Workout while fasting

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(pete69 @ May 02 2008,11:29)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Thanx for the feedback Dan. The reason I ask is because as you know keto diets are mimicking fasting in many ways.

Everything I've seen on fasting suggests the most catabolic effects of fasting/ketogenic diets occur during the initial phase. I believe this is mostly due to the fact that the body is not producing ketones and not adapted to using them, therefore glucose needs are still elevated especially for the brain. And the source of glucose, after hepatic stores become depleted are amino acids, specifially the BCAA's, glutamine and alanine.

Direct measures show loss of aminos from forearm muscle during brief fasting, and some aminos come from the splanchnic bed, but haven't seen any hard numbers quantifying how much protein comes from muscle vs. other sources.

But once adapted to ketosis (which as you know mimics starvation metabolism), glucose needs are down so fatty acids and ketones provide the majority of fuel, lowering need of gluconeogenic precursors from protein. Even though there is always a small need for glucose, it goes down as fasting/ketosis sets in.

My concern is kicking yourself out of ketosis with carbs, switching the brain back to glucose and replacing some of the liver glycogen, while perhaps more anabolic, makes the transition back into ketosis during the next fasting bout more catabolic.

Staying ketogenic, or perhaps doing some moderate level cardio to get back into ketosis, would keep the brain happy during fasting and feeding, as its getting a steady supply of ketones. And perhaps replace some dietary fat with MCT oil.

Probably more sucky and less fun for the dieter, but perhaps better for the brain, mussels, and hunger control overall when intermittent fasting.

Oh, and when eating keto meals, you can eat a surplus of calories and lose weight because calories don't matter when in ketosis, it's insulin and carbs, and those are an evil, deadly duo.  
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Pete,

I'm not seeing how reinstituting ketogenesis is &quot;more&quot; catabolic than the previous bout.

Also I asked in the old &quot;Flexibility&quot; thread if you are still doing a fast or not? (FYI)
 
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(quadancer @ May 02 2008,7:50)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Dan: Pete asked some very good questions I'd like to hear your thoughts on. I would like to see a chart/graph on the body from the beginning of a fast to a replenishment meal and the effects and timing of NB markers, insulin, ketones and so forth pertaining to bodybuilding. Someone should attempt to create a timeline so we can argue it until Hell freezes over, but I think it would be a very interesting thing to see, and useful.
I mean, if I'm on a 16/8 - how close am I to a ketogenic state? If I knew that, I might alter my regimen to include such or not waste time with it. If my main concern was retaining mass, I would like to know my NB marker points, and so forth. You're the only guy I know who could probably pull this straight out of your hat.</div>
I'll post up what charts I have later this evening or this weekend for you. But right now I got to get my *** to my shop and get some work done or I'll be starving for real  
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In the meantime and to suit your purposes go buy some Ketostix at Walmart or Walgreens and monitor your ketones with them.
 
Pete 69

Calories matter even if eating low carb high fat believe, the &quot;metabolic advatange&quot; of Dr. Atkins happens to a degree but not so that you can eat what you want.

I tried the intermittent fasting protocol with the anabolic diet, I tried the 16/8, 24/24, working out while fasting and eating just before workout too.

What I can tell is that for fat loss, intermittent fasting is fantastic because you experience less hunger than when you gradually reduce your cals, insulin is kept very low.

I lost fat to a certain degree but felt it difficult to lose even more (even with carb and cals refeeds).

Working out while fasting gives a real CNS boost from catecholamines, hence strength gains, but very limited LBM gains.

For my part the IF protocol coupled with the anabolic diet worked great for losing fat but not for gaining mass....but I am still waiting for Dan's book on fasting and see more clearly science wised.

Our ancestors lived like that yes but was it optimal for health -&gt; maybe yes but for gaining muscle? -&gt; don't know.
 
Stingblood, you bring up a lot of good points. And for the record, I was joking about calories not mattering. The research is clear on this, and personally, I once went on a VERY low carb bulking diet without refeeds and gained 40 lbs over a 5-6 month period.

I've pretty much low carbed on every stint of IF that i've done. I agree that it would probably be difficult for mass gains, on probably far from ideal. Even if our ancestors did go through periods of feast and famine, and perhaps it will turn out this is optimal for health, our ancestors werent lifting heavy things in the hopes of putting on muscle.

