Protein Guru

Whenever I read the top level research on Protein I keep running into one name – Dr. Donald K. Layman. (His Twitter feed). Here’s some of the studies he has been a part of on the subject of Protein:

I didn’t realize he is in a video lecturing on Protein:

This video is well worth an hour. Key concepts are distribution, amount, timing, quality of protein. Takeaways:

  • It takes about 30 grams of protein in a meal to lead to Muscle Protein Synthesis (MPS). Less than 20 grams of protein on a meal have no effect on MPS. Never eat less than 30 grams of protein in a meal.
  • You are catabolic until you eat protein (breakfast or when you end an Intermittent Fast).
  • Eat at least three meals with greater than 30g of protein per meal.
  • Eat high quality protein with enough Leucine (at least 3g) at each meal
  • Eat protein first then carbs afterwards.
  • Protein burns more energy – commonly attributed to the Thermic Effect of Food -which is the action of MPS. Building muscle burns energy.
  • MPS peaks at 90 mins and is back down to baseline at 180 minutes.
  • MPS eventually declines due to a drop in ATP (energy).
  • Protein accelerates the gain from exercise.
  • Snacks tend to be carbohydrates (without Protein) and lead to fat gain.
  • Skipping breakfast isn’t good. I accommodate this by breaking my fast later in the day (intermittent fasting). I eat at 11:30, 2:30 and when I get home in the evening (typically 5:30 to 7:30). This makes me catabolic about 13 hours a day (10:30 PM to 11:30 AM) and anabolic for 11 hours a day (11:30 AM to 10:30 PM).
  • Reduce carbohydrates to less than 30 grams per meal (I try to do much less than that).
    • Total carbs divided by total fiber < 6 – eat whatever you want.
    • Eliminate food which has carbs divided by total fiber > 10 (bread, grains, etc).

Meals (Using his concepts)

Meets goal of at least 3 grams of Leucine.

Breakfast

  • 4 hard boiled eggs, 4 slices of bacon
    • 36g protein, 32g fat, 2g carbs, 460 calories

Lunch/Dinner

  • 128g Chicken Breast, boneless/skinless
    • 39g protein, 6g fat, 0g carbs, 220 calories
  • 3 medium sized chicken drumsticks
    • 47g protein, 17g fat, 1g carbs, 358 calories
  • 165g Pork Ribs
    • 38g protein,  31g fat, 0g carbs, 479 calories
  • 120g Colby Jack Cheese
    • 31g protein, 41g fat, 2g carbs, 500 calories

Vegetable/Nuts/Fruits Carbs to Fiber Ratios

Carbs with ratios less than 6 are ad libitum (eat as much as you want):

  • Flax Seeds (30g serving) – 8.7/8.2 = 1.06
  • Chia Seeds (1 Tablespoon serving) – 4.2/3.4 = 1.24
  • Mushrooms (85g serving) – 2.8/1.9 = 1.47
  • Cabbage (1 cup) – 7.6/4.7 = 1.61
  • Cauliflower (85g serving) – 4.2/2.5 = 1.68
  • Kale (85g serving) = 7.4/4.4 =  1.68
  • Almond Flour = 5.9/2.6 = 1.79
  • Blackberries (1 cup serving) – 13.8/7.6 = 1.82
  • Asparagus (85g serving) – 3.5/1.8 = 1.94
  • Radish (85g serving) – 2.9/1.4 = 2.07
  • Broccoli (85g serving) – 4.5:2 = 2.25
  • Lettuce Mixed Greens (85g serving) – 2.7/1.1 = 2.45
  • Spinach (85g) – 3.1/1.2 = 2.58
  • Zucchini (medium – 196g) – 6.1/2.0 = 3.05

 

Gaining Muscle During a Cut

Leucine seems to be the central amino acid in muscle protein synthesis.

There’s plenty of interest in gaining muscle while cutting fat. Here’s an interesting item from a paper on that subject (Donald K. Layman, Jamie I. Baum. Dietary Protein Impact on Glycemic Control during Weight Loss. The Journal of Nutrition, Volume 134, Issue 4, 1 April 2004, Pages 968S–973S):

During catabolic periods such as energy restriction, supplementation with leucine or a complete mixture of the 3 BCAAs, leucine, isoleucine, and valine, stimulates muscle protein synthesis (35-37).

