EXAMINATION OF THE HUNGARIAN ELITE ATHLETES USING SELECTED BIOMECHANICAL METHODS

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The Exchange of Tritiated Water Between Zn-A Zeolitevand the Surrounding Water

Zeolites are considered as adsorbents for tritiated waste water. The sorption capacity of 4A zeolite is increased, and the speed of tritium release, as THO, decreased if sodium ions in 4A zeolite are replaced with small divalent cations. The exchange kinetics THO/H20 between Zn-A zeolite containing tritiated water and the surrounding water was investigated at 30-60 De, using zinc-exchanged 4A zeolite beads of 0.8 and 1.6 mm radius. The kinetics was controlled by the diffusion of water in the solid particle and interpreted in terrns of the Boyd - Reichenberg diffusion model. Effective self-diffusion coefficients of water in the zeolite beads were obtained and the kinetic data are discussed from the point of view of using zeolites as sorbents and storage material for tritiated waste water

Does compression sensory axonopathy in the proximal tibia contribute to noncontact anterior cruciate ligament injury in a causative way?—a new theory for the injury mechanism

Anterior cruciate ligament injury occurs when the ligament fibers are stretched, partially torn, or completely torn. The authors propose a new injury mechanism for non-contact anterior cruciate ligament injury of the knee. Accordingly, non-contact anterior cruciate ligament injury could not happen without the acute compression microinjury of the entrapped peripheral proprioceptive sensory axons of the proximal tibia. This would occur under an acute stress response when con-comitant microcracks-fractures in the proximal tibia evolve due to the same excessive and repetitive compression forces. The primary damage may occur during eccentric contractions of the acceleration and deceleration moments of strenuous or unaccustomed fatiguing exercise bouts. This primary damage is suggested to be an acute compression/crush axonopathy of the proprioceptive sensory neurons in the proximal tibia. As a result, impaired proprioception could lead to injury of the anterior cruciate ligament as a secondary damage, which is suggested to occur during the deceleration phase. Elevated prostaglandin E2, nitric oxide and glutamate may have a critical neuro-modulatory role in the damage signaling in this dichotomous neuronal injury hypothesis that could lead to mechano-energetic failure, lesion and a cascade of inflammatory events. The presynaptic modulation of the primary sensory axons by the fatigued and microdamaged proprioceptive sensory fibers in the proximal tibia induces the activation of N-methyl-D-aspartate receptors in the dorsal horn of the spinal cord, through a process that could have long term relevance due to its contribution to synaptic plasticity. Luteinizing hormone, through interleukin-1β, stimulates the nerve growth factor-tropomyosin receptor kinase A axis in the ovarian cells and promotes tropomyosin receptor kinase A and nerve growth factor gene expression and prostaglandin E2 release. This luteinizing hormone induced mechanism could further elevate prostaglandin E2 in excess of the levels generated by osteocytes, due to mechanical stress during strenuous athletic moments in the pre-ovulatory phase. This may explain why non-contact anterior cruciate ligament injury is at least three-times more prevalent among female athletes

Long-term restenosis rate of eversion endarterectomy on the internal carotid artery.

OBJECTIVES: The eversion endarterectomy of the internal carotid artery was introduced in Hungary in 1991. The aim of this study was to define the long-term restenosis rate of this procedure. PATIENTS AND METHODS: Between 1991 and 1993, 171 operations, on 151 patients, were performed by single surgeon: with long-term follow up of 109 patients, which included annual physical and ultrasound examinations. Restenosis rate and plaque morphology were defined. Survival and patency rate were analysed by life-tables. RESULTS: The combined perioperative stroke morbidity and mortality rate was 0.8%. The 5-year patient survival rate was 85%, the recurrent stenosis free rate was 88% at 5 years. Only 9% of the patients had carotid restenosis of more than 70% during this period. Ultrasound plaque morphology showed calcification in one case. Two patients had re-operations, with plaque histology showed myointimal hyperplasia in each case. CONCLUSIONS: Our results for restenosis are compare favourably with the 2-34% restenosis rate reported in the literature. Ultrasound and histological findings suggest that atherosclerosis does not play a significant role in the development of restenosis after the eversion carotid endarterectomy

The redox-associated adaptive response of brain to physical exercise.

