The Role of Diet & Muscle Hypertrophy

Before you start sending hate mail, claiming that MD is against ketogenic diets or low-carb diets, I will open with this statement, “I personally don’t care what diet you are following; use the diet that best fits your needs!” If I said that the best way to increase mass on your thighs would be to squat, I am sure I would get mail saying that I did hack squats and leg presses and got incredible gains better than when I was squatting!

            Every article on MD is meant to provoke thought and make you think outside the box. MD brings you the latest research; you don’t have to necessarily agree with it. Read every article and just think about what was written, but listen to your body and know that your body is like a chemistry experiment. Find the combination that works best for you.

Study Questions How High-fat Diets Impact on Muscle Hypertrophy

            There was a study done on rats, researching how a high-fat diet affects muscle hypertrophy; it has not yet been thoroughly examined. Using rats is easy because you can control their diet and know exactly what scientists are putting in their mouths. Working with humans with diet studies is difficult, because it’s hard to know what they are eating once they leave the lab.

            Many studies have proven that the diet questionnaires that many people are given in diet studies are not worth shit— because people lie! They don’t want the guilt of being in a diet study and saying I drove to McDonald’s last night when I was supposed to be eating healthy. Anyway, the rats were divided into a low-fat diet or a high-fat diet group. The macronutrient breakdown looked like this:

• Low-fat group: 20 percent protein (from casein), 70 percent carbohydrates (from corn starch), 10 percent fats (from saturated and monounsaturated fats).
• High-fat group: 20 percent protein (from casein), 35 percent carbohydrates (from corn starch), 45 percent fats (from saturated and monounsaturated fats).

            The rats then had their muscles placed on tension overload. This is the most extreme form of making muscles grow and not even the most intense workout you have ever had comes close to even remotely resembling this kind of muscle growth. The rats were placed on both diets and placed on muscle overload for 14 weeks, and the scientists examined markers of muscle growth and changes in muscle size.

            At the end of the 14 weeks, both of the groups had increases in muscle hypertrophy, but the rats on the high-fat diet had a decrease in muscle growth, compared to the low-fat group.¹ Specifically, the rats had a decrease in the growth of type II fast-twitch muscles, compared to the low-fat group. The group of rats consuming the high-fat diet had a reduction in the Akt/mTOR pathway, which is a key regulator of muscle protein synthesis. In sum, the high-fat diet blunted the muscle hypertrophy responses to exercise, compared to the low-fat diet.

            Another interesting finding was that 14 weeks on a high-fat diet blunted the Akt/mTOR response; after 30 weeks on the diet, the response was almost completely blunted. The interesting finding is that tension overload is just about the most powerful stimulator of muscle protein synthesis there is, yet a high-fat diet impeded this response.

The researchers did not have an exact mechanism as to how the high-fat diet impeded muscle hypertrophy, but they had a couple of cellular mechanisms. One thing to consider is that a high-fat diet can lead to a decrease in what’s called intramuscular triglycerides, which cause insulin resistance and reduce the actions of insulin. Additionally, high-fat diets can cause oxidative stress, which causes free radical damage and causes cellular damage, which may overwhelm the repair/recuperation machinery.

The other mechanism is a decrease in the Akt/MTOR pathway. A previous study was published in the Journal of Applied Physiology and reported that performing resistance training in a glycogen-depleted state results in impaired genes for muscle hypertrophy.² The study follows a 2005 study in which researchers from the Human Performance Lab in Indiana reported that a glycogen-depletion diet blunts the expression of the muscle protein Akt. Akt, or protein kinase B (PKB), is an important molecule in cellular signaling. Akt is also able to induce protein synthesis pathways and is therefore a key signaling protein in the cellular pathways that lead to skeletal muscle hypertrophy and general tissue growth.

Akt is regulated in response to a wide variety of growth factors, including insulin and more recently, has been associated with rapid activation in response to exercise in human skeletal muscle. In the study, they didn’t use rats or cell cultures; they used resistance-trained athletes. (The athletes had trained for almost eight years, using resistance exercise and had exceptional leg press strength). Resistance-trained males performed resistance exercise in the glycogen-depleted state or with adequate glycogen stores. The next day, the subjects returned to the weight room and completed one-legged leg presses (8 sets of 5 reps ~80 percent of a 1 RM) with one leg that was glycogen-depleted while the other leg was not. Muscle biopsies were taken before exercise, immediately after and three hours after recovery.

