When you place your body in a calorie deficit, your body fat levels drop, but so does your body’s ability to create muscle proteins. Testosterone levels also decline and cortisol levels rise when calories are restricted for extended periods of time.
When you first start weightlifting, your body is hyperresponsive and can gain muscle at a very fast rate.
This “newbie gains” or “honeymoon” phase generally lasts six to eight months for most people, and it can simply overpower the muscle-related disadvantages of a calorie deficit.Eventually this advantage fades, however, and with it goes your ability to effectively “recomp” (short for recomposition) your body.
From that point on, your goal will be to lose fat and not muscle while in a calorie deficit and to gain muscle with minimal fat while in a calorie surplus.
Progressive overload refers to increasing the amount of tension your muscles produce over time, and the most effective way to do this is by progressively increasing the amount of weight that you’re lifting.
The key to gaining muscle and strength isn’t merely changing the types of stimuli your muscles are exposed to—it’s making your muscles work harder.
Your number one goal as a weightlifter should be to increase your whole-body strength over time.
Free weights give you the most muscle-building bang for your buck—far more than machines, bands, and other contraptions in the gym.
Compound exercises are superior to isolation exercises for gaining muscle and strength because they train many muscles at once, allow you to lift heavier weights, and significantly raise testosterone and growth hormone levels.
As enjoyable as pumps are, they’re not a strong muscle-building stimulus—not nearly as strong as mechanical tension, for instance.
If you want to gain muscle and strength as quickly as possible, then you want to limit your cardio because it can interfere with strength and muscle gain by making you more generally fatigued and disrupting cell signaling related to muscle growth.
Cardio does have significant health benefits—some of which you don’t get from resistance training—and it can help you burn more energy, which means faster fat loss and easier weight maintenance.
Clarkson PM, Nosaka K, Braun B. Muscle function after exercise-induced muscle damage and rapid adaptation. Med Sci Sports Exerc. 1992;24(5):512-520.
Trezise J, Collier N, Blazevich AJ. Anatomical and neuromuscular variables strongly predict maximum knee extension torque in healthy men. Eur J Appl Physiol. 2016;116(6):1159-1177. doi:10.1007/s00421-016-3352-8; Delp SL, Maloney W. Effects of hip center location on the moment-generating capacity of the muscles. J Biomech. 26(4-5):485-499.
Chumlea WC, Wisemandle W, Guo SS, Siervogel RM. Relations between frame size and body composition and bone mineral status. Am J Clin Nutr. 2002;75(6):1012-1016. doi:10.1093/ajcn/75.6.1012.
Jeevanandam S, Muthu PK. 2D:4D Ratio and its Implications in Medicine. J Clin Diagn Res. 2016;10(12):CM01-CM03. doi:10.7860/JCDR/2016/21952.9000; Van Etten LM, Verstappen FT, Westerterp KR. Effect of body build on weight-training-induced adaptations in body composition and muscular strength. Med Sci Sports Exerc. 1994;26(4):515-521.
Keogh JWL, Winwood PW. The Epidemiology of Injuries Across the Weight-Training Sports. Sport Med. 2017;47(3):479-501. doi:10.1007/s40279-016-0575-0.
Spinks AB, McClure RJ. Quantifying the risk of sports injury: a systematic review of activity-specific rates for children under 16 years of age. Br J Sports Med. 2007;41(9):548-57; discussion 557. doi:10.1136/bjsm.2006.033605; Moore IS, Ranson C, Mathema P. Injury Risk in International Rugby Union: Three-Year Injury Surveillance of the Welsh National Team. Orthop J Sport Med. 2015;3(7):2325967115596194. doi:10.1177/2325967115596194; Videbæk S, Bueno AM, Nielsen RO, Rasmussen S. Incidence of Running-Related Injuries Per 1000 h of running in Different Types of Runners: A Systematic Review and Meta-Analysis. Sports Med. 2015;45(7):1017-1026. doi:10.1007/s40279-015-0333-8.
Kjaer M. Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading. Physiol Rev. 2004;84(2):649-698. doi:10.1152/physrev.00031.2003.
