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 ...

We investigated the effects of brief leg cooling after moderate exercise on the cardiorespiratory responses to subsequent exercise in the heat. Following 40 min of ergometer cycling [65% peak oxygen uptake (VO(2peak))] at 35 degrees C (Ex. 1), seven male subjects [21.9 (1.1) years of age; 170.9 (1.9) cm height; 66.0 (2.0) kg body mass; 46.7 (2.0) ml kg(-1) min(-1) VO(2peak)] immersed their legs in 35 degrees C (control condition, CONT) or 20 degrees C (cooling condition, COOL) water for 5 min and then repeated the cycling (as before, but for 10 min) (Ex. 2). Just before Ex. 2, esophageal temperature ( T(es)) was lower in COOL than in CONT [36.9 (0.2) vs 37.5 (0.1) degrees C] ( P<0.01), as also were both mean skin temperature [33.9 (0.2) vs 35.2 (0.2) degrees C] ( P<0.01), and heart rate (HR) [93.2 (6.0) vs 102.7 (4.9) beats min(-1)] ( P<0.05). During Ex. 2, no differences between CONT and COOL were observed in oxygen uptake, arterial blood pressure, blood lactate concentration, or ratings of perceived exertion; however, T(es), skin temperature, and HR were lower in COOL than in CONT. Further, during the first 5 min of Ex. 2, minute ventilation was significantly lower in COOL than in CONT [50.3 (2.0) vs 53.4 (2.6) l min(-1)] ( P<0.01). These results suggest that brief leg cooling during the recovery period may be effective at reducing thermal and cardiorespiratory strain during subsequent exercise in the heat.

The purpose of this study was to determine whether the metabolic response and running performance during intermittent graded sprint running were affected by moderate hypobaric hypoxia (H; 2,500 m above sea level) in competitive middle-distance runners. Nine male runners performed intermittent graded sprint running until exhaustion, to evaluate the metabolic response and running performance in H and normobaric normoxia (N). The test constructed of incremental (25 m min(-1)) 20 s running bouts (4 degrees inclination) interspaced with 100 s recovery periods. Maximal running speed was not different between conditions [453 (7) m min(-1) vs. 458 (4) m min(-1) in N vs. H]. V(O2) at each speed was lower in H than N (ANOVA; P < 0.05). Although, oxygen deficit (D(O2)) at each speed was not different between N and H (ANOVA; P = 0.1), total accumulated D(O2) in all bouts was significantly higher in H than N [165 (10) ml kg(-1) in N and 173 (10) ml kg(-1) in H]. The ratio of D(O2).V(O2)(-1) was similar in all bouts, but higher in H than N. These results suggest that intermittent graded sprint running performance is not affected by moderate hypobaria despite a reduction in the energy supplied by aerobic metabolism due to a compensatory increase in the energy supplied by the anaerobic metabolism in competitive middle-distance runners.