powerball pb

akis, fa-mi loc in top

am facut 11.978...

Lyle McDonald - hierarchy of nutrition

Focusing on the insulin response (or lack thereof) is missing the point. 

Your body comp will be determined primarily by your calorie surplus/deficit. Then, below that are issues with macronutrients (essentially, if you are eating enough protein). 

Then below that (MUCH below) are issues with nutrient timing (and being sure to eat carbs+protein around your workout is about all you can do to optimize this) and finally, issues with individual food sub-types (sweet potatos vs white potatos, peanut butter vs. almond butter etc.) are essentially meaningles.

radio misto

profm latino

colesterol

treaba nu e asa de simpla cum pare la prima vedere

it's all about calories in/calories out

un studiu publicat acum in New England Journal of Medicine confirma faptul ca se poate slabi la fel indiferent de compozitia dietei, atata timp cat exista deficit caloric

ABSTRACT

Background The possible advantage for weight loss of a diet that emphasizes protein, fat, or carbohydrates has not been established, and there are few studies that extend beyond 1 year.

Methods We randomly assigned 811 overweight adults to one of four diets; the targeted percentages of energy derived from fat, protein, and carbohydrates in the four diets were 20, 15, and 65%; 20, 25, and 55%; 40, 15, and 45%; and 40, 25, and 35%. The diets consisted of similar foods and met guidelines for cardiovascular health. The participants were offered group and individual instructional sessions for 2 years. The primary outcome was the change in body weight after 2 years in two-by-two factorial comparisons of low fat versus high fat and average protein versus high protein and in the comparison of highest and lowest carbohydrate content.

Results At 6 months, participants assigned to each diet had lost an average of 6 kg, which represented 7% of their initial weight; they began to regain weight after 12 months. By 2 years, weight loss remained similar in those who were assigned to a diet with 15% protein and those assigned to a diet with 25% protein (3.0 and 3.6 kg, respectively); in those assigned to a diet with 20% fat and those assigned to a diet with 40% fat (3.3 kg for both groups); and in those assigned to a diet with 65% carbohydrates and those assigned to a diet with 35% carbohydrates (2.9 and 3.4 kg, respectively) (P>0.20 for all comparisons).Among the 80% of participants who completed the trial, the average weight loss was 4 kg; 14 to 15% of the participants had a reduction of at least 10% of their initial body weight. Satiety, hunger, satisfaction with the diet, and attendance at group sessions were similar for all diets; attendance was strongly associated with weight loss (0.2 kg per session attended). The diets improved lipid-related risk factors and fasting insulin levels.

Conclusions Reduced-calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize. (ClinicalTrials.gov number, NCT00072995[ClinicalTrials.gov] .)

statine

eu zic sa luati cat mai multe

colesterolul si bolile cardiovasculare

corelatia dintre colesterol si bolile cardiovasculare (foarte profitabila de exemplu pentru producatorii de statine) primeste inca o lovitura

studiul de mai jos (care acopera o perioada de 60 de ani) arata ca principalul factor care creste riscul unui infact de miocard nu este colesterolul ci resistenta insulinica. asta este cauzata de o alimentatie "sanatoasa" bazata pe carbohidrati rafinati care include si grasimi "sanatoase" ca margarina 

pe locul doi este hipertensiunea arteriala....

Eddy D, Schlessinger L, Kahn R, et al. Relationship of Insulin Resistance and Related Metabolic Variables to Coronary Artery Disease: A Mathematical Analysis. Diabetes Care 2009; 32 : 361-366 

Abstract

OBJECTIVE — People with diabetes have an increased risk of coronary artery disease (CAD). An unanswered question is what portion of CAD can be attributed to insulin resistance, related metabolic variables, and other known CAD risk factors. 

