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5 for drug effect). Leg blood flow in the active leg decreased at a greater rate during recovery on the control day (?601 �� 141 ml min?1 h?1) versus the blockade find more day (?289 �� 141 ml min?1 h?1; P day (P= 0.14 for drug effect). Likewise, active leg vascular conductance was 1.39 �� 0.38 ml min?1 mmHg?1 lower following exercise on the blockade day when compared with the control day (P Doxorubicin datasheet exercise (Table 2). Leg blood flow (control, 337 �� 35 versus blockade, 365 �� 60 ml min?1; P= 0.5) was similar between study days prior to resistance exercise (Fig. 2). Likewise, leg vascular conductance (control, 4.29 �� 0.46 versus blockade, 4.58 �� 0.73 ml min?1 mmHg?1; P= 0.6) was similar between study days prior to resistance exercise. Postexercise haemodynamics Heart rate and mean arterial pressure had returned to values similar to pre-exercise (P= 0.2) by 10 min postexercise on both control and blockade days (Table 2). As shown in Fig. 2, leg blood flow and leg vascular conductance followed the same pattern of decline following resistance exercise on the blockade day versus the control day (P= 0.2 Sulfatase for drug effect). Figure 3 shows the percentage change (��) in leg vascular conductance values (from pre-exercise to 1 h postexercise) that were derived from protocols 1 and 2, along with historical data from our laboratory on the response to 1 h of cycling at 60% peak oxygen uptake (McCord & Halliwill, 2006). Cycling, which uses a larger muscle mass than the dynamic knee-extension exercises used in the present protocols, elicited a larger rise in leg vascular conductance (P