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Abstract

Parkinson’s disease (PD) is an idiopathic, neurological disorder with impairments in motor and nonmotor physiological functions. Although heat shock proteins (HSPs) may reduce α-synuclein aggregation, central to PD pathology, HSP responses to elevated core temperature and heat-based interventions in PD remain unexplored. PURPOSE: To observe HSP expression, α-synuclein concentration, core body temperature (TC), and nonmotor symptoms of PD following acute aerobic exercise and passive heating in older women with PD. METHODS: Nine women (67.1±4.7 yrs, 27.5±9.4 kg/m2), clinically diagnosed with PD prior to the start of the study, completed a randomized, crossover design including one hour each of treadmill walking (TM), passive heating (HT), TM immediately followed by HT (TM+HT), and a non-exercising control condition (CON). Variables measured in the study include TC, HSPs, α-synuclein, heart rate variability (HRV), cognitive performance, pain, sleep quality, and quality-of-life (QoL). All variables were taken at baseline, immediately post, and 24 hrs after each bout. Wake HRV and sleep HRV were averaged and recorded following each intervention. Multiple repeated measures analyses-of-variance (time x condition) were used to compare variables, with post hoc pairwise comparisons conducted using Fisher’s LSD (α = 0.05). RESULTS: There were no statistical differences for HSP70 or α-synuclein concentration within groups or time (p>0.05). For TC, there was a significant interaction between time and condition (p<0.001), with TC during TM higher than during HT (p=0.036) and control (p=0.031). Only one metric of HRV (high-frequency HRV, HF) was significantly different, with TM+HT showing higher HF power than TM (3.8±1.8 vs 2.5±1.8 ln ms2, p=0.048). There were no differences in cognitive flexibility and reaction time across time or condition (p>0.05). Executive function improved across time (p=0.009), with the immediate (31.9±10.0) and 24 hrs (32.3±8.9) timepoints improving compared to baseline (28.6±8.3). Self-reported pain improved across time (p=0.009), with lower 24 hrs scores (5.0±7.4) than baseline (7.9±8.0, p=0.017) and immediate post (7.9±7.2, p=0.031). Self-reported sleep disruptions decreased 24 hrs post TM (p=0.006) and HT (p=0.025) compared to baseline (TM:12.6±6.6 vs 8.0±6.0; HT:13.7±6.6 vs 7.8±5.1). Self-reported QoL improved across time (p=0.002) between baseline (20.1±19.0) and 24 hrs post (12.8±15.0). CONCLUSION: Although acute hyperthermia did not influence HSP or α-synuclein concentrations, these interventions produced favorable changes in autonomic function, executive function, pain, sleep, and QoL in women with PD. Collectively, these preliminary findings support the potential therapeutic relevance of these interventions for improving nonmotor symptoms in women with PD.

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