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Blood-Brain Barrier and Exercise – a Short Review

100%
Nierwińska K., Malecka E., Chalimoniuk M., Żebrowska A., Langfort J.
Journal of Human Kinetics
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2008
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vol. 19
83-92
EN
Blood-brain barier (BBB) segregates central nervous system (CNS) from the circulating blood. BBB is formed by the brain capillary endothelial cells with complex tight junctions between them as well as by astrocytes and pericytes. BBB is responsible for transport of selected chemicals into and out of the CNS as well as for its protection from fluctuations in plasma composition following meals, during exercise and from circulating agents such as neurotransmitters, xenobiotics and other potentially harmful substances capable to disturb neural function. BBB may be compromised during CNS injury, infection, fever and in some nerodegenerative diseases. The increase of BBB permeability was observed also during exercise as documented by changes of plasma S-100 protein levels, used as a peripheral marker of BBB integrity. Marked change in BBB integrity during exercise may disturb normal brain function and contribute to the development of central fatigue. Moreover, serum S-100β may indicate level of injury in individuals suffering brain injuries during sports. There are also data suggesting that acute effect of physical exercise on serum S100β levels may not be related with CNS injury. Further studies to establish whether training and which type of it may modulate BBB permeability are needed.
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Central and Peripheral Fatigue During Resistance Exercise – A Critical Review

100%
Zając A., Chalimoniuk M., Gołaś A., Lngfort J., Maszczyk A.
Journal of Human Kinetics
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2015
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vol. 49
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issue 1
159-169
EN
Resistance exercise is a popular form of conditioning for numerous sport disciplines, and recently different modes of strength training are being evaluated for health benefits. Resistance exercise differs significantly in nature, and several variables determine the direction and range of adaptive changes that occur in the muscular and skeletal system of the body. Some modes of resistance training can also be effective in stimulating the cardiovascular system. These variables include exercise selection (general, specific, single or multi joint, dynamic, explosive), type of resistance (free weights, variable resistance, isokinetics), order of exercise (upper and lower body or push and pull exercises), and most of all the training load which includes intensity expressed as % of 1RM, number of repetitions, number of sets and the rest interval between sets. Manipulating these variables allows for specific adaptive changes which may include gains in muscle mass, muscle strength or muscle endurance. It has been well established that during resistance exercise fatigue occurs, regardless of the volume and intensity of work applied. The peripheral mechanisms of fatigue have been studied and explained in more detail than those related to the CNS. This review is an attempt to bring together the latest knowledge regarding fatigue, both peripheral and central, during resistance exercise. The authors of this review concentrated on physiological and biochemical mechanisms underlying fatigue in exercises performed with maximal intensity, as well as those performed to exhaustion with numerous repetitions and submaximal load.
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Amyloid beta enhances cytosolic phospholipase A2 level and arachidonic acid release via nitric oxide in APP-transfected PC12 cells

73%
Chalimoniuk M., Stolecka A., Cąkała M., Hauptmann S., Schulz K., Lipka U., Leuner K., Eckert A., Muller W. E., Strosznajder J. B.
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EN
Cytosolic phospholipase A2 (cPLA2) preferentially liberates arachidonic acid (AA), which is known to be elevated in Alzheimer's disease (AD). The aim of this study was to investigate the possible relationship between enhanced nitric oxide (NO) generation observed in AD and cPLA2 protein level, phosphorylation, and AA release in rat pheochromocytoma cell lines (PC12) differing in amyloid beta secretion. PC12 control cells, PC12 cells bearing the Swedish double mutation in amyloid beta precursor protein (APPsw), and PC12 cells transfected with human APP (APPwt) were used. The transfected APPwt and APPsw PC12 cells showed an about 2.8- and 4.8-fold increase of amyloid β (Aβ) secretion comparing to control PC12 cells. An increase of NO synthase activity, cGMP and free radical levels in APPsw and APPwt PC12 cells was observed. cPLA2 protein level was higher in APPsw and APPwt PC12 cells comparing to PC12 cells. Moreover, phosphorylated cPLA2 protein level and [3H]AA release were also higher in APP-transfected PC12 cells than in the control PC12 cells. An NO donor, sodium nitroprusside, stimulated [3H]AA release from prelabeled cells. The highest NO-induced AA release was observed in control PC12 cells, the effect in the other cell lines being statistically insignificant. Inhibition of cPLA2 by AACOCF3 significantly decreased the AA release. Inhibitors of nNOS and γ-secretase reduced AA release in APPsw and APPwt PC12 cells. The basal cytosolic [Ca2+]i and mitochondrial Ca2+ concentration was not changed in all investigated cell lines. Stimulation with thapsigargin increased the cytosolic and mitochondrial Ca2+ level, activated NOS and stimulated AA release in APP-transfected PC12 cells. These results indicate that Aβ peptides enhance the protein level and phosphorylation of cPLA2 and AA release by the NO signaling pathway.
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