Download 408 3 Physiology and Anatomy for the Speed and Power

Sports Science for the Speed
and Power Events
Anatomy and Physiology
The Central Nervous System

The Nervous System. The nervous system is a bioelectrical apparatus and one of the body’s
three primary communication systems, along with the endocrine and fascial systems. The
central nervous system (CNS) comprises the brain and spinal cord. All voluntary movement is
controlled by the brain by complex neural processes.

Anatomy of the Brain

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Cerebrum. The cerebrum is also known as the forebrain. It includes the frontal,
temporal, occipital, and parietal lobes as well as the hippocampus and basal ganglia.
This is the part of the brain that directs all conscious, volitional movements and
functions.
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Basal Ganglia. The Basal Ganglia is located deep in the cerebrum. It receives
environmental and sensory information from various areas of the cerebral cortex,
processes that information, and relays it back to the motor cortex via the Thalamus. The
Basal Ganglia are integral to initiating smooth, well-coordinated movements, which is
evidenced when they are damaged in maladies such as Parkinson’s disease.
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The Cerebellum. The cerebellum is also known as the hindbrain. It is a crucial structure,
storing learned movement sequences for quick recall. The cerebellum also works to
synchronize activities originating from other areas of the brain. Patients with a damaged
cerebellum display precision and timing problems exemplified when trying to grasp an
object. Their hand moves jerkily and may stop short of the object, or accelerate through
the object, knocking it over. The clumsiness and lack of balance seen in drunkenness is
due to the depressive effects of the Cerebellum.
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Forebrain vs. Hindbrain. Forebrain activity is a much slower and more complex process,
so our goal as coaches is to help our athletes automate movements in the cerebellum,
or hindbrain, for a much faster, more coordinated and skilled movement.
Energy Fields in Sport Psychology. Mental rehearsal sets up “anticipatory fields” in the motor
cortex. These fields spread throughout the tissues and into the space around the body. This can
lead to a preconditioning of biochemical pathways, energy reserves, and patterns of information
flow.

Motor Routing. The motor, somatosensory, and posterior parietal areas of the cortex project
massive amounts of neurons to the Pons, which sends its axons to the cerebellum for
coordination. The cerebellum then sends its refined information about required direction, force,
and duration of movement through the ventrolateral nucleus of the thalamus to the motor
cortex. Upon receiving all of this information, the Motor Cortex, located at the rear of the
frontal lobe, decides which muscles to contract. The axons from the motor cortex extend to the
spinal cord where they directly interact with motor neurons.

Neural Fatigue. Sports performance concerns involve prevention of fatigue or deterioration of
movement quality. Studies have shown that in prolonged voluntary contractions reduced force
production could not be improved by direct motor nerve stimulation, indicating that failure of
central drive mechanisms are unlikely a contributor to immediate or short term fatigue.
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Central Fatigue. During fatigues states the CNS is almost never maximally activating all
of the motor units, so central fatigue is likely involved at a more global level. Certain
theories center around the presence of an inhibitory response affecting the CNS under
conditions of peripheral fatigue as an injury prevention mechanism.
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Specificity. When individuals train a two-legged task they become less fatigued when
tested on the two legged task, but not when each leg is tested separately. This carries
with it these implications.
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Unilateral and Bilateral Command Differences. Central motor commands for unilateral
vs. bilateral exercises are significantly different, reiterating the importance of the
principle of specificity.
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CNS Adaptations. Training induced decreases in fatigue involve adaptations within the
CNS as well as in the muscle.
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Training Focus. In speed/power events we are primarily concerned with training the
neuromuscular apparatus (as opposed to energy systems), so deep and prolonged CNS
fatigue is something that we must be well aware of and careful to prevent. It can take
10-14 days to recover from severe central fatigue.
The Peripheral Nervous System

Brain to Body Connection. The peripheral nervous system is comprised of nerves and ganglia,
which connect the CNS to all the organs of the body and to the muscles.

Neurotransmitters
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The Role of Neurotransmitters. Neurotransmitters are chemicals produced by the body
that transmit signals across a synapse from one neuron to either another neuron or a
targeted tissue such as a muscle.
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Types of Neurotransmitters. There are over 50 neurotransmitters that have been
identified. We will only look at the roles of 3, specifically acetylcholine (ACH), dopamine,
and serotonin.
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

Acetylcholine.
Acetycholine is a neurotransmitter released the the
neuromuscular junction to begin the sequence of chemical events that results in
muscular contraction.

Dopamine. Dopamine is a neurotransmitter biosynthesized by the
hydroxylation of the amino acid tyrosine to L-Dopa and then by the
decarboxylation of L-Dopa. In some cases dopamine is further processed into
norepinephrine or epinephrine. Among other things, dopamine increases the
actions of the direct pathway within the basal ganglia improving voluntary
movements.