RESEARCH DESIGN AND METHODS — The Archimedes model was used to estimate the proportion of myocardial infarctions that would be prevented by maintaining insulin resistance and other risk factors at healthy levels. Person-specific data from the National Health and Nutrition Examination Survey 1998–2004 were used to create a simulated population representative of young adults in the U.S. This population was then entered into a series of simulated clinical trials designed to explore the effects of each risk factor. Each trial had a control arm (all risk factors were allowed to progress without interventions) and a treatment arm (a risk factor was held to its value in young healthy adults). The trials continued for 60 years. The effects of these hypothetical "cures" of each risk factor provide estimates of their impact on CAD. 

RESULTS — In young adults, preventing insulin resistance would prevent ~42% of myocardial infarctions. The next most important determinant of CAD is systolic hypertension, prevention of which would reduce myocardial infarctions by ~36%. Following systolic blood pressure, the most important determinants are HDL cholesterol (31%), BMI (21%), LDL cholesterol (16%), triglycerides (10%), fasting plasma glucose and smoking (both ~9%), and family history (4%). 

CONCLUSIONS — Insulin resistance is likely the most important single cause of CAD. A better understanding of its pathogenesis and how it might be prevented or cured could have a profound effect on CAD.

grasimile polinesaturate si cancerul

cu dedicatie pentru madam nutritionist care ieri ne explica ea ce sanatoase sunt grasimile polinesaturate

"The researches used the imaging and cell-counting tools to document that linoleic acid, which is predominant in polyunsaturated fats, caused increasing membrane phase separation, whereas oleic acid, found in monounsaturated fats, did not. Increased membrane phase separation could improve the opportunity of circulating tumor cells to adhere to blood vessel walls and escape to organs far from the original tumor site. The new findings support earlier evidence from other research that consuming high amounts of polyunsaturated fat may increase the risk of cancer spreading."

nutritionista cu acte in regula

cat de haotica e madam

in anul 2009 inca mai exista un nutritionist care spune ca untul este rau dar margarina e buna

care ne spune ca uleiul de floarea soarelui e bun, dar grasimea din carne si din lactate e rea

cica grasimile sunt principalii furnizori de energie

ba ne laaasi

taking questions

astept intrebari legate de nutritie si antrenament

daca tot am o pana de inspiratie poate intrebarile voastre sa ma trezeasca

Fedor the almighty

beavis and butthead

o parte dintr-un articol interesant din EJCN

Which are the greatest recent discoveries and the greatest future challenges in nutrition?

Discoveries

The discovery that folic acid prevents birth defects was judged to be the greatest discovery in nutrition science since 1976. It was a discovery in which neither the speakers nor the audience had been actively involved. In fact, the discovery that periconceptional supplementation with folic acid prevents most cases of spina bifida and anencephaly was not made by nutrition scientists, but by British doctors working on the prevention of birth defects (Smithells et al., 1976; MRC Vitamin Study Research Group, 1991). The story of this discovery spans 50 years (Willett, 1998). A synthesis of data from clinical observations, biochemistry, epidemiology, genetics and randomized clinical trials was required to establish that periconceptional folic acid prevents birth defects. The discovery also overturned the dogma that an apparently balanced diet provides enough of all nutrients. The subsequent addition of folic acid to staple foods in North America clearly reduced the incidence of this most common of the major congenital abnormalities (Persad et al., 2002).

The discovery ranked no. 2 was the health effects of trans fatty acids. Three of the five speakers had been involved in this discovery (Mensink and Katan, 1990;Willett et al., 1993), so there may be bias here. But the discovery of the adverse effects of trans fatty acids on blood lipoproteins and incidence of heart disease continues to affect both nutritional guidelines and food composition worldwide. Throughout the twentieth century, the partial hardening of oils with the concomitant production of trans fatty acids had been a pillar of the food industry, with huge investments in research and factories (Korver and Katan, 2006). All that is being phased out now, and the replacement of partially hydrogenated by unprocessed oils is likely to prevent many myocardial infarctions.

No. 3 was the nutritional regulation of gene transcription. Examples of this are the way dietary fatty acids regulate hepatic fatty acid synthesis and breakdown via nuclear receptors (Shulman and Mangelsdorf, 2005), but the discoveries go beyond that. Molecular biology is opening up the black box of the regulation of intermediary metabolism (Desvergne et al., 2006), and this has consequences for our understanding of vitamin, protein, lipid and carbohydrate metabolism, and of disease development.

