Role of physical activity in preventing cognitive disorders

Regular physical activity induces a range of adjustment changes, particularly in the circulatory system and metabolism. Numerous publications on single exertion and increased physical activity more and more frequently confirm their positive influence on the shaping of cognitive functions. Anatomic and functional changes, such as increased cerebral blood flow, angiogenesis and neurogenesis as well as increased volume of the grey matter in the frontal and temporal cortices, are the basis of this positive influence. Physical exertion stimulates the production of trophic factors, among which the brain-derived neurotrophic factors and insulin-like growth factors are crucial for cognitive processes, synaptic plasticity as well as for the improvement of the neurogenesis signalling pathways and vascular functioning. Physical activity induces enhanced expansion of the brain-derived neurotrophic factor. This has a positive influence on energy processes and activates numerous cerebral energy centres which positively modify the synaptic potential for processing information that is important for developing cognitive functions. Exertion reduces inflammation by decreasing the blood concentration of proinflammatory cytokines that can contribute to the development of neurodegenerative processes. Moreover, it reduces metabolic syndrome risk factors, particularly hypertension and insulin resistance thus decreasing the risk of cognitive dysfunctions, improving brain functioning, delaying the onset and decelerating the development of disorders in neurodegenerative syndromes, including Alzheimer’s and Parkinson’s diseases. Taking these mechanisms into consideration, it seems that physical activity is indispensable for maintaining normal cognitive functions at any age.Regularna aktywność ruchowa wywołuje szereg zmian adaptacyjnych, zwłaszcza w układzie krążenia i przemianie materii. W licznych pracach na temat pojedynczego wysiłku i wzmożonej aktywności fizycznej pojawia się coraz więcej potwierdzeń ich korzystnego wpływu na kształtowanie funkcji poznawczych. U podstaw mechanizmów związanych z tym wpływem leżą zmiany anatomiczne i funkcjonalne, m.in. zwiększenie przepływu krwi przez mózg, angiogenezy i neurogenezy, objętości istoty szarej w korze czołowej i skroniowej. Wysiłek pobudza wydzielanie czynników troficznych, wśród których dla procesów poznawczych, plastyczności synaptycznej, poprawy szlaków sygnałowych neurogenezy i funkcji naczyniowych kluczowe są czynnik troficzny pochodzenia mózgowego i insulinopodobny czynnik wzrostowy. Aktywność ruchowa wywołuje wzmożoną ekspresję czynnika troficznego pochodzenia mózgowego, co pozytywnie wpływa na procesy energetyczne i aktywuje w mózgu wiele układów energetycznych, które korzystnie modyfikują potencjał synaptyczny przetwarzania informacji ważnych w kształtowaniu funkcji poznawczych. Wysiłek redukuje stan zapalny przez obniżenie we krwi stężenia cytokin prozapalnych, mogących się przyczyniać do rozwoju procesów neurodegeneracyjnych. Redukuje czynniki ryzyka zespołu metabolicznego, a zwłaszcza nadciśnienie i insulinooporność, więc zmniejsza ryzyko wystąpienia zaburzeń czynności poznawczych, poprawia funkcjonowanie mózgu, opóźnia początek i spowalnia rozwój zaburzeń w chorobach neurodegeneracyjnych, a wśród nich w chorobie Alzheimera i chorobie Parkinsona. Za sprawą wymienionych mechanizmów aktywność ruchowa wydaje się niezbędna do zachowania prawidłowych funkcji poznawczych w każdym wieku

Psychomotor Performance after 30 h of Sleep Deprivation Combined with Exercise

Sleep deprivation (SD) usually impairs psychomotor performance, but most experiments are usually focused on sedentary conditions. The purpose of this study was to evaluate the influence of 30 h of complete SD combined with prolonged, moderate exercise (SDE) on human psychomotor performance. Eleven endurance-trained men accustomed to overnight exertion were tested twice: in well-slept and non-fatigued conditions (Control) and immediately after 30 h of SDE. They performed a multiple-choice reaction time test (MCRT) at rest and during each workload of the graded exercise test to volitional exhaustion. At rest, the MCRT was shorter after SDE than in the Control (300 ± 13 ms vs. 339 ± 11 ms, respectively, p p p = 0.06). In conclusion, SDE is different from SD alone; however, well-trained men, accustomed to overnight exertion can maintain psychomotor abilities independently of the extent of central fatigue. Exercise can be used to enhance psychomotor performance in sleep-deprived subjects in whom special caution is required in order to avoid overload