And all the paleo guru claims of humans being these muscular specimens and fierce hunters, its more likely we were smart group hunters, could use our endurance to fatigue prey, chase them off a cliff, or use weapons to throw at the tasty critters.

Pics of Masai, Inuit, ALL the pics from Weston Prices book didn't show anyone at risk of taking home a trophy even at a local amateur bodybuilding competition.

And I also agree with your personal experience, once can gain significant strength with no mass gains to show for it. Frustratingly, i've had the same experience myself.
 
Pete, after giving the ketosis question some thought I still have to say, I don't think so.

One reason, which you mention, is the anabolism seen with insulin; something we would want at that time.

Also even though the increase in glycogen may throw one out of ketosis coming back into it would be no more protein catabolic than the intitial, which I've stated is shown to be much smaller than thought so IMOO I would rather have the insulin mediated increase in protein uptake than the small amount of catabolism.
 
I found some info on the importance on post-wo protein supplementation timing. Although it is a study done on elderly it gives some insight into how important the timing is: <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">J Physiol. 2001 Aug 15;535(Pt 1):301-11.
Timing of postexercise protein intake is important for muscle hypertrophy with resistance training in elderly humans.
Esmarck B, Andersen JL, Olsen S, Richter EA, Mizuno M, Kjaer M.
Sports Medicine Research Unit, Bispebjerg Hospital, Denmark. bep01@bbh.hosp.dk

1. Age-associated loss of skeletal muscle mass and strength can partly be counteracted by resistance training, causing a net synthesis of muscular proteins. Protein synthesis is influenced synergistically by postexercise amino acid supplementation, but the importance of the timing of protein intake remains unresolved.
2. The study investigated the importance of immediate (P0) or delayed (P2) intake of an oral protein supplement upon muscle hypertrophy and strength over a period of resistance training in elderly males.
3. Thirteen men (age, 74 +/- 1 years; body mass index (BMI), 25 +/- 1 kg m(-2) (means +/- S.E.M.)) completed a 12 week resistance training programme (3 times per week) receiving oral protein in liquid form (10 g protein, 7 g carbohydrate, 3 g fat) immediately after (P0) or 2 h after (P2) each training session. Muscle hypertrophy was evaluated by magnetic resonance imaging (MRI) and from muscle biopsies and muscle strength was determined using dynamic and isokinetic strength measurements. Body composition was determined from dual-energy X-ray absorptiometry (DEXA) and food records were obtained over 4 days. The plasma insulin response to protein supplementation was also determined.
4. In response to training, the cross-sectional area of m. quadriceps femoris (54.6 +/- 0.5 to 58.3 +/- 0.5 cm(2)) and mean fibre area (4047 +/- 320 to 5019 +/- 615 microm(2)) increased in the P0 group, whereas no significant increase was observed in P2. For P0 both dynamic and isokinetic strength increased, by 46 and 15 %, respectively (P &lt; 0.05), whereas P2 only improved in dynamic strength, by 36 % (P &lt; 0.05). No differences in glucose or insulin response were observed between protein intake at 0 and 2 h postexercise.
5. We conclude that early intake of an oral protein supplement after resistance training is important for the development of hypertrophy in skeletal muscle of elderly men in response to resistance training.

PMID: 11507179 [PubMed - indexed for MEDLINE] PMCID: PMC2278776
</div> The study can be obtained for free via  PubMed.
Note 1: The subjects did not exercise in a fasted state but I believe that the study is equally important for this topic.  
Note 2: The P0 subjects lost LBM during the 12 week experiment while the P2 subjects gained LBM.

Here is quote from the study that raises a question: <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">In the present study subjects in the two groups received the same controlled protein supplementation per body weight (0.13 g kg-1) and per lean body mass (0.19 g kg-1) after every training bout. Hence, the findings do seem to indicate that the timing of the protein intake is of utmost importance for protein synthesis and muscle hypertrophy.</div>Both the net LBM gain and CSA gain in the study was small (1.8 ± 0.7 %) and (7 ± 1 %) respectively. This may be a result of a low protein diet in combination with that the subjects were elderly. Or? Another quote from the study, comparing protein intake: <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Moreover, in the elderly it has been found that the protein requirements probably are not increased above normal dietary intake on non-training days as the myofibrillar protein synthesis was found to be similar in an exercised leg 23 h postexercise whether high-protein (28 E %) or isocaloric low-protein meals (7 E %) were ingested (Welle &amp; Thornton, 1998). </div>Does this mean that we do not need a lot of protein to gain? I'm not sure. As the findings I posted earlier said, we gain some even if we are dieting, but the gains can be moderated by nutrient intake. Or is it timing that matters the most?
 
