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Work in Progress Dove postare il proprio programma di preparazione atletica, le proprie esperienze, il proprio diario personale.
Ciao amico visitatore, cosa aspetti? Apri una discussione subito nella sezione Work in Progress |
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(#61)
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One of Us
Messaggi: 36
Data registrazione: Dec 2007
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29-01-2008, 09:04 PM
ottimo il sistema gironda soprattutto quando ci si vuole riprendere da un periodo di abbuffatte o si vuole riprendere subito forma quando si e' appannatucci....l'8x8 e' un po' piu' statico...io l ho provato....qui invece in questi sistemi si cerca di aumentare sempre il peso...si incide anche sulla forza oltre che sul pump....allora greatescape appena hai l allenamento posta che ti do il mio parere.... |
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(#62)
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One of Us
Messaggi: 36
Data registrazione: Dec 2007
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29-01-2008, 09:08 PM
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(#63)
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Ruan
Messaggi: 1,806
Data registrazione: Mar 2005
Località: catanisi sugnu
Età: 42
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29-01-2008, 09:14 PM
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A domani, le mie ali nn aspettano altro... |
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(#64)
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ParentalAdvisoryMember
Messaggi: 288
Data registrazione: Dec 2006
Località: Italia
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29-01-2008, 11:07 PM
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Ragazzi (@metabolic, @Antò) mettete pure qualche fotuzza se potete (non per mancanza di fiducia...tutt'altro: per apprezzare i vostri progressi...non prendetela cm frase da guy, che non lo sono ) |
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(#65)
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One of Us
Messaggi: 36
Data registrazione: Dec 2007
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29-01-2008, 11:39 PM
[quote=spot86;27481]ma questa smania per la chetosi è a puro scopo sperimentale? O per spremere ancor di + l'organismo ad utilizzar gli FFA ? Ragazzi (@metabolic, @Antò) mettete pure qualche fotuzza se potete (non per mancanza di fiducia...tutt'altro: per apprezzare i vostri progressi...non prendetela cm frase da guy, che non lo sono )[/QUOTE ok spot al piu' presto...cioe' non appena raggiungiamo i risultati voluti...ancora c'e' un po' da sudare....io pensavo cmq di provare il sistema da te consigliato...cioe' mi faccio un altro po' di cheto...e poi cmq provo psmf.....vediamo se scendo un altro po'...certo la forza che ho in questo periodo con la cheto e' incredibile....non l avrei con la psmf ma potrebbe farmi scendere ancora quando stallo con la cheto.... |
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(#66)
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One of Us
Messaggi: 36
Data registrazione: Dec 2007
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29-01-2008, 11:42 PM
ah proposito spot se vai su msn....ti devo far vedere delle foto e poi mi dai dei pareri.....magari ci becchiamo la ok?a presto |
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(#67)
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One of Us
Messaggi: 36
Data registrazione: Dec 2007
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29-01-2008, 11:45 PM
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(#68)
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ParentalAdvisoryMember
Messaggi: 288
Data registrazione: Dec 2006
Località: Italia
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30-01-2008, 12:51 AM
[quote=metabolicboy;27489] Quote:
ehehe...ma l'approccio da me consigliatomi era cmq partorito da Antò ehehehe...te lo dissi, no? Boh cmq, me lo son scritto perché sembra validissimo... Scsa se ho risp solo ora caxx.!! Su MSN magari domani,nn so... Per le fot, io dicevo qualcuna dell'inzio qualcuna della fine proprio per vedere i progressi ehehe |
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(#69)
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Ruan
Messaggi: 1,806
Data registrazione: Mar 2005
Località: catanisi sugnu
Età: 42
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30-01-2008, 08:31 AM
[quote=spot86;27499] Quote:
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(#70)
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ParentalAdvisoryMember
Messaggi: 288
Data registrazione: Dec 2006
Località: Italia
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31-01-2008, 06:38 PM
eheh ragazzi ma ancora non vi riprendete?? Antò volevo farti una domanduzza: stimolanti come la caffeina in genere quanto tempo prima del refeed andrebbero staccati? +in particolare mi interessava sapere, QUANTO influisce staccare o meno la caffeina sulla sens. insulinica (mi interessa xké son in CKD, ricarico dal sabato mattina e stacco con the, caffè, the verde, coca light già giovedì, cioè 48h prima)... P.S.: un po' OT, ma so che questo 3ed lo vedi di sicuro..spero non dispiaccia. |
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(#71)
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Guybrush
Messaggi: 3,950
Data registrazione: Feb 2005
Età: 39
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31-01-2008, 07:57 PM
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(#72)
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One of Us
Messaggi: 36
Data registrazione: Dec 2007
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01-02-2008, 01:25 AM
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(#73)