Willis LH, Slentz CA, Bateman LA, et al. Effects of aerobic and/or resistance training on body mass and fat mass in overweight or obese adults. J Appl Physiol. 2012;113(12):1831-1837. doi:10.1152/japplphysiol.01370.2011.
Umpierre D, Stein R. Hemodynamic and vascular effects of resistance training: implications for cardiovascular disease. Arq Bras Cardiol. 2007;89(4):256-262.
Church DD, Hoffman JR, Mangine GT, et al. Comparison of high-intensity vs. high-volume resistance training on the BDNF response to exercise. J Appl Physiol. 2016;121(1):123-128. doi:10.1152/japplphysiol.00233.2016.
Westcott WL. Resistance Training is Medicine. Curr Sports Med Rep. 2012;11(4):209-216. doi:10.1249/JSR.0b013e31825dabb8.
Guadalupe-Grau A, Fuentes T, Guerra B, Calbet JAL. Exercise and bone mass in adults. Sports Med. 2009;39(6):439-468.
Russo CR, MD. The effects of exercise on bone. Basic concepts and implications for the prevention of fractures. Clin Cases Miner Bone Metab. 2009;6(3):223-228.
Pratley R, Nicklas B, Rubin M, et al. Strength training increases resting metabolic rate and norepinephrine levels in healthy 50- to 65-yr-old men. J Appl Physiol. 1994;76(1):133-137. doi:10.1152/jappl.1994.76.1.133.
Simão R, Lemos A, Salles B, et al. The Influence of Strength, Flexibility, and Simultaneous Training on Flexibility and Strength Gains. J Strength Cond Res. 2011;25(5):1333-1338. doi:10.1519/JSC.0b013e3181da85bf.
Zito CI, Qin H, Blenis J, Bennett AM. SHP-2 Regulates Cell Growth by Controlling the mTOR/S6 Kinase 1 Pathway. J Biol Chem. 2007;282(10):6946-6953. doi:10.1074/jbc.M608338200.
Mäestu J, Eliakim A, Jürimäe J, Valter I, Jürimäe T. Anabolic and Catabolic Hormones and Energy Balance of the Male Bodybuilders During the Preparation for the Competition. J Strength Cond Res. 2010;24(4):1074-1081. doi:10.1519/JSC.0b013e3181cb6fd3; Rossow LM, Fukuda DH, Fahs CA, Loenneke JP, Stout JR. Natural bodybuilding competition preparation and recovery: a 12-month case study. Int J Sports Physiol Perform. 2013;8(5):582-592.
Demling RH, DeSanti L. Effect of a Hypocaloric Diet, Increased Protein Intake and Resistance Training on Lean Mass Gains and Fat Mass Loss in Overweight Police Officers. Ann Nutr Metab. 2000;44(1):21-29. doi:10.1159/000012817; Nindl BC, Harman EA, Marx JO, et al. Regional body composition changes in women after 6 months of periodized physical training. J Appl Physiol. 2000;88(6):2251-2259. doi:10.1152/jappl.2000.88.6.2251.
Goldberg AL, Etlinger JD, Goldspink DF, Jablecki C. Mechanism of work-induced hypertrophy of skeletal muscle. Med Sci Sports. 1975;7(3):185-198.
Schwanbeck S, Chilibeck PD, Binsted G. A Comparison of Free Weight Squat to Smith Machine Squat Using Electromyography. J Strength Cond Res. 2009;23(9):2588-2591. doi:10.1519/JSC.0b013e3181b1b181.
Schick EE, Coburn JW, Brown LE, et al. A Comparison of Muscle Activation Between a Smith Machine and Free Weight Bench Press. J Strength Cond Res. 2010;24(3):779-784. doi:10.1519/JSC.0b013e3181cc2237.
Escamilla RF, Fleisig GS, Zheng N, et al. Effects of technique variations on knee biomechanics during the squat and leg press. Med Sci Sports Exerc. 2001;33(9):1552-1566.
Kraemer W, Fry A, Warren B, et al. Acute Hormonal Responses in Elite Junior Weightlifters. Int J Sports Med. 1992;13(02):103-109. doi:10.1055/s-2007-1021240.
