| |||||||
| Low-Carb L'angolo delle diete a basso contenuto di carboidrati o se si desidera basate su grassi e proteine |
![]() |
| | LinkBack | Strumenti Discussione | Cerca in questa Discussione | Modalità Visualizzazione |
| |
| |||
| i tre studi che seguono non sono stati reperiti da me, ma da un bravissimo medico tedesco che segue atleti. tali studi supportano la convinzione che l'acidosi metabolica possa inficiare l'anabolismo ed agevolare il catabolismo. Il dato, stando alle ricerche di questo medico tedesco, successivamente supportate da ulteriori studi di un ricercatore americano (anch'egli appassionato di bbing)è di fondamentale importanza. ci sono diversi fattori che inducono a ritenere che l'acidosi metabolica sia più alta nei soggetti che si allenano per diversi motivi, tra cui: 1)assunzione di grandi quantità di proteine 2)allenamento anaerobico 3)assunzione di cibo prima di dormire 4)uso di bevande acide tipo coca-light in particolare è opportuno osservare, stando alle parole del medico tedesco, che "protein by itself isn’t acidic, because NH3 from the amino acids can act as a H+-buffer, it’s the sulphur and phosphate content of the typical amino acids e.g. in meat. Whey is better against acidosis because of a lesser content of these amino acids." deve tuttavia precisare cosa debba intendersi per sostanza acida. questo non è il mio terreno preferito, quindi sarò sisntetico: una sostanza è acida quando produce H+-. a questo punto cosa accade? riportiamo ancora le parole del doc.: " To eliminate the excess acids the body has to bind the H+-ions to NH3 which it gets from catabolizing tissue (mostly muscle). " in sostanza, sembrano esserci due vie cataboliche in seguito all'acidosi: 1)incremento del cortisolo (del quale aumento non si capisce bene l'origine) 2)uso delle proteine per portare il corpo in uno stato alkalino. Am J Physiol Renal Physiol 2003 Jan;284(1):F32-F40 Neutralization of Western diet inhibits bone resorption independently of K intake and reduces cortisol secretion in humans. Maurer M, Riesen W, Muser J, Hulter HN, Krapf R. Medizinische Universitatsklinik und Zentrallabor, Kantonsspital Bruderholz, CH-4101 Bruderholz/Basel; Institut fur klinische Chemie und Hamatologie, Kantonsspital, CH-9007 St. Gallen, Switzerland; and Genentech, Incorporated, South San Francisco, California 94080-4990. A Western-type diet is associated with osteoporosis and calcium nephrolithiasis. On the basis of observations that calcium retention and inhibition of bone resorption result from alkali administration, it is assumed that the acid load inherent in this diet is responsible for increased bone resorption and calcium loss from bone. However, it is not known whether the dietary acid load acts directly or indirectly (i.e., via endocrine changes) on bone metabolism. It is also unclear whether alkali administration affects bone resorption/calcium balance directly or whether alkali-induced calcium retention is dependent on the cation (i.e., potassium) supplied with administered base. The effects of neutralization of dietary acid load (equimolar amounts of NaHCO(3) and KHCO(3) substituted for NaCl and KCl) in nine healthy subjects (6 men, 3 women) under metabolic balance conditions on calcium balance, bone markers, and endocrine systems relevant to bone [glucocorticoid secretion, IGF-1, parathyroid hormone (PTH)/1,25(OH)(2) vitamin D and thyroid hormones] were studied. Neutralization for 7 days induced a significant cumulative calcium retention (10.7 +/- 0.4 mmol) and significantly reduced the urinary excretion of deoxypyridinoline, pyridinoline, and n-telopeptide. Mean daily plasma cortisol decreased from 264 +/- 45 to 232 +/- 43 nmol/l (P = 0.032), and urinary excretion of tetrahydrocortisol (THF) decreased from 2,410 +/- 210 to 2,098 +/- 190 &mgr;g/24 h (P = 0.027). No significant effect was found on free IGF-1, PTH/1,25(OH)(2) vitamin D, or thyroid hormones. An acidogenic Western diet results in mild metabolic acidosis in association with a state of cortisol excess, altered divalent ion metabolism, and increased bone resorptive indices. Acidosis-induced increases in cortisol secretion and plasma concentration may play a role in mild acidosis-induced alterations in bone metabolism and possibly in osteoporosis Swiss Med Wkly 2001 Mar 10;131(9-10):127-32 Metabolic and endocrine effects of metabolic acidosis in humans. Wiederkehr M, Krapf R. Medizinische Universitatsklinik Bruderholz, Bruderholz/Basel, Switzerland. Metabolic acidosis is an important acid-base disturbance in humans. It is characterised by a primary decrease in body bicarbonate stores and is known to induce multiple endocrine and metabolic alterations. Metabolic acidosis induces nitrogen wasting and, in humans, depresses protein metabolism. The acidosis-induced