Druckbare Version
guten abend
sie scheinen gut involviert zu sein :winke:
nicht die einnahme sondern der dadruch induzierte "zeitdruck" etwas in ein vorher definierten zeitspanne zu tun , könne mE zu einer vermehrten "stresslage" im körper führen
halten sie die supplemention von n-acetylcystein prinzipiell ebenfalls für sinnvoll?
es wirkt ja antioxidativ
mfg
hi
könnte es theoretisch nicht auch sein dass stress zur apoptose führen könnte??beim stress werden doch Mastzellen durch Substanz-P zur vermehrten Zytokinausschüttung angeregt.Das macht dann die selben Endfaktoren wie hormonell nachgeschaltet.Wenn du bereits angegriffene zellen hast dann besteht kein Unterschied zwischen den Schäden der Stresshormone und den Schäden der Androgene aber auch eine chronische Stressituation bei noch gesunder zelle könnte jedoch ein organ auf dauer multihormonell schädigen/empfindlich auf stress machen?
hier wäre auf jeden fall eine n-acetylcystein supplementierung sinnvoll
Texas researchers have found a naturally occurring hormone that can extend the lifespan of mice by as much as 30 percent, a discovery that opens a new avenue of research into human longevity.
The hormone has a drawback, however - it decreases fertility and increases susceptibility to diabetes, the team reported Thursday in the online edition of the journal Science.
The hormone - called Klotho after one of the Greek fates who controlled the length of human life - is produced in the brain and kidney in a variety of species, but leaks out into the blood stream.
Pathologist Dr. Makoto Kuro-o and his colleagues at the University of Texas Southwestern Medical Center, who discovered the hormone, had previously reported that mice lacking the gene for Klotho begin showing signs of premature aging at around three to four weeks of age and die after about two months, compared to a normal mouse lifespan of two years.
The team genetically engineered mice to produce excess amounts of the hormone. They reported that the genetically engineered males lived 31 percent longer than normal males, while genetically engineered females lived 19 percent longer than their normal counterparts.
The team also found that the hormone produces its effect by increasing the body's resistance to insulin, a phenomenon that has previously been shown to correlate with extended lifespan.
Low-calorie diets that prolong life, for example, also increase insulin resistance.
But insulin resistance is also a symptom of diabetes - although the altered mice were not found to have unusually high levels of glucose in their blood, the primary symptom of the disease.
The hormone is also found in humans, and researchers are now beginning to look to see if long-lived people have above-average levels in their blood.
da igf -1 ja durch sport vermehrt ausgesendet wird, könnte sport schädlich sein
mfg
hi
diese studie hier untermauert die schädlichkeit von IGF -1 noch mehr
*ironie an* "Sport ist Mord" *ironie aus*
"Role of insulin/insulin-like growth factor 1 signaling pathway in longevity"
"Human
Although human ageing is more complicated than C.elegans and rodents, centenarian, sporadic mutations, and diseases studies have given significant insight on the role of the insulin/IGF-1 signaling in human longevity. In humans, insulin sensitivity normally declines during aging, and insulin resistance is an important risk factor associated with a variety of intermediate phenotypes (hypertension, atherosclerosis, obesity) strongly affecting morbidity, disability, and mortality among the elderly [3,31].
Roth et al.[32], reported that the most people with insulin levels live longer. More recently, data from 466 healthy subjects with a wide age range (range 28-110 years) demonstrated a significant reduction of insulin resistance in subjects 90-100 year old[33]. These data suggest an intriguing peculiarity of this age category and indicate that an efficient insulin response has an impact on human longevity.
Interestingly, polymorphisms at IGF-IR, PI3KCB, IRS-1, FOXO1A have been investigated[34]. IGF-I plasma levels, which decrease significantly with age, are affected by the polymorphisms at IGF-IR and PI3CKB genes, both alone and in combination. In particular, individuals bearing at least one allele A at the IGF-IR locus (IGF-IR A+) have lower plasma IGF-I levels than the rest of the population. Also, IGF-IR A+ subjects are found in increased proportion in long-lived individuals. Moreover, genotype combinations of an A allele at the IGF-IR locus and a T allele at the PI3CKB locus (A+/T+ subjects) affect IGF-I plasma levels (having A-/T- individuals the highest free IGF-I plasma levels), as well as longevity, and the proportion of A+/T+ subjects significantly increased among long-lived individuals.