When they examined the muscle biopsies, the researchers found that depleted muscle glycogen concentrations reduced the gene expression of muscle hypertrophy genes. Some of the more disturbing findings were that resting levels of genes involved in muscle hypertrophy (Myogenin and IGF-1) were lower in the glycogen-depleted muscle.³ Akt expression was similar in both groups before and immediately after exercise (after 10 minutes of recovery in the high-carbohydrate trial).

The Akt/mTOR regulates muscle hypertrophy and is down-regulated during muscle atrophy. Akt phosphorylation increased 1.5-fold after resistance exercise with glycogen. During the low-glycogen trial after exercise, Akt remained unchanged.²The study concluded that commencing resistance exercise with depleted muscle glycogen does not enhance the activity of genes implicated in promoting hypertrophy.

Things to Consider!

            Before you jump to the conclusion that I am bashing high-fat/low-carb diets, this study has some severe limitations. First, the protein content was only 20 percent, much lower than a bodybuilder would use. Second, the study was done in rats; of course I would love to see a study done with bodybuilders but fat chance that will ever happen. Third, we still don’t know that different fats have different effects (monounsaturated versus saturated).

            More research needs to be conducted of course, but at least there is no evidence to suggest a high-fat diet may not be the best diet for muscle growth. To be unbiased, there was also recently a study published in humans that showed that low-carbohydrate diets had no impact on muscle hypertrophy in untrained men, but we still don’t know whether long-term low-carb diets have any impact on muscle hypertrophy.

References:

1. Sitnick M, Bodine SC, Rutledge JC. Chronic high fat feeding attenuates load-induced hypertrophy in mice. J Physiol. 2009 Dec 1;587(Pt 23):5753-65.

2. Creer A, Gallagher P, Slivka D, Jemiolo B, Fink W, Trappe S. Influence of muscle glycogen availability on ERK1/2 and Akt signaling after resistance exercise in human skeletal muscle. J Appl Physiol, 2005 Sep;99(3):950-6.
4. Churchley EG, Coffey VG, Pedersen DJ, Shield A, Carey KA, Cameron-Smith D, Hawley JA. Influence of preexercise muscle glycogen content on transcriptional activity of metabolic and myogenic genes in well-trained humans. J Appl Physiol, 2007 Apr;102(4):1604-11.

High-Fat Diet Impairs Muscle Health Before Impacting Function

            Scientists from School of Medicine at McMaster University reported that when mice are fed a high-fat diet, muscle function is not impacted, even though the muscle has sustained cellular damage. The lead scientist Thomas Hawke reported, “Based on the way the muscles performed, you would think that they're still healthy, but the fact is, the muscle is not healthy. It's undergone a lot of pathological changes.

            “What our results tell us is that, initially, skeletal muscle appears to respond positively to the high-fat diet. By changing the size or type of its muscle fibers, the muscle adapts to the high-fat diet by saying ‘Let's burn more of this fuel,’” Hawke said. “But with continued high-fat feeding, we're giving the muscle more fuel than it can handle. So, even though it has made these initial, positive changes, continued high-fat feeding is more than the muscle can cope with. That's when a downward spiral starts.”

            The researchers also discovered that not all muscles responded in the same way to obesity. Some adapted by changing their fiber type, while others altered the size of their fibers. But, in all cases analyzed, a high-fat diet decreased the ability of skeletal muscle to use fat or glucose as fuel. When the researchers looked at function, and examined the maximum effort the muscles could generate, they discovered no difference between the high-fat diet group and the control group, which was eating a diet significantly lower in fat. However, if the muscles were fatigued and then were required to work, the high-fat diet group didn't recover as quickly as the control group.

Reference:

Shortreed KE, Krause MP, Huang JH, Dhanani D, Moradi J, Ceddia RB, Hawke TJ. Muscle-specific adaptations, impaired oxidative capacity and maintenance of contractile function characterize diet-induced obese mouse skeletal muscle. PLoS One, 2009 Oct 6;4(10):e7293.

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