Thermogenic Effect of Glucose in Hypothyroid Subjects

The importance of thyroid hormone, catecholamines, and insulin in modification of the thermogenic effect of glucose (TEG) was examined in 34 healthy and 32 hypothyroid subjects. We calculated the energy expenditure at rest and during oral glucose tolerance test. Blood samples for determinations of glucose, plasma insulin, adrenaline (A), and noradrenaline (NA) were collected. It was found that TEG was lower in hypothyroid than in control group (19.68±3.90 versus 55.40±7.32 kJ, resp., P<0.0004). Mean values of glucose and insulin areas under the curve were higher in women with hypothyroidism than in control group (286.79±23.65 versus 188.41±15.84 mmol/L·min, P<0.003 and 7563.27±863.65 versus 4987.72±583.88 mU/L·min, P<0.03 resp.). Maximal levels of catecholamines after glucose ingestion were higher in hypothyroid patients than in control subjects (Amax—0.69±0.08 versus 0.30±0.07 nmol/L, P<0.0001, and NAmax—6.42±0.86 versus 2.54±0.30 nmol/L, P<0.0002). It can be concluded that in hypothyroidism TEG and glucose tolerance are decreased while the adrenergic response to glucose administration is enhanced. Presumably, these changes are related to decreased insulin sensitivity and responsiveness to catecholamine action

Thermogenic Effect of Glucose in Hypothyroid Subjects

The importance of thyroid hormone, catecholamines, and insulin in modification of the thermogenic effect of glucose (TEG) was examined in 34 healthy and 32 hypothyroid subjects. We calculated the energy expenditure at rest and during oral glucose tolerance test. Blood samples for determinations of glucose, plasma insulin, adrenaline (A), and noradrenaline (NA) were collected. It was found that TEG was lower in hypothyroid than in control group (19.68 ± 3.90 versus 55.40 ± 7.32 kJ, resp., &lt; 0.0004). Mean values of glucose and insulin areas under the curve were higher in women with hypothyroidism than in control group (286.79 ± 23.65 versus 188.41 ± 15.84 mmol/L⋅min, &lt; 0.003 and 7563.27 ± 863.65 versus 4987.72 ± 583.88 mU/L⋅min, &lt; 0.03 resp.). Maximal levels of catecholamines after glucose ingestion were higher in hypothyroid patients than in control subjects (Amax-0.69 ± 0.08 versus 0.30 ± 0.07 nmol/L, &lt; 0.0001, and NAmax-6.42 ± 0.86 versus 2.54 ± 0.30 nmol/L, &lt; 0.0002). It can be concluded that in hypothyroidism TEG and glucose tolerance are decreased while the adrenergic response to glucose administration is enhanced. Presumably, these changes are related to decreased insulin sensitivity and responsiveness to catecholamine action

Efficacy of the sun exposition and oral supplementation.

<p>The concentration of 25(OH)D in SUN and SUPL groups in comparison with OUTD subjects in winter; mean ± SE, the dashed line represents the concentration level considered to be adequate; * denotes significant differences between OUTD and other groups: *** p<0.001; ^x denotes significant differences between SUN and SUPL groups: ^xxx p<0.001.</p

Annual distribution of serum 25(OH)D concentration.

<p>Annual distribution of 25(OH)D concentration in serum demonstrated as mean value for consecutive months and seasons in all athletes (mean ± SE, OUTD and IND groups together, n = 1011); the dashed line represents the concentration level considered to be adequate; * denotes a significant difference between summer and other seasons: ***p<0.001.</p