by Siim Land
However, not all workouts are created equal and they’re going to cause different responses in the body. You don’t want to be training randomly because you’ll be getting random results. Not all types of exercise suit intermittent fasting either. That’s why you have to know how to train to meet the nuances of TIF.
Generally, TIF works best with resistance training that focuses on strength and hypertrophy. It’s meant to shield your muscles against catabolism while boosting recovery. You don’t need any protein or calories if you’re doing low-intensity exercise or cardio because you’ll be utilizing primarily fat for fuel. Chapter XVIII will talk about the different types of intermittent fasting, including TIF.
Post-Workout Nutrition While Fasting
When working out fasted, it’s important to get adequate nutrition and drive protein synthesis post-workout to not cause muscle loss.
In fasting conditions, protein NET balance tends to be negative and resistance training induces further muscle breakdown. That’s why it’s not a good idea to fast for too long after working out if your goal is muscle growth.
Muscle protein synthesis requires protein and amino acids. Just raising insulin or blood sugar isn’t enough to stimulate MPS, which is why you’d need adequate protein intake from food[437].
However, eating immediately afterwards isn’t ideal because you may be still under the influence of cortisol and digestive stress, which can promote gut issues and fat gain. Protein synthesis doesn’t peak immediately after you finish your last set either as it takes a bit of time for the body to respond and shift from a sympathetic state into a parasympathetic one. The sweet spot for muscle protein synthesis and avoiding catabolism seems to be between 60-195 minutes after training but not before 60 minutes[438].
Will chugging down a protein shake with leucine right after dropping the weights make you build more muscle? Maybe it will if it’s going to increase the overall daily nitrogen balance but maybe it won’t if your other macros aren’t on point. It’s definitely not necessary as you have at least 1-2 hours post-workout wherein you won’t be losing muscle thanks to increased ketones and growth hormone, but it won’t be bad for you either.
Dietary protein supplementation has been shown to significantly increase muscle strength and size during prolonged resistance training in healthy adults[439]. It’s another one of those things that’s not necessary as long as your other variables are met but it can still be useful for driving up muscle protein synthesis after the workout. Use it only if your diet lacks whole food complete protein sources.
The timing of protein supplementation in the context of anabolic autophagy may be inconvenient or at least problematic. You definitely don’t want to be consuming any protein or amino acids during fasting because it will break the fast, blunt growth hormone, and block autophagy. Protein shakes would have the most effect either immediately before or intra-workout ala targeted intermittent fasting. If you wait for 2 hours and eat, then it’d be better to get your amino acids from real food but if you don’t have access to those conditions, then the shake is a great alternative.
When taking any fitness supplements, you have to be wary of their ingredients and content. You definitely want to avoid artificial sweeteners like sucralose, saccharin, fructose, and aspartame because they’re linked to insulin resistance and other diseases. They’re still going to spike insulin and even disrupt the microbiome by promoting the proliferation of certain gut buts that can extract more calories from the food you eat. That’s something you can’t read from a nutrition label. Instead, you’d want to use natural protein powders with no additional flavorings or sweeteners. The taste might not be as good but to hell with that! It’s not supposed to taste like chocolate mint ginger-bread berry blast…it’s fuel.
How fast you drive into the anabolic mode post-workout depends on how long you’ve been fasted for, what kind of a workout you had, what are your physique goals, and how efficiently your body responds to ketosis.
If you’re working out on a 20-24 hour fast, then it’s more important to get some protein and building blocks into your system faster than if you were to work out between the 12-16 hour mark. In the case of the latter, you have higher energy stores from the previous feeding thus your buffer zone is also larger wherein you can get away with continuing to fast for longer.
In general, workout somewhere between the 16-20 hour mark of fasting and wait at least 60-120 minutes before eating anything. The fear of missing out on this so-called “anabolic window” wherein you’ll start building exponentially more muscle is futile. There might be some truth to it and it’s relevant in the context of targeted intermittent fasting but the timeframe expands itself for a much longer time than you’d think. Protein synthesis after resistance training can stay elevated for up to 24-48 hours.
What about other macronutrients like carbs and fats? That would depend on the particular individual, what kind of fuel was used during the workout, overall goals, and general anabolic-catabolic homeostasis.
Re-feeding after fasting, especially on carbohydrates, raises the thermic effect of food, which produces excess body heat and can lead to a positive result in body composition[440]. This is ideal for protocols like carb backloading and the cyclical ketogenic diet wherein you have some days of higher carb intake to promote insulin and muscle growth. How often to do it and when will be discussed in Chapter XIII.
On a daily basis, you’d want to still limit your insulin production and control for blood sugar. That’s why the keto template is amazing for maintaining lean muscle while being at a very pro-longevity state of chaperone-mediated autophagy.
Chaperon-Mediated Autophagy (CMA) differs from macroautophagy. CMA responds to increased ketone body production, which will help to salvage fuel for the organs that can’t use ketones for energy[441]. Ketone bodies also protect against muscle catabolism and avoid lean tissue breakdown[442]. This adds an additional layer to the autophagic process in which you can still gain a lot of its benefits without having to fast for too long. The best thing about it is that you’ll be able to send your body the signal to promote muscle growth without shutting down autophagy completely. Certain ketogenic fat sources like MCT oil and coconut oil have been shown to even promote autophagy in small amounts[443].
