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Precorrina-3B_sintasi: definition of Precorrina-3B_sintasi and synonyms of Precorrina-3B_sintasi (Italian)

Precorrina-3B sintasi Da Wikipedia, l'enciclopedia libera.

La precorrina-3B sintasi è un enzima appartenente alla classe delle ossidoreduttasi, che catalizza la seguente reazione:

L'enzima è una proteina ferro-zolfo. Un atomo di ossigeno dal diossigeno è incorporato nel macrociclo al C-20. Nel meccanismo di biosintesi aerobico della cobalamina, quattro enzimi sono coinvolti nella conversione della precorrina-3A in precorrina-6A. La prima delle quattro reazioni è catalizzata dalla precorrina-3B sintasi (CobG), generando precorrina-3B come prodotto. Questo è seguito da tre reazioni di metilazione, che introducono un gruppo metilico al C-17 (CobJ; numero EC 2.1.1.131), C-11 ,(CobM; numero EC 2.1.1.133) ed al C-1 (CobF; numero EC 2.1.1.152) del macrociclo, generando rispettivamente precorrina-4, precorrina-5 e precorrina-6A.

Bibliografia
  • Scott, A.I., Roessner, C.A., Stolowich, N.J., Spencer, J.B., Min, C. and Ozaki, S.I. (1993). Biosynthesis of vitamin B12. Discovery of the enzymes for oxidative ring contraction and insertion of the fourth methyl group . FEBS Lett. 331: 105–108. Entrez PubMed8405386.
  • Debussche, L., Thibaut, D., Cameron, B., Crouzet, J. and Blanche, F. (1993). Biosynthesis of the corrin macrocycle of coenzyme B12 in Pseudomonas denitrificans . J. Bacteriol. 175: 7430–7440. Entrez PubMed8226690.
  • Warren, M.J., Raux, E., Schubert, H.L. and Escalante-Semerena, J.C. (2002). The biosynthesis of adenosylcobalamin (vitamin B12) . Nat. Prod. Rep. 19: 390–412. Entrez PubMed12195810.

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Meccanismo aerobico sportsbook

Caffeine

DESCRIZIONE

La caffeina è la 'droga' psicoattiva più consumata in tutto il mondo. I consumatori abituali sono più dell'80% della popolazione. La caffeina è un alcaloide naturale e la si trova in più di 60 piante, ma le fonti maggiori sono il caffè e il the, seguite dal cioccolato, matè, cola ed energy drinks (anche alcuni farmaci la contengono, es.analgesici e diuretici) .Il caffè contiene il 50-70% in più di caffeina rispetto al the. Il valore di caffeina per tazza di caffè varia molto, ma si aggira intorno ai 100-150 mg.

CLASSIFICAZIONE

La caffeina é una metilxantina (1,3,7 trimetilxantina)

così come la teobromina (3,7 dimetilxantina) e la teofillina (1,3 dimetilxantina).

E' un farmaco stimolante il SNC e il metabolismo.

INDICAZIONI

La caffeina migliora la soglia di attenzione, e le capacità intellettive. Migliora le prestazioni fisiche, riduce la fatica e ritarda l'insorgenza del sonno.

METABOLISMO

la caffeina è assorbita dal tratto gastrointestinale velocemente e completamente.

Si ha assorbimento completo dopo 1 h dall'ingestione.

Non subisce modificazioni da first-pass nel circolo splancnico. Il picco plasmatico è raggiunto dopo 15 120 min dall'ingestione.

Generalmente l'attività fisica non influenza la farmacocinetica della caffeina.

La caffeina é così idrofobica da passare attraverso tutte le membrane plasmatiche ed è rapidamente distribuita in tutti i tessuti del corpo. La distribuzione di caffeina nel plasma segue una cinetica lineare di primo ordine.

Per dosi superiori a 250mg si ha saturazione del metabolismo, e la comparsa di effetti indesiderati.

La caffeina viene metabolizzata dal sistema microsomiale epatico (CytP450). Sono stati identificati almeno 25 metaboliti. Il più importante meccanismo matabolico porta alla formazione di 3 dimetilxantine attraverso reazioni di demetilazione : paraxantina (80%), teobromina(11%), teofillina(5%). Il restante 5% viene trasformato in acido trimetilurico e trimetiluracile o eliminato inmodificato con le urine.

