Carotid baroreflex regulation of sympathetic nerve activity during dynamic exercise in humans

Fadel, Paul J.; Ogoh, Shigehiko; Watenpaugh, Donald E.; Wasmund, Wendy L.; Olivencia‐Yurvati, Albert H.; Smith, Michael L.; Raven, Peter B.

doi:10.1152/ajpheart.2001.280.3.h1383

Cited by 98 publications

(120 citation statements)

References 29 publications

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“…If we then add the average resting value observed in hypoxia to that curve, we can see that the subjects operated in hypoxia on the same baroreflex curve as in normoxia, with a displacement of the operating point along the curve toward the threshold. This is a result of the decrease in P induced by peripheral vasodilation, to which the subjects responded with an increase in f H , supporting the notion that peripheral vascular changes play a significant role in the baroreflex response of resting humans (17,35). If indeed hypoxemia induces vasodilation in peripheral circulation via ␤ 2 -sympathetic stimulation, then we can propose a role for peripheral chemoreflexes in the displacement of the baroreflex operating point in hypoxia.…”

Section: Discussionsupporting

confidence: 72%

Phase I dynamics of cardiac output, systemic O₂ delivery, and lung O₂ uptake at exercise onset in men in acute normobaric hypoxia

Lador¹,

Tam²,

Kenfack³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6 Ϯ 3.4 yr, 82.1 Ϯ 13.7 kg, maximal aerobic power 330 Ϯ 67 W), we determined beat-by-beat cardiac output (Q ), oxygen delivery (Q a O 2 ), and breathby-breath lung oxygen uptake (V O2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O 2 ϭ 0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Q st, by model flow) and heart rate (fH, electrocardiography), and Q a O 2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state f H and Q were higher, and Qst and V O2 were unchanged. Q a O 2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A 1) for V O2 was unchanged. For fH, Q and Q a O 2 , A1 was lower. Phase I time constant (1) for Q a O 2 and V O2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Q st kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A 1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Q st. Thus the dual origin of the phase I of Q and Q a O 2 , neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed. cardiovascular response ALTHOUGH OUR KNOWLEDGE of the central (neural) control of the cardiovascular system at the exercise steady state is quite well established (19,42,57), how the circulatory readjustments upon exercise onset occur and match the increase in pulmonary oxygen uptake (V O 2 ) is less understood, as are the mechanisms underlying this matching. The kinetics of V O 2 at exercise onset were seen for a long time as reflecting essentially the metabolic adaptations in the working muscles (15,31,33). Some authors, however, soon identified two components of the V O 2 kinetics: 1) a rapid, almost immediate phase (phase I) (5, 54, 55), which they attributed to an immediate increase in cardiac output (Q ) at exercise start; and 2) a subsequent slower phase (phase II), to which they restricted the influence of muscle metabolic adjustments. The strongest support to this view came from the demonstration that the kinetics of Q (12, 13, 16, 60) and arterial O 2 flow (Q a O 2 ) (27) are very rapid.The concept of a close correspondence between V O 2 and muscle O 2 consumption was further undermined by the recent demonstration that, upon the onset of light exercise, the V O 2 kinetics are faster than the kinetics of muscle O 2 consumption estimated from the monoexponential decrease in phosphocreatine concentration (7,14,43). This would imply dissociation of the kinetics of V O 2 and muscle O 2 consumption, which should respond to different control mechanisms.Our postulate is that the V O 2 kinetics are dictated by ...

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Section: Discussionsupporting

confidence: 72%

Phase I dynamics of cardiac output, systemic O₂ delivery, and lung O₂ uptake at exercise onset in men in acute normobaric hypoxia

Lador¹,

Tam²,

Kenfack³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Although a linear relationship between spontaneous fluctuations in MSNA and DAP has been demonstrated in previous studies (10,11,33), spontaneous blood pressure fluctuations are not particularly large and so the baroreflex stimulus response range that can be examined by this method is limited (within 20 mmHg). Although this is a narrower range than those obtained with other methods, such as the neck chamber technique (3,8,22,37) or invasive pharmacological manipulation (6, 9), a 20-mmHg change in blood pressure is within the physiological range and should be a good reflection of the arterial baroreflex control of MSNA under physiological conditions. Furthermore, to investigate the reflex effect elicited when two or more inputs are summed (e.g., baroreceptor and muscle metaboreceptor inputs in this study) it is important to use inputs that are small enough not to cause saturation of the output because of any inherent limitation in the effector responses of the system (25).…”

