The effects of 12 weeks of Cardiovascular Exercise on Sleep Architecture and Corticospinal Excitability in Parkinson’s Disease: a mechanistic insight

Regular exercise is a safe adjunct to standard pharmacological treatment and may improve common sleep architecture alterations observed in Parkinson’s disease (PD). However, research in this area is limited, and it is unclear which potential underlying mechanisms are involved. We conducted a proof-of-concept study to investigate whether 12 weeks (3 days/week) of moderate-to-vigorous cardiovascular training (CT) improves sleep architecture and non-rapid-eye-movement (NREM) sleep oscillations in PD. Additionally, we explored potential underlying mechanisms, focusing on measures of intracortical inhibition mediated by gamma-aminobutyric acid (GABA), given its critical role in sleep physiology and dysfunction in PD. We recruited 15 participants at early-to-moderate disease stages (66.0 ± 9.0 years; Female = 3). Participants “On” antiparkinsonian medications were tested before and after the CT program. Cardiorespiratory fitness level was assessed with a symptom-limited cardiopulmonary exercise test. Sleep was evaluated with polysomnography. Intracortical inhibition was assessed using transcranial magnetic stimulation measures, including short intracortical inhibition (SICI) and the cortical silent period (CSP). Explorative outcomes included hypnodensity-related metrics, subjective sleep quality, cognition, motor signs severity, and fatigue. Following CT, we observed significant improvements in cardiorespiratory fitness level, the duration of NREM sleep stage 3, NREM stable sleep (hypnodensity-derived variable), SICI, and cognitive function. In contrast, there were no significant changes in other polysomnographic sleep outcomes, subjective sleep quality, CSP, motor signs severity, and fatigue. Although our findings require replication in RCTs, they expand previous research and suggest that CT may be a long-term, cost-effective strategy to mitigate common alterations in sleep and intracortical inhibition in PD.