si ma a questo punto ti fai una cheto... e ti assicuro si puo fare molto molto piu "salutare"...tra virgolette perchè è assolutamente impropio parlare di salutare con queste diete...
Mr Italia
In Stretching
si ma a questo punto ti fai una cheto... e ti assicuro si puo fare molto molto piu "salutare"...tra virgolette perchè è assolutamente impropio parlare di salutare con queste diete...
Principiante
Allora precisiamo un po le cose :
1 - Ripeto che questa dieta che ho postato è una specie di dieta di "riparazione" x chi ha bisogno di effetti veramente immediati.
2 - Preciso ulteriolmente che NON va protratta per piu' di 2 settimane!!! magari a qualkuno basta anke una settimana, è soggettivo.
3 - Si soffre molto meno la fame
4 - Ovvio che è una dieta per definizione e per chi ha appena iniziato a fare del bb nn è assolutamente adatta!!!
5- E' sicuramente meno salutare e della cheto (nn ho mai scritto che lo fosse) ma molto piu' efficace in breve tempo.
6 - Provare per credere!!
Brandon Curry
Quasi Istruttore
Ripeto il concetto a scanso di ulteriori equivoci.
Se è andata bene per Te, Kurt, me ne compiaccio.
Per gli altri: occorre adattarla, in base a tanti fattori, età., peso, sedentarietà, attività sportiva, fabbisogno, e così via.
E' inutile dire: provatela perché su di me ha funzionato. Il sequitur "...e quindi può funzionare sugli altri" non è assolutamente garantito.
Queste cose le lasciamo scrivere alle riviste di BB e affini perché devono vendere. Qui invece, poiché non si vende nulla, l'esperienza diretta va bene, ma deve essere limitata a questo.
Stop.
Mr Italia
In Stretching
Originariamente Scritto da tattoos
super quoto
Principiante
Raga ma è facile fare un conto delle calorie e ricamare questa dieta su se stessi!!! Ovvio che NON intendevo convincere nessuno ad usare certe determinate quantita' di carbo pro e grassi!! E' lo schema della dieta l'importante, poi calcolare le dosi è soggettivo!!
Mr Olympia
Ciclo di Forza
...bene..ottimo....adesso spiega la teoria che vi è dietro questo approccio alimentare...
.....guarda come imposto io un nuovo piano alimentare, nn mi limito ad affermare "questa doeta è pefetta", ma spiego da dove ho estrapolato alcune teorie:
riporto da un mio post su fituncesored:
il mio schema è
4 o 5 gg
2gr protidi/kg LBM
6 gr O3 o 10gr olio di lino
da 20 a 50gr di CHO post wo
verdure fibrose
12 / 24 ore refeeding
25 / 50gr di grassi max
5-8 / 10-16gr cho/kg LBM
2gr protidi/kg LBM
le differenze sono da riportarsi alla propria FM (fat mass), + è alta meno voluminoso ed intenso deve essere il refeeding
15% bf -> i valori + bassi, 5 gg digiuno controllato
< 15% -> valori medi (12 ore refeeding a 8gr cho/kg lbm) 5 gg digiuno controllato
12% -> 24 ore di refeeding a 10gr cho/kg lbm, 4 gg digiuno controllato
<12% -> i valori + alti, 5 gg digiuno controllato
lunedì-> allenamento A
martedì->allenamentoB
mercoledì-> rest o cardio
giovedì->rest o cardio
venerdi-> full body , refeeding dal post wo a sabato (12 ore)
sabato-> rest, terminate le 12 ore rientri in dieta
domenica->rest, dieta isocalorica (40-30-30 o 33-33-33...cho-fat-pro) con un deficit del 20 o 30%
"la domenica la dieta è variabile per adattarla alla persona ed ai suoi bisogni, con uno schema 5 + 1 ci si dovrebbe allenare la domenica e ricarica il giovedì PM o venerdì, per molti tale approccio nn è fattibile (il sabato si esce e ci si vuole rilassare, la domenica la si passa in famiglia..ecc...)"
somiglia alla ud2, ma è + restrittiva n termini calorici..cmq è abbastanza variabile...ad esmpio, invece di farti 12 ore di refeeding te ne fai solo 5 ore ( con la metà dei CHO naturalemnte) ogni 2 gg e 1/2 o 3 (2 refeeding a settimana da 5 ore con 4 o 5 gr di cho/kg LBM)..