Section: Discussionmentioning

confidence: 81%

“…Total activity is dependent on both burst number and burst strength and represents the level of MSNA more accurately than either of these variables (26,30,32,36). It has been reported that during exercise, the arterial baroreflex operating pressure is reset to a higher pressure than at rest (3,10,22,23,24). Central command, the muscle mechanoreflex, and the muscle metaboreflex have been regarded as possible mechanisms responsible for this resetting (9,10,16,17,(22)(23)(24).…”

Section: Discussionmentioning

confidence: 99%

Modulation of arterial baroreflex control of muscle sympathetic nerve activity by muscle metaboreflex in humans

Ichinose¹,

Saito²,

Wada³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Ichinose, Masashi, Mitsuru Saito, Hiroyuki Wada, Asami Kitano, Narihiko Kondo, and Takeshi Nishiyasu. Modulation of arterial baroreflex control of muscle sympathetic nerve activity by muscle metaboreflex in humans. Am J Physiol Heart Circ Physiol 286: H701-H707, 2004; 10.1152/ajpheart.00618.2003.-We aimed to investigate the interaction [with respect to the regulation of muscle sympathetic nerve activity (MSNA) and blood pressure] between the arterial baroreflex and muscle metaboreflex in humans. In 10 healthy subjects who performed a 1-min sustained handgrip exercise at 50% maximal voluntary contraction followed by forearm occlusion, arterial baroreflex control of MSNA (burst incidence and strength and total activity) was evaluated by analyzing the relationship between beatby-beat spontaneous variations in diastolic arterial blood pressure (DAP) and MSNA both during supine rest (control) and during postexercise muscle ischemia (PEMI). During PEMI (vs. control), 1) the linear relationship between burst incidence and DAP was shifted rightward with no alteration in sensitivity, 2) the linear relationship between burst strength and DAP was shifted rightward and upward with no change in sensitivity, and 3) the linear relationship between total activity and DAP was shifted to a higher blood pressure and its sensitivity was increased. The modification of the control of total activity that occurs in PEMI could be a consequence of alterations in the baroreflex control of both MSNA burst incidence and burst strength. These results suggest that the arterial baroreflex and muscle metaboreflex interact to control both the occurrence and strength of MSNA bursts. skeletal muscle metaboreflex; arterial blood pressure; exercise STATIC AND DYNAMIC EXERCISE is accompanied by increases in arterial blood pressure, heart rate (HR), and sympathetic nerve activity (SNA). These cardiovascular responses are hypothesized to be mediated by a number of factors: 1) central command (24), 2) feedback mechanisms via the afferent nerves (group III and IV fibers) arising from the working skeletal muscles (16,17,23), and 3) arterial and cardiopulmonary baroreflexes (23,24). It has been hypothesized that during heavy exercise the arterial baroreflexes and muscle metaboreflexes are both activated and that they interact to regulate the responses shown by blood pressure, HR, and SNA levels (8-10, 18, 21, 22, 29, 31).Two types of interaction between arterial baroreflexes and muscle metaboreflexes in the control of cardiovascular responses have been demonstrated. The first involves arterial baroreflexes opposing the pressor response elicited via the muscle metaboreflexes (18,21,29,31). Evidence for this opposing effect of the arterial baroreflexes has been obtained during dynamic exercise in dogs (31) as well as during static handgrip exercise (29) and postexercise muscle ischemia (PEMI) in humans (18). The second type of interaction is a modulation of arterial baroreflex function during muscle metaboreflex activation (8-10, 22). Indeed, Papelier et al....

