Changes in hydration status of soccer players competing in the 2008 European Championship.

AIM: Body composition is highly modifiable through exercise and may be changed by the physical stress of soccer training and competition. Especially body water as a constituent of body composition is assumed to be subjected to changes. It is speculated that during the most important soccer championship the combination of heat and the strenuous competitive program could lead to the development of a chronic state of hypohydration. However, no one tested this hypothesis. Therefore, the purpose of present work was to investigate the impact of the European Soccer Championship 2008 on players' body composition. METHODS: Participants were 14 players of one team, split into Starters (N.=7) and Non-Starters (N.=7). Starters participated in the games, while Non-Starters served as substitutes, with marginal playing times. Body composition was examined by bioelectrical impedance analysis before the championship and 36 hours after the first and second game. RESULTS: After the first game, Starters and Non-Starters showed decreased extra-cellular mass (-3.3% and -5.5%) and body cell mass (-4.1% and -6.1%) compared to prechampionship measurements. The impedance vector graph showed a significant lengthening in both groups (Starters T²=30.5, P=0.000; Non Starters T²=39.0, P=0.000). After the second game, extra-cellular mass (-3.4%) and body weight (-1.1%) decreased in Starters only. ANOVA revealed a significant difference in extra-cellular mass between Starters and Non-Starters (P=0.027). The impedance vector graph was lengthened in the Starters only (T²=17.5, P=0.000). The distance covered during the games was correlated to the percent drop in extra-cellular mass between the end of games 1 and 2 (r=-0.602; P=0.023). CONCLUSION: Players competing in the European championship games experienced a decrease in extra-cellular mass and body weight. The impedance vector graph showed a lengthening, indicating fluid loss. Therefore, proper hydration of players requires diligent attention.

Deltamethrin differentially affects neuronal subtypes in hippocampal primary culture.

The effects of deltamethrin on neuronal development and survival were studied using primary mouse hippocampal neurons in culture. Repeated applications of deltamethrin (between 2 nM and 2000 nM) decreased the number of neurons by 16-40%, respectively. Neuronal death was accompanied by an overall decrease of synaptic proteins. Deltamethrin treatment increased the K(+)-stimulated release of amino acid transmitters, GABA and glutamate. The release of the latter might also contribute to neuronal damage. A considerable number of neurons survived treatment with high concentrations of deltamethrin (200-2000 nM) and still displayed characteristics of mature neurons such as synaptic contacts or the expression of members of the Kv1 channel family. When analyzing subtypes of neurons calbindin- as well as somatostatin-positive neurons decreased by 50% after repeated treatment with 2 nM deltamethrin. Under the same conditions neuropeptide Y-positive neurons were up-regulated by 250%.Taken together these data show that deltamethrin at concentrations relevant in human toxicology differentially affects survival of neuronal subtypes by exerting either deleterious or supportive effects. We conclude that deltamethrin disturbs fine-tuning of neuronal efficiency in neuronal networks and might also interfere with the correct wiring during development.

Acute toxicity and mutagenicity of the copper complex of pyruvaldehyde-bis (N-4-methylthiosemicarbazone), Cu-PTSM.

Cu-PTSM is a potential imaging agent for the heart and brain when labeled with either 64Cu or 62Cu. Unlabeled Cu-PTSM was evaluated for its acute toxicity and mutagenicity. Cu-PTSM had an i.v. LD50 of 26 mg kg-1 in the rat and 2 mg kg-1 in the rabbit. At necropsy, rats exhibited severely hemorrhagic lungs, histological findings of acute pulmonary congestion, hemorrhage and edema, and mild congestion in kidney, liver and brain. The rabbit displayed marked polymorphonuclear infiltration in alveoli, peribronchial and periarterial areas with marked macrophage hyperplasia, congestion and mild hemorrhage into alveolar spaces. No effects were found in kidney, liver, testes or brain. Administration of 2.16 micrograms kg-1 day-1 for 5 days per week for 2 weeks resulted in no changes in histopathology, hematology or clinical chemistry parameters. This daily dose is at least 300 times the diagnostic dose intended for use in man. Cu-PTSM was not mutagenic when tested in the absence of S9 supernatant, but elicited a weakly mutagenic response in the presence of S9. Since acute effects in the lung occur at doses approaching 300,000 times the diagnostic dose, it is highly unlikely that the clinical use of Cu-PTSM would result in any acute adverse effects.