Recently, Anisimov et al.[35], firstly reported that mutation located downstream to daf-16 in human insulin signal transduction system is associated with longevity. They invested a group of 137 elderly individuals and concluded that a greater frequency of the apolipoprotein C-III-455C allele was correlated with aging (P<0.005). Also, it is worth noting that centenarians display lower degree of resistance to insulin and lower degree of oxidative stress as compared with elderly persons before 90 years[36]. Moreover, Ruiz-Torres and Soares de Melo Kirzner compared ageing parameters of young (up to 39 years) and old (over 70 years) individuals having similar IGF-1 blood levels, the result was that old males with IGF-1 levels similar to young ones do not show the age-dependent decrease in serum testosterone and lean body mass, nor the increase in fat body mass. This provides powerful evidence on the important life-potential role of this peptide[37].
DISCUSSION
From the data presented, the insulin/IGF-1 pathway has the similar characters in C.elegans, D.melanogaster, rodents and humans, which include the constitution of the gene, the role in regulation of aging and longevity. All these can be concluded that the pathway exists long ago and the mechanism of aging is evolutionarily conserved.
Reviewing the available data on the benefits and adverse effects of caloric restriction and genetic modifications Longo and Finch suggested three categories of drugs which may have the potential to prevent or postpone age-related diseases and extend life span: drugs that (1) stimulate dwarf mutations and therefore decrease pituitary production of GH; (2) prevent IGF-1 release from the liver, or (3) decrease IGF-1 signaling by the action on either extracellular or intracellular targets[18]. According to this, Anisimov concluded and reported that effects of antidiabetic biguanides seems to be more adequate in the prevention of age-related deteriorations in glucose metabolism and in insulin signaling pathway as well as in such important for longevity parameters as a fertility and a resistance to oxidative stress and tumorigenesis than those induced by caloric restriction and genetic manipulations[25].
Although, the insulin/IGF-1 pathway can regulate the life span in different species, the molecular mechanism largely remains unknown. The most possible is that the pathway can enhance the stress resistance. Murakami et al., reported that fibroblasts from Snell dwarf mice show resistance to a variety of forms of lethal injury, including ultraviolet light, heat, paraquat, H2O2, and the toxic metal cadmium. This cellular stress resistance may lead to resistance to late-life diseases and frailty, and thereby increase longevity[38]. Using DNA microarray analysis, Murphy et al.[39], found the insulin/IGF-I pathway not only do cells function non-autonomously to regulate life span but also exert their effect on life span by upregulating a wide variety of genes, including cellular stress-response, antimicrobial and metabolic genes, and by downregulating specific life-shortening genes. In human, Barbieri et al.[36], suggest that centenarians may have been selected for appropriate insulin regulation as well as for the appropriate regulation of tyrosine hydroxylase gene, whose product is rate limiting in the synthesis of catecholamines, stress-response mediators. It was shown that catecholamine may increase free radical production through induction of the metabolic rate and auto-oxidation in diabetic animals[25,40].
On the other hand, although the insulin/IGF-1 pathway is evolution conserved, the pathway in mammals is more complicated than other low animals. While disruption of the insulin/IGF-1 receptor in nematodes and flies increases lifespan significantly, mammals with genetic or acquired defects in insulin signaling pathway are at a risk for age-related diseases and increased mortality. This contradiction can be explained by the acquisition of more complicated metabolic pathways in mammalians over evolution. Mammals have insulin/IGF-1 receptors in many organs, but their functions are opposite if they are located in the central nervous system or in the periphery; whereas lower species have insulin/IGF-1 receptors signaling mainly through the nervous system. Furthermore, mammalians have different and very specific receptors for insulin and IGF-1, with distinct pathways and diverse functions[41].