References

The three references (35-37) are:

35. Li, J. B. & Jefferson, L. S. (1978) Influence of amino acid availability on protein turnover in perfused skeletal muscle. Biochim. Biophys. Acta 544:351–359.
36. Buse, M. G. & Reid, S. S. (1975) Leucine. A possible regulator of protein turnover in muscle. J. Clin. Invest. 56:1250–1261.
37. Hong, S. C. & Layman, D. K. (1984) Effects of leucine on in vitro protein synthesis and degradation in rat skeletal muscle. J. Nutr. 114:1204–1212.

All three were rat studies. From 36.

The data presented indicate that leucine may act as a regulator of the turnover of protein in muscle cells. They are compatible with the hypothesis that leucine inhibits protein degradation and promotes protein synthesis in muscle.

Human Studies

Lundholm K, Edström S, Ekman L, Karlberg I, Walker P, Scherstén T. Protein Degradation in Human Skeletal Muscle Tissue: The Effect of Insulin, Leucine, Amino Acids. Clin Sci (Lond). 1981 Mar;60(3):319-26.

Satoshi Fujita,et.al. Effect of insulin on human skeletal muscle protein synthesis is modulated by insulin-induced changes in muscle blood flow and amino acid availability  Am J Physiol Endocrinol Metab. 2006 Oct; 291(4): E745–E754.

Changes in muscle protein synthesis were strongly associated with changes in muscle blood flow and phenylalanine delivery and availability. In conclusion, physiological hyperinsulinemia promotes muscle protein synthesis as long as it concomitantly increases muscle blood flow, amino acid delivery and availability.

 

Protein is not insulinogenic

In other words, Protein has minimal effect on your Insulin levels (Donald K. Layman Jamie I. Baum. Dietary Protein Impact on Glycemic Control during Weight Loss. The Journal of Nutrition, Volume 134, Issue 4, 1 April 2004, Pages 968S–973S.):

These data suggest that amino acids have minimal impact on plasma insulin concentrations when entering the body via the GI tract.

There’s data which shows a large effect of protein on Insulin but that protein was mainlined into the veins of the test subjects. Unless you are injecting your protein, you’ve got nothing to fear from protein.

Most of these studies used direct intravenous infusion of amino acids into the human forearm under fasted conditions and used euglycemic clamp techniques to measure glucose uptake and insulin resistance. Using these techniques, investigators found that acute increases in plasma amino acid concentrations resulted in higher plasma glucose concentrations, lower glucose uptake, and elevated plasma insulin levels.

Here’s one experiment cited which makes that point:

One of the first studies of the differences in amino acid metabolism between i.v. administration and oral intake was by Floyd et al. (51,52). These investigators evaluated the insulin response to i.v. infusion of amino acids or glucose (51) and also examined the insulin response to oral intake of protein (52). They found that infusion of 30 g of amino acids produced a 3-fold higher insulin response (∼180 μU/mL) than infusion of 30 g of glucose (∼50 μU/mL), suggesting a dramatic hyperinsulinemic effect of amino acids.

However, these investigators also examined the same measurements after subjects consumed a meal of 500 g of beef liver and found that the peak insulin response to the protein meal was only 30 μU/mL. Assuming that leucine is 1 of the most potent insulin secretagogues, the i.v. infusion provided <5 g of leucine while the beef meal provide >14 g of leucine (52). These data suggest that amino acids have minimal impact on plasma insulin concentrations when entering the body via the GI tract.

BCAAs may be the exception since the reach the bloodstream directly like carbohydrates…

The primary exceptions to this pattern of modifications are the BCAA, with over 80% of dietary content of leucine, valine, and isoleucine directly reaching blood circulation.

I wonder if that’s part of their popularity as a supplement?

Speed has an effect too:

For glucose, the postprandial handling occurs mostly within the first 2 h (43); however for amino acids the rate of disposal is much slower with <20% of the dietary amino acids degraded within the first 2 h (48). Thus, direct comparison of a high carbohydrate diet vs. a high protein diet is that the carbohydrate diet requires rapid equilibration of the glucose and insulin metabolic system with dramatic shifts between hepatic vs. peripheral regulations, while a high protein diet serves to stabilize the glycemic environment with delayed metabolism and less reliance on peripheral insulin actions.

And most relevantly to this page:

…diets with reduced carbohydrates and higher protein stabilize glycemic control during weight loss

This part gets really interesting since it describes metabolically broken folks like us…

As expected, as the subjects lost weight (∼6.3 kg) during the 10-wk energy restriction and they improved glycemic control as measured by reduced postprandial insulin response to the test meal. For the CHO Group, average values at wk 0 = 77 μU/mL and at wk 10 = 38 μU/mL. On the other hand, subjects consuming the moderate protein diet achieved normal values for 2-h insulin response after only 4 wk on the diet with average values at wk 0 = 75 μU/mL and at wk 10 = 12 μU/mL. These changes appear to be beneficial associated with the overall risk patterns of obesity and Metabolic Syndrome (57,58).

