in patients with HFpEF, though emerging data reveal heightened sympathetic activation and attenuated skeletal muscle blood flow during exercise in this patient population that may be attributable to dysregulated neural control of the circulation. The overall goal of this review is to provide a brief overview of the current understanding of disease-related alterations in the integrative neural cardiovascular responses to exercise in both HFrEF and HFpEF phenotypes, with a focus on sympathetic nervous system regulation during exercise. [ABSTRACT FROM AUTHOR]

The cardiovascular response to exercise is largely determined by neurocirculatory control mechanisms that help to raise blood pressure and modulate vascular resistance which, in concert with regional vasodilatory mechanisms, promote blood flow to active muscle and organs. These neurocirculatory control mechanisms include a feedforward mechanism, known as central command, and three feedback mechanisms, namely, 1) the baroreflex, 2) the exercise pressor reflex, and 3) the arterial chemoreflex. The hemodynamic consequences of these control mechanisms result from their influence on the autonomic nervous system and subsequent alterations in cardiac output and vascular resistance. Although stimulation of the baroreflex inhibits sympathetic outflow and facilitates parasympathetic activity, central command, the exercise pressor reflex, and the arterial chemoreflex facilitate sympathetic activation and inhibit parasympathetic drive. Despite considerable understanding of the cardiovascular consequences of each of these mechanisms in isolation, the circulatory impact of their interaction, which occurs when various control systems are simultaneously activated (e.g., during exercise at altitude), has only recently been recognized. Although aging and cardiovascular disease (e.g., heart failure, hypertension) have both been recognized to alter the hemodynamic consequences of these regulatory systems, this review is limited to provide a brief overview on the action and interaction of neurocirculatory control mechanisms in health. [ABSTRACT FROM AUTHOR]

Fifty percent of patients with postural tachycardia syndrome (POTS) are hypocapnic during orthostasis related to initial orthostatic hypotension (iOH). We determined whether iOH drives hypocapnia in POTS by low BP or decreased cerebral blood velocity (CBv). We studied three groups; healthy volunteers (n = 32, 18 ± 3 yr) were compared with POTS, grouped by presence [POTSlow end-tidal CO2 (;ETCO2), n = 26, 19 ± 2 yr] or absence [POTS-normal upright end-tidal carbon dioxide (nlCO2), n = 28, 19 ± 3 yr] of standing hypocapnia defined by end-tidal CO2 (ETCO2) 30 mmHg at steady-state, measuring middle cerebral artery CBv, heart rate (HR), and beat-to-beat blood pressure (BP). After 30 min supine, subjects stood for 5 min. Quantities were measured prestanding, at minimum CBv, minimum BP, peak HR, CBv recovery, BP recovery, minimum HR, steady-state, and 5 min. Baroreflex gain was estimated by a index. iOH occurred with similar frequency and minimum BP in POTS-;ETCO2 and POTSnlCO2. Minimum CBv was reduced significantly (P < 0.05) in POTS-;ETCO2 (48 ± 3 cm/s) preceding hypocapnia compared with POTS-nlCO2 (61 ± 3 cm/s) or Control (60 ± 2 cm/s). The anticipatory increased BP was significantly larger (P < 0.05) in POTS (8 ± 1 mmHg vs. 2 ± 1) and began 8 s prestanding. HR increased in all subjects, CBv increased significantly (P < 0.05) in both POTSnlCO2 (76 ± 2 to 85 ± 2 cm/s) and Control (75 ± 2 to 80 ± 2 cm/s) consistent with central command. CBv decreased in POTS-; ETCO2 (76 ± 3 to 64 ± 3 cm/s) correlating with decreased baroreflex gain. Cerebral conductance [meanCBv/mean arterial blood pressure (MAP)] was reduced in POTS-;ETCO2 throughout. Data support the hypothesis that excessively reduced CBv during iOH may intermittently reduce carotid body blood flow, sensitizing that organ and producing postural hyperventilation in POTS-; ETCO2. Excessive fall in CBv occurs in part during prestanding central command and is a facet of defective parasympathetic regulation in POTS. [ABSTRACT FROM AUTHOR]

Abstract It remains unclear whether cardiac baroreflex function is preserved or suppressed at the onset of standing up. To answer the question and, if cardiac baroreflex is suppressed, to investigate the mechanism responsible for the suppression, we compared the sensitivity of the arterial cardiac baroreflex at the onset of voluntary and passive hindlimb standing in conscious cats. Cardiac baroreflex sensitivity was estimated from the maximal slope of the baroreflex curve between the responses of systolic arterial blood pressure and heart rate to a brief occlusion of the abdominal aorta. The systolic arterial blood pressure response to standing up without aortic occlusion was greater in the voluntary case than in the passive case. Cardiac baroreflex sensitivity was clearly decreased at the onset of voluntary standing up compared with rest (P = 0.005) and the onset of passive standing up (P = 0.007). The cardiac baroreflex sensitivity at the onset of passive standing up was similar to that at rest (P = 0.909). The findings suggest that central command would transmit a modulatory signal to the cardiac baroreflex system during the voluntary initiation of standing up. Furthermore, the present data tempt speculation on a close relationship between central inhibition of the cardiac baroreflex and the centrally induced tachycardiac response to standing up.