Serotonin. Serotonin is another important neurotransmitter. Biochemically
derived from the amino acid tryptophan, serotonin largely regulates mood,
appetite, and sleep. As serotonin levels increase, fatigue also increases.
Simultaneously, dopamine levels decrease as fatigue progresses.
Effects of Neurotransmitters. Stimulating dopamine or serotonin has demonstrated an
attenuation or amplification of fatigue, respectively. Administering an opioid antagonist,
Naloxone (which essentially decreases dopamine), during exercise resulted in decreased
time of exercise, total work, and peak VO2, and increased perceived exertion.2 The
conclusion was drawn that work capacity was limited by perceived exertion and this
may have more to do with endogenous opioids than physiological limits.
The Role of Nutrition. Serotonin levels are affected by diet. Diets rich in carbohydrate and low
in protein increase serotonin as insulin levels rise. Likewise, high ratios of tryptophan to
phenylalanine and Leucine increase serotonin levels; and the inverse is also true. Because of
these ratios, bananas, dates, and papaya will raise serotonin levels; while whole wheat and rye
breads will lower serotonin levels.
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Chronic Fatigue. One will find depressed dopamine levels and enhanced serotonin levels in
prolonged CNS fatigue or overtraining states, reiterating the role and significance of these
neurohormones.
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Training Adjustments. Throughout training sessions, it’s vital to keep power output levels high.
If power begins to drop, exercises should be simplified or ended. This will help to keep
dopamine levels high, preventing micro or macro overtraining.
Muscle

Muscle Anatomy and Hierarchical Structure. Muscle anatomy, or architecture, refers to the
arrangement of muscle fibers and tendon and their effects on force generation abilities. Muscles
show a tiered or hierarchical structure with the largest unit being the whole muscle and the
smallest contractile unit being the sarcomere. Sarcomeres are arranged end to end along the
length of the muscle, creating an organized banding pattern that can be seen using a light
microscope. This is why skeletal muscle is also referred to as striated muscle. The two main
components of a sarcomere are myosin (the thick filament) and actin (the thin filament). A pair
of Z lines, or Z disks, form the boundary between two, adjacent sarcomeres, and are comprised
of interconnecting proteins to which actin and titin, a protein that holds together the sarcomere
during lengthening, are anchored.

Actin and Myosin. The actin protein is comprised of globular subunits, which combine to form a
helical strand called filamentous actin. Myosin is made up of six subunits: one pair of heavy
chains (MHC) and two pairs of light chains. The light chains contain actin binding sites and
ATPase and are located on the head of the myosin molecule. The binding of myosin and actin is
a major step in muscle contraction and this process is regulated through the nervous system.

Force-Generating Parameters. When many sarcomeres contract at once, the entire muscletendon unit shortens and pulls on the bone, transmitting force and producing movement. The
amount of force the muscle is capable of generating is dependent on these factors.
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Optimal Fiber Length. Optimal fiber length describes the length of a muscle fiber at
which there is an optimal overlap of myosin and actin at the level of the sarcomere
(optimal sarcomere length), allowing maximum force production. In a given posture, not
every muscle or muscle fiber is at optimal length, and thus, cannot produce maximal
force. Each muscle crossing a joint may achieve optimal fiber length in a different
posture, allowing force to be generated across the entire range of motion of a joint.
Optimal fiber length changes with the number of sarcomeres in series. Increasing the
number of sarcomeres in series also increases the potential velocity of the contraction,
while the potential for force generation increases with the number of sarcomeres in
parallel.
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Pennation Angle. The number of sarcomeres per unit of muscle tissue volume can be
influenced by two features of muscle architecture: pennation angle and cross-sectional
area. Placing the sarcomeres at an angle to the length of the muscle results in a trade
off. Although this allows for the addition of more sarcomeres, it also means that the
force production is at angle to the tendon. This means that some of the force produced
by the muscle is lost. An analogy is a very strong athlete who has poor mechanics – they
are still able to apply more force to the ground, but some of the force is lost because it
is not applied in the proper direction.
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Cross Sectional Area. Adding cross-sectional area, also increases the number of
sarcomeres in parallel, and therefore, increases the maximal force production possible.
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Tendon Slack Length. Tendon slack length is the length of the tendon at which it
passively develops force in tension. A long tendon may store a lot of energy, but may be
slower to react as compared to a very quick athlete who may have shorter tendons and
can generate force more quickly.

