We tested the hypothesis that muscle vasoregulatory mechanisms respond rapidly to step increases and decreases in exercise intensity from steady state. 10 men and 9 women (21.8 ±3.6 yrs) performed repeated step‐transitions between 4 min bouts of low (L) and moderate (M) forearm handgrip exercise intensities. Forearm blood flow (FBF; Doppler ultrasound), mean arterial pressure (MAP, finometer), and heart rate (HR; ECG) were measured beat by beat. A cardiac cycle during each relaxation of the duty cycle (1s contract/2s relax) was used to quantify forearm hemodynamics (FBFrelax ml/min; forearm vascular conductance, FVCrelax ml/min/100 mmHg). Data mean ± SD. FBFrelax increased rapidly following a step increase in exercise intensity (L steady state 243.1 ±103.6 vs. 1st M relaxation 262.0 ±78.1, P = 0.075 vs. 2nd M relaxation 289.8 ±82.2, P<0.001). This was due to a rapid vasodilation (FVCrelax L steady state 258.8 ±93.0 vs. 1st M relaxation 279.6 ± 71.8, P = 0.058; vs. 2nd M relaxation 304.7 ±74.0, P<0.001). The same rapid responses were observed with decreases in exercise intensity (FVCrelax M steady state 462.3 ± 120.5 vs. 1st L relaxation 435.8 ±103.3, P<0.001; vs. 2nd L relaxation 420.4 ±99.0, P<0.001). We conclude that vasoregulatory mechanisms are able to alter muscle blood flow rapidly and with little delay in response to sudden increases and decreases in exercise intensity from steady state. Supported by NSERC Canada.