Mr Olympia
Ciclo di Forza
Questo per dare un minimo di credibilità alla mie ipotesi...
(l'ho postato anche su bodyweb, dove ne staimo discutendo con duch)
Resting energy expenditure in short-term starvation is increased as
a result of an increase in serum norepinephrine1,2
Christian Zauner, Bruno Schneeweiss, Alexander Kranz, Christian Madl, Klaus Ratheiser, Ludwig Kramer, Erich Roth,
Barbara Schneider, and Kurt Lenz
ABSTRACT
Background: The effects of food restriction on energy metabolism
have been under investigation for more than a century. Data
obtained are conflicting and research has failed to provide conclusive
results.
Objective: The objective of this study was to test the hypothesis
that in lean subjects under normal living conditions, shortterm
starvation leads to an increase in serum concentrations of
catecholamines and thus to an increase in resting energy
expenditure.
Design: Resting energy expenditure, measured by indirect
calorimetry, and hormone and substrate concentrations were
measured in 11 healthy, lean subjects on days 1, 2, 3, and 4 of an
84-h starvation period.
Results: Resting energy expenditure increased significantly
from 3.97 ± 0.9 kJ/min on day 1 to 4.53 ± 0.9 kJ/min on day 3
(P < 0.05). The increase in resting energy expenditure was
associated with an increase in the norepinephrine concentration
from 1716. ± 574 pmol/L on day 1 to 3728 ± 1636 pmol/L
on day 4 (P < 0.05). Serum glucose decreased from 4.9 ± 0.5
to 3.5 ± 0.5 mmol/L (P < 0.05), whereas insulin did not change
significantly.
Conclusions: Resting energy expenditure increases in early starvation,
accompanied by an increase in plasma norepinephrine.
This increase in norepinephrine seems to be due to a decline in
serum glucose and may be the initial signal for metabolic changes
in early starvation. Am J Clin Nutr 2000;71:1511–5.
4 gg di digiuno (solo h20) aumentono il RMR di circa 360 calorie in + al giorno
Naturalmente come Benedict notò nel 1915 il digiuno prolungato porta ad calo del BMR di circa il 20 o 30% (ciò è da ricollegarsi anche alla perdita di peso)
Questo sfata il mito che il digiuno nel breve termine porti ad un calo del metabolicmo.
Adesso occupiamoci della perdita di massa grassa che tutto voi BB (io pratico arrampicata sportiva e come Duch nn me ne frega nulla dello stimolo ipertrofico)
Elevation of Plasma Epinephrine Concentrations Inhibits Proteolysis
and Leucine Oxidation in Man via @i-Adrenergic Mechanisms
M. E. Kraenzlin, U. Keller, A. Keller, A. Thelin,* M. J. Arnaud, and W. Stauffacher
Department ofMedicine, University Hospital, CH-4031 Basel, Switzerland; and *Nestec SA, CH-1800 Vevey, Switzerland
Abstract
The role of elevated plasma epinephrine concentrations in the
regulation of plasma leucine kinetics and the contribution of
,8-receptors were assessed in man. Epinephrine (50 ng/kg per
min) was infused either alone or combined with propranolol
(f,-blockade) into groups of six subjects fasted overnight; leucine
flux, oxidation, and net plasma leucine forearm balance
were determined during 180 min. Constant plasma insulin and
glucagon concentrations were maintained in all studies by infusing
somatostatin combined with insulin and glucagon replacements.
Plasma leucine concentrations decreased from
baseline during epinephrine infusion by 27±5 gmol/liter (P
< 0.02) due to a 22±6% decrease in leucine flux (P < 0.05 vs.
controls receiving saline) and to an increase in the metabolic
clearance rate of leucine (P < 0.02). Leucine oxidation decreased
by 36±8% (P < 0.01 vs. controls). fl-Blockade abolished
the effect of epinephrine on leucine flux and oxidation.