Another study points to when the muscle protein synthesis increases after a bout: <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">J Appl Physiol 104: 1452-1461, 2008.
Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging
Micah J. Drummond,1 Hans C. Dreyer,1,2 Bart Pennings,4 Christopher S. Fry,1 Shaheen Dhanani,3,4 Edgar L. Dillon,3,4 Melinda Sheffield-Moore,3,4 Elena Volpi,3,4 and Blake B. Rasmussen1,2,4
1Division of Rehabilitation Sciences, 2Departments of Physical Therapy and 3Internal Medicine, and 4Sealy Center on Aging, University of Texas Medical Branch, Galveston, Texas
Submitted 10 January 2008 ; accepted in final form 5 March 2008

Skeletal muscle loss during aging leads to an increased risk of falls, fractures, and eventually loss of independence. Resistance exercise is a useful intervention to prevent sarcopenia; however, the muscle protein synthesis (MPS) response to resistance exercise is less in elderly compared with young subjects. On the other hand, essential amino acids (EAA) increase MPS equally in both young and old subjects when sufficient EAA is ingested. We hypothesized that EAA ingestion following a bout of resistance exercise would stimulate anabolic signaling and MPS similarly between young and old men. Each subject ingested 20 g of EAA 1 h following leg resistance exercise. Muscle biopsies were obtained before and 1, 3, and 6 h after exercise to measure the rate of MPS and signaling pathways that regulate translation initiation. MPS increased early in young (1–3 h postexercise) and later in old (3–6 h postexercise). At 1 h postexercise, ERK1/2 MNK1 phosphorylation increased and eIF2 phosphorylation decreased only in the young. mTOR signaling (mTOR, S6K1, 4E-BP1, eEF2) was similar between groups at all time points, but MNK1 phosphorylation was lower at 3 h and AMP-activated protein kinase- (AMPK) phosphorylation was higher in old 1–3 h postexercise. We conclude that the acute MPS response after resistance exercise and EAA ingestion is similar between young and old men; however, the response is delayed with aging. Unresponsive ERK1/2 signaling and AMPK activation in old muscle may be playing a role in the delayed activation of MPS. Notwithstanding, the combination of resistance exercise and EAA ingestion should be a useful strategy to combat sarcopenia. </div>The older you get, the longer the delay before MPS increases.
 
Hi Dan. This was another issue that I forgot to address earlier regarding fasting. The insulin resistance that occurs related to the increase in intramuscular triglycerides during a fast. Now even though training acutely increases insulin sensitivity, i'm not sure it overcomes the overall rise in insulin resistance to fasting.

I've also come across some research looking at training in a fasted state after a low carb diet and a rise in intramuscular triglycerides increasing exponentially, seemingly filling in the role of glycogen when food and carbs are low. I know this goes against basic knowledge on muscle physiology, but perhaps this can partially explain why many people CAN train just fine in a constant low carb state.

Effect of short-term starvation versus high-fat diet on intramyocellular triglyceride accumulation and insulin resistance in physically fit men
Nathan A. Johnson1, Stephen R. Stannard2, David S. Rowlands2, Phillip G. Chapman1, Campbell H. Thompson3, Helen O'Connor1, Toos Sachinwalla4 and Martin W. Thompson1

1 The School of Exercise and Sport Science, The University of Sydney, Australia 2 Institute of Food, Nutrition and Human Health, Massey University, New Zealand 3 General Medicine, Flinders Medical Centre, Flinders University, Australia 4 Rayscan Imaging, 40–46 Goulburn Street, Liverpool, Australia