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Ruan
Messaggi: 1,806
Data registrazione: Mar 2005
Località: catanisi sugnu
Età: 42
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01-02-2008, 10:01 AM
Coffee acutely modifies gastrointestinal hormone secretion and glucose tolerance in humans: glycemic effects of chlorogenic acid and caffeine1,2,3 Kelly L Johnston, Michael N Clifford and Linda M Morgan The objective of this study was to assess whether the consumption of dietary amounts of CGA in coffee had any effects on plasma concentrations of glucose, insulin, GIP, and GLP-1 in humans. Welsch et al (9) postulated that 5-CQA–mediated dissipation of the Na+ electrochemical gradient was responsible for the observed decrease in glucose uptake in rat BBM vesicles; therefore, we suggest that coffee consumption in humans would have similar effects on intestinal glucose transport. This study showed that both caffeinated and decaffeinated coffee drinks significantly attenuated postprandial GIP secretion compared with the control beverage. Postprandial secretion of GIP occurs in the proximal region of the small intestine and is stimulated by the absorption of nutrients from the gut rather than by their presence in the intestinal lumen (12). The rate of absorption of glucose determines the magnitude of the GIP response (15); therefore, these data strongly suggest that coffee decreases the rate of intestinal absorption of glucose. Glucose homeostasis is known to be achieved by a coordinated physiologic response to the ingestion of food, the 2 main effectors of which are 1) limitations on the delivery of glucose into the pool, ie, the maximum rate of glucose absorption, and 2) the rate of disposal of glucose into the tissues, which is itself mainly a consequence of increased insulin action (16). Up until 30 min, the increase in plasma glucose concentrations can be attributed solely to increased delivery into the circulation as a result of increased intestinal absorption in response to the load. Once this has peaked, peripheral metabolism of glucose (ie, delivery into muscle and fat tissue in addition to hepatic glucose metabolism) will have a significant effect on overall plasma concentrations and, thus, any differences seen cannot be solely attributed to effects on absorption (17). Glucose, insulin, and GIP profiles were therefore analyzed over the initial postprandial time period. Differences in GLP-1 were additionally assessed during the latter parts of the study, because this hormone is secreted from the distal region of the small intestine (18). Plasma glucose concentrations were significantly higher after consumption of caffeinated coffee than after consumption of the control beverage or decaffeinated coffee when a comparison of the means and of the TAUCs was made. The nature of the interaction between coffee consumption and glucose tolerance remains controversial. However, most of the physiologic effects of coffee can be attributed to the presence of caffeine (19). The physiologic effects of coffee began to receive attention when caffeine was first shown to inhibit the action of phosphodiesterase, an enzyme involved in the catabolism of cyclic adenosine monophosphate (cAMP) (20). Increased concentrations of cAMP have been shown to increase glycogenolysis, which may be partially responsible for the significantly impaired glucose tolerance seen after consumption of the caffeinated coffee compared with both the control and the decaffeinated coffee beverages. Caffeine is also an adenosine receptor antagonist (21) and therefore can inhibit muscle glucose uptake, even in the presence of insulin (22). Moreover, Sharp and Debnam (23) have shown that acute luminal exposure of enterocytes to cAMP in vivo has stimulatory effects on sugar transport across the BBM and the basolateral membrane, and Debnam et al (24) provided evidence for a similar effect of cAMP in the regulation of sodium-dependent glucose transporter–mediated glucose transport across isolated rat renal BBM. Taking into consideration the known actions of caffeine, we propose that the differences in plasma glucose profiles further confirm the potent pharmacologic actions of caffeine but also imply that CGA has an antagonistic effect on glucose transport, because integrated glucose concentrations were lowest after consumption of the decaffeinated coffee beverage. Pizziol et al (25) previously suggested that caffeine causes impaired glucose tolerance by inducing a rise in blood glucose concentrations that is independent of insulin. However, these authors use the terms caffeine and coffee interchangeably and do not consider the action of other biologically active components present in coffee, namely CGA. In our study, plasma insulin concentrations showed small differences in the early part of the postprandial period, which were consistent with the mildly impaired glucose tolerance seen after consumption of the caffeinated beverage compared with the decaffeinated beverage. However, the small differences in plasma insulin observed in this study lack the statistical power to refute the claims by Pizziol et al with any confidence. Although glucose is the major regulator of insulin secretion, incretin gut factors have been estimated to be responsible for as much as 50% of the insulin secretion observed after an oral glucose load and the term "enteroinsular axis" was introduced to encompass the gut factors responsible for this (26–28). The secretion of the incretin hormones GIP and GLP-1 were significantly altered in response to the test beverages compared with the control. GIP secretion was attenuated after consumption of both the caffeinated and decaffeinated coffees compared with that after consumption of the control beverage. GLP-1, in contrast with GIP, is secreted from the distal portion of the small intestine and responds to the presence of nutrients in the gut lumen