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1.
J Sleep Res ; : e14240, 2024 05 19.
Artigo em Inglês | MEDLINE | ID: mdl-38764179

RESUMO

People with Parkinson's disease experience reduced sleep quality compared with their peers. Levodopa may have a direct effect on sleep macrostructure or may improve sleep by enhancing nocturnal motor performance. Therefore, it is important to understand the acute effects of withdrawing levodopa on sleep measures in Parkinson's disease. The purpose of this study was to compare the estimated objective and subjective sleep measures of people with Parkinson's disease sleeping under (ON-night) versus without (OFF-night) the effects of the last daily dopaminergic medication before going to bed. A total of 23 people with Parkinson's disease were instructed to wear an actigraphy device for 4 consecutive nights to objectively measure the sleep behaviour. Subjective sleep measure was assessed each morning using a Likert scale. Participants slept for 3 nights on ON-night and 1 night on OFF-night. They were instructed not to take their last dose of levodopa before going to bed in OFF-night. Sleeping in ON- versus OFF-night increased total sleep time (7.8%, p = 0.032) and sleep efficiency (3.7%, p = 0.019), and decreased duration and number of wakes after sleep onset (22.3%, p = 0.050; and 29.2%, p = 0.013, respectively). However, subjective sleep analysis indicated no significant differences between the two conditions. From a clinical point of view, our results suggest that sleeping on ON-night resulted in an improvement in estimated objective sleep measures compared with sleeping on OFF-night. From a methodological point of view, our findings emphasize the importance of relying on objective sleep measurements to accurately assess OFF-night sleep behaviour in people with Parkinson's disease.

2.
Int J Exerc Sci ; 15(2): 289-299, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36895795

RESUMO

The aim of this study is to verify the influence of the intensity on muscle and hepatic glycogen depletion and recovery kinetics of Wistar rats, submitted to three acute training sessions with equalized loads. 81 male Wistar rats performed an incremental test to determine maximal running speed (MRS) and divided into 4 groups: baseline group (Control; n = 9); low intensity training session (GZ1; n = 24; 48 minutes at 50% of MRS); moderate intensity group (GZ2; n = 24; 32 minutes at 75% of MRS) and high intensity group (GZ3; n = 24; 5x5 minutes and 20 seconds at 90% of MRS). Immediately after the sessions and after 6, 12 and 24 hours, 6 animals from each subgroup were euthanized for glycogen quantification in soleus and EDL muscles and liver. A Two-Way ANOVA and the Fisher's Post-hoc test was used (p < 0.05). Glycogen supercompensation occurred between 6 and 12 hours after exercise in muscle tissue and 24 after exercise in the liver. The muscle and hepatic glycogen depletion and recovery kinetics are not modulated by exercise intensity since the load was equalized, but effects were distinct in different tissues. Hepatic glycogenolysis and muscle glycogen synthesis processes seem to run in parallel.

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