Strength Improvements. Pennation and tendon attachment provide leverage advantages but
are largely genetically determined with little adaptation to training. Further, studies show that
we do not increase the number of muscle fibers with training (hyperplasia). This is of little
concern though because we do add sarcomeres and myofibrils during muscular hypertrophy,
which is a relatively easy adaptation.

Hypertrophy. This is the increase in the size of muscle fibers. A common misconception is that
all hypertrophy leads to an increase in overall size of the athlete. This is not true – we can have
hypertrophy without unwanted gains in overall size. Eccentric resistance exercises, particularly
through a full range of motion, result in stronger and thicker Z-lines of the sarcomere and more
sarcomeres added in series, as well as in parallel, due to the significant strain placed on the soft
tissues.

Tension
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Time Under Tension. In addition to the magnitude of tension, the volume or time under
tension (TUT) of a particular exercise stimulates hypertrophy.
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Importance of Tension in Tissue Remodeling and Healing. When muscle tissue is torn,
wound repair begins with the formation of a clot containing fibrin filaments. If there is
no ‘prevailing’ tension, the fibers orient in no organized pattern. As the clot dissolves,
fibers that are not under tension are dissolved first, leaving behind a web of oriented
fibrin fibers. Fibroblasts then migrate into this area and deposit collagen along tension
lines. Tensions created through the muscle create piezoelectric charges that the
polarized collagen fibers use to orient themselves along the lines of pull. In immobilized
tissues, randomly oriented fibers persist and disused muscles begin to stick to each
other. This means that one of the worst things you can do following an injury is take
complete rest. Rather, as soon as possible, one should begin using the muscle in a
functional manner.
Connective Tissue

Connective Tissue. Connective tissue is one of the four traditional classes of tissues, in addition
to nervous, muscle, and epithelial tissue. It is found throughout the body; composed of cells,
fibers, and extracellular matrix, making up a variety of structures: most notably fascia, tendons,
ligaments, bone, and blood. Most connective tissue cells are spread through an extracellular
fluid composed of ‘ground substance’, a clear, viscous fluid. There are two main fibers, collagen
and elastin, the former of which makes up about 25% of the protein in the human body.

Tensegrity. Connective tissue makes up a tensegrity (tension-integirity) structure. It refers to
structures that maintain their integrity due primarily to a balance of continuous tensile forces
through the structure, as opposed to leaning on continuous compressive forces. The
compression pushes outward against the tension that pulls inward. As long as the two sets of
forces are balanced, the structure is stable. Load one corner of a tensegrity structure and the
whole structure will give a little to accommodate. Load it too much and it’ll eventually break,
but not necessarily anywhere near where the load was placed.

Roles of Connective Tissue. Best known for its supportive and structural role in the human
body, connective tissues provide the series elastic components through which the stretchshortening cycle operates. Beyond this, it serves another imperative function as a
communication system, faster than the endocrine or nervous systems.

Bone. Our muscles attach via tendons to bone. The quality and structure of our bones plays a
large role in athletics. Athletes without sufficient bone density are at great risk for overuse
injuries such as stress fractures. Lifting and plyometric exercises can help promote bone health
by placing stress on the bones and stimulating bone growth to increase bone density. Bone
length affects an athlete’s ability to generate force and momentum.

Tendon. Tendons connect muscles to bones. As previously discussed, the length of the tendon
affects the ability of a muscle to produce force. Overuse tendon injuries can occur in speed
power athletes. It is important to include exercises in your training plan that address these
tissues. For example, eccentric movements can promote good tendon health. If and when
injuries such as patellar tendonitis do occur, individuals that specialize in modalities such as
Active Release Techniques and Graston can be beneficial in the rehabilitation process.

Ligaments. Ligaments connect bone to bone. They are often injured during a joint injury –
knees, ankles, shoulders, elbows, and wrists all have a lot of ligaments holding them together.
Ligaments take longer to heal than muscles or tendons because they have less blood supply.
When ligaments are damaged proper rehabilitation is needed to make sure the joint is stable
and the athlete’s proprioception for that joint is restored. A common example of where this
goes wrong is when an athlete sprains the same ankle many times in one season or year. Each
time an injury occurs, the athlete loses some of their proprioceptive ability in that joint, making
it more likely they will reinjure it in the future.

Myofascia. Surrounding every component of muscle is connective tissue. Connective tissue is
composed primarily of collagen and secondarily elastin. Muscle fibers are encased in
endomysium and several fibers come together to form a fascicle, which is surrounded by
perimysium. Groups of fascicles constitute a muscle collectively encased in epimysium.

