PULSE TRANSIT TIME – RELIABLE MARKER FOR SLEEP DISTURBANCES AMONG ATHLETES

Sleep is essential for everyone and is important for the normal human functioning. Lack of sleep, called sleep deprivation, is a condition leading to poor sports training and achievements. Different factors contribute to sleep deprivation among athletes. Respiratory sleep disorders such as Upper airway resistance syndrome (UARS) and Obstructive Sleep Apnea (OSA) are factors that rebound most to sleep deprivation for certain groups of athletes such as wrestlers, judokas and sumo wrestlers. The present study investigates the UARS and OSA occurrence in the above mentioned groups of athletes using Pulse Transit Time (PTT) as an early noninvasive indicator of respiratory effort and sympathetic nervous system activity. Sixty-seven elite athletes, practicing wrestling, sumo wrestling and judo were screened by enquiry for sleep breathing disturbances. The study involved the most suspicious ten cases for sleep-disordered breathing symptoms. They underwent full standard polysomnographic (PSG) examination using Alice 5 System Philips - Respironics Inc. with the registration of PTT. Among all athletes, regardless of the presence of changes in hemoglobin saturation or apnea-hypopnea index changes (AHI), a significant drop in the PTT value with more than 8-15 ms for sleep stages N1 and N2 (p<0.005) was observed, as well as with more than 6-8 ms for sleep stage N3 (p<0.005). We found bigger dependence of PTT by Arousal Index (ArI) than AHI and Desaturation Index (DI). Therefore, PTT can be used as a good indicator of sleep fragmentation before the development of the clinical picture of UARS and OSA.As a good indicator for inspiratory effort and sympathetic changes in UARS and OSA, PTT gives an opportunity for early diagnosis of respiratory sleep disorders among athletes. Prevention, timely detection and appropriate treatment of sleep disorders before the development of their full clinical picture will improve the processes of recovery and performance in sports practice

The current state of knowledge about the dipping and non-dipping hypertension

Ambulatory blood pressure monitoring provides information about the day-night blood pressure profile, which can be divided into dipping and non-dipping pattern. Non-dipping hypertension is recently thought to have increased cardiovascular risk and outcomes than dipping hypertension. The dipping pattern is explained by physiological changes in circadian rhythm, while the pathomechanism of non-dipping hypertension is not fully understood. Is it considered to be a result of many factors, such as: sympathetic nervous system overactivation, which can be accompanied by impaired parasympathetic nervous system response, obesity, concurrent diabetes mellitus and metabolic syndrome. Moreover abnormalities of hormones levels such as melatonin, catecholamines, thyroid and parathyroid hormones are connected to occurrence of non-dipping hypertension. Other widely discussed problem is obstructive sleep apnoea and its influence on circadian rhythm changes. Also dysfunction in activity of renin-angiotensin-aldosterone axis is thought to cause non-dipping pattern. There are some studies that indicate on role of inappropriate sodium intake in mentioned pathology. The chronic kidney disease and relationship with non-dipping hypertension will be also described. The last considered factor is influence of age on the development of non-dipping hypertension

Sleep Disordered Breathing, Obesity and Atrial Fibrillation: A Mendelian Randomisation Study.

Funder: National Institute for Health Research (NIHR)It remains unclear whether the association between obstructive sleep apnoea (OSA), a form of sleep-disordered breathing (SDB), and atrial fibrillation (AF) is causal or mediated by shared co-morbidities such as obesity. Existing observational studies are conflicting and limited by confounding and reverse causality. We performed Mendelian randomisation (MR) to investigate the causal relationships between SDB, body mass index (BMI) and AF. Single-nucleotide polymorphisms associated with SDB (n = 29) and BMI (n = 453) were selected as instrumental variables to investigate the effects of SDB and BMI on AF, using genetic association data on 55,114 AF cases and 482,295 controls. Primary analysis was conducted using inverse-variance weighted MR. Higher genetically predicted SDB and BMI were associated with increased risk of AF (OR per log OR increase in snoring liability 2.09 (95% CI 1.10-3.98), p = 0.03; OR per 1-SD increase in BMI 1.33 (95% CI 1.24-1.42), p < 0.001). The association between SDB and AF was not observed in sensitivity analyses, whilst associations between BMI and AF remained consistent. Similarly, in multivariable MR, SDB was not associated with AF after adjusting for BMI (OR 0.68 (95% CI 0.42-1.10), p = 0.12). Higher BMI remained associated with increased risk of AF after adjusting for OSA (OR 1.40 (95% CI 1.30-1.51), p < 0.001). Elevated BMI appears causal for AF, independent of SDB. Our data suggest that the association between SDB, in general, and AF is attributable to mediation or confounding from obesity, though we cannot exclude that more severe SDB phenotypes (i.e., OSA) are causal for AF