Stimulation of the mesencephalic locomotor region elicits exaggerated sympathetic nerve and pressor responses in spontaneously hypertensive rats (SHR) as compared with normotensive Wistar-Kyoto rats (WKY). This suggests that central command or its influence on vasomotor centers is augmented in hypertension. The decerebrate animal model possesses an ability to evoke intermittent bouts of spontaneously occurring motor activity (SpMA) and generates cardiovascular responses associated with the SpMA. It remains unknown whether the changes in sympathetic nerve activity and hemodynamics during SpMA are altered by hypertension. To test the hypothesis that the responses in renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) during SpMA are exaggerated with hypertension, this study aimed to compare the responses in decerebrate, paralyzed SHR, WKY, and normotensive Sprague-Dawley (SD) rats. In all strains, an abrupt increase in RSNA occurred in synchronization with tibial motor discharge (an index of motor activity) and was followed by rises in MAP and heart rate. The centrally evoked increase in RSNA and MAP during SpMA was much greater (306 ± 110%) in SHR than WKY (187 ± 146%) and SD (165 ± 44%). Although resting baroreflex-mediated changes in RSNA were not different across strains, mechanically or pharmacologically induced elevations in MAP attenuated or abolished the RSNA increase during SpMA in WKY and SD but had no effect in SHR. It is likely that the exaggerated sympathetic nerve and pressor responses during SpMA in SHR are induced along a central command pathway independent of the arterial baroreflex and/or result from central command-induced inhibition of the baroreflex. [ABSTRACT FROM AUTHOR]

Patients with type-2 diabetes mellitus (T2DM) have exaggerated sympathetic activity and blood pressure responses to exercise. However, the underlying mechanisms for these responses, as well as how these responses change throughout disease progression, are not completely understood. For this study, we examined the effect of the progression of T2DM on the exercise pressor reflex, a critical neurocardiovascular mechanism that functions to increase sympathetic activity and blood pressure during exercise. We also aimed to examine the effect of T2DM on reflexive cardiovascular responses to static contraction, as well as those responses to tendon stretch when an exaggerated exercise pressor reflex was present. We evoked the exercise pressor reflex and mechanoreflex by statically contracting the hindlimb muscles and stretching the Achilles tendon, respectively, for 30 s. We then compared pressor and cardioaccelerator responses in unanesthetized, decerebrated University of California Davis (UCD)-T2DM rats at 21 and 31 wk following the onset of T2DM to responses in healthy nondiabetic rats. We found that the pressor response to static contraction was greater in the 31-wk T2DM [change in mean arterial pressure (∆MAP) = 39 ± 5 mmHg] but not in the 21-wk T2DM (∆MAP = 24 ± 5 mmHg) rats compared with nondiabetic rats (∆MAP = 18 ± 2 mmHg; P < 0.05). Similarly, the pressor and the cardioaccelerator responses to tendon stretch were significantly greater in the 31-wk T2DM rats [∆MAP = 69 ± 6 mmHg; change in heart rate (∆HR) = 28 ± 4 beats/min] compared with nondiabetic rats (∆MAP = 14 ± 2 mmHg; ∆HR = 5 ± 3 beats/min; P < 0.05). These findings suggest that the exercise pressor reflex changes as T2DM progresses and that a sensitized mechanoreflex may play a role in exaggerating these cardiovascular responses.NEW & NOTEWORTHY This is the first study to provide evidence that as type-2 diabetes mellitus (T2DM) progresses, the exercise pressor reflex becomes exaggerated, an effect that may be due to a sensitized mechanoreflex. Moreover, these findings provide compelling evidence suggesting that impairments in the reflexive control of circulation contribute to exaggerated blood pressure responses to exercise in T2DM.

The lack of a testable model explaining how ventilation is regulated in different exercise conditions has been repeatedly acknowledged in the field of exercise physiology. Yet, this issue contrasts with the abundance of insightful findings produced over the last century and calls for the adoption of new integrative perspectives. In this review, we provide a methodological approach supporting the importance of producing a set of evidence by evaluating different studies together—especially those conducted in 'real' exercise conditions—instead of single studies separately. We show how the collective assessment of findings from three domains and three levels of observation support the development of a simple model of ventilatory control which proves to be effective in different exercise protocols, populations and experimental interventions. The main feature of the model is the differential control of respiratory frequency (fR) and tidal volume (VT); fR is primarily modulated by central command (especially during high-intensity exercise) and muscle afferent feedback (especially during moderate exercise) whereas VT by metabolic inputs. Furthermore, VT appears to be fine-tuned based on fR levels to match alveolar ventilation with metabolic requirements in different intensity domains, and even at a breath-by-breath level. This model reconciles the classical neuro-humoral theory with apparently contrasting findings by leveraging on the emerging control properties of the behavioural (i.e. fR) and metabolic (i.e. VT) components of minute ventilation. The integrative approach presented is expected to help in the design and interpretation of future studies on the control of fR and VT during exercise. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Standing up can cause hypotension and tachycardia. Accumulated evidence poses the simple question, does the cardiac baroreflex operate at the onset of standing up? If the cardiac baroreflex is suppressed, what mechanism is responsible for baroreflex inhibition?What is the main finding and its importance?In cats, we found blunting of cardiac baroreflex sensitivity in the pressor range at the onset of voluntary hindlimb standing, but not of passive hindlimb standing. This finding suggests that central command suppresses pressor‐evoked bradycardia at the onset of standing up, probably in advance, to prevent or buffer orthostatic hypotension. It remains unclear whether cardiac baroreflex function is preserved or suppressed at the onset of standing up. To answer the question and, if cardiac baroreflex is suppressed, to investigate the mechanism responsible for the suppression, we compared the sensitivity of the arterial cardiac baroreflex at the onset of voluntary and passive hindlimb standing in conscious cats. Cardiac baroreflex sensitivity was estimated from the maximal slope of the baroreflex curve between the responses of systolic arterial blood pressure and heart rate to a brief occlusion of the abdominal aorta. The systolic arterial blood pressure response to standing up without aortic occlusion was greater in the voluntary case than in the passive case. Cardiac baroreflex sensitivity was clearly decreased at the onset of voluntary standing up compared with rest (P = 0.005) and the onset of passive standing up (P = 0.007). The cardiac baroreflex sensitivity at the onset of passive standing up was similar to that at rest (P = 0.909). The findings suggest that central command would transmit a modulatory signal to the cardiac baroreflex system during the voluntary initiation of standing up. Furthermore, the present data tempt speculation on a close relationship between central inhibition of the cardiac baroreflex and the centrally induced tachycardiac response to standing up. [ABSTRACT FROM AUTHOR]

