The primary objective of this study was to determine whether cardiovascular compensatory response phenotypes exist in the face of a reduced perfusion pressure challenge to exercising muscle oxygen delivery (O2D), and whether these responses might be exercise intensity (EI) dependent. Ten healthy men (19.5 ± 0.4 yr) completed two trials of progressive forearm isometric handgrip exercise to exhaustion (24.5 N increments every 3.5 min) in each of forearm above and below heart level [forearm arterial perfusion pressure (FAPP) difference of 29.5 ± 0.97 mmHg]. At the end of each EI, measurements of forearm blood flow (FBF; ml/min) via brachial artery Doppler and echo ultrasound, mean arterial blood pressure (MAP; mmHg) via finger photoplethysmography, and exercising forearm venous effluent via antecubital vein catheter revealed distinct cardiovascular response groups: n = 6 with compensatory vasodilation vs. n = 4 without compensatory vasodilation. Compensatory vasodilators were able to blunt the perfusion pressure-evoked reduction in submaximal O2D in the arm-above-heart condition, whereas nonvasodilators did not (−22.5 ± 13.6 vs. −65.4 ± 14.1 ml O2/min; P < 0.05), and in combination with being able to increase O2 extraction, nonvasodilators defended submaximal V̇o2 and experienced less of an accumulated submaximal O2D deficit (−80.7 ± 24.7 vs. −219.1 ± 36.0 ml O2/min; P < 0.05). As a result, the compensatory vasodilators experienced less of a compromise to peak EI than nonvasodilators (−24.5 ± 3.5 N vs. −52.1 ± 8.9 N; P < 0.05). In conclusion, in the forearm exercise model studied, vasodilatory response phenotypes exist that determine individual susceptibility to hypoperfusion and the degree to which aerobic metabolism and exercise performance are compromised.