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Strength 101: Part I Strength and the Body

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Overview T he Westside Method is perhaps the best example of strength program that requires its user to have some knowledge of physics, biology, anatomy, and specialized sport science. T he f ollowing series is intended to give new lif ters some general inf ormation on major aspects of weightlif ting science. Part I: Strength and the Body

Part II: Methods of Strength Development Part III: Periodization: History and Early Models Part IV: Advanced Periodization Models

Strength and the Body

From a practical perspective, strength is the bodys ability to generate f orce. It is created through a complex interaction between the nervous system, skeletal muscles, bones, and energy systems. To understand how to maximize the neural and muscular components of strength, a little background on the body can be usef ul bef ore moving on to methods and arrangement. Our knowledge of these two systems is incomplete, though the f ollowing aspects are generally agreed upon. Nerve and Muscle Nerve cells are called neurons. Like most cells, their hub is a round structure that contains a nucleus and other structures necessary f or communication, growth, repair, and division. Where neurons dif f er f rom the average cell is that they possess long, branching tubes that are f illed with cellular f luid; when viewed through a microscope, it looks like the nucleus has roots. T he f luid, cytoplasm , conducts electricity, which is important since every movement message in your body is sent via electro-chemical pulse. An inert membrane f orms the structure of the tube and prevents the current f rom leaking. Because much of the human body is made of cytoplasm, the coating is essential to make sure that signals traveling back and f orth along the nerves get to their intended location.[i] Its no surprise that nerves are of ten compared to electrical wiring. Both conduct electrical currents and have conductive cores surrounded by a sheath; this correlation actually leads neurological science to look like a cross between biology and engineering. A more specialized def inition might be to compare a nerve to an underwater internet cable: much like a nerve, such a cable carries inf ormation through a highly conductive environment to distant end destinations that actively receive and propagate these signals.

Muscle consists of sequential rows of protein-heavy elements that contract when signaled, and it is the regulated contraction and relaxation of these cells that leads to movement. Muscle cells are unusual, which means a lot of what we know about typical cells gets thrown out the window. One key way theyre odd is that theyre multinucleated. T his means that unlike our neurons f rom earlier, muscle cells have more than one nucleus, and these multiple nuclei seem to be both connected to sarcoplasm [ii] (a nutrient-rich cousin of cytoplasm) and essential to hypertrophy, as they divide bef ore a muscle actually grows.[iii] Another key dif f erence is that muscle tissue also has partial cells called satellite cells, which are single-nucleus cells that repair muscle damage and seem to be excited by a lot of the same hormonal activity associated with training and hypertrophy. T hese cells f use into complete muscles cells, which is why the f ull cell is multinucleated. T he major structures of the muscle look roughly similarlong and ropey, with all of their elements running in the same directionso its a bit like your muscles are Russian nesting dolls of protein threats. Down at the micro-level of muscle are contractile elements called sarcomeres, which are stacked into strands myofibrils, which are grouped together into the actual muscle cell or fiber. T he f ibers are themselves grouped together into fascicles, and these are collected into a f ull muscle like a pec or hamstring.[iv] Sarcoplasm surrounds the f ibers and helps provide the muscle with nutrients f or energy and repairs. Neurons that reach out into these muscle f ibers are called motor neurons; a motor neuron and all of the muscle f ibers it touches is called a motor unit. T his is important to know because when a motor neuron sends a signal to its muscle f ibers, it causes each f iber to contract. Very roughly, there are two kinds of motor units: fast-twitch and slow-twitch. Fast-twitch units are large, used f or f orcef ul movements, have low endurance, and are only used when needed; slow-twitch units are smaller, are used f or low-strength movements, dont f atigue quickly, and are used in all movements. T here is actually a continuum between the two types, and the units can change characteristics depending on the activity theyre exposed to.[v] T his means that lif ting heavy weights will cause slow-twitch units to behave more like f ast units, while practicing f or a marathon will cause f aster units to act more like slow units.[vi] T his is just a snapshot of muscle cellsI imagine that bef ore its all said and done, therell probably be a dozen or more distinct pathways and processes that all work together in a knotted mess to make muscles larger. If youre interested in learning more about the micro-level stuf f , look up IGF-1, myosin heavy chain expression, and the mT OR pathway. You should be busy f or a while. Neural Strength When it comes to movement, the brain doesnt have a lif t this slowly signal or a lif t this explosively signal where a brain message of x millivolts lets you gently pick up your child, and a stronger signal of y millivolts causes you to f ling him through the ceiling. Motor units actually respond to the f requency of the nerve impulses they receive. T his means that most of our movements arent completely smooth actions, but the result of millions of microscopic mini-contractions within our muscle f ibers. T he less time the f ibers take between a mini-contraction the stronger the entire muscle contracts. When the muscle is actively shortening, this is called the concentric portion of a movement; when the muscle is static, this is an isometric contraction; and when the muscle is lengthening, the movement is called the eccentric portion.