Fascial Meridians. There are superhighways of fascia that run throughout the body and are
congruent with the meridians of energy flow described in acupuncture. Looking at these tissues,
one will see that they are shiny. If you’ve never dissected a cadaver to observe this, you may
have carved a turkey and seen this shiny connective tissue at musculotendinous junctions or in
the myofascia. This shininess or light reflection is due to the atoms having free electrons in their
outermost orbitals (valance electrons). These electrons are responsible for absorbing and
emitting photons (i.e. reflection) and are responsible for the conduction of electricity.

The Importance of Tension (Again). As discussed above, tension is the largest stimulant for
tissue growth. Resistance training stimulates increased bone mineral density due to the added
tension that gravity places on the system. Common lines of pull stimulate tendons, ligaments,
and connective tissue to thicken and strengthen.


Piezoelectric Properties. Connective tissue is piezoelectric (pressure electricity). It generates
electricity when it is compressed. Deformations of bones, tendons, blood vessel walls, muscles,
and skin all create electric fields as a result of the piezoelectric effect. These signals are not
byproducts, but are communications that inform neighboring cells of what’s happening in
different parts of the body. In the same way that proprioception works within the nervous
system, the same communications happen even faster through the connective tissue. It is also
well known that the magnitude and duration of tension (piezoelectricity) on various tissues
directly stimulates them to become stronger.
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Piezoelectric Effect at Work. An application point putting the piezoelectric effect to
work would be to have a jumper do weighted calf stretches for a long period of time (1
minute) to strengthen the Achilles tendon, preventing ruptures.
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Electromagnetic Healing. Pulsing electromagnetic fields (PEMF) can stimulate the
healing process and are frequently used to mend fracture nonunions. Each tissue
responds to a particular frequency, so methods are being developed to repair ligaments,
nerves, and so on. PEMF’s operate by initiating a signaling cascade from the cellular
membrane to the cytoplasm, nucleus, and DNA, activating cellular processes.
Training Modalities That Improve Tissue Quality. Complimentary practitioners and coaches
alike may recognize that tissue that is ‘normal’ from the medical perspective can be
compromised in a variety of ways, lacking a certain quality, tone, or vibrancy; revealed in
patterns of movement, asymmetries, range of motion, texture, or other indicators. Tissue that is
medically acceptable can range from barely alive to fully vibrant and radiant. Medicine ball
training, hurdle mobility, general strength, resistance training, and a variety of other modalities
can bring tissues toward a peak of order and aliveness that is difficult to quantify physiologically,
but necessary in order to achieve the highest pinnacles of performance.
The Neuromuscular System

Motor Neurons. A motor neuron is a nerve cell which innervates skeletal muscle tissue. Motor
neurons are capable of stimulating contraction in the muscle fibers they innervate. The soma, or
body, of the neuron contains the nucleus and various organelles. Dendrites receive signals from
other neurons, and axons transmit signals to their target.

Anatomy of the Motor Unit. Each motor neuron typically innervates several muscle fibers. A
single motor neuron and all of the muscle fibers that it innervates are collectively termed a
motor unit.

The Resistor: The Cell Membrane. Cellular membranes are composed of a dual layer of
phospholipids with hydrophobic heads facing the interior and exterior of the cell and hydrophilic
tails constituting the center of the membrane. This biphospholipid membrane acts as a dielectric
(insulator) between two conducting media, the interstitial fluid and cytosol; which are aqueous
solutions composed mostly of water, similarly to the alkaline solution in a battery. The insulating
effect of the cell membrane would essentially represent Ohms, or resistance, of an electrical
circuit.

Motor Unit Size. Motor units that control gross movements innervate hundreds or thousands of
muscle fibers, such as in the quadriceps. Motor units that control precise coordination, such as
in the eye, may innervate as few as 10 muscle fibers.

Motor Unit Types. α-motor neurons innervate extrafusal (regular) muscle fibers, whereas γmotor neurons innervate the small intrafusal muscle fibers within the muscle spindles.

Nervous System Function. The nervous system acts much like a rechargeable battery. A battery
is constructed of two different chemical mixtures soaked in an alkaline solution. When
connected in a circuit, switching it on, the chemical reactions produces voltage, causing
electrons to flow. The reactions use up the chemicals and produce others that inhibit the
process.

Recharging. Rechargeable batteries are rechargeable because the chemical reaction that leads
to the flow of current is reversible by passing a current through the battery. When the battery is
charged the current can flow through a resistive load. The battery loses power as the chemicals
lose efficiency at making the electrons flow.

Bioelectrics. In neurons (and muscle fibers), there are electrical potentials that exist across the
surface membranes, with potassium (K+) ions being more concentrated inside the cell and
Sodium (Na+) and Chlorine (Cl-) ions having a greater concentration outside the cell. This creates
a resting potential with a sum positive charge outside the cell and a negative charge inside the
cell, similar to the positive and negative polarities of a battery.