It is currently believed that intramyocellular triglyceride (IMTG) accumulation and insulin resistance are a consequence of dietary fat ingestion and/or the elevated circulating lipid levels associated with chronic fat surplus. The purpose of this study was to compare the effect of short-term starvation versus low-carbohydrate (CHO)/high-fat diet on IMTG accumulation and the development of insulin resistance in physically fit men. Intramyocellular triglyceride content, measured as intramyocellular lipid (IMCL) by proton magnetic resonance spectroscopy (1H-MRS), and glucose tolerance/insulin sensitivity, assessed by frequently sampled intravenous glucose tolerance test (IVGTT), were determined after 67 h of: (a) water-only starvation (S); and (b) very low-CHO/high-fat diet (LC). These diets had in common significant restriction of CHO availability but large differences in fat content. All results were compared with those measured after a mixed CHO diet &copy;. Dietary interventions were administered by cross-over design. The level of dietary-induced IMTG accumulation (P = 0.46), insulin resistance (P = 0.27) and glucose intolerance (P = 0.29) was not different between S and LC treatments. Intramyocellular triglyceride content and insulin sensitivity were negatively correlated (r = –0.63, P &lt; 0.01). Therefore, whilst insulin resistance may be due to fat accumulation at a cellular level, in the integrated human organism this outcome is not exclusively a function of dietary fat intake. The comparable level of IMTG accumulation and insulin resistance following S and LC may suggest that these metabolic perturbations are largely a consequence of the increased lipolytic response associated with CHO restriction.

Effects of acute starvation on insulin resistance in obese patients with and without type 2 diabetes mellitus

František Duškaa, Corresponding Author Contact Information, E-mail The Corresponding Author, Michal And&amp;#283;la, Aleš Kub&amp;#283;naa and Ian A. Macdonaldb

aDepartment of Internal Medicine II, The 3rd Faculty of Medicine, Šrobárova 50, Královské Vinohrady University Hospital, Charles University, Prague, Czech Republic

bSchool of Biomedical Sciences, University of Nottingham, Nottingham, United Kingdom

Received 22 February 2005;
accepted 11 August 2005.
Available online 26 September 2005.

Purchase the full-text article



References and further reading may be available for this article. To view references and further reading you must purchase this article.

Summary
Background &amp; Aims

Starvation decreases insulin sensitivity and glucose tolerance in both lean and obese (OB) non-diabetic subjects. Influence of drastic calorie reduction on insulin resistance in patient with type 2 diabetes (T2DM) is not known.
Methods

We enrolled 10 T2DM (diabetes duration 11.1±7.9 years) and 10 OB age and weight-matched subjects and performed isoglycaemic hyperinsulinaemic clamp (two 120 min phases of 60 and 120 mIU min&amp;#8722;1 m&amp;#8722;2 i.v. insulin) with indirect calorimetry at baseline and after 60 h of fasting.
Results

After starvation insulin-mediated glucose disposal decreased significantly in both hyperinsulinaemic phases in T2DM (phase 1: from 46±28 to 33±17, P&lt;0.04; phase 2 from 122±47 to 80±30 &amp;#956;g kg&amp;#8722;1 min&amp;#8722;1, P&lt;0.01) as well as in OB (phase 1: from 94±52 to 52±24, P&lt;0.04; phase 2: from 131±46 to 106±43 &amp;#956;g kg&amp;#8722;1 min, P&lt;0.01). Both oxidative and non-oxidative components of glucose disposal tended to be reduced after fasting. A change of insulin sensitivity was found to be highly dependent upon pre-starvation conditions: more insulin resistant subjects tended to maintain (or modestly improve) insulin resistance whilst subjects with better insulin sensitivity tended to worse it.
Conclusion

Insulin sensitivity worsens similarly in both T2DM and OB subjects during 60-h fast. The change is probably predictable according to pre-starvation insulin sensitivity.
 
On fasted lifting

http://jn.nutrition.org/cgi/content/full/137/4/985

Resistance Training Reduces Fasted- and Fed-State Leucine Turnover and Increases Dietary Nitrogen Retention in Previously Untrained Young Men1
Daniel R. Moore2,3, Nicole C. Del Bel2,3, Kevin I. Nizi2,3, Joseph W. Hartman3, Jason E. Tang3, David Armstrong4 and Stuart M. Phillips3,*

3 Exercise Metabolism Research Group, Department of Kinesiology, and 4 Division of Gastroenterology, McMaster University, Hamilton, Ontario, Canada L8S 4K1