Cholesterol has been found to be quite beneficial for muscle growth. In a study by Riechman et al. (2007), 49 elderly people participated in a 12-week strength training program[444]. There was a dose-specific relationship between dietary cholesterol intake and lean body mass increase. The more cholesterol they ate the more muscle they gained. This was confirmed by controlled protein and fat intake as well.
In young healthy adults, a high cholesterol diet (~800 mg/d) has shown 3 times higher MPS rates 22 hours after resistance training compared to a low cholesterol diet (< 200 mg/d) [445].
High cholesterol intake from things like red meat and eggs has been recommended by many bodybuilders from the previous century as well. Vince Gironda from the 1950s became renown for his Steak and Eggs diet where he cycled through 5 days of eating zero carb followed up by a massive carbohydrate refeed on the weekend. According to him, this helped to maintain his leanness year round while still building muscle. Other bodybuilders often go on cycles of consuming a lot of whole eggs and yolks to promote muscle growth with cholesterol. Vince himself said that whole eggs are like natural anabolic steroids. Eggs are also rich in leucine, which will then stimulate MPS further.
Part of the reason why cholesterol helps with muscle growth may have to do with the anti-oxidant properties of cholesterol and the repair mechanisms it triggers. Cholesterol improves membrane stability of cells which enhances their resiliency against muscle damage during exercise. This also controls inflammation during recovery. Cholesterol supports mTOR and IGF-1 signaling by helping with the formation of signaling pathways.
The controversy around eating cholesterol and saturated fat is still controversial and not conclusive. In Chapter X, we’ll go through the past and
current research regarding their effects on heart disease and how you should eat them.
Whatever the case may be, no doubt that cholesterol and saturated fat, especially from meat and eggs are incredibly potent foods for muscle growth and anabolism. Saturated fat is a building block for cholesterol, which in turn promotes testosterone production as well.
Low saturated fat intake is associated with reduced testosterone production. For instance, men who go from a high saturated fat diet with 40% calories coming from fat to a low saturated fat diet with 25% fat saw their total and free testosterone levels drop[446]. Funny enough, going back to the high saturated fat diet made their testosterone increase again.
In the context of doing resistance training and practicing intermittent fasting, your body needs more anabolic foods to repair the damage it’s received. That’s why the idea that certain foods give you cancer is completely out of context when doing the Metabolic Autophagy Protocol. If you fast most of the day and lift weights, then you actually want to drive anabolism for recovery.
The upcoming chapters will delve deeper into the topic of what exact foods to eat for anabolism as well as catabolism. Remember that both of them are good in some situations but not all the time.
That’s it for protein and fasting. Hopefully, you’ve now realized that the body is incredibly adaptable in finding out how to produce energy and still build muscle. With smart and strategic nutrient timing you’ll make the absurd a reality and push that boulder across the hill. Now let’s turn to the general overview of healthy nutrition.
Chapter X
Food Fallacy
Dwight: Through concentration, I can raise and lower my cholesterol at will.
Pam: Why would you want to raise your cholesterol?
Dwight: So I could lower it.
The Office
After the Second World War, the United States went through drastic changes in its dietary landscape. The country was booming economically, influentially, as well as nutritionally. People got access to a lot of commercial privileges they’d been deprived of during the conflict. Instead of sticking to meager rations and eating home-made dishes, a lot of the foods people used to eat were replaced by different kind of inventions of the food industry.
Unfortunately, all did not go well as many in the Western population started to suffer from a devastating tidal wave of deaths caused by cardiovascular disease and its derivatives. In today’s day and age, 1 out of 4 deaths in the United States is caused by heart disease, making it one of the biggest dangers to people’s health. How the hell did we get here?
Enter the Lipid Hypothesis
In the 1940s, a researcher from the University of Minnesota, Ancel Keys, hypothesized that the sudden rise in heart attacks amongst Americans was caused by their diet and lifestyle.
Keys first did a 15-year long prospective study on Minnesotan business professionals. The study began in 1947 and was followed up in 1963. It confirmed the results of some earlier studies, indicating that the biggest risk factors of heart disease were high blood pressure, cholesterol levels, and smoking[447].
In 1958, Keys collaborated with other researchers from 7 selectively picked countries to try and see a cross-cultural comparison of heart disease risk in the male population. The Seven Countries Study as it was called recruited 12 763 men, 40-59 years of age, living in the United States, Finland, the Netherlands, Greece, Italy, Yugoslavia, and Japan, with a follow-up from 1958-1964[448]. Results showed that the risk of heart attack and stroke were directly correlated with the total level of serum cholesterol, blood pressure, and obesity. See Figure 64.