Ad un dosaggio basso il citocromo P450 sottotipo 1A2 e 2E1, è interamente responsabile della formazione delle dimetilxantine.

In caso di intossicazione (>200 microM/l) vengono reclutati altri sottotipi di CYT P450.

L'emivita della caffeina è di 2,5-10 h nell'adulto, si prolunga notevolmente nel neonato (60-100 h) a causa dell'immaturità del suo sistema enzimatico.

La caffeina viene filtrata a livello renale, ma riassorbita a livello tubulare. Solo 0,5-3% della caffeina plasmatica è elimitata come tale nelle urine.

C'è una enorme variabilità interindividuale nella concentrazione urinaria di caffeina, questo è dovuto per il 70% alla variabilità individuale del CYT P450 A2.

I valori di concentrazione urinaria,negli atleti agonisti, non devono superare 12microg/mL nelle misurazioni dopo gara, come imposto dall'International Olympic Committee.

MECCANISMO D'AZIONE
  • Inibizione dell'enzima fosfodiesterasi (PDE) portando le concentrazioni di cAMP intracellulare a livelli più alti. Questo spiegherebbe la stimolazione cardiaca e il rilasciamento della muscolatura liscia.
    • Inattivazione (in sinergismo con il glucosio) della glicogenolisi (nel muscolo scheletrico) e attivazione della glicogeno sintetasi.
  • Inibizione dei recettori per l'adenosina con antagonismo recettoriale. (l'adenosina è capace di contrarre la muscolatura liscia bronchiale ed aumentare il rilascio di istamina dalle cellule presenti nel polmone.)
  • Induzione del rilascio di ioni calcio dal reticolo sarcoplasmatico attivando il canale RyR.
EFFETTI COLLTERALI E TOSSICITA'

100-200mg (1-2 tazze di caffè) leggera stimolazione corticale, con aumento dell'attenzione e diminuzione del senso di fatica.

1g (5-10 caffè) determina nervosismo, ansietà,cambiamenti di umore, tremori, insonnia, aritmie cardiache,disturbi gastroenterici.

1.5g (>12) agitazione,ansietà,tremori.

2.5g (16-40)stimolazione bulbare e convulsioni.

10g (100) dose letale.

PERFORMANCE FISICHE

E' noto da più di cento anni il fatto che la caffeina migliori le prestazioni fisiche e riduca il tempo di recupero dalla fatica. I suoi effetti ergogenici sono sfruttati da molte diverse discipline sportive, che coinvolgano sia esercizi aerobici che di resistenza.

performance di lunga durata (corsa o ciclismo con 30-60 min al 60-80% del VO2 max), migliora il 'time to exhaustion' del 20-50%, mentre ha effetti irrilevanti sulla velocità e sulla forza.

performance di breve durata, (lavoro aerobico intenso della durata inferiore a 30 min con un VO2 max >90%), aumenta il 'time to exhaustion', in maniera ridotta rispetto ad un esercizio di lunga durata;

lavoro aerobico intenso (100% della VO2 max della durata di 5 min), gli effetti sul 'time to exhaustion' sono minimi.

sprint di corsa ( >150% della vo2max) non si hanno più effetti positivi.

D'A lessandro Rossella & Kakaa Omar

Caffeine as a pain-reliever aid Global vision on caffeine chemical properties

Pharmacokinetics

Caffeine is completely absorbed by the stomach and small intestine within 45 minutes of ingestion. The time in which maximum plasmatic concentration is obtained (Tmax) is 30–45 minutes. The half-life of caffeine varies widely among individuals according to such factors as age, liver function, pregnancy, some concurrent medications, and the level of enzymes in the liver needed for caffeine metabolism. Other factors such as smoking can shorten caffeine's half-life.

Metabolism

The hepatic cytochrome P-450 (CYP) isoenzyme metabolizes most of the caffeine (95%) into more than 25 metabolites in humans, the primary of those are three dimethylxanthines, that have their own effects on the body

  • Paraxanthine (84 %) is the result of a demethylation in N-3 Has the effect of increasing lipolysis, leading to elevated glycerol and free fatty acid levels in the blood plasma.
  • Theobromine (10 %) is the result of demethylation in N-1 and acts as a mild stimulant, a mild diuretic and by relaxing the smooth muscles of the bronchi in the lungs and therefore it has been beneficial to those with asthma. It acts also dilating blood vessels and on colon smooth muscle as a relaxant.
  • Theophylline (5%) is the result of demethylation in N-7 and acts as a vascular, bronchiole, muscular, and respiratory relaxant.

