Creatine is mostly synthesized in the liver via AGAT and GAMT[29][33] (the other locations are neurons,[35] the pancreas, and kidneys[34]) despite it not being stored in high levels in the liver like glycogen or adipose would be. Supplemental creatine is known to suppress AGAT by downregulating transcription,[31] which probably occurs in humans (since the products of AGAT are reduced with creatine supplementation).[39]

This suppression of creatine synthesis is thought to actually be beneficial, since creatine synthesis requires S-adenosylmethionine as a cofactor and may use up to 40-50% of SAMe for methylation[36][37][123] (initially thought to be above 70%, but this has since been re-evaluated[123]) though the expected preservation of SAMe may not occur with supplementation.[487] Reduced creatine synthesis, via preserving methyl groups and trimethylglycine (which would normally be used up to synthesize SAMe), is also thought to suppress homocysteine levels in serum,[38] but this may also not occur to a practical level following supplementation.[487]

Creatine is mostly synthesized in the liver. Supplementation of creatine will suppress subsequent production of creatine in the body, since high levels of creatine will suppress its own synthesis, by downregulating the enzymes of synthesis. This is a reversible suppression.
In regard to liver fat buildup (steatosis), which is normally associated with reduced availability of S-adenosyl methionine[495][496] and a suppression in expression of genes involved in fatty acid oxidation (PPARα and CPT1), creatine supplementation at 1% of the rat diet alongside a diet that induces fatty liver is able to fully prevent (and nonsignificantly reduce relative to the control given standard diets) the aforementioned changes and the state of steatosis, as well as changes in serum biomarkers (glucose and insulin) that accompany steatosis.[126]

These protective effects are similar to those seen with trimethylglycine, since they both cause an increase in liver concentrations of phosphatidylcholine (PC, causing an increase in vLDL production and efflux of triglycerides from the liver).[497] Both TMG and creatine are thought to work indirectly by preserving SAMe concentrations,[126][498] since PC synthesis requires SAMe as well (via PEMT[499]) and genes involved in fatty acid metabolism in the liver that were not affected by the diet (VLCAD and CD36) were unaffected by creatine.[126]

Creatine supplementation appears to be somewhat similar to TMG supplementation in the sense that they both promote localized synthesis of phosphatidylcholine, effluxing triglycerides from the liver into serum and thus potently protecting from diet-induced fatty liver. The concentration at which this occurs is within the range supplemented by humans.
Rats beginning an exercise program are known to experience increased serum levels of some liver enzymes (ALT and GGT). Supplementation of high levels of creatine at 4% of the diet over 60 days does not modify this effect.[500]

Young adult athletes who reported creatine usage for over two years prior to the study (retrospective design) were not significantly different than controls.[501] Elsewhere, in a similar cohort of athletes reporting creatine usage for up to four years, failed to note significant differences in liver enzymes, although a nonsignificant reduction in LDH was noted.[502]

Minor liver lesions (grade I, no grade II or III, pathology not indicative of toxicity) have been studied in SOD1 G93A transgenic mice (a research model for amyotrophic lateral sclerosis or ALS, but used in this study to assess a state of chronic pro-oxidative stress) for 159 days with 2% of feed intake and in CD-1 rats (seen as normal) over 56 days with 0.025-0.5mg/kg in CD-1 mice, although in Sprague-Dawley rats (normal controls) there were no significant differences noted even after 2% of feed intake for 365 days.[503] These observations appear to be due to the strain of the rodents used,[504][503] and human studies on ALS (what the SOD1 G93A transgenic mice are thought to represent) lasting from nine to sixteen months with subjects supplementing with up to 10g of creatine daily have failed to find any abnormalities in serum biomarkers of liver or kidney health.[505][506][507]

There appear to be species-related responses to creatine supplementation in rat livers, where some strains experience non-pathological lesions, which are minor, but indicative of hepatitis. These do not appear to influence all strains, and the human condition it is thought to mimick, ALS, does not appear to be negatively affected.

Yogi120 napísal:Aký čas ubehol od jedla ako si začal cvičiť ? Co si jedol?

LukasqoO napísal:treba pit vela vody po cely den a hlavne popri treningu, nedavaj si zbytocne rychle tempo (zhorsuje sa technika a skorej dojde k urazu), pred cvicenim nejest a po cviceni dat sachre aby ti nebolo zle a doplnil svalovy glykogen
a kedze zacinas, nezabudni na dolezity fakt: pi aj mineralne vody (napr. gemerka, magnesia, budis) - lepsie sa budes regenerovat, taktiez mozes pridat aj nejake horcikove tablety - predides krcom a taktiez zlepsi regeneraciu
drzim palce, hlavne sa nevzdavaj a ked ti aj pride zle, tak si kludne oddychni a docvic neskor (poznam aj takych, ktorym prislo az tak zle, ze sa museli ist vyvracat... ale docvicili )
//horcik uzivam aktualne tento https://www.iherb.com/pr/KAL-Magnesium- ... lets/70143
//skoro by som bol zabudol, nezabudni pri cviceni spravne dychat!

hughito napísal:Pred tréningom aspoň dve hodiny nejedz.

A keď si nikdy nič nerobil a zrazu začneš "makať," tak sa takéto čosi dá aj očakávať. Veľa ľudí pri ťažkej fyzickej námahe aj grcia (to ale skôr pri bojových športoch). Ako nováčik by si mal začať zľahka, nič ti neujde a nezabudni, "svalovica" nie je žiadny znak, že cvičíš dobre. Svalovica je negatívny jav. Musíš cvičiť tvrdo, ale niekedy je menej viac, môže sa dokonca dospieť do stavu pretrénovania a to ta odpíše na pár dní (stalo sa mi to raz v živote).