We aimed to determine the impact of intense resistance training, designed to increase lean body mass (LBM), on both fasted and fed whole body protein kinetics in untrained young men. Twelve healthy males (22 ± 2 y of age; BMI, 24.3 ± 2.4 kg/m2) participated in a 12-wk (5-d/wk) resistance training program. Before and after training, a primed constant infusion of [1-13C]leucine was used to measure whole body leucine turnover, protein breakdown, and nonoxidative leucine disposal in the fasted and fed states. Participants were studied during 5-d controlled diet periods that provided a moderate protein intake [1.4 g/(kg body wt · d)]. We estimated protein turnover and nitrogen balance. Training increased LBM (61.6 ± 6.9 vs. 64.8 ± 6.7 kg, P &lt; 0.05). After training, whole body leucine turnover was reduced (P &lt; 0.01) in both fasted (167 ± 18 vs. 152 ± 17) and fed (197 ± 23 vs. 178 ± 21) states [all values µmol/(kg LBM · h)]. Training-induced decreases (P &lt; 0.01) in protein breakdown occurred in the fasted (165 ± 18 vs. 144 ± 17) and fed (111 ± 23 vs. 93 ± 20) states. Following training, nonoxidative leucine disposal was similarly reduced (P &lt; 0.01) in the fasted (144 ± 18 vs. 126 ± 18) and fed (151 ± 20 vs. 133 ± 19) states. Nitrogen balance was more positive after training (13.7 ± 8.1 vs. 33.4 ± 12.5 g/(kg LBM · d), P &lt; 0.01) indicating an increased retention of dietary nitrogen. Intense resistance training alters whole body protein kinetics in novice weightlifters regardless of feeding status. The increase in nitrogen balance after training demonstrates a more efficient utilization of dietary nitrogen, suggesting that protein requirements for novice weightlifters are not elevated.


On low glycogen and changes in genes in IIA muscle fibers

Skeletal muscle heterogeneity in fasting-induced upregulation of genes encoding UCP2, UCP3, PPARgamma and key enzymes of lipid oxidation.

Samec S, Seydoux J, Russell AP, Montani JP, Dulloo AG.

Department of Medicine, University of Fribourg, Rue du Musée 5, 1700 Fribourg, Switzerland.

The uncoupling protein homologs UCP2 and UCP3 have been proposed as candidate genes for the regulation of lipid metabolism. Within the context of this hypothesis, we have compared, from fed and fasted rats, changes in gene expression of skeletal muscle UCP2 and UCP3 with those of carnitine palmitoyltransferase I and medium-chain acyl-CoA dehydrogenase, two key enzymes regulating lipid flux across the mitochondrial beta-oxidation pathway. In addition, changes in gene expression of peroxisome proliferator-activated receptor gamma, a nuclear transcription factor implicated in lipid metabolism, were also investigated. The results indicate that in response to fasting, the mRNA levels of UCP2, UCP3, carnitine palmitoyltransferase I and medium-chain acyl-CoA dehydrogenase are markedly increased, by three- to sevenfold, in the gastrocnemius and tibialis anterior (fast-twitch muscles, predominantly glycolytic or oxidative-glycolytic), but only mildly increased, by less than twofold, in the soleus (slow-twitch muscle, predominantly oxidative). Furthermore, such muscle-type dependency in fasting-induced transcriptional changes in UCP2, UCP3, carnitine palmitoyltransferase and medium-chain acyl-CoA dehydrogenase persists when the increase in circulating levels of free fatty acids during fasting is abolished by the anti-lipolytic agent nicotinic acid - with blunted responses only in the slow-twitch muscle contrasting with unabated increases in fast-twitch muscles. Independently of muscle type, however, the mRNA levels of peroxisome proliferator-activated receptor gamma are not altered during fasting. Taken together, these studies indicate a close association between fasting-induced changes in UCP2 and UCP3 gene expression with those of key regulators of lipid oxidation, and are hence consistent with the hypothesis that these UCP homologs may be involved in the regulation of lipid metabolism. Furthermore, they suggest that in response to fasting, neither the surge of free fatty acids in the circulation nor induction of the peroxisome proliferator-activated receptor gamma gene may be required for the marked upregulation of genes encoding the UCP homologs and key enzymes regulating lipid oxidation in fast-twitch muscles.
 
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(nkl @ May 04 2008,4:28)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Does this mean that we do not need a lot of protein to gain? I'm not sure. As the findings I posted earlier said, we gain some even if we are dieting, but the gains can be moderated by nutrient intake. Or is it timing that matters the most?</div>
Personally I have always believed that timing is more important that eating vast amounts but again when eating vast amounts of protein timing may not be an issue at all since you would (in theory) be ingesting protein throughout the day.