Net forearm release of leucine increased during epinephrine (P
< 0.01), suggesting increased muscle proteolysis; the fall of
total body leucine flux was therefore due to diminished proteolysis
in nonmuscle tissues, such as splanchnic organs. Nonoxidative
leucine disappearance as a parameter of protein synthesis
was not significantly influenced by epinephrine. Plasma
glucose and FFA concentrations increased via f,-adrenergic
mechanisms (P < 0.001). The results suggest that elevation of
plasma epinephrine concentrations similar to those observed in
severe stress results in redistribution of body proteins and
exerts a whole body protein-sparing effect; this may counteract
catabolic effects of other hormones during severe stress.
Come si nota l'aumento di catecolamine tende a preservare la massa magra, questo adattamento naturalemente dura poco (ricollegandoci al primo studio, circa 4 o 5 gg). Aumentando il digiuno e quindi i fattori stressori avremo dei livelli sovrafisiologici di cortisolo, vero ormone proteolitico (a livelli sovrafisiologici)
Mr Olympia
Ciclo di Forza
Effect of ,0-Hydroxybutyrate on Whole-Body Leucine Kinetics and Fractional
Mixed Skeletal Muscle Protein Synthesis in Humans
K. Sreekumaran Nair, Stephen L. Welle, David Halliday,* and Robert G. Campbell
Department ofMedicine, University ofRochester School ofMedicine and Dentistry, Rochester NY 14603;
and the *Nutrition Group, Clinical Research Centre, Harrow HA] 3UJ, United Kingdom
Abstract
Because intravenous infusion of 0-hydroxybutyrate (8-OHB)
has been reported to decrease urinary nitrogen excretion, we
investigated in vivo metabolism of leucine, an essential amino
acid, using L-11-'3Cjleucine as a tracer during t9-OHB infusion.
Leucine flux during ,B-OHB infusion did not differ from leucine
flux during normal saline infusion in nine normal subjects,
whereas leucine oxidation decreased 1841% (mean = 30%)
from 18.1±1.1 pmol * kg-' * h-1 (P < 0.01), and incorporation
of leucine into skeletal muscle protein increased 5-17% (mean
= 10%) from 0.048 + 0.003%/h (P < 0.02). Since blood pH
during jt-OHB infusion was higher than the pH during saline
infusion, we performed separate experiments to study the effect
of increased blood pH on leucine kinetics by infusing sodium
bicarbonate intravenously. Blood pH during sodium bicarbonate
infusion was similar to that observed during the
,B-OHB infusion, but bicarbonate infusion had no effect on
leucine flux or leucine oxidation. We conclude that #-OHB
decreases leucine oxidation and promotes protein synthesis in
human beings.
Altra cosa: l'aumento di beta-idrossibutirrato, un corpo chetonico, che si ha durante la restrizione glicidica tende a preservare l'ossidazione della leucina (amino essenziale nel messoggio di disponibilità proteica). I + alti livelli di BHB li abbiamo in ketosi, ma il problema è che una dieta alta in grassi fa si che la ketogenesi venga attivata dai grassi esogeni, durante il digiuno, invece, la sintesi di KB (ketone body) avviene dai soli grassi endogeni e quindi avremo un vero e proprio smantellamento delle riserve adipose. Essere in ketosi durante il digiuno vuole dire ossidare solo i propri grassi.
Il problema è che + un soggetto è magro + il suo corpo è restio a rilasciare FFA dal tessuto adiposo, questo per vari adattamenti ormonali che inibiscono la lipolisi (come ha spiegato Duch).
Quindi diventa indispensabile aumentare intensità e tempistica dei refeeding con il diminuire della BF.
Regulation of Energy Balance and Carbohydrate/Lipid
Metabolism
Peter J. Havel
Hormones produced by adipose tissue play a critical role
in the regulation of energy intake, energy expenditure,
and lipid and carbohydrate metabolism. This review will
address the biology, actions, and regulation of three adipocyte
hormones—leptin, acylation stimulating protein
(ASP), and adiponectin—with an emphasis on the most
recent literature. The main biological role of leptin appears
to be adaptation to reduced energy availability
rather than prevention of obesity. In addition to the
well-known consequences of absolute leptin deficiency,
subjects with heterozygous leptin gene mutations have
low circulating leptin levels and increased body adiposity.
Leptin treatment dramatically improves metabolic abnormalities
(insulin resistance and hyperlipidemia) in patients
with relative leptin deficiency due to lipoatrophy.
