Ever since the discovery that the degeneration of midbrain DA neurons (mDANs) projecting to the striatum underlies bradykinesia (i.e., slowness of movement) in Parkinson’s disease (PD), DA has become synonymous with motor vigor. However, the mechanisms through which DA contributes to the speed and amplitude of individual voluntary movements are still debated. Initial investigations suggested a somewhat slow or permissive role for DA, but recent experiments in rodents proposed a stronger and faster role for DA in the dynamic control of the gain of motor commands. In this presentation, I will describe our attempts at better understanding how dopamine contributes to motor vigor through the study of release patterns, lesions, and optogenetic and pharmacological manipulations. Our findings call into question the widely-held view that phasic fluctuations in extracellular dopamine control the vigor of ongoing movements, constraining the kinds of mechanisms and timescales that dopamine likely acts on to modify behavior.