We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflexes (as reflected by alterations in the dynamic responses shown by muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) in humans. In nine healthy subjects (eight male, one female) who performed a sustained 1 min handgrip exercise at 50 % maximal voluntary contraction followed by forearm occlusion, a 5 s period of neck pressure (NP) (30 and 50 mmHg) or neck suction (NS)(_30 and _60 mmHg) was used to evaluate carotid baroreflex function at rest (CON) and during post-exercise muscle ischaemia (PEMI). In PEMI (as compared with CON): (a) the augmentations in MSNA and MAP elicited by 50 mmHg NP were both greater; (b) MSNA seemed to be suppressed by NS for a shorter period, (c) the decrease in MAP elicited by NS was smaller, and (d) MAP recovered to its initial level more quickly after NS. However, the HR responses to NS and NP were not different between PEMI and CON. These results suggest that during muscle metaboreflex activation, the dynamic arterial baroreflex response is modulated, as exemplified by the augmentation of the MSNA response to arterial baroreflex unloading (i.e. NP) and the reduction in the suppression of MSNA induced by baroreceptor stimulation (i.e. NS).

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....

-To investigate local bloodflow regulation during orthostatic maneuvers, 10 healthy subjects were exposed to Ϫ20 and Ϫ40 mmHg lower body negative pressure (LBNP; each for 3 min) and to 60°head-up tilt (HUT; for 5 min). Measurements were made of blood flow in the brachial (BFbrachial) and femoral arteries (BF femoral) (both by the ultrasound Doppler method), heart rate (HR), mean arterial pressure (MAP), cardiac stroke volume (SV; by echocardiography), and left ventricular enddiastolic volume (LVEDV; by echocardiography). Comparable central cardiovascular responses (changes in LVEDV, SV, and MAP) were seen during LBNP and HUT. During Ϫ20 mmHg LBNP, Ϫ40 mmHg LBNP, and HUT, the following results were observed: 1) BFbrachial decreased by 51, 57, and 41%, and BFfemoral decreased by 40, 53, and 62%, respectively, 2) vascular resistance increased in the upper limb by 110, 147, and 85%, and in the lower limb by 76, 153, and 250%, respectively. The increases in vascular resistance were not different between the upper and lower limbs during LBNP. However, during HUT, the increase in the lower limb was much greater than that in the upper limb. These results suggest that, during orthostatic stimulation, the vascular responses in the limbs due to the cardiopulmonary and arterial baroreflexes can be strongly modulated by local mechanisms (presumably induced by gravitational effects). blood flow; orthostatic stress; baroreflex IT IS KNOWN THAT, DURING ORTHOSTATIC stress, peripheral vascular resistance and/or heart rate (HR) increase (mainly via cardiopulmonary and arterial baroreflexes), serving to maintain arterial blood pressure (1, 3-5, 7, 8, 17, 27, 36, 37, 39, 42, 44, 47). Furthermore, it has been suggested that, during orthostatic stress, differential vascular responses occur between the arms and legs (9, 12, 16). The proposed explanations for the latter phenomenon include differences in 1) "local" mechanisms stimulated by the increments in transmural pressure (11,12,18), 2) norepinephrine spillover (13), and 3) the effectiveness of ␣-or ␤-receptors (26). However, those mechanisms are not well understood.Various ways can be used to simulate orthostatic stress in humans. These include application of lower body negative pressure (LBNP) and head-up tilt (HUT), which are known to increase the pooling of blood in the lower body, leading to a decreased blood volume in the central circulation and a consequent unloading of cardiopulmonary and arterial baroreceptors. LBNP is usually applied with the subject in the horizontal posture, and the negative pressure affects mainly the superficial veins, less so the arteries, so arterial blood pressure is almost constant throughout the whole body. In contrast, during HUT, the arterial and venous pressures increase in proportion to the distance from the heart. Thus LBNP and HUT represent two possible ways of decreasing the central blood volume and enhancing sympathetic nervous activity, but they differ in the extent of the change in hydrostatic pressure (local pressure) in the dependent ...

It has frequently been demonstrated that prior heavy cycling exercise facilitates pulmonarẏ VO 2 kinetics at the onset of subsequent heavy exercise. This might be due to improved muscle perfusion via acidosis-induced vasodilating effects. However, it is difficult to measure the blood flow (BF) to the working muscles (via the femoral artery) during cycling exercise. We therefore selected supine knee extension (KE) exercise as an alternative, and investigated whether the fasterVO 2 kinetics in the 2nd bout was matched by proportionally faster BF kinetics to the exercising muscle. Nine healthy subjects (aged 21-44 years) volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate: 70-75% of peak power) separated by a 6-min baseline rest (EX1 to EX2). During the protocol, a pulsed Doppler ultrasound technique was utilized to continuously measure the BF in the right femoral artery. The protocol was repeated at least 6 times to characterize the precise kinetics. In agreement with previous studies using cycling exercise, theVO 2 kinetics in the 2nd bout were facilitated compared with that in the 1st bout [mean ± S.D. of the 'effective' time constant (τ ): EX1, 68.6 ± 15.9, versus EX2, 58.0 ± 14.4 s. Phase II-τ : EX1, 48.7 ± 9.0, versus EX2, 41.2 ± 13.3 s. Empirical index of the slow component (∆VO 2(6-3) ): EX1, 78 ± 44, versus EX2, 57 ± 36 ml min −1 (P < 0.05)]. However, no substantial difference was observed for the facilitation of the femoral artery BF response to the 1st and 2nd exercise bouts [i.e. the 'effective' τ of the femoral artery BF: EX1, 40.8 ± 16.9, versus EX2, 39.0 ± 17.1 s (P > 0.05)]. It was concluded that the faster pulmonaryVO 2 kinetics during heavy KE exercise following prior heavy exercise was not associated with a similar modulation in the BF to the working muscles.