Leptin production is primarily regulated by insulin-induced
changes of adipocyte metabolism. Dietary fat and
fructose, which do not increase insulin secretion, lead to
reduced leptin production, suggesting a mechanism for
high-fat/high-sugar diets to increase energy intake and
weight gain. ASP increases the efficiency of triacylglycerol
synthesis in adipocytes leading to enhanced postprandial
lipid clearance. In mice, ASP deficiency results in reduced
body fat, obesity resistance, and improved insulin sensitivity.
Adiponectin production is stimulated by thiazolidinedione
agonists of peroxisome proliferator-activated
receptor- and may contribute to increased insulin sensitivity.
Adiponectin and leptin cotreatment normalizes insulin
action in lipoatrophic insulin-resistant animals.
These effects may be mediated by AMP kinase–induced fat
oxidation, leading to reduced intramyocellular and liver
triglyceride content. The production of all three hormones
is influenced by nutritional status. These hormones, the
pathways controlling their production, and their receptors
are promising targets for managing obesity, hyperlipidemia,
and insulin resistance. Diabetes 53 (Suppl. 1):
S143–S151, 2004
Poi guarda questo studio. L'overfeeding a base di CHO (50% surplus) aumenta la DNL (de novo lipogenesi) di soli 5gr al giorno. Ed i soggetti dello studio nn conducevano alcuna attività fisica.
Short-Term Alterations in Carbohydrate Energy Intake in Humans
Striking Effects on Hepatic Glucose Production, De Novo Lipogenesis, Lipolysis, and Whole-Body
Fuel Selection
Jean-Marc Schwarz,* Richard A. Neese,*" Scott Tumer,* Doris Dare,* and Marc K. Hellerstein**
*Department of Nutritional Sciences, University of California, Berkeley, California 94720-3104; and tDivision of Endocrinology and
Metabolism, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, California 94110
Abstract
Short-term alterations in dietary carbohydrate (CHO) energy
are known to alter whole-body fuel selection in humans,
but the metabolic mechanisms remain unknown. We used
stable isotope-mass spectrometric methods with indirect calorimetry
in normal subjects to quantify the metabolic response
to six dietary phases (5 d each), ranging from 50%
surplus CHO (+50% CHO) to 50% deficient CHO (-50%
CHO), and 50% surplus fat (+50% fat). Fasting hepatic
glucose production (HGP) varied by > 40% from deficient
to surplus CHO diets (1.78+0.08 vs 2.43+0.09 mg/kg per
min, P < 0.01). Increased HGP on surplus CHO occurred
despite significantly higher serum insulin concentrations.
Lipolysis correlated inversely with CHO intake as did the
proportion of whole-body lipolytic flux oxidized. Fractional
de novo hepatic lipogenesis (DNL) increased more than 10-
fold on surplus CHO and was unmeasurable on deficient
CHO diets; thus, the preceding 5-d CHO intake could be
inferred from DNL. Nevertheless, absolute hepatic DNL accounted
for < 5 g fatty acids synthesized per day even on
+50% CHO. Whole-body CHO oxidation increased sixfold
and fat oxidation decreased > 90% on surplus CHO diets.
CHO oxidation was highly correlated with HGP (r2 = 0.60).
HGP could account for 85% of fasting CHO oxidation on
+25% CHO and 67% on +50% CHO diets. Some oxidation
of intracellular CHO stores was therefore also occurring.
+50% fat diet had no effects on HGP, DNL, or fuel selection.
We conclude that altered CHO intake alters HGP specifically
and in a dose-dependent manner, that HGP may
mediate the effects of CHO on whole-body fuel selection
both by providing substrate and by altering serum insulin
concentrations, that altered lipolysis and tissue oxidation
efficiency contribute to changes in fat oxidation, and that
surplus CHO is not substantially converted by the liver to
fat as it spares fat oxidation, but that fractional DNL may
nevertheless be a qualitative marker of recent CHO intake.
(J. Clin. Invest. 1995. 96:2735-2743.)
Inoltre l'ipernutrizione a base di carbo aumenta di circa 11% il RMR e quindi la termogenesi
Stimulation of Thermogenesis by
Carbohydrate Overfeeding
EVIDENCE AGAINST SYMPATHETIC NERVOUS SYSTEM MEDIATION
STEPHEN WELLE and ROBERT G. CAMPBELL, Endocrine-Metabolism Unit, Monroe
Community Hospital, Department of Medicine, University of Rochester
School of Medicine and Dentistry, Rochester, New York 14603
A B S T R A C T Daily carbohydrate intake of seven men
with normal weight was limited to 220-265 g/d for
6 d and then increased to 620-770 g/d for 20 d, while
intake of protein, fat, and sodium remained constant.