Arguably, this discovery might have been combined with no. 6, the LDL receptor and its regulation by diet. The regulation of the activity of the LDL receptor by dietary cholesterol was elaborated by Brown and Goldstein around 1976 in a model of brilliant simplicity and predictive power (Kovanen et al., 1981). Unfortunately, we still lack a similar insightful explanation of why the structure of dietary fatty acids affects blood lipid levels. Why do saturated and trans-unsaturated fatty acids raise and cis-unsaturated fatty acids lower LDL cholesterol? Many mechanisms have been proposed, but none entirely satisfactory (Spritz et al., 1965; Spritz and Mishkel, 1969; Beynen and Katan, 1985; Fox et al., 1987; Lin et al., 2005).

Discovery nos. 4 and 5 both represent gains made in obesity research. Essential to discovery no. 4, progress in measuring energy intake, was the doubly labeled water technique for estimating energy expenditure and intake. Application of this technique to humans (Schoeller and van Santen, 1982) showed that traditional dietary history and recall methods underestimated energy intake, and that this bias increases with increasing body fatness. The paradox that the more obese a person is, the less they appeared to eat had puzzled scientists, but it took many doubly labeled water measurements plus years of heated debate before it was accepted that obese people eat more than lean people, at least in populations with limited variation in physical activity. The issue was sensitive because the results of the doubly labeled water studies seemed to put the blame on obese subjects, and in addition, they appeared to discredit the recall techniques so widely used in nutrition and dietetics.

Discovery no 5, fat tissue as an endocrine organ, was heralded by the discovery of leptin and its absence in a genetic model of rodent obesity (Zhang et al., 1994). Leptin was followed by tumor-necrosis factor-, adiponectin, resistin and other hormones. These have drastically changed our view of adipose tissue metabolism and have given important insights into the mechanisms linking obesity with type II diabetes, atherosclerosis and other diseases (Rosen and Spiegelman, 2006; Trujillo and Scherer, 2006).

No. 7, obesity is a normal response to an abnormal environment, represents a step forward in a different area of the obesity issue, namely the role of the environment. Until recently, the search for causes of weight gain focused on genetic or metabolic abnormalities of obese people. Also, obese individuals were considered to lack the willpower to eat less or exercise more (Prentice and Jebb, 1995). But from a public health point of view, obesity can be also be viewed as a normal reaction to an abnormal environment (Egger and Swinburn, 1997) instead of a disorder. Attempts to improve individual diet and exercise habits may not be enough to curb the obesity epidemic; we may also need to create healthier school environments, transportation systems and town planning.

No. 8, alcohol causes breast cancer (Williams and Horm, 1977), and no. 9, body fatness is the second most avoidable cause of cancer (Lew and Garfinkel, 1979), together represent the major known dietary causes of cancer. Implicitly, they also illustrate the problems and frustrations of the diet and cancer field. Early in our 30-year time frame, observations on carotenes and on dietary fat seemed to offer hope of reducing the incidence of cancer through changes in nutrient intake (Petoet al., 1981), but new research has shown that the prospects for reducing cancer through a change of nutrient intake are more limited (WCRF, 2007). There remains a real possibility that we have not investigated the critical periods in life. Effects of diet during childhood and early adult life on later risk of cancer remain to be explored, as are effects of various foods and nutrients. But such research will not come easily. As it is, reductions in alcohol intake and in obesity could already have a marked impact on the incidence of cancer of the breast and other organs. Both doctors and the general public are little aware of the alcohol–cancer link.