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Purpose: This study evaluated whether central motor drive during fatiguing exercise plays a role in determining performance and the development of neuromuscular fatigue during a subsequent endurance task. Methods: On separate days, 10 males completed three constant-load (80% peak power output), single-leg knee-extension trials to task failure in a randomized fashion. One trial was performed without preexisting quadriceps fatigue (CON), and two trials were performed with preexisting quadriceps fatigue induced either by voluntary (VOL; involving central motor drive) or electrically evoked (EVO; without central motor drive) quadriceps contractions (~20% maximal voluntary contraction (MVC)). Neuromuscular fatigue was assessed via pre–post changes in MVC, voluntary activation (VA), and quadriceps potentiated twitch force (Q tw,pot). Cardiorespiratory responses and rating of perceived exertion were also collected throughout the sessions. The two prefatiguing protocols were matched for peripheral fatigue and stopped when Q tw,pot declined by ~35%. Results: Time to exhaustion was shorter in EVO (4.3 ± 1.3 min) and VOL (4.7 ± 1.5 min) compared with CON (10.8 ± 3.6 min, P < 0.01) with no difference between EVO and VOL. ΔMVC (EVO: −47% ± 8%, VOL: −45% ± 8%, CON: −53% ± 8%), Δ Q tw,pot (EVO: −65% ± 7%, VOL: −59% ± 14%, CON: −64% ± 9%), and ΔVA (EVO: −9% ± 7%, VOL: −8% ± 5%, CON: −7% ± 5%) at the end of the dynamic task were not different between conditions (all P > 0.05). Compared with EVO (10.6 ± 1.7) and CON (6.8 ± 0.8), rating of perceived exertion was higher (P = 0.05) at the beginning of VOL (12.2 ± 1.0). Conclusions: These results suggest that central motor drive involvement during prior exercise plays a negligible role on the subsequent endurance performance. Therefore, our findings indicate that peripheral fatigue–mediated impairments are the primary determinants of high-intensity single-leg endurance performance. [ABSTRACT FROM AUTHOR]

It remains undetermined whether the cardiac component of the entire arterial baroreflex is blunted even at the onset of low‐intensity exercise. We sought to examine the moment‐to‐moment sensitivity of the cardiac baroreflex during walking at different speeds and the presumed mechanisms responsible for baroreflex modulation in conscious cats. Arterial baroreflex sensitivity for heart rate was estimated from the baroreflex ratio between changes in systolic arterial blood pressure and heart rate and from the slope of the baroreflex curve between the cardiovascular responses to brief occlusion of the abdominal aorta. Treadmill walking was performed for 1 min at three levels of speed (low: 20–30 m/min, moderate: 40 m/min, and high: 50–60 m/min) or for 3 min at the stepwise change of speed (low to high to low transition). Cardiac baroreflex sensitivity was blunted at the onset of walking, irrespective of speed. Thereafter, the blunted cardiac baroreflex sensitivity was restored around 15 s of walking at any speed, while the blunting occurred again at 45 s of high‐speed walking. The inhibition of cardiac baroreflex sensitivity also occurred (1) during the speed transition from low to high and (2) at 45 s of high‐speed exercise of the stepwise exercise. The blunted cardiac baroreflex sensitivity was restored immediately to the resting level during the speed transition from high to low, despite sustained pressor and tachycardiac responses. Therefore, moment‐to‐moment modulation of the cardiac baroreflex during exercise would occur in association with motor intention (i.e., exercise onset) and effort (i.e., treadmill speed). [ABSTRACT FROM AUTHOR]

Abstract It remains undetermined whether the cardiac component of the entire arterial baroreflex is blunted even at the onset of low‐intensity exercise. We sought to examine the moment‐to‐moment sensitivity of the cardiac baroreflex during walking at different speeds and the presumed mechanisms responsible for baroreflex modulation in conscious cats. Arterial baroreflex sensitivity for heart rate was estimated from the baroreflex ratio between changes in systolic arterial blood pressure and heart rate and from the slope of the baroreflex curve between the cardiovascular responses to brief occlusion of the abdominal aorta. Treadmill walking was performed for 1 min at three levels of speed (low: 20–30 m/min, moderate: 40 m/min, and high: 50–60 m/min) or for 3 min at the stepwise change of speed (low to high to low transition). Cardiac baroreflex sensitivity was blunted at the onset of walking, irrespective of speed. Thereafter, the blunted cardiac baroreflex sensitivity was restored around 15 s of walking at any speed, while the blunting occurred again at 45 s of high‐speed walking. The inhibition of cardiac baroreflex sensitivity also occurred (1) during the speed transition from low to high and (2) at 45 s of high‐speed exercise of the stepwise exercise. The blunted cardiac baroreflex sensitivity was restored immediately to the resting level during the speed transition from high to low, despite sustained pressor and tachycardiac responses. Therefore, moment‐to‐moment modulation of the cardiac baroreflex during exercise would occur in association with motor intention (i.e., exercise onset) and effort (i.e., treadmill speed).

