PURPOSEWe tested the hypothesis that manipulating perfusion pressure (PP) impacts forearm critical power (fCP).METHODS9 healthy young (23 ± 2.6 yrs) males completed 10 min fCP tests in each of arm above (A) and below (B) heart level (forearm PP A < B by ~30 mmHg). fCP (average of force impulse in last 30 s of test), forearm blood flow (FBF; echo and Doppler ultrasound), arterial pressure (MAP; finger photoplethysmography), O2 consumption (VO2; venous blood samples, Fick eqn) were measured during exercise.RESULTSmean ± SD. Responders (all with compromised fCP in A vs. B; 21 ± 7 vs. 30 ± 6 kg·s, p=0.01) and non‐responders (no compromise to fCP in A vs. B; 29 ± 17 vs. 27 ± 16 kg·s, P=0.14) were identified. Responders exhibited O2D compromise in A vs. B (164 ± 60 vs. 178 ± 65 ml O2/min, p=0.04), and all had lower VO2 in A vs. B but this was not statistically significant (VO2 88 ± 30 ml/min vs. 104 ± 40 ml/min, p=0.12). Non‐responders had no compromise to O2D in A vs. B (153 ± 26 vs. 164 ± 28 ml O2/min, p=0.53), nor any compromise to VO2 (99 ± 21 ml/min vs. 106 ± 28 ml/min, p=0.58). No clear pattern regarding pressor or vasodilatory compensation to protect O2D was found (Responders A vs. B, ΔFVC p=0.01, ΔMAP p=0.12; Non‐responders A vs. B ΔFVC p=0.22, ΔMAP p=0.37).CONCLUSIONSReductions in perfusion pressure can reduce forearm critical power in individuals who cannot defend O2D. These data highlight the importance of O2D to fCP. NSERC