Motor units are also recruited f rom the smallest available unit to the largest as the f requency increases. Imagine a man taking a leisurely walk. He could keep up the walk f or hours using only slow-twitch motor units, which burn stored body f at f or f uel. If he wants to move to a quick jog, the brain sends a f aster series of signals to the muscle which causes slightly f aster slow-twitch units to be brought in. If he picks up the pace, the signal rate climbs and even f aster units are added; these use glycogen f or f uel. Finally, if the jogger breaks into running so that af ter a f ew seconds his heart f eels ready to explode, the signal rate increases to the point that all the motor units are moving, with the f reshest units using small AT P and creatine phosphate stores f or f uel. If he starts a f ull-on sprint or explosively jumping, there arent any additional motor units to recruit; the brain compensates f or this by increasing the signal f requency even more. Our example above showed two ways the nervous system creates strength. Recruitment is the act of enlisting a greater number of motor units, and can occur up to about 80% of persons maximum ef f ort at a given activity. Rate coding is an increase of signal f requency, which can continue increasing even af ter all of a muscles motor units are active. A third method, synchronization, exists beyond these two. Normally, motor units are activated to produce a smooth movement, though high-level athletes have the ability to simultaneously contract all their f ibers, causing a sudden burst of power.[vii],[viii] T his synchronization appears to have been reduced in humans as a course of evolution; compared to closely-related mammals, humans have superb endurance but poor maximal strength, as well as additional structural def icits and inhibitory mechanisms that hamper our ef f orts at meeting our strength potential. Bef ore moving away f rom the nervous system, I want to talk a little about movement. T he super-simple example of strength f rom the beginning could be made more specif ic to athletes by saying that strength is the bodys ability to produce f orce as part of creating and/or resisting movement. Imagine the squat: while the leg muscles act upon the f emur, tibia, and pelvis to create movement (raising and lowering the bar), the abdominal and spine muscles are f ighting to resist movement in the spine (unwanted f lexion). T he learned movements are called motor skills. Strength is nothing without the guidance of movement, as the body cant apply f orce without f irst being rehearsed in its movement. Lif ters experience this in a very shortterm manner when warming up; even though the involved muscles should be f atigued af ter the f irst warm-up reps, perf ormance of a lif t will actually improve as the nervous system re-grooves the pattern. T he importance of motor skills is just as evident when you try a new exercise (or even a new load f or a f amiliar exercise) and f ind that your reps go up with every set despite being f atigued f rom the earlier reps. When applied to moving weights, lif ters ref er to motor skills broadly as technique. Technique is of ten ref erenced as an individual act, but not so much as a component of strength or strength programming. I hope to address that as this series continues, because the Westside method is very smart in how it grooves technique. Muscle Strength