We previously demonstrated that muscle sympathetic nerve activity (MSNA) increases to contracting muscle as well as to non-contracting muscle, but this was only assessed during isometric exercise at ∼10% of maximum voluntary contraction (MVC). Given that high-intensity isometric contractions will release more metabolites, we tested the hypothesis that the metaboreflex is expressed in the contracting muscle during high-intensity but not low-intensity exercise. MSNA was recorded continuously via a tungsten microelectrode inserted percutaneously into the right common peroneal nerve in 12 participants, performing isometric dorsiflexion of the right ankle at 10, 20, 30, 40, and 50% MVC for 2 min. Contractions were immediately followed by 6 min of post-exercise ischemia (PEI); 6 min of recovery separated contractions. Cross-correlation analysis was performed between the negative-going sympathetic spikes of the raw neurogram and the ECG. MSNA increased as contraction intensity increased, reaching mean values (± SD) of 207 ± 210 spikes/min at 10% MVC (P = 0.04), 270 ± 189 spikes/min at 20% MVC (P < 0.01), 538 ± 329 spikes/min at 30% MVC (P < 0.01), 816 ± 551 spikes/min at 40% MVC (P < 0.01), and 1,097 ± 782 spikes/min at 50% MVC (P < 0.01). Mean arterial pressure also increased in an intensity-dependent manner from 76 ± 3 mmHg at rest to 90 ± 6 mmHg (P < 0.01) during contractions of 50% MVC. At all contraction intensities, blood pressure remained elevated during PEI, but MSNA returned to pre-contraction levels, indicating that the metaboreflex does not contribute to the increase in MSNA to contracting muscle even at these high contraction intensities. [ABSTRACT FROM AUTHOR]

We previously demonstrated that muscle sympathetic nerve activity (MSNA) increases to contracting muscle as well as to non-contracting muscle, but this was only assessed during isometric exercise at ∼10% of maximum voluntary contraction (MVC). Given that high-intensity isometric contractions will release more metabolites, we tested the hypothesis that the metaboreflex is expressed in the contracting muscle during high-intensity but not low-intensity exercise. MSNA was recorded continuously via a tungsten microelectrode inserted percutaneously into the right common peroneal nerve in 12 participants, performing isometric dorsiflexion of the right ankle at 10, 20, 30, 40, and 50% MVC for 2 min. Contractions were immediately followed by 6 min of post-exercise ischemia (PEI); 6 min of recovery separated contractions. Cross-correlation analysis was performed between the negative-going sympathetic spikes of the raw neurogram and the ECG. MSNA increased as contraction intensity increased, reaching mean values (± SD) of 207 ± 210 spikes/min at 10% MVC (P = 0.04), 270 ± 189 spikes/min at 20% MVC (P < 0.01), 538 ± 329 spikes/min at 30% MVC (P < 0.01), 816 ± 551 spikes/min at 40% MVC (P < 0.01), and 1,097 ± 782 spikes/min at 50% MVC (P < 0.01). Mean arterial pressure also increased in an intensity-dependent manner from 76 ± 3 mmHg at rest to 90 ± 6 mmHg (P < 0.01) during contractions of 50% MVC. At all contraction intensities, blood pressure remained elevated during PEI, but MSNA returned to pre-contraction levels, indicating that the metaboreflex does not contribute to the increase in MSNA to contracting muscle even at these high contraction intensities.

Objective: To investigate whether the changes in the corticospinal excitability contribute to the anticipatory postural adjustments (APAs) in the lower limb muscles when performing the ballistic upper limb movement of the dart throwing. Methods: We examined the primary motor cortex (M1) excitability of the lower limb muscles [tibialis anterior (TA) and soleus (SOL) muscles] during the APA phase by using transcranial magnetic stimulation (TMS) in the healthy volunteers. The surface electromyography (EMG) of anterior deltoid, triceps brachii, biceps brachii, TA, and SOL muscles was recorded and the motor evoked potential (MEP) to TMS was recorded in the TA muscle along with the SOL muscle. TMS at the hotspot of the TA muscle was applied at the timings immediately prior to the TA onset. The kinematic parameters including the three-dimensional motion analysis and center of pressure (COP) during the dart throwing were also assessed. Results: The changes in COP and EMG of the TA muscle occurred preceding the dart throwing, which involved a slight elbow flexion followed by an extension. The correlation analysis revealed that the onset of the TA muscle was related to the COP change and the elbow joint flexion. The MEP amplitude in the TA muscle, but not that in the SOL muscle, significantly increased immediately prior to the EMG burst (100, 50, and 0 ms prior to the TA onset). Conclusion: Our findings demonstrate that the corticospinal excitability of the TA muscle increases prior to the ballistic upper limb movement of the dart throwing, suggesting that the corticospinal pathway contributes to the APA in the lower limb in a muscle-specific manner. [ABSTRACT FROM AUTHOR]

Objective: To investigate whether the changes in the corticospinal excitability contribute to the anticipatory postural adjustments (APAs) in the lower limb muscles when performing the ballistic upper limb movement of the dart throwing.Methods: We examined the primary motor cortex (M1) excitability of the lower limb muscles [tibialis anterior (TA) and soleus (SOL) muscles] during the APA phase by using transcranial magnetic stimulation (TMS) in the healthy volunteers. The surface electromyography (EMG) of anterior deltoid, triceps brachii, biceps brachii, TA, and SOL muscles was recorded and the motor evoked potential (MEP) to TMS was recorded in the TA muscle along with the SOL muscle. TMS at the hotspot of the TA muscle was applied at the timings immediately prior to the TA onset. The kinematic parameters including the three-dimensional motion analysis and center of pressure (COP) during the dart throwing were also assessed.Results: The changes in COP and EMG of the TA muscle occurred preceding the dart throwing, which involved a slight elbow flexion followed by an extension. The correlation analysis revealed that the onset of the TA muscle was related to the COP change and the elbow joint flexion. The MEP amplitude in the TA muscle, but not that in the SOL muscle, significantly increased immediately prior to the EMG burst (100, 50, and 0 ms prior to the TA onset).Conclusion: Our findings demonstrate that the corticospinal excitability of the TA muscle increases prior to the ballistic upper limb movement of the dart throwing, suggesting that the corticospinal pathway contributes to the APA in the lower limb in a muscle-specific manner.