alterations in various endocrine systems include decreases in IGF-1 levels due to peripheral growth hormone insensitivity, a mild form of primary hypothyroidism and hyperglucocorticoidism. Metabolic acidosis induces a negative calcium balance (resorption from bone) with hypercalciuria and a propensity to develop kidney stones. Metabolic acidosis also results in hypophosphataemia due to renal phosphate wasting. Negative calcium balance and phosphate depletion combine to induce a metabolic bone disease that exhibits features of both osteoporosis and osteomalacia. In humans at least, 1,25-(OH)2 vitamin D levels increase, probably through phosphate depletion-induced stimulation of 1-alpha hydroxylase. The production rate of 1,25-(OH)2 vitamin D is thus stimulated, and parathyroid hormone decreases secondarily. There is experimental evidence to support the notion that even mild degrees of acidosis, such as that occurring by ingestion of a high animal protein diet, induces some of these metabolic and endocrine effects. The possible role of diet-induced acid loads in nephrolithiasis, age-related loss of lean body mass and osteoporosis is discussed. Kidney Int 1997 Jan;51(1):216-21 Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: new cause of growth hormone insensitivity in humans. Brungger M, Hulter HN, Krapf R. Klinik B fur Innere Medizin, Kantonsspital, St. Gallen, Switzerland. The effects of metabolic acidosis on growth hormone and IGF-1 are poorly understood. We investigated the effects of chronic metabolic acidosis (induced by administration on NH4Cl, 4.2 mmol/kg body wt/day) on the growth hormone/IGF-1 endocrine axis in 6 normal male volunteers during metabolic balance conditions. NH4Cl administration resulted in hyperchloremic metabolic acidosis with plasma bicarbonate decreasing from 25 +/- 0.4 to 15.5 +/- 0.9 mmol/liter (P < 0.001). Metabolic acidosis significantly decreased serum IGF-1 concentration from 45 +/- 6 to 33 +/- 6 nmol/liter (P = 0.002), while serum IGF binding protein 3 concentration was not affected significantly. The growth hormone response to growth hormone releasing factor administration (1 microgram per kg body wt, intravenous bolus) was enhanced significantly during acidosis. The IGF-1 response to growth hormone administration (0.1 U kg body wt subcutaneously, every 12 hr for 48 hr) was blunted significantly during acidosis. Apparent endogenous serum half-life and metabolic clearance rates of growth hormone were not altered significantly by acidosis. Metabolic acidosis in humans results in a significant decrease in serum IGF-1 concentration without a demonstrable effect on IGF binding protein 3, and is related to a resistance to the hepatocellular action of growth hormone. The primary defect in the growth hormone/IGF-1 axis occurs via an impaired IGF-1 response to circulating growth hormone with consequent diminution of normal negative feedback inhibition of IGF-1 on growth hormone, as evidenced by the exaggerated growth hormone response to growth hormone releasing factor administration. SEGUE.... zaeus direbbe"LA PROSSIMA VOLTA, PRIMA DI ELEGGERE FALSI MITI, saranno fulmini e saette!" io dico: il prossimo che si permette di paragonarmi a certi personaggi...si becca un fulmine nelle chiappe!
__________________ Ultimate bodyopus system |
| |||
| Perdonate l'intromissione,pur essendo nuovo vorrei intervenire. Volevo constatare che anche gli allenamenti aerobici molto prolungati producono acidosi. Ve lo posso garantire perchè controllo giornalmente(anzi controllavo,ora lo faccio solo in concomitanza ad allenamenti molto pesanti)il ph delle urine ed integro di conseguenza(regobasic ecc..). Cmq l'acidosi comporta la perdita di calcio che va ovviamente reintegrato(nn dai formaggi possibilimente perchè generano anch'essi acidosi,parmigiano in primis,che è l'alimento piu acido in assoluto)i citrati servono solo a tamponare l'acidosi,ma se il calcio è già stato perso allora va reintegrato. Tra l'altro l'acidosi compromette,o perlomeno rallenta,il recupero,per evitarla cmq basta avere un alimentazione ricca di cibi alcalini(frutta,verdura,patate e uva sultanina in primis). Carne,pesce,formaggi,cereali sono alimenti acidificanti,andrebbero sempre accompagnati da alimenti alcalinizzanti(come direbbe il buon cordain,e tanti altri) |
| |||
| Ciao, scusate se mi intrometto, ma vorrei chiedervi un consiglio. Da 7 gg sto seguendo una dieta solo proteica (solo il mattino a colazione mangio una fetta di pane di segale + proteine) per una durata totale di 10 gg. Solo che da tre giorni mi sento molto stanca, assonnata e le gambe indolenzite Come potrei integrare? Ci sono delle vitamine che dovrei assumere? ![]() Grazie. Chicca |
![]() |
| Strumenti Discussione | Cerca in questa Discussione |
| Modalità Visualizzazione | |
| |