Exercising muscle blood flow (BF) may be an indicator of oxygen supply change allowing increased muscle energy metabolism through the circulatory response between central and peripheral hemodynamics. During exercise an increase in cardiac output may represent the interplay of alterations in both blood pressure and vascular conductance. Dynamic muscle contractions lead to an increase in cardiac output and promote venous return at the onset of exercise, and concurrently lead to enhanced muscle vasodilatation (and thus increased muscle BF) due to metabolites, neurological responses and/or other mechanisms, causing exercise hyperaemia. Doppler ultrasound can non-invasively detect with high resolution the temporal pulsatile blood velocity profiles in the conduit artery at rest as well as during muscle contractions. Based on this technique, it has been shown that alterations in the physiological blood velocity profile related to cardiac systole-diastole and fluctuations in the beat-by-beat blood velocity profile are due to rapid changes in the blood velocity profile concurrent with muscle contraction and/or relaxation during exercise (dynamic/static) or respiratory cycle, in different states (muscle contraction time/frequency or workload), or of any other type of vasodilatation/vasoconstriction. Muscle contraction-induced alterations in the blood velocity profile may be due in general to the magnitude of intramuscular pressure variation (mechanical factors) and the superimposed influence of perfusion pressure variation (pulsatile hemodynamic factors). This review therefore focuses on methodological considerations for muscle contraction-induced blood velocity/flow variability in the leg conduit artery, which in turn influences the magnitude of exercising BF during dynamic knee extensor exercise.