Patients with diabetes display heightened blood pressure response to exercise, but the underlying mechanism remains to be elucidated. There is no direct evidence that insulin resistance (hyperinsulinemia or hyperglycemia) impacts neural cardiovascular control during exercise. We propose a novel paradigm in which hyperinsulinemia or hyperglycemia significantly influences neural regulatory pathways controlling the circulation during exercise in diabetes. [ABSTRACT FROM AUTHOR]

Emerging evidence suggests that type 2 diabetes (T2D) may impair the ability to properly adjust the circulation during exercise with augmented blood pressure (BP) and an attenuated contracting skeletal muscle blood flow (BF) response being reported. This review provides a brief overview of the current understanding of these altered exercise responses in T2D and the potential underlying mechanisms, with an emphasis on the sympathetic nervous system and its regulation during exercise. The research presented support augmented sympathetic activation, heightened BP, reduced skeletal muscle BF, and impairment in the ability to attenuate sympathetically mediated vasoconstriction (i.e., functional sympatholysis) as potential drivers of neurovascular dysregulation during exercise in T2D. Furthermore, emerging evidence supporting a contribution of the exercise pressor reflex and central command is discussed along with proposed future directions for studies in this important area of research.

Muscle fatigue induced by voluntary exercise, which requires central motor drive, causes central fatigue that impairs endurance performance of a different, nonfatigued muscle. This study investigated the impact of quadriceps fatigue induced by electrically induced (no central motor drive) contractions on single-leg knee-extension (KE) performance of the subsequently exercising ipsilateral quadriceps. On two separate occasions, eight males completed constant-load (85% of maximal power-output) KE exercise to exhaustion. In a counterbalanced manner, subjects performed the KE exercise with no pre-existing quadriceps fatigue in the contralateral leg on one day (No-PreF), whereas on the other day, the same KE exercise was repeated following electrically induced quadriceps fatigue in the contralateral leg (PreF). Quadriceps fatigue was assessed by evaluating pre- to postexercise changes in potentiated twitch force (ΔQtw,pot; peripheral fatigue), and voluntary muscle activation (ΔVA; central fatigue). As reflected by the 57 ± 11% reduction in electrically evoked pulse force, the electrically induced fatigue protocol caused significant knee-extensors fatigue. KE endurance time to exhaustion was shorter during PreF compared with No-PreF (4.6 ± 1.2 vs 7.7 ± 2.4 min; P < 0.01). Although ΔQtw,pot was significantly larger in No-PreF compared with PreF (−60% vs −52%, P < 0.05), ΔVA was greater in PreF (−14% vs −10%, P < 0.05). Taken together, electrically induced quadriceps fatigue in the contralateral leg limits KE endurance performance and the development of peripheral fatigue in the ipsilateral leg. These findings support the hypothesis that the crossover effect of central fatigue is mainly mediated by group III/IV muscle afferent feedback and suggest that impairments associated with central motor drive may only play a minor role in this phenomenon. [ABSTRACT FROM AUTHOR]

Emerging evidence suggests that type 2 diabetes (T2D) may impair the ability to properly adjust the circulation during exercise with augmented blood pressure (BP) and an attenuated contracting skeletal muscle blood flow (BF) response being reported. This review provides a brief overview of the current understanding of these altered exercise responses in T2D and the potential underlying mechanisms, with an emphasis on the sympathetic nervous system and its regulation during exercise. The research presented support augmented sympathetic activation, heightened BP, reduced skeletal muscle BF, and impairment in the ability to attenuate sympathetically mediated vasoconstriction (i.e., functional sympatholysis) as potential drivers of neurovascular dysregulation during exercise in T2D. Furthermore, emerging evidence supporting a contribution of the exercise pressor reflex and central command is discussed along with proposed future directions for studies in this important area of research. [ABSTRACT FROM AUTHOR]

Our laboratory has reported with near-infrared spectroscopy (NIRS) that prefrontal oxygenated-hemoglobin concentration (Oxy-Hb), measured as index of regional cerebral blood flow, increased before and at the onset of arbitrary (i.e., noncued) ergometer exercise in a laboratory environment. In the current study, we hypothesized that naturally occurring over-ground locomotion, despite “very light” motor effort, as indicated by a Borg scale of 8.0 ± 0.3, likewise causes preexercise activation of the prefrontal cortex. Using wireless NIRS, we examined in this study how early and to what extent prefrontal activity changed before the onset of arbitrary walking in 13 subjects. Prefrontal Oxy-Hb increased 2 s before the onset of arbitrary walking, and the increased Oxy-Hb reached a peak at 5 s from walking onset. The preexercise and initial increase in prefrontal Oxy-Hb was absent when over-ground walking was forced to start by cue. The difference in the Oxy-Hb response between arbitrary and cued start, which was considered to be related to central command, became significant 2 s before walking onset, preceding the difference in the heart rate (HR) response by 8 s. This demonstrated a positive relationship with the HR difference in 69% of subjects. Imagery of arbitrary walking was, likewise, able to increase prefrontal oxygenation to the same extent as actual walking. Thus, it is likely that prefrontal oxygenation increases before the onset of naturally occurring walking in daily life, despite “very light” effort. The increased prefrontal oxygenation may contribute at least partly to cardiac adjustment, synchronized with the beginning of motor performance. NEW & NOTEWORTHY We found using wireless near-infrared spectroscopy that prefrontal oxygenation increased before the onset of arbitrary over-ground walking, whereas the preexercise increase was absent when walking was suddenly started by cue. The difference in prefrontal oxygenation between start modes (considered related to central command) preceded heart rate response variances and demonstrated a positive relationship with the difference in heart rate. The central command-related prefrontal activity may contribute to cardiac adjustment, synchronized with the beginning of over-ground walking. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?When performing skilful hand movement, motor command descends especially towards distal arm muscles. Does central command evoke a vascular response selectively in the distal arm muscles during skilful hand movement?What is the main finding and its importance?We found, using near‐infrared spectroscopy, that unilateral skilful hand movement evoked a greater increase in oxygenation of the contralateral forearm muscle compared with that of the upper arm muscles. Mental imagery of the hand movement also increased oxygenation of the forearm muscle. These findings suggest that central command might contribute to the vasodilator response in the non‐contracting forearm muscle during contralateral skilful hand movement. The human hand is a special organ to perform skilful movement in daily life. To meet metabolic demands of the working distal arm muscles, central command might evoke neurogenic vasodilatation in the muscles. Based on our previous demonstration that a centrally generated vasodilator signal is transmitted bilaterally to skeletal muscles during exercise, centrally induced vasodilatation might occur in the non‐contracting distal arm muscles during contralateral skilful hand movement. To examine this possibility, we used near‐infrared spectroscopy to measure the relative concentrations of oxygenated haemoglobin (Oxy‐Hb; as an index of regional blood flow) in the non‐contracting arm muscles during skilful hand movement (two‐ball rotation) in 22 subjects. Two‐ball rotation increased Oxy‐Hb of both forearm and upper arm muscles, with little changes in perfusion pressure and cardiac output. The increased Oxy‐Hb was greater in the forearm muscle than in the upper arm muscles. The increased Oxy‐Hb of the forearm muscle during two‐ball rotation was greater than that during one‐armed cranking performed with no load. Mental imagery of two‐ball rotation increased Oxy‐Hb of the forearm and biceps muscles. The increases in Oxy‐Hb of both forearm and upper arm muscles during two‐ball rotation were reduced by decreasing the level of task difficulty. Intravenous administration of atropine attenuated the increases in Oxy‐Hb of the arm muscles during two‐ball rotation. It is likely that contralateral skilful hand movement evokes a selective increase in Oxy‐Hb of the non‐contracting forearm muscle via a sympathetic cholinergic mechanism and that the increase in oxygenation might be mediated, at least in part, by central command. [ABSTRACT FROM AUTHOR]