Anyway

Appl Physiol Nutr Metab. 2007 Dec;32(6):1132-8.Links
Minimal whey protein with carbohydrate stimulates muscle protein synthesis following resistance exercise in trained young men.Tang JE, Manolakos JJ, Kujbida GW, Lysecki PJ, Moore DR, Phillips SM.
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main St. West, Hamilton, ON L8S 4K1, Canada.

Whey protein is a supplemental protein source often used by athletes, particularly those aiming to gain muscle mass; however, direct evidence for its efficacy in stimulating muscle protein synthesis (MPS) is lacking. We aimed to determine the impact of consuming whey protein on skeletal muscle protein turnover in the post-exercise period. Eight healthy resistance-trained young men (age=21+/-1 .0 years; BMI=26.8+/-0.9 kg/m2 (means+/-SE)) participated in a double-blind randomized crossover trial in which they performed a unilateral leg resistance exercise workout (EX: 4 sets of knee extensions and 4 sets of leg press; 8-10 repetitions/set; 80% of maximal), such that one leg was not exercised and acted as a rested (RE) comparator. After exercise, subjects consumed either an isoenergetic whey protein plus carbohydrate beverage (WHEY: 10 g protein and 21 g fructose) or a carbohydrate-only beverage (CHO: 21 g fructose and 10 g maltodextran). Subjects received pulse-tracer injections of L-[ring-2H5]phenylalanine and L-[15N]phenylalanine to measure MPS. Exercise stimulated a rise in MPS in the WHEY-EX and CHO-EX legs, which were greater than MPS in the WHEY-RE leg and the CHO-RE leg (all p&lt;0.05), respectively. The rate of MPS in the WHEY-EX leg was greater than in the CHO-EX leg (p&lt;0.001). We conclude that a small dose (10 g) of whey protein with carbohydrate (21 g) can stimulate a rise in MPS after resistance exercise in trained young men that would be supportive of a positive net protein balance, which, over time, would lead to hypertrophy.
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Personally I have always believed that timing is more important that eating vast amounts but again when eating vast amounts of protein timing may not be an issue at all since you would (in theory) be ingesting protein throughout the day.</div>
Which is good for me, because I can't always time my protein intake. Even the good old handy protein drinks don't work for me - I'm just too lactose intolerant, I crap it out after an hour or so, making me doubt its efficacy in supplying protein to myself. So instead I try to eat a crapload of protein-rich foods every meal or snack (well, not really a crapload, more like 20-40g per meal).
 
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(Dan Moore @ May 11 2008,8:11)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"><div>
(nkl @ May 04 2008,4:28)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Does this mean that we do not need a lot of protein to gain? I'm not sure. As the findings I posted earlier said, we gain some even if we are dieting, but the gains can be moderated by nutrient intake. Or is it timing that matters the most?</div>
Personally I have always believed that timing is more important that eating vast amounts but again when eating vast amounts of protein timing may not be an issue at all since you would (in theory) be ingesting protein throughout the day.
...
We conclude that a small dose (10 g) of whey protein with carbohydrate (21 g) can stimulate a rise in MPS after resistance exercise in trained young men that would be supportive of a positive net protein balance, which, over time, would lead to hypertrophy.</div>
If we would ingest small amounts of protein during the day, say 10 g every 2 hours all day long, would the MPS continue to be elevated throughout? Perhaps. MPS is dependent on availability of amino acids, especially essential amino acids.

Would these small amounts of protein meals disturb the fasted metabolism much? I would not believe so, as protein is part of a low carb diet with similar metabolism and the small insulin rise from 10 grams of protein would not make much of a difference to the overall metabolism. But adding carbs would disturb the 'fasting' metabolism. Carbs can be eaten when we break the fast (if you eat carbs at all).

Pete69, if memory serves me right, exercise make us more insulin sensitive. Wouldn't this even out the insulin resistivity gained during fast? I actually believed that fasting made us more insulin sensitive, from what Martin Berkhan said in an interview here and in his bloghere. What is the truth here?
 
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(nkl @ May 12 2008,4:52)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">I actually believed that fasting made us more insulin sensitive</div>
That has always been my understanding also....Fasting and/or low carb = increased insulin sensitivity.
 
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(Bulldog @ May 12 2008,5:44)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"><div>
(nkl @ May 12 2008,4:52)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">I actually believed that fasting made us more insulin sensitive</div>
That has always been my understanding also....Fasting and/or low carb = increased insulin sensitivity.</div>
isn't fasting more beneficial when following a high carb diet (as the low carb diet already mimics fasting in certain ways)?
 
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