ABSTRACT
BACKGROUND: Excessive daytime sleepiness is a prevalent and sustained symptom that contributes to untoward physiologic and psychologic outcomes among stroke survivors. Mechanisms of excessive daytime sleepiness post-stroke are not fully understood. Chronic systemic inflammation may contribute to impaired mitochondrial functioning and thereby reduce cellular energy metabolism which may contribute to symptoms of excessive daytime sleepiness in stroke survivors. OBJECTIVES: This pilot study aimed to assess the relationship between systemic inflammation and cellular energy metabolism to post-stroke excessive daytime sleepiness. METHODS: This descriptive pilot study explored the relationship between excessive daytime sleepiness, systemic inflammation, and aerobic energy metabolism of platelets in 22 chronic stroke survivors. The Epworth Sleepiness Scale was used to measure excessive daytime sleepiness. Systemic inflammation was measured by assessing pro-inflammatory cytokines IL-6, IL-1ß and TNF-α and the inflammatory marker C-reactive protein. Aerobic energy metabolism was measured by assessing oxygen consumption rates of platelets. Simple linear regression was used to test the influence of oxygen consumption rates and inflammation on excessive daytime sleepiness. Correlations were analyzed using Spearman rho correlation coefficients. RESULTS: Excessive daytime sleepiness was recognized in 27.3% of the sample. Systemic inflammation was associated with excessive daytime sleepiness in women but not men. We found no significant relationship between excessive daytime sleepiness and energy metabolism of platelets. However, all oxygen consumption rates were numerically higher in persons with excessive daytime sleepiness. DISCUSSION: Systemic inflammation may be related to excessive daytime sleepiness symptoms with a notable effect among women. Future larger studies are needed to further explore the sexually dimorphic relationship of post-stroke excessive daytime sleepiness to systemic inflammation. Numerically higher platelet oxygen consumption rates may indicate higher energy demands for stroke survivors with excessive daytime sleepiness.
ABSTRACT
BACKGROUND: Fatigue is a prominent symptom of heart failure (HF). However, underlying mechanisms remain poorly understood. Fluid volume status has been suggested as a physiologic mechanism of HF-related fatigue. Serum osmolality may fluctuate with changes in volume status associated with neurohormonal dysregulation. The relationship of fatigue to serum osmolality has not been assessed in adults with HF. OBJECTIVES: Describe the relationship between serum osmolality and fatigue in adults with HF. METHODS: We analyzed two waves of cross-sectional data from the National Health and Nutrition Examination Survey (2015-2016 and 2017-2018). Adults who self-reported having HF without select co-morbid conditions known to contribute to fatigue were included. Data were weighted to provide US national estimates, and complex sample design used for analyses. Sequential logistic regression was used to isolate the effect of serum osmolality on the odds of having fatigue. RESULTS: Data from the sample represented 1.4 million Americans with HF (58.5 % male; median age 68 years), of whom 1,001,589 (67.9 %) reported fatigue. Participants with fatigue had lower serum osmolality compared to those without fatigue (t = -3.04, p = .009). Higher serum osmolality was associated with 8.8 % lower odds of experiencing fatigue when controlling for sex and body mass index (OR = 0.912, p = .007, CI 0.857 - 0.972). CONCLUSIONS: HF-related fatigue is associated with lower serum osmolality. Low serum osmolality may indicate excess volume and the presence of a heightened neurohormonal response, both of which may influence fatigue. Alternatively, serum osmolality may directly affect other physiologic changes that may contribute to fatigue.