Improving neuromuscular performance in young basketball players: plyometric vs. technique training.

AIM: The aim of this study was to compare the effects of plyometric training versus basketball technique training on improving neuro-muscular performance. METHODS: Thirty-six (age 14.9±0.9 years, body height 164.0±7.6 cm, body weight 54.0±8.7 kg, BMI 20.1±2.4 kg·m-2) basketball players girls were randomly allocated to 2 groups: Basketball Plyometric Training (BPT, N.=18) and Basketball Technique Training (BTT, N.=18). The players were tested by two specific tests: counter movement jump (CMJ) and squat jump (SJ) before and after 6 training weeks. RESULTS: The jump height, as dependent variable, showed a different trend as an effect of the different training protocols, in contrast with the current knowledge. Manova did not show significant interactions between the two groups for the height of jumps, while significant differences were found for interaction time × training (P<0.05) and for main effect × time (P<0.001). After training, the BPT group increased significantly CMJ performance by 11.3% (P<0.05), whereas the BTT group increased by 4.6%. Likewise, the BPT group demonstrated a significant greater improvement of jump height than BTT group (an increase of 15.4% vs. 7.5%, P<0.01; respectively). CONCLUSION: These results suggest that both training protocols proposed in this study improved vertical jump performance. However, a combination of the two protocols, plyometric training and sport-specific-exercises, could be useful to optimize performance by an easy transition from controlled a-specific to sport-specific performance requirements. In conclusion, BPT is a safe and effective method of achieving a favourable neuro-muscular performance than BTT in female basketball players.

Psychological well-being and social participation assessment in visually impaired subjects playing Torball: a controlled study.

The aim of this study was to evaluate the differences in psychological well-being, symptomatic psychological disorders and social participation, between blind Torball players and non-players. Thirty blind male participants were recruited, 17 Torball players (aged 36.27±3.46) and 13 non-players (aged 34.80±2.53), and evaluated for social participation level, psychological well-being and symptomatic psychological disorders, using three validated self-report questionnaires: Participation Scale (PS), Psychological Well-Being Scale (PWBS) and Symptom Checklist 90 R (SCL-90-R) respectively. ANOVA showed significant overall differences between the two groups. The social restriction score in the non-player group was significantly higher (p<0.01) than the player group. The Torball player group showed significant better scores than non-player group in 5 of the 6 dimensions of the PWB Scale (p<0.01) and in 8 of the 10 dimensions of the SCL-90-R (7 dimensions p<0.01; 1 dimension p<0.05) and in the three global scores of the SCL-90-R (p<0.01). The results of this study showed a relationship between psychological well-being and social skills of visually impaired people and their Torball practice.

Long-term treatment with S-adenosylmethionine induces changes in presynaptic CaM kinase II and synapsin I.

BACKGROUND: According to current hypotheses, antidepressant drug action is the result of adaptive changes in neuronal signaling mechanisms rather than a primary effect on neurotransmitter transporters, receptors, or metabolic enzymes. Among the signaling mechanisms involved, protein kinases and phosphorylation have been shown to be modified by drug treatment. Presynaptic signaling (calcium/calmodulin-dependent protein kinase II [CaMKII]) and the protein machinery regulating transmitter release have been implicated in the action of these drugs. METHODS: We investigated the effect of S-adenosylmethionine (SAM), a compound with putative antidepressant activity, on presynaptic CaMKII and its synaptic vesicle substrate synapsin I. The activity of CaMKII was assayed in synaptic subcellular fractions prepared from hippocampus (HI), frontal cortex (FCX), striatum (STR), and parieto-temporal cortex. RESULTS: The kinase activity was increased after SAM treatment in the synaptic vesicle fraction of HI (31.7%), FCX (35.9%), and STR (18.4%). The protein level of CaMKII was also increased in synaptic vesicles of HI (40.4%). The synapsin I level was unchanged in synaptic vesicles but markedly increased in synaptic cytosol of HI (75.8%) and FCX (163.0%). No changes for both CaMKII and synapsin I level were found in homogenates, suggesting that synaptic protein changes are not explained by an increase in total level of proteins, but rather by translocation to nerve terminals. CONCLUSIONS: Similar to typical antidepressant drugs, SAM induces changes in CaMKII activity and increases synapsin I level in HI and FCX nerve terminals, suggesting a modulatory action on transmitter release.