All other things being equal, a bigger muscle is a stronger muscle. Just how the muscle gets bigger isnt quite as clear, which goes back to our earlier look at muscle anatomy, as the way other cells work doesnt carryover as much. Whatever triggers it, there are two main types of muscle growth: hypertrophy is the process of enlarging existing muscle f ibers, while hyperplasia is the act of growing new muscle f ibers. Hyperplasia seems to be the lesser of two f orms.[ix] Several studies indicating statistically signif icant hyperplasia af ter weight training were muddled by chemical use.[x] Youll also hear about old studies ref erencing f iber-number dif f erences between bodybuilders and powerlif ters, though as above, these are muddled by androgen use or are likely to represent inherent genetic dif f erences between the dif f erent kinds of lif ters. It seems hyperplasia could happen in an average Joe, but not to a signif icant extent, and its appearance is linked to standalone hormonal processes. Hypertrophy has also been controversial. An older model of hypertrophy held that there were two methods of enlarging muscles: myofibrillar hypertrophy, which involved making actual muscle f ibers larger; and sarcoplasmic hypertrophy, which involved increasing the volume of sarcoplasm around the muscle f ibers. T he theory went that lif ting in the 1-5 RM range triggered usef ul hypertrophy that made the working parts of the musclethe myof ibrilslarger, which is why powerlif ters appeared to be stronger than similarly-sized bodybuilders. Meanwhile, reps closer to the 10 RM range just swelled a muscle with cytoplasm, and had little ef f ect on increasing the size of a muscles working parts, or of increasing its strength. T he takeaway thought was that working in the 10 RM range (or with even less weight) had no positive ef f ect on athletic perf ormance. Some older studies did back up the theory, though newer work downplays their conclusions. Of course, looking at the neural sources of strength, its easy to understand that a bodybuilder using 10-15 RMs (which are about 75% or less of a one-rep max) wouldnt regularly be improving his rate coding or synchronization, or as f orcef ully engaging and converting his motor units towards the f astest end of the spectrum. On the other hand, strength athletes and recreational lif ters alike have long used similar reps to get bigger and stronger, with biopsies on both populations showing f iber hypertrophy. What seems more likely is that both bodybuilding and powerlif ting rep ranges stimulate myof ibrillar hypertrophy and neural strength gains. In addition to being connected to muscle f iber nuclei, sarcoplasmic hypertrophy may correlate to a combination of nutrient depletion, nutrient ingestion, and resistance training.[xi],[xii] It may be that sarcoplasmic hypertrophy is more connected with the metabolic demands of an activity than anything else, and may be largely absent in activities that dont have great metabolic demands (such as a one-rep max bench press). T he common f actor of seemingly all ef f ective strength programs is a general increase in the amount of total weight lif ted over time. Well explore this topic better in later parts. Bef ore leaving muscles behind, an interesting physical aspect should be noted. If the eccentric portion of a lif t is rapid enough, the stretched muscle unit can actually store energy like an elastic band.[xiii] T his ef f ect known as the stretch-shortening cycleis why pausing at the bottom of a lif t is hard. Bouncing a squat out of the hole is an example of how to take advantage of the stretch-shortening cycle. Looking Ahead Just as complicated as the components of strength is how it is expressed and built-up. Part II of this series will examine dif f erent kinds of strength and the basic methods f or improving it. [i] Keynes, R.J. and Aidely, D.J. (2001). Nerve and Muscle: T hird Edition. New York: Cambridge UP. [ii] Allen, DL et al. (1999). Myonuclear domains in muscle adaptation and disease. Muscle Nerve, 22(10), 135060.

[iii] Bruusgaard JC, et al. (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proceedings of the National Academy of the Sciences of the United States of America , 107(34), 15111-6. [iv] Ibid [v] Z atsiorsky, Vladimir M. (1995). Science and Practice of Strength Training. Champaign, IL: Human Kinetics. [vi] Vila-Cha, C. et al. (2010). Motor unit behavior during submaximal contractions f ollowing six weeks of either endurance or strength training. Journal of Applied Physiology , November,109(5), 1455-66. [vii] Z atsiorsky [viii] Schmied A., and Descarreaux M. (2010). Inf luences of contraction strength on single motor unit synchronous activity. Clinical Neurophysiology, 121 (10), 1624-32. [ix] McCall, G.E., et al. (1996) Muscle f iber hypertrophy, hyperplasia, and capillary density in college men af ter resistance training. Journal of Applied Physiology , 81(5), 2004-12. [x] McDonald, L. (2010). Categories of weight training: part II. Bodyrecomposition. Retrieved f rom http://www.bodyrecomposition.com/training/categories-of -weight-training-part-2.html. [xi] Cuthbertson, D.J., et al. (2006). Anabolic signaling and protein synthesis in human skeletal muscle af ter dynamic shortening or lengthening exercise. American Journal of Physiology, Endocrinology, and Metabolism , 290(4), E731-8. [xii] Moore, D.R., et al. (2009). Dif f erential stimulation of myof ibrillar and sarcoplasmic protein synthesis with protein ingestion at rest and af ter resistance exercise. Journal of Physiology, 587(pt. 4), 897-904. [xiii] I use muscular unit here as a non-scientif ic acknowledgement that there is debate over whether energy storage occurs in the muscle belly or the tendon.