In summary:

In summary, use of diets with higher protein and reduced carbohydrates appears to enhance weight loss with greater loss of body fat and reduced loss of lean body mass. Beneficial effects of high protein diets may be increased satiety, increased thermogenesis, sparing of muscle protein loss, and enhanced glycemic control. Specific mechanisms to explain each of the observed outcomes remain to be fully elucidated. We suggest that a key to understanding the relationship between dietary protein and carbohydrates is the relationship between the intakes of leucine and glucose. Leucine is now known to interact with the insulin-signaling pathway with apparent modulation of the downstream signal for control of protein synthesis resulting in maintenance of muscle protein during periods of restricted energy intake. Leucine also appears to modulate glucose use by skeletal muscle. While total protein is important in providing substrates for gluconeogenesis, leucine appears to regulate oxidative use of glucose by skeletal muscle through stimulation of glucose recycling via the glucose-alanine cycle. These mechanisms appear to provide a stable glucose environment with low insulin responses during energy-restricted periods.

 

 

Are the Protein RDA Values Enough?

A metabolic unit study was performed to determine the effects of eating higher protein levels than the RDA and weight loss. (Pasiakos, S. M., Cao, J. J., Margolis, L. M., Sauter, E. R., Whigham, L. D., McClung, J. P., Rood, J. C., Carbone, J. W., Combs, G. F., Jr., Young, A. J. Effects of high-protein diets on fat-free mass and muscle protein synthesis following weight loss: a randomized controlled trial. FASEB J. 27, 3837–3847 (2013).) The study:

…assessed body composition and muscle protein synthesis responses to controlled diets manipulating protein intake over a range that spans the current acceptable macronutrient distribution range during short-term Energy Deficit (ED).

The study concluded:

…determined that consuming dietary protein at levels exceeding the RDA may protect fat-free mass (FFM) during short-term weight loss.

In summary, consuming twice the amount of dietary
protein than current recommendations measurably
protects FFM and promotes the loss of body fat during
short-term weight loss, likely through the maintenance
of muscle anabolic sensitivity to protein ingestion.
However, consuming dietary protein at 3 times the
RDA does not appear to confer any additional protective
advantage.

 

Muscle Protein Synthesis in the Elderly

Here’s a good study/article on Protein and the Elderly (Adv Nutr. 2014 Sep; 5(5): 599S–607S. Published online 2014 Sep 1. doi: 10.3945/an.113.005405
PMCID: PMC4188243. Keeping Older Muscle “Young” through Dietary Protein and Physical Activity. Daniel R. Moore*). One of the points

…35 g (∼0.45 g/kg) of whey protein stimulates mixed muscle protein synthesis in older adults, whereas 10 and 20 g (∼0.13 and ∼0.28 g/kg, respectively) do not.

And:

Individuals who more frequently elicit a maximal stimulation of muscle protein synthesis throughout a daily meal feeding cycle would be more likely to maintain muscle mass and possibly function. This could explain in part the greater retention of lean body mass in older adults who consume more than the current RDA for protein [i.e., ≥1.2 g/(kg ⋅ d)] relative to those who habitually consume a suboptimal amount [i.e., <0.8 g/(kg ⋅ d)]

 

Muscle Protein Synthesis from Eating Protein

From (Muscle for Life. The Truth About Protein Absorption: How Often You Should Eat Protein to Build Muscle. Michael Matthews):

When you eat protein, your stomach uses its acid and enzymes to break it down into its building blocks, amino acids. These molecules are transported into the bloodstream by special cells that line the small intestine, and are then delivered to various parts of the body. Your small intestine only has so many transporter cells, which limits the amount of amino acids that can be infused into your blood every hour.

The article goes on to say that different proteins sources are absorbed at different rates.

According to one review, whey clocks in at 8 to 10 grams absorbed per hour, casein at ~6.1 g/hr, soy at ~3.9 g/hr, and cooked egg at ~2.9 g/hr.

Here’s a really interesting point that I didn’t know about:

For instance, the presence of protein in the stomach stimulates the production of a hormone that delays “gastric emptying” (the emptying of the food from the stomach). This slows down intestinal contractions and thus how quickly the food moves through the small intestine, where nutrients are absorbed. This is one of the ways your body “buys the time” it needs to absorb the protein you eat.