Relationships between conformational behaviour and binding affinity towards beta 1 and beta 2 adrenoceptors of some chiral phenoxypropanolamines with bulky N-substituents.

The optical isomers of a series of phenoxypropanolamine compounds with N-substituents bulkier than isopropyl have been synthesized, and their binding affinity towards beta 1 and beta 2-adrenoceptors has been determined. A computational study, including a Molecular Dynamics (MD) simulation and quenching in water and a GRID analysis provided some useful suggestions for possible interpretation patterns for the different affinity exhibited by the compounds studied.

Molecular properties of the WB4101 enantiomers and of its chiral methyl derivatives for alpha 1-adrenoceptor recognition.

The optical isomers of the well known alpha 1-antagonist WB4101 and of its derivatives with a methyl group in the oxyethyl moiety were prepared for the evaluation of their alpha-adrenoceptors binding affinity. By means of a detailed computational analysis, the present work shows that the introduction of a methyl group affects the behaviour of WB4101 in different ways. A limitation of the conformational freedom in certain regions of the torsional subspace of the potential energy function, differences in the reactivity of the protonated species towards a model proton acceptor and the quality of the superposition with the rigid template for alpha 1 antagonists, corynanthine, are examined and discussed in order to select a candidate bioactive form and possible features which act as modulators of the recognition process at the alpha 1-adrenoceptors.

Regulation of prolactin secretion during suckling: involvement of the hypothalamo-pituitary GABAergic system.

Previous results demonstrated that GABA exerts a dual control on PRL secretion, one excitatory mediated in part by the impairment of the tubero-infundibular dopaminergic (TIDA) system function, the other inhibitory occurring at the level of the anterior pituitary (AP), where 3H-GABA and 3H-Muscimol (3H-M) recognition sites have been described. This report provides evidence for a physiological role of the tubero-infundibular GABAergic system (TI-GA-BA) on PRL secretion in the rat. In lactating rats separated for 4 h from their pups reinstitution of suckling for different periods resulted in an increase either in glutamic acid decarboxylase (GAD) activity in the mediobasal hypothalamus (MBH) or in AP-GABA content. Dynamic changes of the GABAergic function in the MBH-AP system seemed to have a certain degree of specificity because suckling did not affect GAD activity in the caudate nucleus. In lactating rats 2, 4, 8 and 24 h after removal of the offsprings AP-GABA concentrations and plasma PRL titers significantly decreased with respect to values present in rats never separated from their pups. Since it has been demonstrated that the PRL lowering effect of GABA is a receptor-mediated event, we have investigated the plasticity of AP-GABA receptors during suckling. The inhibitory action of GABA seems to be mediated mainly by the activation of the high affinity binding sites. This proposition is supported by the fact that in lactating rats, where only the high affinity receptor population is present, M was still able to decrease significantly plasma PRL concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Cyclic nucleotides in experimental and human brain tumors.

It is well known that the system of cyclic nucleotides plays an important role in cell differentiation and proliferation. Cyclic AMP is capable of stimulating cell growth, and cyclic GMP is thought to control cell division and growth. The authors measured adenylcyclase activity (AC) and cGMP content in the tumor latency period and in early neoplastic proliferations in rats with brain tumors induced by transplacental ethylnitrosourea (ENU). AC activity, which is high during the first days of life, decreases until it reaches, at the 60th day, levels lower than those in control animals. Cyclic GMP, on the contrary, increases during the first month in treated animals and remains consistently higher than controls up to the 45th day. In fully developed experimental brain tumors (mixed gliomas, isomorphic and polymorphic oligodendrogliomas) the percentage of reduction in AC activity is significantly higher. AC activity was measured also in human tumoral tissue. In malignant tumors it is markedly lower than in benign tumors. In the same patients cAMP in the cerebrospinal fluid was measured with results similar to those obtained in tissues. These findings confirm that the system of cyclic nucleotides is implicated in all the developmental phases of brain tumors and therefore may reveal how research can clarify the first transformations of tumoral cells.

Metabolism and brain uptake of gamma-aminobutyric acid in galactosamine-induced hepatic encephalopathy in rats.