Human longevity is mysterious. Though we have found the role of insulin/IGF-1 pathway in regulation of longevity, further investigation would shed light on the molecular mechanism of the pathway so that we will get more methods to decrease the age-related diseases and everyone will be centenarians."
1) Haushaltszucker ist KEIN NaturproduktZitat:
Zitat von Joop75
2) 1g/KG alle 1-2h ist auch viel zu viel und ein hoher GI ist auch nicht nötig
http://www.ncbi.nlm.nih.gov/entrez/q...838&query_hl=4
Hier wird sind die Werte für CHo, die als hoch und moderat gelten für post exercise gelten noch ander eGesetze, aber die Studie find´ ich gerade net.
hi
hier die antwort vom herrn moosburger , facharzt für innere medizin und sportarzt zu whey
das ist zu hinterfragen. heißt "schneller" automatisch "effizienter? schneller im blut heißt noch lange nicht schneller im muskel. alles, was resorbiert wird, gelangt zunächst mal in die leber. und die entscheidet dann darüber, was und wieviel in den großen kreislauf und damit zu den organe gelangt.
außerdem betrifft das "open window" die glykogenresynthese und nicht die proteinsynthese innerhalb der muskelzelle - diese ist ein viel längerdauernder prozess, der praktisch rund um die uhr abläuft (parallel zum proteinabbau. es kommt also auf die N-bilanz an, und diese ist, so wie die energiebilanz, ein überdauernder prozess). wieviel gramm muskelmasse, glaubst du, kann man pro tag aufbauen? warum also der "stress", innerhalb 30-45 minuten eine menge protein ins blut zu bringen?
keine frage, whey-protein ist ein biologisch hochwertiges protein. aber ist es wirklich "besser" als alle anderen tierischen proteine? ich habe oben eine studie präsentiert, die gezeigt hat, dass milchprotein (casein) effizienter ist. warum also nicht ein großes glas (fettreduzierte) milch oder buttermilch vor und/oder nach dem training trinken? und denk bitte an das ei-protein, das die höchste biologische wertigkeit aller lebensmittel hat (wenn man von kombinationen absieht - klassisches beispiel ei + kartoffel, siehe den abschnitt über die proteinqualität in meinem artikel "der proteinstoffwechsel").
machen wir nicht den fehler und sind der nahrungsergänzungsmittelindustrie hörig! mit einer zweckmäßigen ernährung kann man dem körper alles bieten, und das mindestens so gut wie mit einem supplement. außerdem spart es geld. die meisten supplemente sind sowieso fakes. glaub mir, es "geht" auch ohne proteinshakes, wenn man sich vernünftig ernährt.
und das, worauf man sich besonders konzentrieren sollte, ist der trainingsreiz. die trainingseffizienz lässt bei vielen zu wünschen übrig. ineffektives training lässt sich mit keinem supplement kompensieren. wer "ganz normal" zwei- bis dreimal am tag isst und effizient trainiert, wird allemal den größeren trainingseffekt erzielen als jemand, der vor lauter angst vor "muskelschwund" alle 3 stunden isst und sich mit whey-protein zuschüttet.
gruß, kurt
p.s.: wenn schon eine proteinsupplementation, würde ich ein präparat bevorzugen, das aus molke- und milchprotein besteht.
der doc hat sicher recht, der Trainingsreiz ist (eine gute ernährung vorausgesetzt) sicher entscheidender. Aber man will ja immer das optimum rausholen, also noch ein whey nach dem Train und 2h Später Eiweisshaltig essen. So seh ich das.
Gruss
Der einzige sinn von protein supplements besteht darin die eiweissreiche ernaehrung angenehmer zu machen. wer versucht hat uber laenger zeit grosse mengen von fleisch, quark und eier zu jeder tages- und nachtzeit zu essen weiss wovon ich rede - man fuehlt sich wie ein Zombi!
irgendwann ekelt es einen an. shakes bringen ein bisschen fun in die sache.
Hab hier noch nen feinen Artikel:
http://www.natural-bb.de/phpBB_CMS/i...opic=2&post=27