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Parkinson’s disease (PD) is generally associated with abnormally increased beta band oscillations in the cortico-basal ganglia loop during walking. PD patients with freezing of gait (FOG) exhibit a more distinct, prolonged narrow band of beta oscillations that are locked to the initiation of movement at ∼18 Hz. Upon initiation of cycling movements, this oscillation has been reported to be weaker and rather brief in duration. Due to the suppression of the overall beta band power during cycling and its continuous nature of the movement, cycling is considered to be less demanding for cortical networks compared to walking, including reduced need for sensorimotor processing, and thus unimpaired continuous cycling motion. Furthermore, cycling has been considered one of the most efficient non-pharmacological therapies with an influence on the subthalamic nucleus (STN) beta rhythms implicative of the deep brain stimulation effects. In the current review, we provide an overview of the currently available studies and discuss the underlying mechanism of preserved cycling ability in relation to the FOG in PD patients. The mechanisms are presented in detail using a graphical scheme comparing cortical oscillations during walking and cycling in PD.