Omega- 3 Fatty Acids for Muscle Growth: Promising Potential. Since most people's eyes glaze over when someone starts talking cell biology, imagine your cell as an avocado. Picture the avocado with myriads of pins buried in it. This is your cell. The pins are membrane proteins, some of which are nutrient transporters for glucose, amino acids, and so forth. The dark skin and the edible green flesh is the plasma membrane, which consists of two thin layers made of fatty acids.
N- 3 supplementation has the potential of altering this part of the cell. Generally speaking, plasma membranes with a higher % EPA and DHA enrichment are healthier; they have the potential of modulating signals in between the white pins/plasma proteins and the avocado core.
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Let's take a look at what they do. Omega- 3 Fatty Acids: Effects on Health Controlled studies have clearly established the positive influence of n- 3 intake on cardiovascular health. The role of n- 3 as a modulator of inflammation is also well recognized and the fact that omega- 3 fats down- regulate genes involved in chronic inflammation makes it likely that n- 3 intake can reduce the risk of atherosclerosis.
Dietary epidemiology have also shown a link between n- 3 and mentally debilitating disorders such as Alzheimer's and depression. Furthermore, n- 3 may affect the development of many facets tied to brain function, such as intelligence, vision and mood. For example, infants who do not get enough n- 3 from their mothers during pregnancy might be at risk for developing vision and nerve problems.
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Other epidemiological trials have suggested a protective effect of n- 3 on cancer and tumour growth; in particular, prostate, breast and colon cancer. Omega- 3 Fatty Acids: Effects on Body Composition.
Freedom from disease and a sharper mind is all good and well, but what what about biomakers related to body composition? Results from studies on n- 3 intake and insulin sensitivity are mixed. In summary, people with poor insulin sensitivity (obese) usually see an improvement with n- 3, while lean subjects see no or only modest improvements. I have not seen a single study which shows that adding n- 3 alone will generate fat loss in lean subjects, but overweight/obese subjects sometimes see a small - but clinically significant - effect of n- 3 supplementation.
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There are some exceptions to this, i. However, I'll note that it's a profound flaw to look at the effects of n- 3 and fat loss in lean subjects and conclude that there is no benefit. Because the effect of n- 3 on fat metabolism and adipose tissue is not acute. It takes approximately 4- 6 weeks of n- 3 supplementation to change the fatty acid composition of the cell membrane, and controlled interventions on n- 3 supplementation and fat loss have never been longer than 1. In the case of Brilla, et al., who looked at fat loss in lean subjects, it was 1.
The implication of this is that the study, or studies, on n- 3 intake and fat loss in lean subjects might be too short in duration to show a clinically significant effect. The n- 3 supplements simply didn't . Furthermore, any greater weight loss, as a percentage of body weight, is always harder to spot in lean subjects in comparison to obese subjects, unless you have a large sample size (Brilla, et al., used only 8 subjects in the fish oil + exercise group).
In conclusion, there simply aren't any good trials on n- 3 supplementation and their role in fat loss yet. Oh sure, there are studies looking at fish intake and so forth, but I'm talking controlled interventions without a bunch of variables (fish protein, outpatient trials with poor control, etc.). Omega- 3 Fatty Acids: What We Know So Far. In summary of a vast area of research on n- 3 and health, the scientific evidence is indisputable for a positive effect on cardiovascular health and chronic inflammation. These are things you can measure and track, and find a clinically significant effect on within 1. Keep in mind that it's impossible to provide hard data on these aspects of human health. You can't put people in a lab, give some of them some fish oil pills, and look at who got Alzheimer's or cancer 8 weeks later.
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Instead you look at things like fish consumption in thousands of individuals, sometimes over several years, and compare the disease trends relative to fish or seafood consumption. When you do this, you often see positive associations between n- 3 saturation of the phospholipid membranes and greater health. This positive association seems independent of other factors that affect health; meaning that, in an imaginary scenario where we compare two people with the exact same stats, such as body fat percentage and lifestyle habits, with the exception of n- 3 intake or fish intake, the person with a higher n- 3 intake will be healthier.
