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Strength 101: Part I Strength and the Body

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Overview

The Westside Method is perhaps the best example of strength program that requires its user to have someknowledge of physics, biology, anatomy, and specialized sport science. The f ollowing series is intended to givenew lif ters some general inf ormation on major aspects of weightlif t ing 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 body’s ability to generate f orce. It is created through a complexinteraction between the nervous system, skeletal muscles, bones, and energy systems. To understand how tomaximize the neural and muscular components of strength, a litt le background on the body can be usef ulbef ore moving on to methods and arrangement. Our knowledge of these two systems is incomplete, thoughthe 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 otherstructures necessary f or communication, growth, repair, and division. Where neurons dif f er f rom the averagecell is that they possess long, branching tubes that are f illed with cellular f luid; when viewed through amicroscope, it looks like the nucleus has roots. The f luid, cytoplasm, conducts electricity, which is importantsince every movement message in your body is sent via electro-chemical pulse. An inert membrane f orms thestructure of the tube and prevents the current f rom leaking. Because much of the human body is made ofcytoplasm, the coating is essential to make sure that signals traveling back and f orth along the nerves get totheir intended location.[i]

It ’s no surprise that nerves are of ten compared to electrical wiring. Both conduct electrical currents and haveconductive cores surrounded by a sheath; this correlation actually leads neurological science to look like across between biology and engineering. A more specialized def init ion might be to compare a nerve to anunderwater internet cable: much like a nerve, such a cable carries inf ormation through a highly conductiveenvironment 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 theregulated contraction and relaxation of these cells that leads to movement. Muscle cells are unusual, whichmeans a lot of what we know about typical cells gets thrown out the window. One key way they’re odd is thatthey’re multinucleated. This means that unlike our neurons f rom earlier, muscle cells have more than onenucleus, and these multiple nuclei seem to be both connected to sarcoplasm[ii] (a nutrient-rich cousin ofcytoplasm) and essential to hypertrophy, as they divide bef ore a muscle actually grows.[iii] Another keydif f erence is that muscle tissue also has partial cells called satellite cells, which are single-nucleus cells thatrepair muscle damage and seem to be excited by a lot of the same hormonal activity associated with trainingand hypertrophy. These cells f use into complete muscles cells, which is why the f ull cell is multinucleated.

The major structures of the muscle look roughly similar—long and ropey, with all of their elements running inthe same direction—so it ’s a bit like your muscles are Russian nesting dolls of protein threats. Down at themicro- 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. The f ibers are themselves grouped togetherinto fascicles, and these are collected into a f ull muscle like a pec or hamstring.[iv] Sarcoplasm surrounds thef 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 themuscle f ibers it touches is called a motor unit. This is important to know because when a motor neuron sends asignal 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, andare only used when needed; slow-twitch units are smaller, are used f or low-strength movements, don’t f atiguequickly, and are used in all movements. There is actually a continuum between the two types, and the units canchange characteristics depending on the activity they’re exposed to.[v] This means that lif t ing heavy weightswill cause slow-twitch units to behave more like f ast units, while practicing f or a marathon will cause f asterunits to act more like slow units.[vi]

This is just a snapshot of muscle cells—I imagine that bef ore it ’s all said and done, there’ll probably be adozen or more distinct pathways and processes that all work together in a knotted mess to make muscleslarger. If you’re interested in learning more about the micro- level stuf f , look up IGF-1, myosin heavy chainexpression, and the mTOR pathway. You should be busy f or a while.

Neural Strength

When it comes to movement, the brain doesn’t 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 millivoltscauses you to f ling him through the ceiling. Motor units actually respond to the f requency of the nerveimpulses they receive. This means that most of our movements aren’t completely smooth actions, but theresult of millions of microscopic mini-contractions within our muscle f ibers. The less time the f ibers takebetween 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 ofsignals 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 breaksinto running so that af ter a f ew seconds his heart f eels ready to explode, the signal rate increases to the pointthat all the motor units are moving, with the f reshest units using small ATP and creatine phosphate stores f orf uel. If he starts a f ull-on sprint or explosively jumping, there aren’t any additional motor units to recruit; thebrain 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 enlistinga greater number of motor units, and can occur up to about80% of person’s maximum ef f ort at a given activity. Ratecoding is an increase of signal f requency, which can continueincreasing even af ter all of a muscle’s motor units are active.A third method, synchronization, exists beyond these two.Normally, motor units are activated to produce a smoothmovement, though high- level athletes have the ability tosimultaneously contract all their f ibers, causing a suddenburst of power.[vii],[viii] This synchronization appears to havebeen reduced in humans as a course of evolution; comparedto closely-related mammals, humans have superb endurance but poor maximal strength, as well as additionalstructural 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 litt le about movement. The super-simpleexample of strength f rom the beginning could be made more specif ic to athletes by saying that strength is thebody’s ability to produce f orce as part of creating and/or resisting movement. Imagine the squat: while the legmuscles act upon the f emur, t ibia, and pelvis to create movement (raising and lowering the bar), the abdominaland spine muscles are f ighting to resist movement in the spine (unwanted f lexion).