Water. Surrounding every molecule in the body is a highly organized film of water and ions
organized by electrical fields surrounding the charged groups on proteins. This order comes
about because water molecules are dipolar: their electrical field is unbalanced (oxygen end
strongly electronegative relative to the hydrogen atoms) causing them to rotate and align with
the lines of force of an electric or magnetic field.

The Importance of Water. We already know that water is essential for life. If you take water
away from proteins, they change from being semiconductors to being insulators. A 10% change
in water content can trigger a million-fold change in charge transport along a protein, reiterating
the importance of hydration.

On/Off Switch. The resting membrane is semipermeable, allowing K+ and Cl- ions to diffuse
through while blocking Na+ ions. This allows Na+ channels to operate as the mechanical switch,
allowing or stopping depolarization, while the Na+/K+ pump is the battery charger.

Peripheral Fatigue. This is a possible cite of fatigue as K+ ions accumulate outside the cell
causing the battery to lose charge. It has been demonstrated that as extracellular K+
accumulates force production is significantly reduced.

Time to Recharge. There is not exact science determining neural recovery times. Time to
recharge will be determined by intensity, density, and volume of neural activities. Anecdotally, it
takes about 30 seconds for 50% recovery, 3 minutes for 90%, 5-7 minutes for 95%, 10-15
minutes for 98%, and could take 10-14 days for a supramaximal effort such as a new world
record.

Holistic Communications. Even within the nervous system there are likely two parallel and
distinct mechanisms for the transmission of sensory and movement information: a fast
mechanism, involving waves of conformational changes in the microtubules, and the slower,
classic mechanism involving ionic currents and action potentials.

Depolarization vs. Sounds Waves. In a large myelinated fiber signals are conducted at up to
120m/sec, slowed by 0.5ms for each synapse. In contrast, sound (phonons) travels at 330m/sec
in tissues.

The Neuromuscular Junction. Motor neurons do not come into direct contact with muscle cells.
The space between the axon terminal and the motor end plate is termed the neuromuscular
junction (NMJ). Upon stimulation of the nerve, acetylcholine (ACh) is released from the axon
terminal, transverses the NMJ, and binds with receptors on the Na+/K+ channel of the motor end
plate to stimulate muscle depolarization. Acetylcholinesterase then hydrolyzes ACh to end
depolarization.

Myelin. Schwann cells lay down a spiral wrapping of membranes on axons which creates myelin
sheaths. Myelin is an insulator around axons, but the Nodes of Ranvier allow action potentials to
jump from one node to the next, making signal transmission exponentially faster. One could
think of myelin as being the insulation around an electrical cord. If you want to send greater
currently, you need a larger gauge of wire with greater insulation around it.
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Myelination. As the nerve is used, Schwann cells are stimulated to myelinate the
neuron. If poor motor patterns are developed these neural networks will become
myelinated, making this the most readily used motor pattern. Consequently, this makes
it that much harder to teach proper technique after bad habits are already formed.
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Proper Rehabilitation. If a nerve is damaged or severed, when it grows back, it does not
have the myelin sheath initially. Accordingly, to rehabilitate an injury, not only do the
soft tissues need to be addressed, but a wealth of proprioceptive and coordination
training to fully restore the injured area to full health.
Neuromuscular Physiology


Muscle Activation. Muscle activation starts with a signal from the nervous system, which is
propagated along the length of a motor neuron and terminates at the motor end plate on a
muscle. If the signal is large enough it triggers the depolarization of the muscle membrane,
which leads to a cascade of events ending in muscle contraction.
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Starling’s Law – All or None. Starling’s Law dictates that either the stimuli to a nerve
achieve a threshold allowing the nerve to fire, or they do not and it remains quite.
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Depolarization. Depolarization of the muscle spreads longitudinally along the cell
membrane, but also travels deep within the cell by the T-tubules so that the sarcomeres
are all working together simultaneously.
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Speed of Depolarization. A small muscle fiber (slow twitch) has a narrower core of the
highly conductive cytosol and hence a higher electrical resistance, causing it to
depolarize more slowly than a large fiber.
Muscle Contraction. There are five steps in this process:
1. Acetylcholine Release. The release of the neurotransmitter acetylcholine at the
neuromuscular junction stimulates (via depolarization) the release of calcium from the
sarcoplasmic reticulum (SR).
2. Calcium Release. Ca2+ is released from the Sarcoplasmic Recticulum and binds with
troponin, resulting in a conformational change, shifting tropomyosin, and exposing the
binding sites for myosin heads to bind with actin and form a cross bridge.
3. ADP and Pi Release. ADP + Pi are released from the cross bridge during the ‘power
stroke’ as the myosin head ratchets itself, pulling actin towards the center of the
sarcomere shortening the muscle.
4. ATP Binding. An ATP molecule binds to the cross bridge allowing it to dissociate from
actin. If ATP is not available, the cross bridge cannot disconnect from actin, hence rigor
mortis.
5. Hydrolyzation. Myosin ATPase, an enzyme located on the myosin head, hydrolyzes ATP
to split to ADP + Pi reenergizing the cross bridge for another cycle by returning to its
starting position. This mechanism of contraction is called the sliding filament
mechanism. While the sliding filament mechanism is the most widely understood and
accepted theory. It is worth noting that there are several other theories of muscle
contraction.

