Objectives:Poor sleep quality may contribute to autonomic dysfunction in older adults, but evidence regarding its effect on stress-associated baroreflex sensitivity (BRS), an important physiological indicator, is limited. Methods:data were derived from the MIDUS 3 Biomarker Project (2017-2022). Stress-associated BRS was measured using the sequence method while participants are taking a math-task (used as a psychological stressor) to solve in prespecified limited time. Sleep quality was assessed via the Pittsburgh Sleep Quality Index (PSQI). Multiple linear regression analyses were conducted to examine the association between sleep quality and stress-associated BRS, adjusting for insulin resistance (measured using HOMA-IR), age, sex, smoking history, physical activity, systolic blood pressure (SBP) measured during stress, body mass index (BMI), total cholesterol-to-HDL ratio, medications, respiratory rate measured during stress, and anxiety and depression (measured as a composite of general distress-anxiety and depression scales from Mood and Symptom Questionnaire (MASQ)). Log transformation was applied to BRS values to meet analysis assumptions. Results:The final sample included 401 participants (58.6% female; mean age 63.9 ± 8.6 years). In crude analysis, sleep quality was not associated with BRS. After adjustment, poorer sleep quality was significantly associated with impaired stress-associated BRS (Beta = -0.121; 95% CI: [-0.233 to -0.008], P = 0.035). In addition, higher SBP was the only covariate associated with significant decrease in BRS (Beta = -0.117; 95% CI: [-0.214 to -0.019], P = 0.019). Mediation analysis revealed that heart rate fully mediated the association between sleep quality and BRS, with near-significant total association and significant indirect association (estimate = -0.01; 95% CI: [-0.0160 to -0.003], P = 0.003). Conclusion:Poor sleep quality is associated with impaired stress-associated BRS in older adults, with important mediating role for autonomic arousal represented by heart rate.
Background:Type 2 diabetes mellitus and metabolic diseases are increasing worldwide and are closely linked to mitochondrial dysfunction. Mitochondrial-derived peptides (MDPs), such as humanin and MOTS-c, play a role in regulating energy balance and cellular stress responses. Exercise is known to improve metabolic function and stimulate MDP synthesis through mitochondria-dependent signaling pathways. Understanding these mechanisms has the potential to uncover new therapeutic targets for the treatment of metabolic diseases. Research objectives:This study sought to ascertain how physical activity affected MDPs levels. Methods:This systematic review searched four electronic databases, PubMed, Scopus, Web of Science, and ScienceDirect, for studies published between 2016 and 2025 that examined MDPs and exercise. A total of 435 records were identified. After screening according to predefined inclusion and exclusion criteria following PRISMA guidelines, nine studies were included in the final analysis. Results:Of the nine studies included in this systematic review, most reported a trend toward increased MDP levels after exercise. However, these findings should be interpreted with caution due to the limited number of studies and variations in study design, subject characteristics, and exercise protocols. Conclusion:Available evidence suggests that physical exercise has the potential to increase MDP levels, which may be associated with improved metabolic function, increased insulin sensitivity, and the efficiency of cellular energy metabolism. However, current evidence is limited, particularly in human studies. Therefore, further research, particularly controlled clinical trials and longitudinal studies, is needed to confirm these findings and evaluate MDP's potential as a therapeutic target in the prevention and management of metabolic diseases.
Purpose:To determine whether short-term dehydration and hyperhydration affect OCT-derived retinal thickness in healthy young adults in a randomized cross-over design. Methods:Sixty volunteers aged 18-35 years completed two morning sessions ≥7 days apart: 12-h fluid restriction, representing relative dehydration, and water loading, defined as ≥2 L within 4 h. Spectral-domain OCT (Zeiss Cirrus HD-OCT 7000) was performed by a masked examiner. Primary outcomes were central subfield thickness (CST) and mean peripapillary retinal nerve fiber layer (RNFL) thickness; secondary outcomes were cube average thickness (CAT) and ganglion cell-inner plexiform layer (GCL-IPL) thickness. Hydration was documented using a self-reported thirst scale and recorded water intake. Within-subject comparisons used the Wilcoxon signed-rank test. Results:Median age was 28.5 years and 65% of participants were female. Thirst was higher during dehydration than hyperhydration (P < 0.001). After review of OCT outputs and exclusion of outlying paired observations for GCL-IPL and CAT, the direction and statistical interpretation of the findings remained unchanged. CAT was slightly lower during dehydration in both eyes. CST was lower during dehydration in the left eye, with a similar non-significant trend in the right eye. RNFL thickness did not differ between hydration states in either eye. GCL-IPL thickness showed only a small right-eye difference and no significant difference in the left eye. Conclusions:Acute fluid restriction was associated with small reductions in macular OCT thickness measures, whereas RNFL thickness remained stable. The magnitude of these changes was modest and close to expected OCT test-retest variability, suggesting limited clinical relevance for routine individual interpretation but potential relevance for highly standardized research or longitudinal imaging settings.
Background:Propranolol (a non-selective β-blocker), metoprolol (a β1-selective blocker), and nebivolol (a β1-selective blocker with nitric oxide (NO)-releasing properties) are widely used in the treatment of various cardiovascular diseases. Based on their distinct pharmacological profiles at β-adrenergic receptors, we aimed to comparatively evaluate their effects on chronotropic, inotropic, and vascular responses in isolated rat atria and thoracic aorta preparations. Methods:In this study, isolated right, left atria and thoracic aorta preparations were used and mounted in organ bath systems. The right atrium was used to assess spontaneous beating rate (chronotropic responses), whereas the left atrium was used to evaluate contractile force (inotropic responses). Cumulative concentration-response curves were obtained by administering increasing concentrations (10-9-10-5 M) of propranolol, metoprolol, and nebivolol in noradrenaline (NA)-stimulated atrial preparations. To determine the contribution of NO, nebivolol-induced negative chronotropic and inotropic responses were also examined in the presence of the NO synthase inhibitor L-NAME (10-5 M). In endothelium-intact thoracic aorta rings, NA-induced contractile responses were also evaluated in the presence of each β-blocker with different concentrations (10-7, 10-6, 10-5 M). Results:Propranolol, metoprolol, and nebivolol produced negative chronotropic and inotropic effects in a concentration-dependent manner in isolated right and left atrial preparations. The negative chronotropic and inotropic effects of nebivolol were significantly attenuated in the presence of L-NAME (P < 0.05). NA induced a concentration-dependent increase in contractile responses in endothelium-intact aortic rings. Propranolol, metoprolol, and nebivolol caused rightward shifts of the NA concentration-response curves and Schild plot analysis revealed pA2 values of 6.64 ± 0.47, 6.47 ± 0.46, and 6.95 ± 0.35, respectively. Conclusion:These findings demonstrate that propranolol, metoprolol, and nebivolol show differential pharmacological profiles affecting atrial and vascular responses under NA stimulation in isolated rat atrial and aorta preparations. Notably, NO appears to be a key mediator of nebivolol's cardiac effects, reflected in its pronounced negative chronotropic and inotropic responses in isolated atrial tissues.
Assessment of cutaneous microcirculation contributes to studying pathophysiological mechanisms and the progression of systemic and local diseases. However, the available quantitative data demonstrate heterogeneity across studies by different authors. In this narrative review, we briefly discuss the main factors influencing heterogeneity in cutaneous microcirculation assessment. We divided all factors into three groups: (1) factors related to microcirculation per se; (2) factors influencing the thickness of individual skin layers and, consequently, the depth of blood vessels; and (3) factors associated with the measurement technique.