Figure 64 The more dietary fat consumed the more deaths from heart disease
The Lipid Hypothesis postulates that the main cause of heart disease are saturated fat and cholesterol that cause clogging of the arteries or atherosclerosis, which eventually will lead to a stroke or a heart attack. Based on that, lowering blood cholesterol and dietary fat intake decreases the risk of coronary heart disease and is healthier. By the 1980s, the lipid hypothesis or the Diet Heart Hypothesis was widely accepted and considered almost like a medical law[449].
That was a huge red light for the traditional way of eating that included eggs, full-fat dairy, red meat, butter, cream, and other foods high in cholesterol and saturated fat. Instead, inspired by the findings of Keys and other similar researchers, the public dietary guidelines shifted more towards promoting whole wheat grains, fresh fruits and vegetables, low-fat dairy, lean cuts of meat, egg substitutes, juices, and many other processed foods.
Over the course of the following decades, the situation didn’t get any better as the obesity epidemic actually got even worse after the introduction of the diet heart hypothesis. There are more people with diabetes, insulin resistance, and cardiovascular events than ever before. Granted the average American still eats a crappy diet with processed carbs and fats but the general population hasn’t gotten any healthier despite the change in dietary advice.
The Seven Countries Study has received a lot of criticism since its origin. In the 1950s, other researchers such as John Gofman from Berkeley California agreed that reducing dietary fat might be beneficial for heart disease patients[450]. Others were more skeptical, saying that the cause could be fat and cholesterol or it could also be the elevation of triglycerides from carbohydrates and sugar.
In 1973, Raymond Reiser found several methodological errors in Keys’ work, namely misinterpreting the connection of saturated fat and cholesterol with atherosclerosis and confusing it with trans fats[451]. It does pose the question of why ancestral diets with high meat and fat consumption found in Alaskan Eskimos, Tanzanian Maasai, and others don’t have such an epidemic of heart disease.
There’s also the French Paradox or the Mediterranean Diet, which is relatively high in saturated fat, animal protein, wine, cheeses, and other „heart attack foods“. Despite the high amounts of cholesterol and fat in their diet, French have quite low rates of heart disease compared to other Western countries.
Keys had selected those particular 7 countries out of the potential 22 for which he had available data as to fit his narrative. That’s why he didn’t include France into the study and chose populations with already lower levels of physical activity and poorer lifestyle habits. See Figure 65.
There have been many critiques of the diet heart hypothesis but no serious progress had been made until the 2000s. More data emerged that started to point the blame not on cholesterol or saturated fat but on sugar, processed carbs, vegetable oils, and trans fats.
Figure 65 Note how the relationship between fat consumption and heart disease gets skewed when you include all the other 22 countries
On August 2017, True Health Initiative pointed out many of Keys’ inaccuracies in the Seven Countries Study[452]. They refuted 4 false ideas: (1) the countries were selected to fit the expected outcome; (2) France was intentionally excluded as to avoid the French Paradox; (3) the data from Greece was taken during Lent, which created discrepancies; (4) sugar or carbohydrates were not considered as a possible contributor to heart disease.
Death By Cholesterol
So, is cholesterol really that bad for you that it’ll give you heart disease? Should you be eating foods high in cholesterol and saturated fat or not?
It is true that people who have heart disease tend to have higher cholesterol and blood pressure. But that’s not the only thing that matters and it’s potentially not the most important variable. In fact, low cholesterol is associated with mortality from heart disease, strokes, and cancer, whereas higher cholesterol has not been seen to be a bigger risk factor[453][454].
Cholesterol is an organic molecule produced by all animal cells. It’s an essential component of cell membrane and helps with its functioning. It’s also a steroid hormone that promotes hormone, bile, and vitamin D synthesis. Because of its molecular substance, cholesterol doesn’t mix with blood and it’s carried around the body by lipoproteins. There are different types of them:
&
nbsp; Very Low Density Lipoprotein (VLDL) – VLDL delivers triglycerides and cholesterol throughout the body to be stripped off from energy or for storage.
Intermediate Density Lipoprotein (IDL) – IDL helps the transport of cholesterol and fats but its density is between that of LDL and VLDL.
Low Density Lipoprotein (LDL) – LDL carries energy through the bloodstream and directs nutrients into the cells.
High Density Lipoprotein (HDL) – HDL collects unused cholesterol from the blood and brings it back to the liver for recycling.
HDL is considered the healthy one and LDL the bad one because it prevents the clogging of arteries and accumulation of cholesterol.
Figure 66 Different types of cholesterol
The amount of cholesterol in your blood is irrelevant to how it affects atherosclerosis and risk of heart disease because the build-up of plaque in the arteries is mostly driven by inflammation. If you suffer from higher inflammation and oxidative stress, then you’ll also have more free radicals in the blood which can oxidize LDL. Oxidation of LDL by free radicals is associated with an increased risk of cardiovascular disease[455].
Free radicals and high inflammation damages the arterial lining called the endothelium, which the cholesterol then gets stuck to. Over the long run, this leads to the accumulation of plaques and increased risk of heart disease. Additionally, higher VLDL is considered a better predictor of heart disease risk than LDL[456].