Later the caffeine metabolites are filtered by the kidneys and they are excreted in the urine with a first order kinetic.

Global vision on caffeine effects in the human body

Mechanisms of action

Caffeine acts in the body’s cells by different mechanisms of action and on a wide range of molecular targets. It intervenes as:

  • an antagonist of the adenosine receptors;
  • an competitive nonselective phosphodiesterase inhibitor, provoking the raise of the

    intracellular cAMP, the actvivation of PKA and begin the phosphorylation of specific enzymes;

  • a sensitizer of calcium liberation channels;
  • a GABA receptor antagonist.

Other cardiovascular processes are related to the reduction of cytoplasmic Ca2+ in the VSMC through CAMP and the increase of the same in the endothelial cell, favoring the synthesis of NO .

For caffeine is both water-soluble and lipid-soluble, it readily crosses the blood–brain barrier . Once in the brain, caffeine mainly acts as a nonselective antagonist of adenosine receptors. Infact, its molecule is structurally similar to adenosine one and binds to adenosine receptors on the surface of cells, acting as a competitive inhibitor.

Usually, adenosine is found in every part of the body, but it has special functions in the brain, where it is an inhibitor neurotransmitter that suppresses activity in the central nervous system. It's shown that increasing levels of adenosine are related to various of metabolic stress such as anoxia or ischemia. The are also evidence that indicates that brain adenosine protect the brain by suppressing neural activity and also by increasing blood flow through A2A and A2B receptors located on vascular smooth muscle.

There are reasons to believe that adenosine may be more specifically involved in control of the sleep-wake cycle wake-promoting neurons via A1 receptors, and activation of sleep-promoting neurons via indirect effect on A2A receptors.

Several classes of adenosine receptors have been described, with different anatomical distributions.

  • A1 receptors : are widely distributed and act to inhibit calcium uptake.
  • A2A receptors : are heavily concentrated in the basal ganglia, an area that plays a critical role in behavior control, but can be found in other parts of the brain as well, in lower densities. There is evidence that A 2A receptors interact with the dopamine system, which is involved in reward and arousal. (A2A receptors can also befound on arterial walls and blood cell membranes.)

This explains how caffeine's effect works, so that's why caffeine has a generally disinhibitory effect on neural activity (Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects, 1992) causing the increase of arousal and alertness. Moreover caffeine blocks adenosine receptor A2 , that has a vasodilatator effect, promoting cerebral vasoconstriction . (Caffeine's Vascular Mechanisms of Action, 2010)

Caffeine in migraine pain relieving – The vascular Theory

Centrally, in the brainstem and spinal cord, adenosine is a painkiller, but peripherally, in the outer reaches of the nervous system, it causes pain.

Adenosine applied to the skin causes localized pain and vasodilation.

Adenosine dilates blood vessels in the head and neck.

Many researches have demonstrated that, during migraine episodes, the concentration of adenosine in the head and neck is increased above normal, causing vascular dilatation of the area. The dilation provokes an increase pressure on nerves, causing the headache.

Physiologically, norepinephrine action is to constrict blood vessels, whereas adenosine inhibits its release from noradrenergic neurons, and therefore causes vasodilation.

Caffeine alters this situation by blocking adenosine receptor A2, prevents adenosine from inhibiting norepinephrine release, so caffeine increases the amount of norepinephrine released by neurons, and thereby causes vasoconstriction. As a result, caffeine restores blood pressure of the area relieving the pain . (The analgesic effects of caffeine in headache, 1991)

However, the vascular theory has several problems, one of them is the observation that many times blood vessels routinely constrict and dilate without causing pain. Infact, experiments in which blood pressure in the brain was artificially increased failed to produce migraine-like symptoms. The new scientific consensus is that migraine is a neurovascular disorder, the modified idea being that a central nervous system dysfunction leads to the vascular dilation. Many lay authors, however, still assume the vascular dilation directly generates migraine pain.