Reactive oxygen species (ROS) are continuously generated during metabolism. ROS are involved in redox signaling, but in significant concentrations they can greatly elevate oxidative damage leading to neurodegeneration. Because of the enhanced sensitivity of brain to ROS, it is especially important to maintain a normal redox state in brain and spinal cord cell types. The complex effects of exercise benefit brain function, including functional enhancement as well as its preventive and therapeutic roles. Exercise can induce neurogenesis via neurotrophic factors, increase capillarization, decrease oxidative damage, and enhance repair of oxidative damage. Exercise is also effective in attenuating age-associated loss in brain function, which suggests that physical activity-related complex metabolic and redox changes are important for a healthy neural system

Master athletes have higher miR-7, SIRT3 and SOD2 expression in skeletal muscle than age-matched sedentary controls.

Regular physical exercise has health benefits and can prevent some of the ageing-associated muscle deteriorations. However, the biochemical mechanisms underlying this exercise benefit, especially in human tissues, are not well known. To investigate, we assessed this using miRNA profiling, mRNA and protein levels of anti-oxidant and metabolic proteins in the vastus lateralis muscle of master athletes aged over 65 years and age-matched controls. Master athletes had lower levels of miR-7, while mRNA or protein levels of SIRT3, SIRT1, SOD2, and FOXO1 levels were significantly higher in the vastus lateralis muscle of master athletes compared to muscles of age-matched controls. These results suggest that regular exercise results in better cellular metabolism and antioxidant capacity via maintaining physiological state of mitochondria and efficient ATP production and decreasing ageing-related inflammation as indicated by the lower level of miR-7 in master athletes

Impact of Treadmill Running and Sex on Hippocampal Neurogenesis in the Mouse Model of Amyotrophic Lateral Sclerosis

Hippocampal neurogenesis in the subgranular zone (SGZ) of dentate gyrus (DG) occurs throughout life and is regulated by pathological and physiological processes. The role of oxidative stress in hippocampal neurogenesis and its response to exercise or neurodegenerative diseases remains controversial. The present study was designed to investigate the impact of oxidative stress, treadmill exercise and sex on hippocampal neurogenesis in a murine model of heightened oxidative stress (G93A mice). G93A and wild type (WT) mice were randomized to a treadmill running (EX) or a sedentary (SED) group for 1 or 4 wk. Immunohistochemistry was used to detect bromodeoxyuridine (BrdU) labeled proliferating cells, surviving cells, and their phenotype, as well as for determination of oxidative stress (3-NT; 8-OHdG). BDNF and IGF1 mRNA expression was assessed by in situ hybridization. Results showed that: (1) G93A-SED mice had greater hippocampal neurogenesis, BDNF mRNA, and 3-NT, as compared to WT-SED mice. (2) Treadmill running promoted hippocampal neurogenesis and BDNF mRNA content and lowered DNA oxidative damage (8-OHdG) in WT mice. (3) Male G93A mice showed significantly higher cell proliferation but a lower level of survival vs. female G93A mice. We conclude that G93A mice show higher hippocampal neurogenesis, in association with higher BDNF expression, yet running did not further enhance these phenomena in G93A mice, probably due to a ‘ceiling effect’ of an already heightened basal levels of hippocampal neurogenesis and BDNF expression

Long Term Running Biphasically Improves Methylglyoxal-Related Metabolism, Redox Homeostasis and Neurotrophic Support within Adult Mouse Brain Cortex