Securing large areas specifically establishments of national importance like military areas, nuclear site or parliament etc. from unauthorized intrusion is difficult, complex and costly. In this paper, we propose Integrated Peripheral Security System for different areas based on specific data rate exchange. This system overcomes the limitations of conventional security systems. Data rate based peripheral security system has been confined to local command unit formerly. In the proposed system, central authority can visualize, control and update the security information on local command, and provide a cost-effective solution compared to existing systems. [ABSTRACT FROM AUTHOR]

In this study, the subjects were asked to track the low-frequency rhythm of amplitude-modulated acoustic white noise in the series that required the varying degrees of periodic concentration of sensory and motor attention. We measured heart rate variability (HRV), frequency and depth of chest excursions, blood flow perfusion in the skin of the wrist and fingertip, and their spectral characteristics. The study included women and men aged 18–25 years with normal blood pressure and without skin disorders, cardiovascular or respiratory diseases. It has been found that mental activity in the form of periodic concentration of sensory and motor attention in combination with arbitrary periodic muscular activity has a significant effect on the rhythmic structure of oscillations in the central and peripheral components of the cardiovascular system. For HRV, the dependence of the amplitude of induced oscillations on the frequency of exposure has resonant properties and is described by a bell-shaped curve with a maximum in the range of 0.07–0.1 Hz. For the skin blood flow, the frequency dependence has a non-linear nearly S-shaped pattern. We suppose that induced oscillations of the microcirculatory blood flow in the skin under conditions of periodic concentration of attention are mainly due to the central modulation of the neurogenic (sympathetic) mechanisms of the vascular tone. [ABSTRACT FROM AUTHOR]

Central command (CC) and the exercise pressor reflex (EPR) regulate blood pressure during exercise. We previously demonstrated that experimental stimulation of the CC and EPR pathways independently contribute to the exaggerated pressor response to exercise in hypertension. It is known that CC and EPR modify one another functionally. Whether their interactive relationship is altered in hypertension, contributing to the generation of this potentiated blood pressure response, remains unknown. To address this issue, the pressor response to activation of the CC pathway with and without concurrent stimulation of the EPR pathway, and vice versa, was examined in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. In decerebrated, paralyzed animals, activation of the CC pathway was evoked by electrical stimulation of the mesencephalic locomotor region (MLR; 20–50 μA in 10-μA steps). Electrical stimulation of the sciatic nerve (SN, 3, 5, and 10 × motor threshold; MT) was used to activate hindlimb afferents known to carry EPR sensory information. In both WKY and SHR, the algebraic sum of the pressor responses to individual stimulation of the MLR and SN were greater than when both inputs were stimulated simultaneously. Although the blood pressure response to a constant level of SN stimulation was not significantly affected by concurrent MLR stimulation at variable intensities, the pressor response to a constant level of MLR simulation was significantly attenuated by concurrent SN stimulation in WKY but not in SHR. These findings suggest the interactive relationship between CC and the EPR is inhibitory in nature in both WKY and SHR. However, the neural occlusion between these central and peripheral pressor mechanisms is attenuated in hypertension.

During both static and dynamic exercise hypertensive subjects can experience robust increases in arterial pressure to such an extent that heavy exercise is often not recommended in these patients due to the dangerously high levels of blood pressure sometimes observed. Currently, the mechanisms mediating this cardiovascular dysfunction during exercise in hypertension are not fully understood. The major reflexes thought to mediate the cardiovascular responses to exercise in normotensive healthy subjects are central command, arterial baroreflex and responses to stimulation of skeletal muscle mechano-sensitive and metabo-sensitive afferents. This review will summarize our current understanding of the roles of these reflexes and their interactions in mediating the altered cardiovascular responses to exercise observed in hypertension. We conclude that much work is needed to fully understand the mechanisms mediating excessive pressor response to exercise often seen in hypertensive patients.