No. 10, plant stanols/sterols and lipid metabolism, was not a discovery of the period 1976–2006 proper, as the effect of plant sterols on cholesterol was already known in the 1950s (Wilkinson et al., 1955). But it took until the 1990s before large amounts of plant stanols could be incorporated into margarine in a way that conserves or even enhances their cholesterol-lowering potency. The effect of such margarines on cholesterol equals that of the rest of the diet combined (Miettinen et al., 1995; Jenkins et al., 2003). Products with sterols and stanols became the paradigm for branded foods with health claims, and they remain one of the few 'functional foods' with proven efficacy in reducing a biomarker for a disease. But they have to compete with a class of drugs with an unbeatable record for clinical effectiveness and safety, that is, the statins. Sterols/stanols owe their market position more to the fact that they are perceived as a food than to superior efficacy in preventing heart disease. There is also some concern that absorption of sterols may promote the very disease that they aim to prevent. The prototype of such an effect of absorbed sterols on atherosclerosis is phytosterolemia or sitosterolemia (Bhattacharyya and Connor, 1974). Patients with homozygous phytosterolemia overabsorb plant sterols, and they develop massive xanthomas and atherosclerosis.

No. 11, diabetes can be prevented by diet and lifestyle, builds on another observation made before 1976, namely that obesity causes type II diabetes. But in spite of the huge impact of obesity on diabetes risk seen in observational studies, the efficacy of lifestyle changes in trials still came as a surprise. A non-randomized study of modest levels of exercise and weight reduction from Sweden found a remission rate in diabetics of over 50% (Eriksson and Lindgarde, 1991), and in a Chinese study, the number of patients progressing from impaired glucose tolerance to frank diabetes was reduced by 36% (Pan et al., 1997). The first large randomized trial was done in Finland (Tuomilehto et al., 2001), closely followed by one in the United States, (Knowler et al., 2002) and both found that fairly small changes in diet, activity and weight reduced diabetes incidence by 58%. Diet and weight loss were clearly more efficacious than the standard drug treatment, metformin. (Knowler et al., 2002) How can 20 to 30 min of moderate exercise per day plus a 3- to 6-kg weight loss reduce the incidence of type II diabetes by more than half? We do not know. But an even more urgent question is how we can change our world so that more patients receive and comply with this most powerful of diabetes treatments.

Discovery no. 12 was interaction of carbohydrate/glycemic load with insulin resistance. There is controversy over diets with a low glycemic index for the treatment of diabetes. However, the effect of glycemic index on postprandial blood glucose levels in diabetics is incontrovertible (Jenkins et al., 1983). New research is extending the concept of glycemic index beyond the treatment of diabetics to prevention of diabetes (Salmeron et al., 1997), but the data are still incomplete and therefore controversial.

Discovery no. 13 deals with the finding that something does not work: after high hopes for antioxidants, large randomized trials showed that vitamin E does not reduce cardiovascular disease, at least not in patients who have the disease or are at high risk for it. (The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group, 1994) It still remains possible that vitamin E has a role in the primary prevention of cardiovascular disease, but the issue is unlikely to be settled by clinical trial evidence.

No. 14, the effect of fish oil fatty acids to reduce mortality in coronary heart disease patients, has been a topic of interest ever since the initial observation that Eskimos (Inuit) have a high fat intake but low rates of coronary heart disease. (Bang et al., 1971) It received support from Nobel prize-winning research on fatty acids and prostaglandins, was strengthened by observational findings in Zutphen (Kromhout et al., 1985) and many subsequent epidemiological studies, and was initially upheld by clinical trials. Recent trial data have, however, been less consistent (Brouwer et al., 2006). More trials are in the pipeline.

No. 15, the multisystemic role of vitamin D, is still at an early stage. Reported effects of vitamin D on cancer, diabetes and muscle function are intriguing but not yet established beyond doubt (Garland et al., 1985; Martinez et al., 1996;Holick, 2006).

Challenges

The speakers and the audience together nominated 17 challenges. As some of these were similar, we collated them into the 14 challenges.

According to the audience, controlling obesity and insulin resistance through activity and diet, was the greatest challenge for nutrition research in the coming 30 years; it received 48 of the 128 votes. But is it a challenge for nutrition science or for society as a whole? After all, the causes of obesity are clear: too many dietary calories and too little energy expenditure. Still, the debate is raging whether some foods or nutrients exacerbate the problem, and other foods help to limit caloric intake. These questions seem simple, but the record of the past 30 years shows they are not, as witnessed by the long-standing controversy over the role of dietary fat in obesity (Connor and Connor, 1997; Katan et al., 1997;Astrup et al., 2000). We obviously need more thorough tests of proposed remedies. Such testing should involve large, well-controlled trials that last several years, and, even more demanding, the studies should ideally be double-blind, because food intake is highly sensitive to suggestion. That will be hard to achieve with most foodstuffs: what is the placebo for an apple?