Calcium Pumps. Interestingly, one of the biggest differentiators between the superiority of
speed/power athletes is the quality and number of their Calcium (Ca2+) pumps. Ca2+ pumps
remove calcium from the myoplasm, returning it to the SR, ceasing contraction. All athletes are
able to contract muscle in a similar amount of time. Better athletes are able to relax their
muscles much faster due to enhanced quality and quantity of Ca2+ pumps. This is a trainable
feature through intramuscular coordination, but like all physiology, it’s limited by genetic
expression.

Neural Control of Force Modulation. While the anatomic properties of muscle discussed in
detail earlier determine the maximum force-generating capacity of muscle, the nervous system
regulates how much of this force is generated during a muscle contraction. Force production can
be controlled by the nervous system two ways, frequency modulation and orderly recruitment.
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Rate Coding - Frequency Modulation. Rate Coding involves using the frequency of
action potentials (signals from the nervous system) to control force production. When a
single action potential is sent by the nervous system, the calcium released from the SR is
quickly sequestered and therefore, the muscle does not stay activated. This produces
what is referred to as a muscle twitch. If more than one action potential is sent by the
nervous system, calcium is re-released, and we get a second twitch. As the action
potentials from the nervous system become more closely spaced together in time, the
twitches begin to come together so that when many action potentials are sent in short
succession, the twitches fuse and a state of muscle tetanus is reached. This method of
force regulation is limited because 1) there can only be a 4-fold change in force and 2) if
the muscle is not stimulated to tetanus, a tremor is elicited, which is definitely not ideal
in athletics.
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
Orderly Recruitment. The second way in which the nervous system regulates force is
through is referred to as Henneman’s recruitment principle. This principle states that
motor units are recruited based on size and fatigability. Smaller, less fatigable motor
units are activated first and larger more fatigable motor units are activated last. This
method allows for fine gradations of force and stable force output.
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The Henneman Size Principle. According to the Henneman size principle, slow
twitch motor units with the thinnest neurons are always the first to fire due to
their lower activation threshold. Fast twitch motor units with large motor
neurons will fire faster, but later. The Henneman size principle demonstrates
the need for maximum effort in training sessions of speed/power athletes; if
lackadaisical work is performed, the largest, fastest, most powerful motor units
will not be utilized or trained.
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Possible Exceptions. There is conflicting evidence in the literature as to whether
or not there are exceptions to this rule. Some believe that the order of
recruitment can be reversed in tasks where there is a high demand for power
and therefore, type IIb motor units.11 These researchers hypothesize that order
is actually reversed, activating fast twitch motor units first. However, more
recent findings refute these hypotheses and demonstrate that even in explosive
movements orderly recruitment is maintained46.
Increasing Force Production Through Training
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Intramuscular Coordination. Force production can be increased by training, resulting in
a more efficient pattern of stimulation of the individual motor units that comprise the
muscle. Intramuscular coordination is enhanced.
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Intermuscular Coordination. Force production can be increased by training, resulting in
a more efficient pattern of stimulation of the individual muscles that comprise the
kinetic chain. Intermuscular coordination is enhanced through improved harmony
amongst synergistic muscles and decreased resistance from antagonistic muscle groups.
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Practical Applications. Improvements in intermuscular and intramuscular coordination
can be achieved by performing tasks with higher coordination and power output
demands, respectively. Including a macrocycle in your fall training program that is
focused on power can lead to large improvements in these attributes and may lead to
greater strength gains in the long run. The first 10-12 weeks of adaptation to strength
training is neural adaptation largely due to inter and intra muscular coordination.
Strength gains due to hypertrophy don’t begin until at least 10 weeks into training.3
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Fiber Types. In addition to the architecture of muscle, the type of motor units and muscle fibers
affect contraction. There are two primary ways to classify muscle; one is fiber typing: type I, IIa,
IIb, IIc, and IIx by staining for metabolic enzymes, another is classifying the motor units as fast
twitch or slow twitch based upon the innervation of motor units.
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Muscle Qualities Dictated by Neurons. Like the electrical cord analogy, a large, fast
twitch neuron is required to operate a very large motor unit of say 2000 muscle fibers
that can be found in the gastrocnemius. However in the same muscle, there may be
narrow, unmyelinated neurons conducting the activities of a slow twitch motor unit
possessing as few as 15 muscle fibers. Interestingly enough, if a muscle fiber becomes
deinnervated for whatever reason and is then reinnervated by a neuron of a different
motor unit, the muscle fiber will take on the characteristics of this new motor unit.
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Identification via Metabolic Enzymes. Motor neurons can be repeatedly stimulated
followed by muscle biopsy and staining for glycogen depletion. In the more common
method of determining fiber type, scientists stain muscle fibers to determine the
amount of aerobic (e.g. Malate and succinate dehydrogenase) or anaerobic (e.g.
phosphorylase and myosin ATPase) enzymes they contain.
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IIb Fibers. Type IIb fibers, also called white fibers, are almost exclusively
anaerobic, possessing large amount of glycolytic enzymes, few mitochondria,
and having a low capillarity surrounding them. Consequently, these fibers
produce large amounts of force quickly, but also fatigue quickly.