Carbohydrate overfeeding increased body weight by
4.8%, basal oxygen consumption (Vo2) by 7.4%, BMR
by 11.5%, and serum triiodothyronine levels by 32%.
Overfeeding did not affect the thermic effect of a standard
meal. Intravenous propranolol reduced the
thermic effect of a meal by 22% during the base-line
feeding period, and by 13% during carbohydrate overfeeding,
but did not affect preprandial Vo2. Overfeeding
attenuated the rise in plasma glucose and FFA
levels induced by infusion of norepinephrine, but had
no effect on the increase in Vo2 induced by norepinephrine.
Overfeeding did not alter 24-h urinary excretion
of vanillylmandelic acid, supine plasma catecholamine
levels (pre- and postprandial), blood pressure,
or plasma renin activity, but increased peak
standing plasma norepinephrine levels by 45% and
resting pulse rate by 9%. Even though short-term carbohydrate
overfeeding may produce modest stimulation
of sympathetic nervous system activity in man,
the increase in thermogenesis induced by such overfeeding
is neither suppressed by beta adrenergic blockade
nor accompanied by an increased sensitivity to the
thermogenic effects of norepinephrine. These data do
not support an important role for the sympathetic nervous
system in mediating the thermogenic response to
carbohydrate overfeeding.
è anche vero che il fasting tende ad abbassare la sensibilità nsulinica.
Ma questo problema nn rigurda gli atleti. L'allenamento migliora la sensibilità insulinica upregolando gli IR (recettori insulinici) ed stimolando degli8 adattamenti che fanno si che la membrana cellulare diventi maggiormente permeabili al glucosio e stimolando l'aumento dei trasportatori si glusoio GLUT-4 sulle membrane cellulari
Differential regulation of metabolic genes in skeletal muscle during starvation and refeeding in humans
Littlewood, Ian Macdonald and Andrew Bennett
Kostas Tsintzas, Kirsty Jewell, Mo Kamran, David Laithwaite, Tantip Boonsong, Julie
Abstract
This study investigated the molecular alterations underlying the physiological adaptations to starvation and refeeding in human skeletal muscle. 48 h starvation reduced whole body insulin sensitivity by 42% and produced marked changes in expression of key carbohydrate (CHO) regulatory genes and proteins: SREBP1c and hexokinase II (HKII) were downregulated 2.5- and 5-fold respectively whereas the pyruvate dexydrogenase kinase 4 (PDK4) was upregulated 4-fold. These responses were not dependent on the phosphorylation status of Akt and FOXO1. On the other hand, starvation and the concomitant increase in circulating free fatty acids did not upregulate the expression of transcription factors and genes involved in fat metabolism. 24 h refeeding with a CHO-rich diet completely reversed the changes in PDK4, HKII and SREBP1c expression in human skeletal muscle but failed to fully restore whole body insulin sensitivity. Thus, during starvation in healthy humans, unlike rodents, regulation of fat metabolism does not require an adaptive response at transcriptional level, but adaptive changes in gene expression are required to switch off oxidative glucose disposal. Lack of effect on key proteins in insulin-signalling pathway may indicate that changes in intracellular substrate availability/flux may be responsible for these adaptive changes in glucose metabolism. This may represent an important aspect of the molecular basis of the development of insulin resistance in metabolic conditions characterised by energy restriction.
Adesso unisci il tutto in un piano dietetico composto da 2 estremi:
1)fortissima restrizione calorica o meglio "digiuno controllato" poichè si assumono solo protidi (2gr/kg LBM) e grassi essenziali (6gr O3 da pesce o 10gr olio di lino) potratta per 4 o 5 gg dove ciò che ossidi sono solo i tuoi grassi
2)ricarica intensa di 12 o 24 ore a base di CHO in cui vengono ricaricate solo le riserve muscolari di glicogeno con una DNL di meno di 5gr al giorno (irrisoria)
penso che si possano ottenere migliori e + rapidi risultati rispetto ad una dieta meno restrittiva
Poi questo, che mostra come la sottoalimentazione aumenti il gene Sirt1. Il quale inibisce i PPAR-gamma, recettori deputati alla lipogenesi ed alla differenziazione dei pre adipociti in adipociti. Inoltre fungendo da PPAR-gamma antagonista, il Sirt1 aumenta la lipolisi
Sirt1 promotes fat mobilization in white adipocytes by repressing PPAR-gamma.