The learned movements are called motor skills. Strength is nothing without the guidance of movement, as thebody can’t apply f orce without f irst being rehearsed in its movement. Lif ters experience this in a very short-term manner when warming up; even though the involved muscles should be f atigued af ter the f irst warm-upreps, perf ormance of a lif t will actually improve as the nervous system re-grooves the pattern. The importanceof motor skills is just as evident when you try a new exercise (or even a new load f or a f amiliar exercise) andf ind that your reps go up with every set despite being f atigued f rom the earlier reps. When applied to movingweights, 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 seriescontinues, 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 isn’t quiteas clear, which goes back to our earlier look at muscle anatomy, as the way other cells work doesn’t carryoveras much. Whatever triggers it, there are two main types of muscle growth: hypertrophy is the process ofenlarging existing muscle f ibers, while hyperplasia is the act of growing new muscle f ibers. Hyperplasia seemsto be the lesser of two f orms.[ix] Several studies indicating statistically signif icant hyperplasia af ter weighttraining were muddled by chemical use.[x] You’ll also hear about old studies ref erencing f iber-numberdif f erences between bodybuilders and powerlif ters, though as above, these are muddled by androgen use orare likely to represent inherent genetic dif f erences between the dif f erent kinds of lif ters. It seems hyperplasiacould happen in an average Joe, but not to a signif icant extent, and its appearance is linked to standalonehormonal processes.

Hypertrophy has also been controversial. An older model of hypertrophy held that there were two methods ofenlarging muscles: myofibrillar hypertrophy, which involved making actual muscle f ibers larger; and sarcoplasmichypertrophy, which involved increasing the volume of sarcoplasm around the muscle f ibers. The theory wentthat lif t ing in the 1-5 RM range triggered usef ul hypertrophy that made the working parts of the muscle—themyof ibrils—larger, 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 litt le ef f ect onincreasing the size of a muscle’s working parts, or of increasing its strength. The takeaway thought was thatworking in the 10 RM range (or with even less weight) had no posit ive ef f ect on athletic perf ormance.

Some older studies did back up the theory, though newer work downplays their conclusions. Of course, lookingat the neural sources of strength, it ’s easy to understand that a bodybuilder using 10-15 RMs (which are about75% or less of a one-rep max) wouldn’t regularly be improving his rate coding or synchronization, or asf orcef ully engaging and converting his motor units towards the f astest end of the spectrum. On the otherhand, 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 t ing rep ranges stimulate myof ibrillar hypertrophyand neural strength gains. In addition to being connected to muscle f iber nuclei, sarcoplasmic hypertrophy maycorrelate to a combination of nutrient depletion, nutrient ingestion, and resistance training.[xi],[xii] It may be thatsarcoplasmic hypertrophy is more connected with the metabolic demands of an activity than anything else, andmay be largely absent in activit ies that don’t have great metabolic demands (such as a one-rep max benchpress). The common f actor of seemingly all ef f ective strength programs is a general increase in the amount oftotal weight lif ted over t ime. We’ll 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 tis rapid enough, the stretched muscle unit can actually store energy like an elastic band.[xiii] This ef f ect—known as the stretch-shortening cycle—is why pausing at the bottom of a lif t is hard. “Bouncing” a squat out ofthe 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 willexamine 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: Third Edition. New York: Cambridge UP.

[ii] Allen, DL et al. (1999). Myonuclear domains in muscle adaptation and disease. Muscle Nerve, 22(10), 1350-60.

[iii] Bruusgaard JC, et al. (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not loston detraining. Proceedings of the National Academy of the Sciences of the United States of America , 107(34),15111-6.

[iv] Ibid

[v] Zatsiorsky, 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 eitherendurance or strength training. Journal of Applied Physiology, November,109(5), 1455-66.

[vii] Zatsiorsky

[viii] Schmied A., and Descarreaux M. (2010). Inf luences of contraction strength on single motor unitsynchronous 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 terresistance training. Journal of Applied Physiology, 81(5), 2004-12.

[x] McDonald, L. (2010). Categories of weight training: part II. Bodyrecomposition. Retrieved f romhttp://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 terdynamic 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 withprotein 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 energystorage occurs in the muscle belly or the tendon.