by the ultrasound Doppler method), leg vascular conductance (LVC), mean arterial blood pressure (MAP), and heart rate (HR)] in humans. In 12 healthy subjects (10 men and 2 women), who performed sustained 1-min handgrip exercise at 50% maximal voluntary contraction followed immediately by an imposed postexercise muscle ischemia (PEMI), 5-s periods of neck pressure (NP; 50 mmHg) or neck suction (NS; Ϫ60 mmHg) were used to evaluate carotid baroreflex function both at rest (Con) and during PEMI. First, the decreases in LVC and LBF and the augmentation of MAP elicited by NP were all greater during PEMI than in Con (⌬LVC, Ϫ1.2 Ϯ 0.2 vs. Ϫ1.9 Ϯ 0.2 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; ⌬LBF, Ϫ97.3 Ϯ 11.2 vs. Ϫ177.0 Ϯ 21.8 ml/min; ⌬MAP, 6.7 Ϯ 1.2 vs. 11.5 Ϯ 1.4 mmHg, Con vs. PEMI; each P Ͻ 0.05). Second, in Con, NS significantly increased both LVC and LBF (⌬LVC, 0.9 Ϯ 0.2 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; ⌬LBF, 46.6 Ϯ 9.8 ml/min; significant change from baseline: each P Ͻ 0.05), and, whereas during PEMI no significant increases in LVC and LBF occurred during NS itself (⌬LVC, 0.2 Ϯ 0.1 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; ⌬LBF, 10.8 Ϯ 9.6 ml/min; each P Ͼ 0.05), a decrease was evident in each parameters at 5 s after the cessation of NS. Third, during PEMI, the decrease in MAP elicited by NS was smaller (⌬MAP, Ϫ8.4 Ϯ 1.0 vs. Ϫ5.8 Ϯ 0.4 mmHg, Con vs. PEMI; P Ͻ 0.05), and it recovered to its initial level more quickly after NS (vs. Con). Finally, however, the HR responses to NS and NP were not different between PEMI and Con. These results suggest that during muscle metaboreflex activation in humans, the arterial baroreflex dynamic effect on peripheral vascular conductance is modulated, as exemplified by 1) an augmentation of the NP-induced LVC decrease, and 2) a loss of the NS-induced LVC increase. skeletal muscle metaboreflex; carotid baroreflex; exercise DURING HEAVY EXERCISE, the arterial baroreflexes and the reflexes evoked by activation of those afferent nerve endings in the working skeletal muscles that are sensitive to metabolic changes (the so-called muscle metaboreflex) are hypothesized to be activated and, moreover, to interact in ways that lead to modulation of the primary cardiovascular reflex responses (6 -9, 15, 19, 20, 24, 25, 29, 31). Two types of interaction between these reflexes have been demonstrated to lead to such modulation. In the first type, the arterial baroreflexes act to oppose the pressor response elicited via the muscle metaboreflex (15,19,29,31). Evidence for this effect has been obtained during dynamic exercise in dogs (31) as well as during static handgrip exercise (29) and postexercise muscle ischemia (PEMI) in humans (15). The second type of interaction involves a modulation of arterial baroreflex function during muscle metaboreflex activation (6 -9, 20). However, these interactions (especially the second: viz. modulation of arterial baroreflex function by the muscle metaboreflex) and their consequences are not fully understood.Papelier et al. (20) found that during PEMI-induced muscle metaboreflex activation, the carotid sin...