Three other challenges also drew over 10% of the votes.

The first of these, and no. 2 in the overall ranking, was Can diet delay cognitive decline? Its election may have been helped by the recent completion in Wageningen of the FACIT trial, which showed that folic acid reduced the decline in memory in elderly volunteers (Durga et al., 2007). Further studies in this direction are obviously worthwhile, because the effect of B-vitamins on cognitive decline is far from settled. The effect of n-3 fatty acids from fish on cognitive decline also deserves further exploration (Beydoun et al., 2007; van Gelder et al., 2007).

Challenge no. 3 was restore the balance between private and public control of nutrition research. This had nothing to do with any specific line of research, but it reflected widespread concern that nutrition research has become overly market-oriented and sensitive to commercial interests (Katan, 2007). Over the past 20 years, there has been a strong preference for market forces to take care of research priorities, but some correction may be imminent. For example, the European Research Council is beginning to award research grants based exclusively on scientific excellence; this new program no longer requires the commercial applicability that is a prerequisite for much of the other research funded by the European Union. Although collaboration with industry can yield valuable research results, as testified by the FACIT (Durga et al., 2007) and SOFA (Brouwer et al., 2006) trials, industry-sponsored research will probably not lead to the long-term scientific breakthroughs that we need.

Challenge no. 4 was the reductionistic approach versus the food pattern approach. This sounds philosophical but it is a concrete issue that has been around for many years: should we do research and give dietary recommendations in terms of molecules and their actions, or of foods and diets? The popularity of the 'Mediterranean diet' (800 PubMed hits as of 17 May 2007), shows that the holistic approach is gaining territory among scientists. But when is a diet Mediterranean? That is hard to decide without assigning a number for 'Mediterranean-ness'. On the other hand, the benefits of certain foods are hard to summarize in terms of the molecules in them: the effect of low-fat, high-carbohydrate diet (Schaefer et al., 1995) on weight loss may be due more to their taste and structure than to a particular content of any macro- or micronutrient. Similarly, there is more to corn and pellagra than the low niacin content of corn. Foods are complex and our knowledge is limited, so nutrition and health is unlikely to be reduced entirely to molecular interactions.

Another 10 challenges each gathered a few percentage of the votes. Some referred to practical problems that have been with us for a while, such asimplementing diet in clinical practice and reduction of salt in foods, some were of a more general nature, such as diet and low-grade systemic inflammation, from genetics to epigenetics and the use of substances from plants to prevent disease. Some were methodological, for example, How can we prove that lifestyle interventions work? and How can we measure energy balance in free living people?

Finally, two represent work in progress in the diet-heart field. One is the role of B-vitamins and homocysteine lowering in the prevention of cardiovascular disease.Up till now the results of clinical trials of homocysteine lowering have been disappointing, but the largest trials will only report in the next few years (B-Vitamin Treatment Trialists' Collaboration, 2006). Trials may not provide the final answer, because short-term application of high doses in patients with existing disease may not be equivalent to long-term intake of modest amounts by healthy people. But a trial of the primary prevention of heart disease with B-vitamins in healthy subjects is unlikely to happen because the size and cost would be prohibitive.