Schoenfeld BJ. The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training. J Strength Cond Res. 2010;24(10):2857-2872. doi:10.1519/JSC.0b013e3181e840f3.
Ibid.
Murach KA, Bagley JR. Skeletal Muscle Hypertrophy with Concurrent Exercis
e Training: Contrary Evidence for an Interference Effect. Sport Med. 2016;46(8):1029-1039. doi:10.1007/s40279-016-0496-y.
Jones TW, Howatson G, Russell M, French DN. Performance and Neuromuscular Adaptations Following Differing Ratios of Concurrent Strength and Endurance Training. J Strength Cond Res. 2013;27(12):3342-3351. doi:10.1519/JSC.0b013e3181b2cf39.
9
The 3 Little Big Things about Rapid Fat Loss
For me, life is continuously being hungry. The meaning of life is not simply to exist, to survive, but to move ahead, to go up, to achieve, to conquer.
—ARNOLD SCHWARZENEGGER
Most people view body fat as ugly, greasy flesh that must be ruthlessly exterminated, but it’s actually vital for our survival.
Not only is it an organ that helps in the creation of various important hormones, but many thousands of years ago, it was all that kept our ancient ancestors alive.
They often journeyed for days without food. Starving, they would finally kill an animal and feast, and their bodies prepared for the next bout of starvation by storing excess energy as fat.
This genetic programming is still in us, and it explains in part why so many people are overweight.
For the first time in our history, we have an endless supply of delicious, calorie-dense foods literally at our fingertips—foods that are, in many cases, carefully engineered to be as satisfying and “addictive” as possible.
(Read Michael Moss’s Salt Sugar Fat: How the Food Giants Hooked Us if you want to learn the truth about the “dark side” of food science.)
Fortunately, none of this determines our destinies. Although we can’t “hack” or override this biological hardwiring, we can lose excess and unwanted body fat and maintain aesthetically pleasing (and healthy) body fat levels.
It’s not complicated or difficult, either. As you’ll learn in this chapter, you really only need to understand and abide by three rules to never again struggle to lose fat and keep it off.
Rule #1
Energy Balance Is King
A couple of chapters ago, you learned how energy balance alone dictates your body weight.
Eat more energy than you burn for long enough, and you’ll gain weight. Eat less, and you’ll lose weight. Period.
Although that’s all you really need to know to create a diet plan that gets the types of results that most people are after, it helps to understand how energy balance directly impacts fat storage and burning, so let’s get into that here.
Scientifically speaking, when your body is digesting and absorbing food you’ve eaten, it’s in the postprandial state (post means “after,” and prandial means “having to do with a meal”). This is also called the “fed” state.
When in this state, the body uses a portion of the energy provided by the meal to increase its fat stores. Some people call this the body’s “fat-storing mode.”
Once your body has finished digesting, absorbing, and storing the food eaten, it enters the postabsorptive state (“after absorption”). This is also called the “fasted” state.
When in this state, the body must rely mostly on its fat stores for energy. Some people call this the body’s “fat-burning mode.”
Your body flips between these fed and fasted states every day, storing small amounts of fat after meals, and then burning small amounts after food energy runs out.
Here’s a simple graph that shows this visually:
The lighter portions are the periods where you’ve eaten and provided your body with energy to use and store as fat. The darker portions are the periods where food energy has run out, and your body has to burn fat to stay alive.
You probably also noticed the mention of insulin in the graph, which, as you know, is a hormone that causes muscles, organs, and fat tissue to absorb and use or store nutrients like glucose and amino acids.
Lately, this vital hormone has been under vicious attack by health and diet “gurus,” because it also inhibits the breakdown of fat cells and stimulates fat storage.1
That is, insulin tells the body to stop burning fat for energy, and to start using and storing the energy being provided by food.
This makes sense given what you’ve just learned about fed and fasted states. Insulin tells your body whether it has food to burn or must rely on fat for energy.
This also makes insulin an easy target and scapegoat. Here’s how the story usually goes:
High-carb diet = high insulin levels = burn less fat and store more = get fatter and fatter.