A striking example of this, is the fact that fat Eskimos have significantly lower rates of Diabetes Type 2 compared to equally fat Americans (3. Not a completely valid comparison, due to the inherent problems of dietary epidemiology, but it illustrates the point I'm trying to make, as these health trends are seen across the board in many different populations. It's safe to say that n- 3 is good for us. The Western diet contains too little omega- 3 relative to omega- 6 fats for optimal health, and our low n- 3 intake might certainly be an independent factor influencing the disease trend amongst Westerners compared to other populations with high n- 3 intake (e.
Eskimos, etc.). In terms of dietary protein, . The amino acid leucine is the primary amino acid responsible for triggering muscle protein synthesis. Elderly folks need higher concentrations of leucine to get the same response as young folks. Various feeding strategies that overcomes this problem include: Anyway, so this one study I mentioned earlier showed that 8 weeks of n- 3 supplementation lead to a significant increase in muscle protein synthesis in response to feeding. The same experiment was repeated with younger subjects and the results were released a few weeks ago. Below, I'll do a detailed review of the newly released second study and talk a about the results.
Omega- 3 Fatty Acids and Muscle Protein Synthesis. Here's the study I'm going to talk about now: After obtaining baseline values for anabolic signalling pathways (m. TOR- p. 70s. 6k) and muscle protein synthesis, the participants were given 4 g n- 3/day for 8 weeks. A 6- 8 AM the following morning, they arrived at the laboratory, where they were infused with tracers for four hours. Without going into technical detail, tracer infusion is a technique for tracking the passage of nutrients, i. This is always done prior to infusion of amino acids; e. The amino acid dose was determined to 1.
A one- time . This might seem like a fairly trivial amount, but the the amino acid mixture, Travasol 1. BCAA (leucine, isoleucine, valine) or 1.
EAA (BCAA + 5 essential amino acids). I'll discuss the implications of this later on. During the infusion protocol, blood samples were taken with regular intervals. Three muscle tissue samples were obtained, one prior to the amino acid infusion, and two towards the end. Based on these values, the researchers were able to obtain relevant data points for comparison against the ones obtained 8 weeks prior (the same procedure was performed before the n- 3 intervention).
I just treated myself to an n- 3- intervention. I don't eat a lot of fish, but when I do it's usually salmon with cottage cheese. I find that the salty salmon fits nicely with the cool creamy cottage cheese. This confirmed that compliance was good and that the n- 3 supplementation was effective. For those interested in some raw numbers: EPA: 0.
DHA: 1. 9. 1% vs 4. Values are expressed as percentage of the total fatty acid composition of the phospholid membrane. It's interesting to note that n- 3's displaced n- 6 and monounsaturated fatty acids (MUFA) in the membrane. These were significantly lower (~5. Saturated fatty acid composition remained stable at 3.
What did this result in? Let's start with some health markers: As expected, the concentration of inflammatory markers in plasma was low in this healthycohort of subjects and there were no differences (all P . Recall what I said earlier about n- 3 supplementation and metabolic status. Overweight and obese people often see meaningful improvements in these markers with n- 3 supplementation, but in these normal weight subjects, n- 3 supplementation did not do much in terms of reducing inflammation or altering glucose tolerance.
Glucose rate of disappearance, which shows glucose tolerance but can also be seen as a rough marker for insulin sensitivity, was unchanged. Then again, 8 weeks might also have been too short of a time to see any significant improvements in this area.
The basal muscle protein FSR (calculated by using the muscle free phenylalanine enrichmentas the precursor enrichment) was not different before and after LCn- 3. PUFA supplementation.. I will use MPS instead of FSR to avoid confusion, and it's basically the same thing. Why ? Muscle protein is made out of three fractions; 2/3 myofibrillar protein and 1/3 sarcoplasmic and mithocondrial protein (around 1. Without derailing the topic too much, I'll note that an increase in MPS usually mean that synthesis in all these fractions increase equally in proportion to their volume. Weight training tends to increase synthesis of myofibrillar protein slightly more, relatively speaking, while endurance training increases mithocondrial protein synthesis specifically.
Anyway, MPS in the fasted state was unchanged, which is to be expected. Meaningful changes in MPS are always seen in response to feeding. For example, weight training boosts MPS in response to amino acids in the blood (via pre- workout and/or post- workout meals), but does not alter basal FSR, assuming concentrations of amino acids in the blood are not elevated.
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