The cardiovascular responses to exercise are potentiated in patients with type 2 diabetes mellitus (T2DM). However, the underlying mechanisms causing this abnormality remain unknown. Central command (CC) and the exercise pressor reflex (EPR) are known to contribute significantly to cardiovascular control during exercise. Thus these neural signals are viable candidates for the generation of the abnormal circulatory regulation in this disease. We hypothesized that augmentations in CC as well as EPR function contribute to the heightened cardiovascular responses during exercise in T2DM. To test this hypothesis, changes in mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) in response to electrical stimulation of mesencephalic locomotor region (MLR), a putative component of the central command pathway, and activation of the EPR, evoked by electrically induced hindlimb muscle contraction, were examined in decerebrate animals. Sprague-Dawley rats were given either a normal diet (control) or a high-fat diet (14-16 wk) in combination with two low doses (35 mg/kg week 1, 25 mg/kg week 2) of streptozotocin (T2DM). The changes in MAP and RSNA responses to MLR stimulation were significantly greater in T2DM compared with control (2,739 ± 123 vs. 1,298 ± 371 mmHg/s, 6,326 ± 1,621 vs. 1,390 ± 277%/s, respectively, P < 0.05). Similarly, pressor and sympathetic responses to activation of the EPR in diabetic animals were significantly augmented compared with control animals (436 ± 74 vs. 134 ± 44 mmHg/s, 645 ± 135 vs. 139 ± 65%/s, respectively, P < 0.05). These findings provide the first evidence that CC and the EPR may generate the exaggerated rise in sympathetic activity and blood pressure during exercise in T2DM. [ABSTRACT FROM AUTHOR]

The arterial baroreflex (ABR) resets during exercise in an intensity-dependent manner to operate around a higher blood pressure with maintained sensitivity. This review provides a historical perspective of ABR resetting and the involvement of other neural reflexes in mediating exercise resetting. Furthermore, we discuss potential underlying signaling mechanisms that may contribute to exercise ABR resetting in physiological and pathophysiological conditions. [ABSTRACT FROM AUTHOR]

We have previously shown that the increase in muscle sympathetic nerve activity (MSNA) to contracting muscle during sustained isometric exercise is due primarily to central command and that contracting muscle does not express a metaboreceptor-driven increase in MSNA. Here we tested the hypothesis that MSNA increases to the contracting muscle also during rhythmic isotonic exercise, in which muscle metabolites will not accumulate because the contraction is performed without external load. MSNA was recorded from the common peroneal nerve in 10 participants, and negative-going sympathetic spikes were extracted during 50 cycles of sinusoidal (0.15 Hz) isotonic dorsiflexions of the ipsilateral or contralateral ankle. Electromyographic activity (EMG) was recorded from the tibialis anterior muscle on both sides. Cross-correlation analysis between MSNA and EMG revealed a marked cyclic modulation of MSNA to the contracting (ipsilateral) muscle. This modulation, in which MSNA increased during the contraction phase, was three times greater than that to the noncontracting muscle (modulation index = 27.4 ± 3.2% vs. 9.2 ± 1.5%; P < 0.002). There were no differences in either the intensity or the magnitude of modulation of EMG during ipsilateral and contralateral contractions. We conclude that central command increases MSNA to the contracting muscle during rhythmic isotonic exercise. [ABSTRACT FROM AUTHOR]

The present study examined the effect of muscle metaboreflex on blood flow in different cerebral arteries. Eleven healthy participants performed isometric, one-leg knee extension at 30% maximal voluntary contraction for 2 min. Activated muscle metaboreflex was isolated for 2 min by post-exercise muscle ischemia (PEMI). The contralateral internal carotid (ICA), vertebral (VA), and ipsilateral external carotid arteries (ECA) blood flows were evaluated using Doppler ultrasound. The ICA blood flow increased at the beginning of exercise (P  = 0.004) but returned to the baseline level at the end of exercise (P  = 0.055). In contrast, the VA blood flow increased and it was maintained until the end of the exercise (P = 0.011), while the ECA blood flow gradually increased throughout the exercise (P  = 0.001). These findings indicate that isometric exercise causes a heterogeneous cerebral blood flow response in different cerebral arteries. During PEMI, the conductance of the VA as well as that of the ICA was significantly lower compared with the baseline value (P  = 0.020 and P  = 0.032, at PEMI90), while the conductance of the ECA was not different from the baseline (P  = 0.587), suggesting that the posterior and anterior cerebral vasculature were similarly affected during exercise by activation of muscle metaboreceptors, but not in the non-cerebral artery. Since ECA branches from ICA, the balance in the different influence of muscle metaboreflex on ECA (vasodilation via exercise-induced hypertension) and ICA (vasoconstriction) may contribute to the decrease in ICA blood flow at the end of isometric exercise. [ABSTRACT FROM AUTHOR]

Central command (CC) and the exercise pressor reflex (EPR) regulate blood pressure during exercise. We previously demonstrated that experimental stimulation of the CC and EPR pathways independently contribute to the exaggerated pressor response to exercise in hypertension. It is known that CC and EPR modify one another functionally. Whether their interactive relationship is altered in hypertension, contributing to the generation of this potentiated blood pressure response, remains unknown. To address this issue, the pressor response to activation of the CC pathway with and without concurrent stimulation of the EPR pathway, and vice versa, was examined in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. In decerebrated, paralyzed animals, activation of the CC pathway was evoked by electrical stimulation of the mesencephalic locomotor region (MLR; 20–50 μA in 10-μA steps). Electrical stimulation of the sciatic nerve (SN, 3, 5, and 10 × motor threshold; MT) was used to activate hindlimb afferents known to carry EPR sensory information. In both WKY and SHR, the algebraic sum of the pressor responses to individual stimulation of the MLR and SN were greater than when both inputs were stimulated simultaneously. Although the blood pressure response to a constant level of SN stimulation was not significantly affected by concurrent MLR stimulation at variable intensities, the pressor response to a constant level of MLR simulation was significantly attenuated by concurrent SN stimulation in WKY but not in SHR. These findings suggest the interactive relationship between CC and the EPR is inhibitory in nature in both WKY and SHR. However, the neural occlusion between these central and peripheral pressor mechanisms is attenuated in hypertension. [ABSTRACT FROM AUTHOR]

