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Arterial hypertension (AH) remains the most common disease. One possible way to improve the effectiveness of the primary prevention of AH is to identify and control the preclinical orthostatic disturbances that precede the development of AH. The aim of the study was to determine the feasibility of a new protocol for the head-up tilt test (HUTT) with a standardized hydrostatic column height for the detection of asymptomatic orthostatic circulatory disorders and their racial differences in young African and European adults. Methods. In total, 80 young healthy adults (40 African and 40 European) aged 20–23 years performed the HUTT with a standardized hydrostatic column height of 133 cm. The hemodynamic parameters were recorded using a Task Force Monitor (3040i). The cardio-ankle vascular index (CAVI) was measured using a VaSera VS-2000 volumetric sphygmograph. Results. The baseline and orthostatic hemodynamic changes in both racial groups were within normal limits. Orthostatic circulatory disturbances were not detected in 70% of the European participants and 65% of the African participants; however, preclinical orthostatic hypertension, which precedes AH, was detected using the new HUTT protocol in 32.5% of the African participants and 20% of the European participants. The baseline CAVI was higher in the European group compared to the African group. Conclusion. The results of this study showed the feasibility of the detection of preclinical orthostatic disturbances in young adults and the detection of their racial differences using the HUTT protocol, providing the use of a standard gravity load. Further study on the evolution of preclinical orthostatic disturbances and their relation to increased vascular stiffness is necessary among large samples.

Since disagreement has been found between an objective sleep propensity measured by sleep onset latency (SOL) and subjective sleepiness assessment measured by the Epworth sleepiness scale (ESS) score, distinct underlying causes and consequences were suggested for these two sleepiness measures. We addressed the issue of validation of the ESS against objective sleepiness and sleep indexes by examining the hypothesis that these two sleepiness measures are disconnected due to their differential relationship with the antagonistic drives for sleep and wake.The polysomnographic records of 50-min napping attempts were collected from 27 university students on three occasions. Scores on the first and second principal components of the electroencephalographic (EEG) spectrum were calculated to measure the sleep and wake drives, respectively. Self-assessments of subjective sleepiness and sleep were additionally collected in online survey of 633 students at the same university.An ESS score was disconnected with the polysomnographic and self-assessed SOL in the nap study and online survey, respectively. An ESS score but not SOL was significantly linked to the spectral EEG measure of the sleep drive, while SOL but not ESS showed a significant association with the spectral EEG measure of the opposing wake drive.Each of two sleepiness measures was validated against objective indicators of the opposing sleep-wake regulating processes, but different underlying causes were identified for two distinct aspects of sleepiness. A stronger sleep drive and a weaker opposing drive for wake seem to contribute to a higher ESS score and to a shorter SOL, respectively.

In this work, mechanisms of influence of protein sensibility of an organism on contractile function of the isolated skeletal muscles of the mouse—“fast”—musculus extensor digitorum longus, “mixed”—musculus diaphragma and “slow”— musculus soleus are investigated. It is shown that at a protein sensitization all “fast”, “mixed” and “slow” skeletal muscles change the contractile properties. The vector of these changes for muscles with a various phenotypes carries opposite character. Force of the reduction caused carbacholine at a “slow” and “mixed” muscles increase, at “fast”—decreases. A vector of change of force of reduction on carbacholine at protein sensitization at these skeletal muscles correlates with changes of non-quantum secretion acetylcholine in a zone of a trailer plate. Opposite changes of functional properties of “fast” and “mixed” muscles and “slow” muscles of a shin of the mouse at protein sensitization are caused by dynamics cholinoceptive processes of excitation of membrane muscular fibers. It comes out with the assumption, that change of the contraction functions of skeletal muscles at protein sensitization is caused by changes of cholinoceptive processes of excitation of a membrane of muscular fibers, and other changes in system of electro-mechanical interface.

Disorders in memory and other cognitive functions in Alzheimer's disease (AD) may result from an exhaustion of adaptive reserves in the brain. Therefore it is a challenge to find methods to increase the adaptive reserve of the organism to combat AD. Excitotoxicity, Ca2+ homeostasis disruptions, oxidative stress, disturbed synthesis of NO, and impaired cerebral circulation are suggested as key pathogenic factors of AD. At present it appears that stimulation of the self-defense systems in neural cells is a promising strategy in restricting the progression of AD. These systems include those of antioxidants, heat shock proteins (HSPs), NO, and other so-called stress-limiting systems. Non-drug activation of these systems can be achieved most efficiently by adaptation of the organism to environmental challenges, such as hypoxia. In this paper the potential of methods used in adaptive medicine is explored. The protective mechanisms of adaptation to hypoxia may be related to restriction of oxidative stress in the hippocampus, the limitation of a decrease in NO production induced by beta-amyloid, and increased density of the vascular network in the brain. In this review we selectively present data that support the idea that adaptation to hypoxia is a possible non-drug means in the prevention of AD. In our opinion this strategy may provide a break-through in the clinical approach of this disease.