We tested the hypothesis that peripheral vascular responses (in the lower and upper limbs) to application of lower body positive pressure (LBPP) are dependent on the posture of the subjects. We measured heart rate, stroke volume, mean arterial pressure, leg and forearm blood flow (using the Doppler ultrasound technique), and leg (LVC) and forearm (FVC) vascular conductance in 11 subjects (9 men, 2 women) without and with LBPP (25 and 50 mmHg) in supine and upright postures. Mean arterial pressure increased in proportion to increases in LBPP and was greater in supine than in upright subjects. Heart rate was unchanged when LBPP was applied to supine subjects but was reduced in upright ones. Leg blood flow and LVC were both reduced by LBPP in supine subjects [LVC: 4.8 (SD 4.0), 3.6 (SD 3.5), and 1.4 (SD 1.8) ml·min−1·mmHg−1 before LBPP and during 25 and 50 mmHg LBPP, respectively; P < 0.05] but were increased in upright ones [LVC: 2.0 (SD 1.2), 3.4 (SD 3.4), and 3.0 (SD 2.0) ml·min−1·mmHg−1, respectively; P < 0.05]. Forearm blood flow and FVC both declined when LBPP was applied to supine subjects [FVC: 1.3 (SD 0.6), 1.0 (SD 0.4), and 0.9 (SD 0.6) ml· min−1·mmHg−1, respectively; P < 0.05] but remained unchanged in upright ones [FVC: 0.7 (SD 0.4), 0.7 (SD 0.4), and 0.6 (SD 0.5) ml·min−1·mmHg−1, respectively]. Together, these findings indicate that the leg vascular response to application of LBPP is posture dependent and that the response differs in the lower and upper limbs when subjects assume an upright posture.

We tested the hypothesis that in humans, carotid-baroreflex dynamic responses (evaluated by examining the time course of the carotid-baroreflex-induced alterations in muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) would be altered during mild orthostatic stress in ways that serve to limit orthostatic hypotension. In 12 healthy subjects (10 male, 2 female), 5-s periods of neck pressure (NP) (50 mmHg) and neck suction (NS) (− 60 mmHg) were used to evaluate carotid baroreflex function at rest (CON) and during lower body negative pressure (LBNP) (−15 mmHg). During LBNP (as compared with CON) (a) the augmentations in MSNA and MAP elicited by NP were greater, (b) the NS-induced period of MSNA suppression was, if anything, shorter, (c) the peak decrement in MAP elicited by NS, although not different in amplitude, occurred earlier and recovered to its initial level more quickly after NS, and (d) the HR responses to NP and NS were greater. These results suggest that during mild orthostatic stress, carotid-baroreflex dynamic responses are modulated in ways that should help maintain blood pressure and limit orthostatic hypotension. The nature of the mechanisms involved in blood pressure regulation under conditions of orthostatic stress is an important research issue in physiology, especially in humans who usually adopt an upright posture (Rowell, 1986). With the body in an upright posture, blood in the central circulation is pooled in the peripheral veins, thus decreasing the cardiac filling pressure and leading to a decrease in arterial blood pressure. Increases in peripheral vascular resistance and heart rate (HR), major cardiovascular adjustments to orthostatic stress mediated by the autonomic nervous system (Rowell, 1986), form part of the reflex response patterns elicited via the carotid sinus and aortic baroreceptors (arterial baroreflex) and via stretch receptors in the cardiopulmonary regions (cardiopulmonary baroreflex) (Zoller et al. 1972;Johnson et al.

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It has frequently been demonstrated that prior high-intensity exercise facilitates pulmonary oxygen uptake [Formula: see text] response at the onset of subsequent identical exercise. To clarify the roles of central O(2) delivery and/or peripheral O(2) extraction in determining this phenomenon, we investigated the relative contributions of cardiac output (CO) and arteriovenous O(2) content difference [Formula: see text] to the [Formula: see text] transient during repeated bouts of high-intensity knee extension (KE) exercise. Nine healthy subjects volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate 70-75% of peak power) separated by 6 min of rest. Throughout the protocol, continuous-wave Doppler ultrasound was used to measure beat-by-beat CO (i.e., via simultaneous measurement of stroke volume and the diameter of the arterial aorta). The phase II [Formula: see text] response was significantly faster and the slow component (phase III) was significantly attenuated during the second KE bout compared to the first. This was a result of increased CO during the first 30 s of exercise: CO contributing to 100 and 56% of the [Formula: see text] speeding at 10 and 30 s, respectively. After this, the contribution of [Formula: see text] became increasingly more predominant: being responsible to an estimated 64% of the [Formula: see text] speeding at 90 s, which rose to 100% by 180 s. This suggests that, while both CO and [Formula: see text] clearly interact to determine the [Formula: see text] response, the speeding of [Formula: see text] kinetics by prior high-intensity KE exercise is predominantly attributable to increases in [Formula: see text].