During both static and dynamic exercise hypertensive subjects can experience robust increases in arterial pressure to such an extent that heavy exercise is often not recommended in these patients due to the dangerously high levels of blood pressure sometimes observed. Currently, the mechanisms mediating this cardiovascular dysfunction during exercise in hypertension are not fully understood. The major reflexes thought to mediate the cardiovascular responses to exercise in normotensive healthy subjects are central command, arterial baroreflex and responses to stimulation of skeletal muscle mechano-sensitive and metabo-sensitive afferents. This review will summarize our current understanding of the roles of these reflexes and their interactions in mediating the altered cardiovascular responses to exercise observed in hypertension. We conclude that much work is needed to fully understand the mechanisms mediating excessive pressor response to exercise often seen in hypertensive patients. [ABSTRACT FROM AUTHOR]

The paper analyses the circumstances in which the incumbents of the office of the logothetes tou dromou operated in the first century of this post’s existence. It concludes that in the 8th century the logothetes tou dromou was usually recruited from military ranks and that he could also wield military authority. At this time the system of central command was not yet defined through specific functions, which certainly influenced the competences of leading Byzantine officials such as the logothetes tou dromou. [Project of the Serbian Ministry of Education, Science and Technological Development, Grant no. 177032: Tradicija, inovacija i identitet u vizantijskom svetu]

Sympathetic nerve activity (SNA) contributes appreciably to the control of physiological function, such that pathological alterations in SNA can lead to a variety of diseases. The goal of this review is to discuss the characteristics of SNA, briefly review the methodology that has been used to assess SNA and its control, and to describe the essential role of neurophysiological studies in conscious animals to provide additional insights into the regulation of SNA. Studies in both humans and animals have shown that SNA is rhythmic or organized into bursts whose frequency varies depending on experimental conditions and the species. These rhythms are generated by brainstem neurons, and conveyed to sympathetic preganglionic neurons through several pathways, including those emanating from the rostral ventrolateral medulla. Although rhythmic SNA is present in decerebrate animals (indicating that neurons in the brainstem and spinal cord are adequate to generate this activity), there is considerable evidence that a variety of supratentorial structures including the insular and prefrontal cortices, amygdala, and hypothalamic subnuclei provide inputs to the brainstem regions that regulate SNA. It is also known that the characteristics of SNA are altered during stress and particular behaviors such as the defense response and exercise. While it is a certainty that supratentorial structures contribute to changes in SNA during these behaviors, the neural underpinnings of the responses are yet to be established. Understanding how SNA is modified during affective responses and particular behaviors will require neurophysiological studies in awake, behaving animals, including those that entail recording activity from neurons that generate SNA. Recent studies have shown that responses of neurons in the central nervous system to most sensory inputs are context-specific. Future neurophysiological studies in conscious animals should also ascertain whether this general rule also applies to sensory signals that modify SNA.

Background: Repetitive experiences of certain stresses evoke feedforward cardiovascular responses via central command (CC)--central signals from the higher brain. However, it is unclear whether the anticipatory cardiovascular responses before pain stimulation occur after repetitive pain experiences and how nitrous oxide/oxygen inhalation (N 2 O), a sedative widely used in dentistry, affects the responses. We tested the hypothesis that the repetitive cold pressor test (CPT) alters the anticipatory cardiovascular responses, which are attenuated by N 2 O., Materials and Methods: Beat-to-beat systolic (SBP) and diastolic blood pressure (DBP), heart rate (HR), and finger arterial stiffness ( β -stiffness) were measured during the 5-min rest, 30-s countdown (CD) before CPT, 2-min CPT, and 3-min recovery (CPT [1st] ) in 15 young adults [age, 28 ± 4 years]. The same protocols were repeated randomly with the second CPT (CPT + CC) or placebo test (PLCB + CC)., Results: SBP and DBP increased from baseline in CPT [1st] and CPT + CC under room air (RA) and 40 % N 2 O, while SBP was lower under N 2 O than under RA in CPT [1st] . HR in CPT [1st] was lower under N 2 O than under RA. The change (Δ) in HR was smaller during CPT [1st] than during CPT + CC under N 2 O, and a similar trend was observed under RA. ΔSBP by CD was lower under N 2 O than under RA in CPT [1st] but not in CPT + CC. HR increased with CD in CPT + CC but not in CPT [1st] under both RA and N 2 O. β -stiffness increased by CD regardless of the pain experience, while it was lower under N 2 O., Conclusion: Repetitive pain experiences induce a feedforward HR increase. 40 % N 2 O decreases vascular stiffness, which may attenuate the anticipatory pressor response only when the feedforward HR increase does not exist., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors. Published by Elsevier Ltd.)

The cardiovascular response to exercise is largely determined by neurocirculatory control mechanisms that help to raise blood pressure and modulate vascular resistance which, in concert with regional vasodilatory mechanisms, promote blood flow to active muscle and organs. These neurocirculatory control mechanisms include a feedforward mechanism, known as central command, and three feedback mechanisms, namely, 1 ) the baroreflex, 2 ) the exercise pressor reflex, and 3 ) the arterial chemoreflex. The hemodynamic consequences of these control mechanisms result from their influence on the autonomic nervous system and subsequent alterations in cardiac output and vascular resistance. Although stimulation of the baroreflex inhibits sympathetic outflow and facilitates parasympathetic activity, central command, the exercise pressor reflex, and the arterial chemoreflex facilitate sympathetic activation and inhibit parasympathetic drive. Despite considerable understanding of the cardiovascular consequences of each of these mechanisms in isolation, the circulatory impact of their interaction, which occurs when various control systems are simultaneously activated (e.g., during exercise at altitude), has only recently been recognized. Although aging and cardiovascular disease (e.g., heart failure, hypertension) have both been recognized to alter the hemodynamic consequences of these regulatory systems, this review is limited to provide a brief overview on the action and interaction of neurocirculatory control mechanisms in health.