rather than to their absorption (29). Its secretion can be increased when the absorption of carbohydrate is delayed (30). Circulating GLP-1 concentrations were significantly enhanced after consumption of decaffeinated coffee, later in the postprandial time period. These opposing effects of incretin hormones would have minimized any effects of coffee on insulin secretion. However, the gastrointestinal hormone data are consistent with delayed glucose uptake in the small intestine, ie, uptake occurring further down the small intestine. We suggest that at the level of the BBM, coffee exerts it physiologic effects via CGA-mediated Na+ electrochemical gradient dissipation—the driving force for active glucose assimilation. This is reflected in and supported by the gastrointestinal hormone profiles but not in those for plasma insulin and glucose. However, the potent biological effects of caffeine on both hepatic glucose output and muscular uptake suggest that plasma glucose and insulin concentrations are a poor biomarker when interpreting the gastrointestinal effects of coffee on glucose transport in the small intestine. Our previous work showed that consumption of the same volume of commercial apple juice containing significant amounts of CGA (500 µmol/L) as well as other bioactive dietary phenols, such as phloridzin (60 µmol/L), significantly delays glucose uptake and shifts absorption to a more distal region of the gastrointestinal tract, as indicated by a similar change over time in plasma GIP and GLP-1 concentrations (31). Compared with the present study, in which the test beverages contained 2.5 mmol total CQA/L (the dietary equivalent of 2 small strong cups of coffee), the effects after apple juice consumption were less pronounced but not as much as would be expected if CGA were the only agent responsible given the large difference in CQA concentrations between the 2. It is therefore likely that most of the effects seen after apple juice consumption were mediated by phloridzin, a potent competitive inhibitor of sodium-dependent glucose transporter 1 and one that is commonly used in physiologic studies to abolish glucose transport (32). Recent evidence to support the clinical effects of dietary polyphenols is provided by van Dam and Feskens (33), who showed in a prospective cohort study that the risk of developing clinical type 2 diabetes was 0.5 times as likely in individual persons who drank 7 cups (1659 mL) coffee/d than in those who drank <=" BORDER="0"> 2 cups (474 mL) coffee/d. The results of their study strongly suggest that coffee consumption can have clinical benefits; the results of our study suggest a possible mechanism whereby these benefits might be mediated. IN SINTESI: La caffeina aumenta il Camp inibendo le fosfodiesterase, questo comporat un aumento della glicogenolisi e quindi una inibizione dell'uptake di glucosio da parte delle cellule e la glicogenosintesi. La caffeina è anche un antagonista dei recettori dell'adenosina e ciò blocca l'uptake di glucosio da parte delle cellule muscolari anche in presenza di alti livelli di insulina. Il consumo di caffè aumenta i livelli plasmatici di glucosio ed insulina, ma, a livello intestinale sembra rallentare l'assorbimento del glucosio, o megio, spostarlo nelle porzioni + distali dell'intestino (via inibizione del rilascio degli ormoni incretina, che rispondono al flusso di nutrienti nel tratto gastrointestinale). Questo mi da da pensare che l'aumento della glicemia e dell'insulina dopo 30 min dal'assunzione di caffè sia da riportare alla sola glicogenolisi epatica (EGP- epathic glucose production). Di contro, su altri studi che leggevo, sembrerebe che l'attivazione dei recettori beta2 adrenergici migliori la glicogenosintesi e l'uptake di glucosio, aumentando il trasporto di questo via nn-insulina-mediata (appena li trovo li posto). Caffeina e caffè sono cmq due "bestie" diffreneti. Sembra che il ralentamento dell'uptake di glucosio a livello intestinala dato dal consumo di caffè sia da imputare al suo contenuto di polifenoli ed altre sostanze Quindi, in cKD, direi: caffeina duranyte la scarica, con dosi a scalare (forte dosaggio 2 gg dopo la carica per poi staccare almeno 6/8 pre prima del primo pasto di refeed). Questo dovrebbe velocizzare la glicogenolisi epatica e forzare l'enrata in ketosi. Durante la ricarica andare di the verde ( che come postato da homer, migliora l'uptake di glucosio via trasportatori glut-4). |
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(#74)
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Ruan
Messaggi: 1,806
Data registrazione: Mar 2005
Località: catanisi sugnu
Età: 42
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01-02-2008, 10:15 AM
Stamane sempre in ketosi profonda. Oggi refeed dopo un bel depletion fullbody WO, pensavo di tirarmi 30 serie, 2 ex x gruppo in serie giganti: leg press + leg ext-> 4 x 8/12 (e già vomiterò) distensioni manubri + croci manubri-> 4 x 8/12 pulley + push down braccia tese-> 4 x 8/12 alzate laterali + tirate mento-> 3 x 8/12 se mi sento bene un 3 giri di serie composte x biceps e triceps. Sono indeciso riguardo le gambe, se allenarle o meno (lo farei solo per coinvolgere + grandi gruppi muscolari e deplezionare meglio), ho dolore al soleo sinistro (causa metaboy che mi ha fatto camminare per ore attorno la pista da ballo ed i vari shortini che mi avranno disidratato di brutto..) Colazio andrò di protidi polverose. Aumento insulina e glucagone, aumento glicemia via gluconeogensi e glicogenolisi epatica, uscita dalla ketosi, ma senza un aumento della glicemia per "via diretta"... |
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(#75)
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One of Us
Messaggi: 36
Data registrazione: Dec 2007
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01-02-2008, 11:05 AM
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