That seems to be the mechanism by which protein gets processed by the body. That’s how the area under the curve for protein is so long.

The article goes on to say that:

Carbohydrates and fats can move through your small intestine and be fully absorbed while the protein is still being worked on.

The page then quoted a study (Protein feeding pattern does not affect protein retention in young women) which indicated that it doesn’t matter if the protein is consumed all at one time (Intermittent Fasting style) or over the course of the entire day.

It was higher during the experimental period, but not significantly different in the women fed the spread or the pulse patterns [59 +/- 12 and 36 +/- 8 mg N/(kg fat-free mass. d) respectively]. No significant effects of the protein feeding pattern were detected on either whole-body protein turnover [5.5 +/- 0.2 vs. 6.1 +/- 0.3 g protein/(kg fat-free mass. d) for spread and pulse pattern, respectively] or whole-body protein synthesis and protein breakdown. Thus, in young women, these protein feeding patterns did not have significantly different effects on protein retention.

Interesting…

 

Fat Adapted Athletes

Fat adaptation is the shift from carbohydrates as the primary fuel source to fat as the primary fuel source. Here’s a study of fat adaptation (Helge JW, Watt PW, Richter EA, Rennie MJ, Kiens B. Fat utilization during exercise: adaptation to a fat-rich diet increases utilization of plasma fatty acids and very low density lipoprotein-triacylglycerol in humans. J Physiol. 2001 Dec 15;537(Pt 3):1009-20.). The study:

was carried out to test the hypothesis that the greater fat oxidation observed during exercise after adaptation to a high-fat diet is due to an increased uptake of fat originating from the bloodstream.

The study had 13 male untrained subjects, seven consumed a fat-rich diet (62 % fat, 21 % carbohydrate) and six consumed a carbohydrate-rich diet (20 % fat, 65 % carbohydrate). Note that this was not a low carbohydrate diet (at 21%). The length was 7 weeks of training and diet.

The performance test was 60 min of bicycle exercise performed at 68 +/- 1 % of maximum oxygen uptake. This rate is the maximum rate of fat oxidation from this study (Nutrition. 2004 Jul-Aug;20(7-8):716-727. Optimizing fat oxidation through exercise and diet. Achten J, Jeukendrup AE.). The test measured the RER and found that the high fat group used significantly more fat as fuel:

During exercise, the respiratory exchange ratio was significantly lower in subjects consuming the fat-rich diet (0.86 +/- 0.01, mean +/- S.E.M.) than in those consuming the carbohydrate-rich diet (0.93 +/- 0.02).

An RER of 0.85 indicates that the subject were taking energy equally from fat and carbohydrates so the high fat group was getting about half of their energy from fat and half from carbohydrates. The high carb diet group got much less of their energy from fat.

The leg fatty acid (FA) uptake (183 +/- 37 vs. 105 +/- 28 micromol min(-1)) and very low density lipoprotein-triacylglycerol (VLDL-TG) uptake (132 +/- 26 vs. 16 +/- 21 micromol min(-1)) were both higher (each P < 0.05) in the subjects consuming the fat-rich diet.

Not only was the fatty acid uptake higher in the high fat group the fat oxidation was greater.

Whole-body plasma FA oxidation (determined by comparison of (13)CO(2) production and blood palmitate labelling) was 55-65 % of total lipid oxidation, and was higher after the fat-rich diet than after the carbohydrate-rich diet (13.5 +/- 1.2 vs. 8.9 +/- 1.1 micromol min(-1) kg(-1); P < 0.05).

Burning higher fat rates reduces the amount of muscle glycogen which is used.

Muscle glycogen breakdown was significantly lower in the subjects taking the fat-rich diet than those taking the carbohydrate-rich diet (2.6 +/- 0.5 vs. 4.8 +/- 0.5 mmol (kg dry weight)(-1) min(-1), respectively; P < 0.05), whereas leg glucose uptake was similar (1.07 +/- 0.13 vs. 1.15 +/- 0.13 mmol min(-1)). 4.

The study conclude that

…plasma VLDL-TG appears to be an important substrate source during aerobic exercise, and in combination with the higher plasma FA uptake it accounts for the increased fat oxidation observed during exercise after fat diet adaptation.

If fat is available as fuel the body will use the fat in preference to the glucose. If insufficient fat is available the body will use glucose.

The decreased carbohydrate oxidation was apparently due to muscle glycogen sparing and not to diminished plasma glucose uptake.

 

What is Endurance Training?