Another work in progress is the role of -linolenic acid in prevention of coronary heart disease mortality. This might be solved by the ongoing Alpha Omega Trial (http://clinicaltrials.gov/ct/show/NCT00139464), which is due to report in 2010. Or it might not: certainty does not come easy in nutrition research, but fortunately, 2036 is still a long way off.

powerball

mi-am luat un powerball. foarte misto chestie :-)

informatii aici

deocamdata am facut 10302 de puncte

mancare libaneza misto

mezze

foarte buna mancarea

pe vremea asta livrarea acasa/la serviciu face toti banii

Romanian cities

Afumaţi - Neversober
Urlaţi – Gimme Some Noise
Constanţa - The Steadiness
Slobozia - A Very Wrong Local Tradition
Călăraşi - Silly-dressed Folks on Horses
Piteşti - Youdohide
Oneşti - The Sincere
Huşi - Shoo
Buhuşi - Boo
Satu-Mare - The Rather Roomy Rural Community
Slatina - Slut Tina
Târgu Frumos - The Aesthetically Pleasing Bazaar
Buzău - Really Fat Lip
Năvodari - Networkers
Dor Mărunt - Miniature Melancholy
Baia Mare – Big Bathroom

Voluntari - Town of Unpaid Assistants

repost

tii regim si nu ai rezultate? ia mai uita-te o data la asta 

marele secret al slabitului este ca nu exista nici un secret. cine iti spune altceva are ceva de vandut...

why are we fucked?

despre criza

for the love of house

aici gasiti niste radio-uri online

foame

Lyle McDonald scrie aici despre 9 modalitati de a combate foamea intr-un regim de slabire (proteine, fructe, fibre, grasimi, sport, post intermitent, suplimente care reduc apetitul, flexibilitate si vointa). pe langa astea cred ca se mai poate combate foamea mancand des si putin (cam din 3 in 3 ore) sau band apa/cola light

subiectul este extrem de important, controlul foamei fiind cheia oricarui regim de slabire

multivitamine

conform unui studiu recent pe 161.808 femei intr-o perioada de 8 ani, folosirea multivitaminelor nu a redus in nici un fel risul de cancer, boli cardiovasculare sau mortalitatea

bukres

un site misto

la sala de balet

paine

ne place sau nu suntem obisnuiti sa mancam cu paine. binenteles ca ne putem dezobisnui dar nu cred ca merita efortul. se poate manca foarte sanatos si se poate slabi foarte bine mancand paine

si in cazul asta "the dose makes the poison". una e sa mananci o franzela alba la o masa (sau chiar mai mult, cum imi aduc aminte ca faceam prin liceu) si alta e sa mananci o felie de paine integrala

1-2 felii de paine integrala la o masa sunt ok. in general doua felii de paine integrala au cam 100 de grame, respectiv 250 kcal. daca intr-o zi ai o limita de 1500 kcal si mananci de 4 ori, evident ca nu e ideal sa mananci paine de 1000 kcal

cum arata o paine buna. pai in primul rand nu are faina alba, zahar, coloranti, conservanti, uleiuri vegetale. are minim 5-6 g de fibre la 100 g. daca are si seminte e perfect

imi place o paine fara drojdie de la Greenland si painea de secara de la Natura Land

t mobile

T-Mobile Dance
Încărcat de Delichild

tattoo

organic vs. conventional

desi suna foarte bine, alimentele organice nu sunt intotdeauna de preferat celor obtinute in mod conventional

o analiza interesanta aici

diferentele sunt de fapt foarte mici. sunt plusuri si minusuri pentru ambele categorii de alimente. daca ai bani de mancare organica poti sa-ti cumperi dar nu e necasar sa mananci alimente organice ca sa mananci sanatos

vitamina D

o prezentare interesanta aici

un film frumos

fasting

de doua zile m-am apucat de post intermitent, leangains style

practic mananc doar intre ora 14 si ora 22. orice. oricat

sa vedem ce iese

dupa Martin Berkhan avantajele postului intermitent sunt urmatoarele:

* Increased insulin sensitivity, possibly resulting in superior nutrient partitioning as compared to traditional meal patterns; especially when combined with weightlifting. There are also several other health benefits, including improved blood lipids (scientifically proven).

* Possible to reduce bodyfat and increase lean mass through a cyclic calorie intake.

* No more obsessive thinking about food and worrying about eating every second hour.

* Very liberal approach to calorie intake in the eating window (8 hrs) and post-workout window; you can eat to your hearts content and still lose bodyfat.

* Increased mental focus, energy and productivity during the fast.