Caffeine as an adjuvant ingredient

Many studies have shown that caffeine added in the amount of 100 mg to standard pain relievers, such as aspirin, paracetamol and ibuprofen (Caffeine as an adjuvant to ibuprofen in treating childhood headaches, 2007) , is believed to boosts their speed and effectiveness by 30 to 40 %. One proposed mechanism for the adjuvant effect of caffeine is that caffeine expedites delivery of the other medicines by speeding up absorption through the gut wall into the bloodstream, or by increasing heart rate, thereby speeding the painrelievers in the blood stream . For this reason, caffeine is also a common ingredient in many prescription and over-the-counter headache medications.

The amount of caf feine contained in this caffeinated drugs is the same that half a cup of coffee provides ( 65-70 mg ).

Tolerance and withdrawal

Caffeine tolerance develops very quickly, especially among heavy coffee and energy drink consumers, some studies also suggest that with a daily doses of 250 milligrams of caffeine tolerance quickly develops within four days. That's because caffeine is primarily an antagonist of the central nervous system's receptors for the neurotransmitter adenosine, so the bodies of individuals that regularly consume caffeine adapt to the continuous presence of the drug by substantially increasing the number of adenosine receptors in the central nervous system. This increase in the number of the adenosine receptors makes the body much more sensitive to adenosine, with two primary consequences:

  1. the stimulatory effects of caffeine are substantially reduced, a phenomenon known as a tolerance adaptation.
  1. because these adaptive responses to caffeine make individuals much more sensitive to adenosine, a reduction in caffeine intake _will effectively increase the normal physiological effects of adenosine, resulting in unwelcome withdrawal symptoms in tolerant users (Low-dose caffeine physical dependence in humans, 1990).

The withdrawal cause the blood vessels of the head to dilate, leading to an excess of blood in the head and causing a headaches and nausea. Reduced catecholamine activity may cause feelings of fatigue and drowsiness. A reduction in serotonin levels when caffeine use is stopped can cause anxiety, irritability, inability to concentrate, and diminished motivation to initiate or to complete daily tasks; in extreme cases it may cause mild depression. Withdrawal symptoms may appear within 12 to 24 hours after discontinuation of caffeine intake, peak at roughly 48 hours, and usually last from one to five days, representing the time required for the number of adenosine receptors in the brain to revert to "normal" levels , uninfluenced by caffeine consumption.

Caffeine is the most widely used psychoactive stimulant with prevalent use across all age groups. Caffeine is found in varying quantities in the seeds, leaves, and fruit of some plants, where it acts as a natural pesticide that paralyzes and kills certain insects feeding on the plants. It is most commonly consumed by humans in infusions extracted from the bean of the coffee plant and the leaves of the tea bush, as well as from various foods and drinks containing products derived from the kola nut. Other sources include yerba maté, guarana berries, guayusa, and the yaupon holly. Recently there has been an increase in energy drink consumption leading to caffeine abuse, with aggressive marketing and poor awareness on the consequences of high caffeine use. With caffeine consumption being so common, it is vital to know the impact caffeine has on the body, as its effects can influence cardio-respiratory, endocrine, and perhaps most importantly neurological systems.

Caffeine is synthesized in plants from the purine nucleotides AMP, GMP, and IMP. These in turn are transformed into xanthosine and then theobromine, the latter being the penultimate precursor of caffeine.

Absorption

Caffeine from coffee is absorbed faster than caffeine from cold drinks. Some reasons for this could be: the lower temperature of the beverage may decrease the rate of blood flow within the intestines; phosphoric acid in cold drinks could decrease gastric emptying; absorption rate could increase with caffeine dose; sugar in cold drinks could inhibit gastric emptying of caffeine and delay absorption.

Caffeine disperses throughout the body and penetrates the biological membranes, the blood brain barrier and placenta, however it does not accumulate in the tissues or organs.

Metabolism

Caffeine is converted into dimethylxanthines, dimethyl and monomethyl uric acids, trimethyl and dimethyl-allantoin and uracil derivatives in the liver. Only 2–3% of caffeine is excreted in urine unchanged. While caffeine itself is eliminated overnight from the body, some primary metabolites such as theobromine and theophylline have longer half-lives.