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“…Full carotid-cardiac baroreflex function curves were derived at rest and during moderate-intensity cycling, as previously described (14,30,36). Briefly, following instrumentation for HR and blood pressure measurements, subjects were fitted with a malleable lead neck collar that encircled the anterior 2/3 of the neck for the application of NP and NS.…”

Section: Methodsmentioning

confidence: 99%

Influence of age on cardiac baroreflex function during dynamic exercise in humans

Fisher¹,

Ogoh²,

Ahmed³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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We investigated the influence of aging on cardiac baroreflex function during dynamic exercise in seven young (22 Ϯ 1 yr) and eight older middle-aged (59 Ϯ 2 yr) healthy subjects. Carotid-cardiac baroreflex function was assessed at rest and during moderate-intensity steadystate cycling performed at 50% heart rate reserve (HRR). Five-second pulses of neck pressure and neck suction from ϩ40 to Ϫ80 Torr were applied to determine the operating point gain (GOP) and maximal gain (GMAX) of the full carotid-cardiac baroreflex function curve and examine baroreflex resetting during exercise. At rest, mean arterial pressure (MAP) and heart rate were similar between the younger and older subjects. In contrast, the resting GOP and GMAX were significantly lower in the older subjects. The increase in MAP from rest to exercise was greater in the older subjects (⌬ ϩ20 Ϯ 2 older vs. ⌬ ϩ6 Ϯ 3 younger mmHg; P Ͻ 0.001). However, the GOP was similar in both groups during exercise because of a reduction in the younger subjects. In contrast, GMAX was unchanged from rest and therefore remained lower in older subjects (Ϫ0.19 Ϯ 0.05 older vs. Ϫ0.42 Ϯ 0.05 younger beats ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; 50% HRR; P Ͻ 0.001). Furthermore, exercise resulted in an upward and rightward resetting of the cardiac baroreflex function curve in both groups. Collectively, these findings suggest that the cardiac baroreflex function curve appropriately resets during exercise in older subjects but operates at a reduced GMAX primarily because of age-related reductions in carotidcardiac control manifest at rest. arterial baroreceptors; aging; heart rate HEALTHY AGING HAS BEEN associated with impaired arterial baroreflex control of heart rate (HR; see Refs. 10,17,25,33), vasomotor tone (8), and blood pressure (23) under resting conditions. However, little is known about how aging alters baroreflex function during dynamic exercise. Importantly, alterations noted at rest cannot simply be extrapolated to exercise because peripheral feedback from skeletal muscle (i.e., exercise pressor reflex; EPR) and feedforward central neural inputs (i.e., central command) modulate arterial baroreflex control during exercise, influencing reflex sensitivity and also contributing to the resetting of the baroreflex function curve (13,27). Moreover, EPR function may be attenuated in older subjects (24), thereby leading to decreases in input from the EPR to the baroreflex, potentially altering baroreflex sensitivity and resetting characteristics. In addition, it is possible that an agerelated enhancement of central command may also modify the baroreflex during exercise (5). Thus it is important to consider the influence of healthy aging on baroreflex function and resetting during dynamic exercise. This is particularly relevant from a clinical standpoint since older subjects are increasingly being encouraged to exercise and decreases in baroreflex control of HR can increase the occurrence of ventricular arrhythmias during physical activity (1,38).Limited studies have attempted to investigate ag...

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Carotid baroreflex regulation of sympathetic nerve activity during dynamic exercise in humans

Cited by 98 publications

References 29 publications

Phase I dynamics of cardiac output, systemic O₂ delivery, and lung O₂ uptake at exercise onset in men in acute normobaric hypoxia

Phase I dynamics of cardiac output, systemic O₂ delivery, and lung O₂ uptake at exercise onset in men in acute normobaric hypoxia

Modulation of arterial baroreflex control of muscle sympathetic nerve activity by muscle metaboreflex in humans

Influence of age on cardiac baroreflex function during dynamic exercise in humans

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Carotid baroreflex regulation of sympathetic nerve activity during dynamic exercise in humans

Cited by 98 publications

References 29 publications

Phase I dynamics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men in acute normobaric hypoxia

Phase I dynamics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men in acute normobaric hypoxia

Modulation of arterial baroreflex control of muscle sympathetic nerve activity by muscle metaboreflex in humans

Influence of age on cardiac baroreflex function during dynamic exercise in humans

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Phase I dynamics of cardiac output, systemic O₂ delivery, and lung O₂ uptake at exercise onset in men in acute normobaric hypoxia

Phase I dynamics of cardiac output, systemic O₂ delivery, and lung O₂ uptake at exercise onset in men in acute normobaric hypoxia