* Increased metabolism during the fast. Ironically, most people think it´s the other way around.

* Appetite suppression during the fast. This is particularily beneficial if your main priority is to lose bodyfat.

Lyle despre cofeina

aici

studiu romanesc in Nutrition Journal

publica si romanasii nostri ceva in Nutrition Journal

pe langa faptul ca e un studiu subtireanu rau (studiu e mult spus, un fel de rezumat), la concluzii sunt doua dezacorduri

asta e nivelul

pentru cei care evita grasimea dupa antrenament

P+C eaters, take this:


J Appl Physiol 97: 11–16, 2004.

Adding fat calories to meals after exercise does not alter glucose tolerance.
Amanda K. Fox, Amy E. Kaufman, and Jeffrey F. Horowitz
Division of Kinesiology, The University of Michigan, Ann Arbor, Michigan 48109
Submitted 26 December 2003; accepted in final form 16 February 2004

A single session of exercise increases insulin sensitivity for hours and even days, and dietary carbohydrate ingested after exercise alters the magnitude and duration of this effect. Although increasing systemic fatty acid availability
is associated with insulin resistance, it is uncertain whether increasing dietary fat availability after exercise alters the exercise induced increase in insulin sensitivity. The purpose of this study was to determine whether adding fat calories to meals after exercise alters glucose tolerance the next day. Seven healthy men cycled 90 min at 66 +/- 2% peak oxygen uptake followed by a maximum of five high-intensity intervals. During the hours after exercise, subjects ingested three meals containing either low-fat (5% energy from fat) or high-fat (45% energy from fat) foods (Low-Fat and High-Fat groups, respectively). Each diet contained the same amount of carbohydrate and protein. An oral glucose tolerance test was performed the next morning. Muscle glycogen and intramuscular triglyceride (IMTG) concentrations were measured in muscle biopsy samples obtained immediately before exercise and the next morning. The day after exercise, muscle glycogen concentration was identical in High-Fat and Low-Fat (393 +/-70 and 379 +/- 38 mmol/kg dry wt). At the same time, IMTG concentration was 20% greater during High-Fat compared with Low-Fat (42.5 +/- 3.4 and 36.3 +/- 3.3 mmol/kg dry wt; P 0.05). Despite the addition of 165 g of fat to meals after exercise (1,500 kcal) and a resultant elevation in IMTG concentration, glucose tolerance was identical in High-Fat and Low-Fat (compositeindex: 8.7 +/-
1.0 and 8.4 +/- 1.0). In summary, as long as meals ingested in the hours after exercise contain the same carbohydrate content, the addition of 1,500 kcal from fat to these meals did not alter muscle glycogen resynthesis or glucose tolerance the next day.

un film superb

va recomand din suflet sa vedeti "The Curious Case of Benjamin Button"

nu degeaba este favorit la oscar anul asta

imi aduce aminte de forrest, forrest gump

career change

diet cola for men

raceala

sunt racit

Iulian MD scrie misto despre raceala aici

somn usor

de ce ti se face somn uneori dupa ce mananci?

amino acidul triptofan e de vina. daca mananci o sursa de proteine (implicit de triptofan, de exemplu branza de vaci, piept de pui, oua, fasole, migdale etc.)alaturi de carbohidrati, insulina astfel secretata scoate din circulatie alti aminoacizi facand ca o cantitate mai mare de triptofan sa ajunga la creier si sa fie transformata in serotonina si melatonina, substante care induc somnul

daca ai treaba si nu vrei sa vegetezi dupa ce ai mancat la pranz, incerca sa mananci mai multe proteine si mai putini carbohidrati (evitand carbohidratii cu indice glicemic mare ca paine alba si zaharul)

handstand pushups

vrei sa faci umeri cu o greutate mai mare dar ti-e frica sa nu iti distrugi spatele

o solutie foarte buna este asta:

low carb talibans

un post excelent pe blogul lui Martin Berkhan

discutia s-a aprins...au postat comentarii Lyle McDonald, Tom Venuto si Alan Aragon

s-a bagat in seama si yours truly

branzeturi