Caffeine and its primary metabolites, theobromine, paraxanthine, and theophylline are identified in all body fluids. Paraxanthine is responsible for an increase in the lipolysis process, which releases glycerol and fatty acids into the blood to be used as a source of fuel by the muscles. Theobromine is a vasodilator that increases the amount of oxygen and nutrient flow to the brain and muscles. Theophylline acts as a smooth muscle relaxant that chiefly affects bronchioles and acts as a chronotrope and inotrope that increases heart rate and force of contraction.

Cardiovascular and Respiratory Effects

Experimental studies have shown that administration of coffee or caffeine acutely raises blood pressure, circulating concentrations of (nor)epinephrine, increases arterial stiffness, impairs endothelium dependent vasodilation and inhibits ischemic preconditioning. The adverse effects of chronic coffee consumption on traditional risk factors for coronary heart disease are less consistent: although coffee intake slightly increases blood pressure, and plasma concentrations of homocysteine and cholesterol, there is no association with the incidence of hypertension, and a strong negative association with the incidence of type 2 diabetes mellitus. An increase in the respiration rate (RR) is the prime effect dependent on the plasma caffeine value.

Gastrointestinal Effects

Caffeine can stimulate the secretion of stress hormones (such as epinephrine and norepinephrine), which can increase blood pressure. Moreover, stress hormones activate the body's "fight or flight" reactions, causing the body to redirect blood supply from the digestive system to muscles. In this way, decreased blood flow to the gastrointestinal tract will slow down the absorption rate and lead to indigestion. Moreover, the additional epinephrine increases the secretion of the main gastric hormone gastrin, which will speed up gastric peristalsis and hypersecretion of gastric juice. Additional gastric acid will lead to acidic chyme going into the small intestine and cause intestinal injury. Therefore, it is not recommended for ulcer patients to drink too much coffee.

Urinary Effects

Caffeine intake increases renal excretion of sodium and water. This is caused by both slightly increasing the glomerular filteration rate and inhibiting the tubular reabsorption of sodium and water. Although the ability for caffeine and theophylline to induce diuresis and natriuresis is well established, the mechanisms behind them are not well understood. It has been suggested that inhibition of phosphodiesterases in the proximal tubule may contribute to the diuretic and natriuretic effects of methylxanthines. (Diuretic potential of energy drinks, 2006)

Stress can be defined to when the human body is not able to cope suitably to physical or emotional threats. The brain is the major component of interpreting and responding to potentially stressful events and determines what is stressful.

Studies show that during periods of increased stress, caffeine consumption increases. Caffeine increases cortisol secretion by stimulating the central nervous system so it is advisable to individuals with hypertension to avoid caffeine during periods of stress as this further increases blood pressure. Chronic caffeine consumption causes sensitization of a specific subset of cannabinoid receptors in the striatum, consistent with the psychoactive properties of the compound. This may explain why enhanced relaxation and a sense of well being are some of the reported effects of caffeine use during stressful events.

HOCKEY su ghiaccio by Chiara Giudici on Prezi

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Transcript of HOCKEY su ghiaccio

La resistenza specifica

La resistenza è la capacità di resistere alla stanchezza tollerando sforzi di media o lunga durata.

resistenza generale o di base

Le qualità motorie

Forza veloce o potenza

La forza è la qualità motoria condizonale che permette di esprimere un lavoro in contrapposizione a una resistenza.

La forza nell'hockey si esprime nelle forme:

Nel caso dell'hockey, si parla di resistenza a lunga durata, dove predomina il meccanismo aerobico.

Per allenare la resistenza specifica si

adegua l'allenamento ai particolari obiettivi.

Alcuni metodi di allenamento sono:

lavoro continuo a ritmo costante

metodo ad ondature varie

Un esercizio per allenare la coordinazione può essere il controllo del dischetto con il bastone.

L'equilibrio consiste nella capacità di mantenere una posizione stabile per il proprio corpo in differenti situazioni statiche o dinamiche.

Nel caso dell'hockey si parla di equilibrio dinamico poichè cambia col movimento.

Viene definita come la qualità motoria che ci permette di eseguire un gesto nel minor tempo possibile.

corretta tecnica esecutiva

capacità di concentrazione

Nell'hockey si alternano fasi anaerobiche e fasi aerobiche.

Es. velocità di reazione = lancio del puck all'inizio della partita

La mobilità è la capacità di compiere un movimento utilizzando la massima escursione articolare.

Le principali capacità coordinative generali che vengono coinvolte sono:

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