Oxidative stress and neurotrophic support decline seem to be crucially involved in brain aging. Emerging evidences indicate the pro-oxidant methylglyoxal (MG) as a key player in the age-related dicarbonyl stress and molecular damage within the central nervous system. Although exercise promotes the overproduction of reactive oxygen species, habitual exercise may retard cellular aging and reduce the age-dependent cognitive decline through hormetic adaptations, yet molecular mechanisms underlying beneficial effects of exercise are still largely unclear. In particular, whereas adaptive responses induced by exercise initiated in youth have been broadly investigated, the effects of chronic and moderate exercise begun in adult age on biochemical hallmarks of very early senescence in mammal brains have not been extensively studied. This research investigated whether a long-term, forced and moderate running initiated in adult age may affect the interplay between the redox-related profile and the oxidative-/MG-dependent molecular damage patterns in CD1 female mice cortices; as well, we investigated possible exercise-induced effects on the activity of the brain derived neurotrophic factor (BDNF)-dependent pathway. Our findings suggested that after a transient imbalance in almost all parameters investigated, the lately-initiated exercise regimen strongly reduced molecular damage profiles in brains of adult mice, by enhancing activities of the main ROS- and MG-targeting scavenging systems, as well as by preserving the BDNF-dependent signaling through the transition from adult to middle age

Prevalence of the metabolic syndrome in patients with carotid disease according to NHLBI/AHA and IDF criteria: a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>Metabolic syndrome (MetS) has been related to type 2 diabetes and cardiovascular diseases. Different criteria for diagnosis of MetS have been recommended, but there is no agreement about which criteria are best to use. The aim of the present study was to investigate agreement between the National Heart, Lung, and Blood Institute, American Heart Association (NHLBI/AHA) and the International Diabetes Federation (IDF) definitions of MetS in patients with symptomatic carotid disease and to compare the frequency of cardiovascular risk factor in patients with MetS diagnosed by these two sets of criteria.</p> <p>Methods</p> <p>The study was a cross-sectional one involving 644 consecutive patients with verified carotid disease who referred to the Vascular Surgery Clinic Dedinje in Belgrade during the period April 2006 - November 2007. Anthropometric parameters blood pressure, fasting plasma glucose and lipoproteins were measured using standard procedures.</p> <p>Results</p> <p>MetS was present in 67.9% of participants, according to IDF criteria, and in 64.9% of participants, according to the NHLBI/AHA criteria. A total of 119 patients were categorized differently by the two definitions. Out of all participants 10.7% had MetS by IDF criteria only and 7.8% of patients had MetS by NHLBI/AHA criteria only. The overall agreement of IDF and NHLBI/AHA criteria was 81.5% (Kappa 0.59, <it>p </it>< 0.001). In comparison with patients who met only IDF criteria, patients who met only NHLBI/AHA criteria had significantly more frequently cardiovascular risk factors with the exception of obesity which was significantly more frequent in patients with MetS diagnosed by IDF criteria.</p> <p>Conclusion</p> <p>The MetS prevalence in patients with symptomatic carotid disease was high regardless of criteria used for its diagnosis. Since some patients with known cardiovascular risk factors were lost by the use of IDF criteria it seems that NHLBI/AHA definition is more suitable for diagnosis of MetS. Large follow-up studies are needed to test prognostic value of these definitions.</p

Vitamin C and E Supplementation Effects in Professional Soccer Players Under Regular Training

Exercise training is known to induce an increase in free radical production potentially leading to enhanced muscle injury. Vitamins C and E are well known antioxidants that may prevent muscle cell damage. The purpose of this study was to determine the effects of these supplemental antioxidant vitamins on markers of oxidative stress, muscle damage and performance of elite soccer players. Ten male young soccer players were divided into two groups. Supplementation group (n = 5) received vitamins C and E supplementation daily during the pre-competitive season (S group), while the placebo group (PL group, n = 5) received a pill containing maltodextrin. Both groups performed the same training load during the three-month pre-season training period. Erythrocyte antioxidant enzymes glutathione reductase, catalase and plasma carbonyl derivatives did not show any significant variation among the experimental groups. Similarly, fitness level markers did not differ among the experimental groups. However, S group demonstrated lower lipid peroxidation and muscle damage levels (p < 0.05) compared to PL group at the final phase of pre-competitive season. In conclusion, our data demonstrated that vitamin C and E supplementation in soccer players may reduce lipid peroxidation and muscle damage during high intensity efforts, but did not enhance performance