And then, as a corollary:
Low-carb diet = low insulin levels = burn more fat and store less = stay lean.
This is wrong, and the “evidence” used to sell it is pseudoscience. Eating carbs does trigger insulin production, and insulin does trigger fat storage, but none of that makes you fatter. Only overeating does.
This is why a number of overfeeding studies have confirmed that the only way to cause meaningful weight gain is to eat a large surplus of calories, whether from protein, carbohydrate, or dietary fat.2
Without that energy surplus, no amount of insulin or insulin-producing foods can significantly increase body fat levels.
Another gaping hole in the great insulin conspiracy is the fact that high-protein, low-carb meals can result in higher insulin levels than high-carb meals.3
Research shows that whey protein raises insulin levels more than white bread, and that beef stimulates just as much insulin release as brown rice.4
Furthermore, studies show that both protein and carbohydrate generally produce the same type of insulin response—a rapid rise, followed by a rapid decline.5
Carbohydrate and insulin demonizers also often talk about an enzyme in your fat cells called hormone-sensitive lipase (HSL), which helps release fatty acids to be burned.
Insulin suppresses the activity of HSL and thus is believed to promote weight gain, but dietary fat—the current darling of the mainstream health and diet marketing machines—suppresses it as well.6
And thanks to an enzyme called acylation stimulating protein, your body doesn’t need high levels of insulin to store dietary fat as body fat.7
At this point, you may want to believe what I’m telling you about energy balance, but are hung up on claims that it has been refuted by recent scientific research, or on people’s personal stories about their own experiences that seem to defy my explanations.
Let’s review a few of the more common allegations and anecdotes.
Claim #1
“I lost weight on [insert diet here] and never counted calories.”
It’s easy to find people who’ve lost significant amounts of weight without ever paying attention to how many calories they were eating.
Maybe they went low-carb. Maybe they stopped eating meat, sugar, or animal products. Or maybe they just started eating “cleaner.” And they sure lost weight.
What they don’t realize, though, is that the root cause of their weight loss wasn’t their food choices per se, but how those choices impacted their energy balance.
In other words, they lost weight because their diets kept them in a state of negative energy balance long enough for meaningful weight loss to occur, not because they ate the “right” foods and avoided the “wrong” ones.
Most weight loss diets revolve around food restriction. You have to limit or avoid foods or entire food groups, and this inevitably forces you to cut various higher-calorie fare out of your diet. Many of these higher-calorie foods also happen to be delicious and easy to overeat, like refined carbs and sugars.
Thus, when you stop eating these foods, your calorie intake naturally goes down, and the more it dips below your calorie output (expenditure), the more fat you lose.
What’s more, many people who start dieting to lose weight also start exercising or exercising more, which bumps up energy expenditure and makes it easie
r to maintain the calorie deficit needed to get results.
Claim #2
“I starved myself and didn’t lose weight.”
Every week, I hear from people who report no weight loss despite (allegedly) eating a small number of calories every day.
While their frustration is understandable, this doesn’t mean their metabolisms work in fundamentally different ways from everyone else’s.
What’s actually happening is almost always nothing more than a matter of human error, just like we discussed in chapter seven: accidentally eating too much and “cheating” their progress away.
Water retention is another issue that can throw many dieters for a loop.
When you restrict your calories to lose fat, especially when you do it aggressively, your body tends to retain more water. The reason for this is that calorie restriction increases production of the “stress hormone” cortisol, which in turn increases fluid retention.8
Depending on your physiology, this effect can be negligible and unnoticeable, or it can be so strong that it completely obscures several weeks of fat loss. In this way, people can lose fat for several weeks without losing weight and conclude that calorie counting “doesn’t work.”
Later in this book, you’ll learn how to make sure you don’t make the same mistake.
Claim #3
“If you eat clean, calories don’t matter.”
If all we’re talking about is body weight, then a calorie is very much a calorie, and “clean” calories count just as much as “dirty” ones.
That said, it’s accurate to say that “clean” or “healthy” foods are more conducive to weight loss and maintenance than “dirty” or “unhealthy” ones, because they’re generally lower in calories and harder to overeat.
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