Kinetic studies of [3H]gamma-aminobutyric acid ([3H]GABA) after an intravenous injection were performed in normal rats and in rats with severe degree of hepatic encephalopathy due to fulminant hepatic failure induced by galactosamine. Moreover, plasma and brain GABA levels, and GABA and glutamic acid decarboxylase activity were studied in some brain areas. After intravenous injection, [3H]GABA disappeared very rapidly in the blood of normal rats, with a prompt increase of 3H metabolites. In comatose rats, a delayed disappearance of [3H]GABA was parallelled by a lower amount of metabolites, indirectly indicating a peripheral decrease of GABA-transaminase activity. The amount of [3H]GABA in brain was lightly but constantly lower in comatose rats than in controls, indicating that the change in permeability of the blood-brain barrier in hepatic encephalopathy does not affect the [3H]GABA uptake of the brain. Furthermore, the assay of endogenous GABA in blood, whole brain, and brain areas did not show any significant difference in any of the two groups. The finding that glutamic acid decarboxylase activity in brain was reduced, together with the indirect evidence of a reduction in GABA-transaminase, may account for the steady state of GABA in hepatic encephalopathy. However, the reduction in glutamic acid decarboxylase activity is in favor of a functional derangement at the GABA-ergic nerve terminals in this pathological condition.

Cerebellar cyclic GMP and behavioral effects after acute and repeated administration of benzodiazepines in mice.

The previous finding that benzodiazepine-induced changes in cyclic GMP in the cerebellum were poorly correlated with the impairment of motor function has now been extended further. The effects following acute, and during repeated administration of diazepam, quazepam and flurazepam were studied in mice. A 10 day period of daily treatment with 5 mg/kg p.o. was used in these studies. The content of cGMP was significantly reduced (P less than 0.05) during the chronic administration of quazepam and flurazepam except after 10 days for flurazepam. After diazepam, cGMP levels were lower than in control animals but a significant difference was observed only at the sixth and tenth day because a minimal threshold dose was used. Antagonism of pentylenetetrazol-induced convulsions was significantly (P less than 0.05) effective over the 10 day treatment for all drugs. Spontaneous motor activity was reduced by quazepam given for two days and by diazepam given for one day while this measure was unaffected by flurazepam given at the same dose which was effective in the other tests. These results further supported a lack of association between changes of cGMP content in the cerebellum and sedative or muscle relaxant effects of benzodiazepines, whereas the lowering of cGMP levels seemed to parallel effects that are not subject to tolerance such as the antagonism of pentylenetetrazol-induced convulsions.

Role of central nervous system-derived or circulating gamma-aminobutyric acid on prolactin secretion in the rat.

To investigate the respective role in PRL secretion of gamma-aminobutyric acid (GABA), either derived from the central nervous system or circulating in plasma, experiments were performed using ethanolamine-O-sulfate (EOS), a specific inhibitor of GABA catabolism. Intracerebroventricular injection of EOS (2 mg/kg) induced in unanesthetized male rats 2-8 h post injection a clear-cut rise in hypothalamic, anterior pituitary (AP), and plasma GABA concentrations. Rises in GABA titers occurred earlier in the hypothalamus and AP (2 h) than in the plasma (4 h). Concomitant to alterations of GABA, there was a striking lowering of plasma PRL evident at 2 h and still present 24 h after EOS administration. In contrast, systemic administration of graded doses of EOS (200-400 mg/kg, iv) did not induce significant changes in plasma GABA concentrations 4 h post injection; only the 600 mg/kg dose of EOS increased GABA concentrations 4 h post injection in the hypothalamo-AP system and decreased plasma PRL concentrations. Finally, in hypophysectomized rats bearing ecotopic pituitaries, despite the occurrence of rises in the hypothalamic GABA after intracerebroventricular or systemic (600 mg/kg) administration of EOS, AP, plasma GABA, and plasma PRL concentrations were not altered. In all these findings indicate that: 1) changes in plasma PRL are best correlated to variations in the amino acid titers occurring in the hypothalamo-AP systems; and 2) circulating GABA does not play a functional role in the control of PRL secretion. Finally, since alterations in blood GABA levels after central or systemic administration of EOS appear to reflect primary changes occurring in the brain concentration of the amino acid, circulating GABA may be a reliable indicator of central nervous system GABAergic function.