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This study was designed to measure the electroencephalogram (EEG) after exercise with increasing intensity. In a field test with increments in running velocity a 2-min EEG was recorded, together with blood lactate concentration and heart rate, after each stage. An individual protocol was used, with up to six stages of running to ensure comparability of exercise intensity among the subjects, in each of 19 athletes (17 men, 2 women) experienced in leisure-time running. The exercise consisted initially of three running stages of aerobic exercise intensity without blood lactate accumulation followed by stages with an increase of lactate concentration. The protocol of the field test led to a progressive increase in cortical activity directly after the stages without blood lactate accumulation mainly in the delta frequency band, followed by theta and alpha-1 frequency band, and less pronounced in the alpha-2 and in the beta frequency bands. After the stages with an onset and further increase of blood lactate accumulation significant decreases in the beta-2, beta-1 and alpha-1 frequency bands occurred predominantly in temporal (T3, T4, T5, and T6) and occipital (O1, and O2) electrode positions, indicating a stage-by-stage decrease of activity. This decrease may be explained by feed-back from working muscle, via afferents to the cortex from intero- and proprio-receptors and affective processes. This could suggest that through a higher running intensity indicated by an onset of blood lactate accumulation metabolic and mechanical changes led to alterations within the afferent systems influencing the level of cortical activity.

Muscle damage, recurrent and serious infections or exercise-induced fatigue especially to the end of the playing period in team sport or to the end of preparation for competition in endurance or single sport are the most common symptoms in elite sport demolishing optimal training results. Are micronutrient deficiencies responsible for these symptoms in elite sport. Methods:In 111 elite athletes [male: 50female: 61 / soccer: 21field hockey: 62 -Olympics: 19tennis: 5 -motorsports (DTM-Formula1): 4] blood vitamin D, coenzymeQ10, vitamin B1-B2-B6-B12 and folic acid as well as selenium, ferrum and magnesium intraerythrocytary were determined. In all elite athletes the symptoms muscle damage, infections, sleeping disorder and fatigue were correlated. A Spearman-ranking coefficient of correlation, a chi-quadrat-test by Pearson and an independent t-test were used. Results:In 51, 3% of all elite athletes (N=57/111) a vitamin Ddeficiency (< 30 ng/ml), in 57% (N=61/107) a seleniumdeficiency (< 121 µg/l), in 70% (N=77/110) a coenzymeQ10deficiency (< 750 µg/l) and in 27,1% (N=19/70) a magnesium deficiency intraerythrocytary were established. In cases of young player (< 18) vitamin D and of young national player (U16-U21) ferrum intraerythrocytary compared to national A player were poorly supplied [vitamin D: 25,71 ± 9,58 ng/ml vs 35,87 ± 12,35 ng/ml (p=0,007)ferrum: 407,13 ± 43,09 mg/l vs 460,29 ± 36,69 mg/l (p=0,018)]. Muscle damages (in 73% of all cases) significantly occurred in vitamin D deficiency [29,13 ± 9,38 ng/dl vs 36,27 ± 12,09 ng/dl, p=0,005] and in coenzymeQ10 deficiency [623,31 ± 226,31 µg/l vs 732,93 ± 408,19 µg/l, p=0,039] more frequently. Comparing the settings of vitamin D 40ng/ml [27,50 ± 7,85 ng/ml vs 46,31 ± 6,71 ng/ml, OR=4,53, p=0,007] muscle damage were observed 4,53 times more frequent in the lower group, whereas the settings of vitaminB1-(thiamine) < 50 µg/l vs > 50 µg/l [36,45 ± 7,01 µg/l vs 63,24 ± 24,33 ng/ml, OR=0,38, p=0,045] showed muscle damage in 62% less frequent in the lower group. No significances were observed in infection, sleeping disorder or fatigue. Conclusion:Independantly to the type of sports, except all bvitamines, deficiencies of essential vitamins and trace elements in elite sports were observed. Vitamin D-as well as coenzymeQ10deficiencies and vitaminB1-excess play an important and significant role developing muscle damages. Further studies preventing muscle damages, recurrent infections and fatigue by treating elite athletes with micronutrients to eradicate those deficiencies are necessary.

Muscle injuries and excessive lactate overloads in training or at the end of a season in team sports or at the end of competition preparation in endurance and individual sports are concomitant symptoms in top-level sport, quickly preventing optimal results as well as competition participation. Is whole blood magnesium deficiency responsible for these problems in elite athletes and will magnesium supplementation improve their muscle metabolism or lactate-pyruvate-metabolism? Methods: In 70 elite athletes [male: 35female: 35 / soccer: 19field hockey: 27 -Olympics: 15tennis: 5motorsports (DTM-Formula1): 4] whole blood magnesium were determined. In 25 athletes serum and whole blood magnesium, creatine kinase (CK), venous pyruvate and lactate and the mitochondrial energy level ATP were determined before and after 3 months of daily supplementation with 370mg magnesium and statistically correlated. A Spearman-ranking coefficient of correlation, a chi-quadrat-test by Pearson and an independent t-test were used. p<0.05 was supposed to be significant, p<0.01 highly significant.Results: In 27.1% of all elite athletes (N=19/70) a whole blood magnesium deficiency (vMg<1.29 mmol/l) was proved. Female athletes were significantly worst supplied than the male athletes [vMg: 1.33 ± 0.11 mmol/l vs. 1.41 ± 0.13 mmol/l (p<0.024].Whole blood magnesium (1.31 ± 0.15 mmol/l before vs 1.45 ± 0.09 mmol/l after therapy, p<0.00025), serum magnesium (0.78 ± 0.06 mmol/l before vs 0.93 ± 0.05 mmol/l after therapy, p<0.00025), the venous pyruvate (0.21 ± 0.12 mg/dl before vs 0.39 ± 0.10 mg/dl after therapy, p<0.00025) and mitochondrial ATP (90.56 ± 10.11 %T cells before vs 99.07 ± 1.21 %T cells after therapy, p<0.00025) significantly increased after 3 month supplementation of 370mg magnesiumoxide. Venou slactate (10.62 ± 3.50 mg/dl vs. 8, 08 ± 2.09 mg/dl after therapy, p<0.0025), the pyruvate lactate ratio (69.98 ± 52.81 vs. 22.93 ± 12.29 after therapy, p<0.00025) and the creatine kinase CK (501 ± 323 U/l before vs. 294 ± 161 U/l after therapy, p=0.018) significantly reduced under 3-month of daily magnesium substitution. For each 0.1 mmol/l increase in whole blood magnesium, the pyruvate improves significantly by 0.06 mg/dl and the pyruvate lactate ratio decreases significantly by 90.9. The improvement of the pyruvate as well as the pyruvate lactate ratio leads to a significant improvement in muscle metabolism (CK) [increase by 0.1 mg/dl pyruvate decreases CK by 89.39, p=0.018, reduction of lactate pyruvate ratio decreases CK by 25.45. p=0.008). An absolute risk reduction of 68% (18/25 before vs 1/25 after therapy) could be calculated for muscular injuries. No side effects were reported. Conclusion:The determination of serum magnesium in elite sports is not meaningful. Whole blood magnesium (vMg), on the other hand, plays a significant role in the prevention of muscle injuries, independently to the type of sports, by optimizing pyruvate-lactate-metabolism and thus mitochondrial energy production ATP. Further treatment studies have to prove if op...

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