I Fibers. Type I fibers, also called red fibers because of the large amount of
myoglobin and mitochondria (both are red) found in them, have a great blood
supply and operate primarily aerobically. These fibers take a long time to fatigue
but are unable to produce significant forces extremely fast.

IIa Fibers. Type IIa fibers are an intermediary between type I and IIb, and
respond largely to how one is trained. If a lot of aerobic training is done, IIa
fibers will take on the characteristics of type I fibers; but if training is primarily
strength and power oriented, then IIa fibers will react like IIb fibers. This is
another reason that the principle of specificity in training is so important.

IIc Fibers. Depending on which text or journal you read, some authors also
classify a type IIc fiber which is generally considered a precursor that may
develop into type IIa or IIb, depending on training conditions. However, all fiber
types will adapt to the phenotype of training applied.

IIx Fibers. Other authors classify a type IIx fiber which is supposed to be an
intermediary between IIa and IIb; in reality, there is not an absolute delineation
between fiber types but rather they span the spectrum of possibilities.
o
Myosin Isoforms. In addition to these methods of classification, there are at least five
major heavy chain myosin isoforms and seven light chain forms that have been
identified.10 These isoforms have been used by other authors to classify types I, IIa, IIb,
IIc, and IIx fibers.
o
Myosin ATPase. There are various subcategories of myosin ATPase, and these in part
determine the contraction speed of a fast twitch versus a slow twitch muscle fiber. It is
now known that the myosin ATPase activities of the fibers are related to their rates of
shortening, as measured from force-velocity studies.7
o
Genetic Expression and Myosin Changes. The expression of myosin ATPase can be
modified with specificity of training; which is why it’s necessary to eliminate things like
long, slow running from a speed/power athlete’s training regime.
o
Fiber Type Distribution. These classifications lead to a simplified view of the variations
in fiber type that exist; in reality there is a continuum of fiber types 47. Motor units
typically consist of fibers with identical characteristics; however, mammalian muscles
typically contain a variety of fiber types. Even athletes have a combination of all fiber
types, but certain groups of athletes have higher tendencies in particular areas. These
variances often dictate various training design approaches, especially when certain
lactate markers must be achieved.
Movement Control

Involuntary Movement. Generally when we discuss the neuromuscular system we think about
volitional, voluntary movements. However, there are protocols in place to maintain balance and
prevent injuries that are involuntary. These systems are regulated through proprioception and
reflex pathways and circumvent parts of the Central Nervous System to provide rapid responses
to potentially dangerous situations. These pathways are commonly called reflex arcs.

Proprioception. Proprioception is the process of sensing positions and movements of the body
and its parts. Proprioceptors are muscle receptors that serve to collect and convey this
information. There are four types of muscle receptors that set up peripheral reflexes: muscle
spindles, Golgi tendon organs, Paciniform corpuscles, and free nerve endings.

Types of Proprioceptors
o
Muscle Spindles. Muscle spindles are specialized organs that are sensitive to the rate of
stretch. This helps prevent damage to muscles from overstretching. Muscle spindles are
elegant in that they can sense the rate and magnitude of stretch, but their sensitivity
can also be enhanced by the central nervous system by contraction of the intrafusal
muscle fibers.

Operation. Muscle spindles contain two types of muscle fiber. Nuclear bag
fibers have an extraordinary number of nuclei in the center of the fiber while
nuclear chain fibers have their nuclei spread in series along the length of the
fiber. There are only two bag fibers and as many as 12 chain fibers in a muscle
spindle. Each spindle has one Ia afferent neuron which terminates in
annulospiral endings around each intrafusal muscle fiber; additionally, there is
also a thinner group II afferent sensory fiber that terminates in flower spray
endings on the chain fibers and bag2 fibers.