Picard F, Kurtev M, Chung N, Topark-Ngarm A, Senawong T, Machado De Oliveira R, Leid M, McBurney MW, Guarente L.
Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Calorie restriction extends lifespan in organisms ranging from yeast to mammals. In yeast, the SIR2 gene mediates the life-extending effects of calorie restriction. Here we show that the mammalian SIR2 orthologue, Sirt1 (sirtuin 1), activates a critical component of calorie restriction in mammals; that is, fat mobilization in white adipocytes. Upon food withdrawal Sirt1 protein binds to and represses genes controlled by the fat regulator PPAR-gamma (peroxisome proliferator-activated receptor-gamma), including genes mediating fat storage. Sirt1 represses PPAR-gamma by docking with its cofactors NCoR (nuclear receptor co-repressor) and SMRT (silencing mediator of retinoid and thyroid hormone receptors). Mobilization of fatty acids from white adipocytes upon fasting is compromised in Sirt1+/- mice. Repression of PPAR-gamma by Sirt1 is also evident in 3T3-L1 adipocytes, where overexpression of Sirt1 attenuates adipogenesis, and RNA interference of Sirt1 enhances it. In differentiated fat cells, upregulation of Sirt1 triggers lipolysis and loss of fat. As a reduction in fat is sufficient to extend murine lifespan, our results provide a possible molecular pathway connecting calorie restriction to life extension in mammals.
Naturalmente la ricerca è ancora lunga
questo il link: http://www.fituncensored.com/forums/...ead.php?t=6932
Principiante
Osanno la tua teoria e le fonti da cui la estrapoli ma il concetto che forse non è chiaro è che bisogna SEMPLIFICARE le cose!!! Per chi si avvicina per la prima volta al bb è una tragedia vedere teorie o tabelle teoriche di alimentazione!!! Poi ovvio che ci sono soggetti + inclini ad approfondire l'argometo come te (a meno che tu nn sia un nutrizionista) studiando ed informandosi.
Larry Scott
Ciclo di Massa
Le teorie salutari fanno bene sia a chi le conosce sia a chi non le conosce.
Se hai la bronchite e il medico ti ordina l'antibiotico, non serva che tu sia un chimico..ti farà effetto lo stesso.
Nle bodybuilding LE scorciatoie portano solo a diminuire la salute. Il fisico non ti cambia in 2 settimane.
Fai quello che vuoi tutto l'anno e le ultime 2 settimane prima della spiaggia ricorri alla tua formula magica per risolvere tutto??
Mai sentito parlare di Scienza???? E' una cosa che serve per capire come funzionano le cose! E le cose di solito (ma per il corpo SEMPRE) hanno un solo modo di funzionare.
Ovvio che se togli del tutto i carbo e spari le proteine magari puoi pure perdere 4 kg in 2 settimane..e i reni? e il fegato?? e...metteresti la mano sul fuoco che perdi solo grasso??
Se funzione manda una mail al sito di Coleman...anzichè le sue 12/14 settimane di dieta magari decide di adottare la tua strategia!!!
TRASHHHHHH
Mr Olympia
Ciclo di Forza
...tu riporti un tuo piano alimentare affermando che vada bene per tutti.....poi arriva il primo pollletto di turno e lo va a seguire.....e questo nn fa altro che sviare la comprensione che dieta ed allenamento sono da riportarsi al soggetto.....che nn bisogna crede al primo che arriva ed osanna una dieta bella e fatta che va bene per lui..perchè i neofiti vogliono questo....nessuna cultura, nessuna conoscienza, solo dieta ed allenamento belli e pronti...
mi pare che il mio piano:
1)sia riportato al soggetto
2)abbia un minimo di base scientifica
poi, tranquilli, se qua nn ve ne frega nulla della scienza medica...tranquilli, nn posto + studi.....tutto di guadagnato per me....
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