The Wikipedia definition of Endurance Training is:

The term endurance training generally refers to training the aerobic system as opposed to the anaerobic system.

This chart in the Wikipedia article shows the heart rate range associated with aerobic training as 70-80% of max heart rate.

This is a form of Aerobic Training is also known as “Long slow distance training“.

Richard Diaz on WodCast Podcast Episode 323 talks about why CrossFit fails in the area of aerobic training. He explains how VO2max testing works and why Crossfit doesn’t produce the sort of VO2max numbers that they would expect (I got at the bottom end of good on my VO2max after nearly a year on Crossfit). He also explains the benefits of training aerobically. He has some critiques of Maffetone’s method for competitive athletes.

A helpful page with a descriptive title (Training with the Maffetone Method: 7 Tips for Beginners).

 

Athletic Interference Effects

There have been studies which showed that simultaneous endurance and strength training produce interference effects. The effect is a loss of strength but not of endurance.

An early (1980) study (Hickson RC. Interference of strength development by simultaneously training for strength and endurance. Eur J Appl Physiol Occup Physiol. 1980;45(2-3):255-63.) stated:

The purpose of this study was to determine how individuals adapt to a combination of strength and endurance training as compared to the adaptations produced by either strength or endurance training separately.

There were three exercise groups: a strength group (S) that exercised 30–40 min . day-1, 5 days . week-1, and endurance group (E) that exercised 40 min . day-1, 6 days . week-1; and an S and E group that performed the same daily exercise regimens as the S and E groups.

After 10 weeks of training, VO2max increased approx. 25% when measured during bicycle exercise and 20% when measured during treadmill exercise in both E, and S and E groups. No increase in VO2max was observed in the S group.

There was a consistent rate of development of leg-strength by the S group throughout the training, whereas the E group did not show any appreciable gains in strength. The rate of strength improvement by the S and E group was similar to the S group for the first 7 weeks of training, but subsequently leveled off and declined during the 9th and 10th weeks.

These findings demonstrate that simultaneously training for S and E will result in a reduced capacity to develop strength, but will not affect the magnitude of increase in VO2max.

The graph in Hickson shows the interference effect on strength training. The strength alone group had continued strength gains. The Strength plus Endurance group increased in strength but then declined.

Another study (1985) showed similar interference effects (Dudley GA, Djamil R. Incompatibility of endurance- and strength-training modes of exercise. J Appl Physiol (1985). 1985 Nov;59(5):1446-51.).

Another study (Gustavo A Nader. Concurrent strength and endurance training: from molecules to man. Med Sci Sports Exerc. 2006 Nov;38(11):1965-70.) (PDF) described the interference effect as:

situations when strength and endurance training are performed simultaneously, a potential interference in strength development takes place, making such a combination seemingly incompatible

The paper described a number of possible causes for the interference effect.

 At the molecular level, there seems to be an explanation for the interference of strength development during concurrent training; it is now clear that different forms of exercise induce antagonistic intracellular signaling mechanisms that, in turn, could have a negative impact on the muscle’s adaptive response to this particular form of training. That is, activation of AMPK by endurance exercise may inhibit signaling to the protein-synthesis machinery by inhibiting the activity of mTOR and its downstream targets.

One of the possible reasons is the reduction of glycogen stores from both modes of training. However, this assumes that endurance training is performed at a heart rate level which oxidizes carbohydrates. If endurance training is done in the aerobic zone then carbohydrate stores are not reduced.

This raises the question “What is Endurance Training?”

 

Exercise and Blood Sugar Control

Here’s a meta-analysis that looked at the effect of exercise and blood sugar control in diabetics (Neil J. Snowling, MSC and Will G. Hopkins, PHD. Effects of Different Modes of Exercise Training on Glucose Control and Risk Factors for Complications in Type 2 Diabetic Patients: A meta-analysis. (PDF) Diabetes Care 2006 Nov; 29(11): 2518-2527.) which concluded:

Differences among the effects of aerobic, resistance, and combined training on HbA1c (A1C) were trivial; for training lasting ≥12 weeks, the overall effect was a small beneficial reduction (A1C 0.8 ± 0.3% [mean ± 90% confidence limit]).

There were generally small to moderate benefits for other measures of glucose control.

For other risk factors, there were either small benefits or effects were trivial or unclear, although combined training was generally superior to aerobic and resistance training.

Effects of covariates were generally trivial or unclear, but there were small additional benefits of exercise on glucose control with increased disease severity.

The Low Carb diet has a much more significant effect than exercise. But are there any studies showing the power of the Low Carb diet compared with exercise?