Ia Axon. When the muscle spindle is stretched, the Ia axon fires a high
frequency burst of impulses, and a steady discharge of impulses when the
muscle spindle is held at its new length.

II Axon. The secondary afferent axon has a much higher firing threshold and
only communicates static length of the spindle as compared to dynamic length
change.

Afferent Neurons. The axons of the afferent neurons reach all the way to the
spinal cord, where they interact with an intermediary nerve that directly
stimulates and extrafusal motor neuron to contract the muscle, preventing it
from being overstretched and damaged.

Gamma Motor Neurons. There are two types of γ-motor neurons that innervate
the muscle spindle.

γ1. The γ1 axon innervates the bag fiber and is stimulated to fire in
response to stretch, as the bag fiber contracts in its distal portions it’s
stretched more proximally increasing the sensitivity of the annulospiral
endings.


o
γ2. The γ2 axon innervates the chain fiber and increases impulse
frequency once the spindle is at its new length, ‘resetting’ the spindle so
new stretches will receive an immediate response.
Application to Sport. Understanding how the muscle spindle works, we can
learn how to properly set up the stretch shortening cycle (SSC). The quality of
the SSC is largely determined by how quickly the eccentric phase can be
converted into concentric activity. The SSC should begin with an isometric
contraction of the involved musculature. This sets the muscle spindle so it will
be highly sensitive to the stretch about to ensue and cause even faster recoil. In
addition to setting the muscle spindle, isometric contraction will allow the
muscles to use series elastic components to aid with amortization creating an
earlier and more powerful rebound.
The Golgi Tendon Organ. The Golgi tendon organ (GTO) is another reflex structure
located at the musculotendinous junction in series with the tendon and five to twenty
five muscle fibers. Contrary to muscle spindles, GTO’s are not very sensitive to passive
stretch, but rather the magnitude of tension created by active contraction. GTO’s are
necessary to prevent the tendon from tearing away from the bone.

Ib Axon. When stimulated, the Ib afferent axon sends a signal to the spinal cord
which inhibits α-motor neurons from continuing to fire.

Training Implications. The GTO can be overly inhibitive. Training with high
forces can help the GTO adapt, raising its threshold so that it does not so readily
inhibit contraction.
o
Free Nerve Endings. Free nerve endings innervate almost all structures within the
muscle belly and are sensitive for mechanical stimuli such as pressure or stretching,
changes in temperature or chemical environment.
o
Paciniform Corpuscles. Paciniform corpuscles are small cylindrical encapsulations that
ensheath the end of a sensory neuron. These are mechanoreceptors, sensitive to
pressure, stretch, change in joint angle, and other mechanical stimuli that provide
proprioceptive feedback to the nervous system.

Corpuscle Diversity. Unlike muscle spindles and GTO’s, always found in the
muscle, Paciniform corpuscles may be found in muscle, joint capsules, between
fascial layers, and near blood vessels.


Sensory Organ Stimuli. Even though sensory receptors are specialized
(mechanoreceptors, chemoreceptors, thermoreceptors, etc), they may be
excited by more than one kind of stimulus. For example, the retina can respond
to both light and magnetic fields. Sensory receptors differ from conventional
neurons in that neurons have an all-or-none response, whereas electrical fields
develop across the membranes of receptor cells in a direct relationship to
stimulus intensity, not propagated along the attached afferent nerves unless the
stimulus reaches a critical intensity.
Reflexes. A reflex is an involuntary and nearly instantaneous movement in response to a
stimulus. There are many types of reflexes. Some are found in the muscle and peripheral
nervous system while others are built in to the brain. The most common is the myostatic or
stretch reflex generated by muscle spindles. There are four important reflexes that occur in the
central nervous system, reciprocal inhibition, the flexion reflex, the crossed extension reflex,
and the stumble reflex.
o
Reciprocal Inhibition. Reciprocal inhibition is when an agonist is contracted the
antagonist is inhibited so the body is not working against itself becoming less efficient
and risking injury.
o
Therapeutic applications. Reciprocal inhibition is imperative in all athletic endeavors,
but is not as well understood or applied in therapeutic situations. For example, if the
iliopsoas muscle is hypertonic, locked short and tight, the ipsilateral gluteal will be
inhibited and not fire properly. Coaches may see that the gluteals are not working as
they should, but they might not understand that the problem is not in the gluteal but
rather in the illiopsoas.
o
Specific Reflexes

The Flexion Reflex. The flexion reflex is well known when someone touches a
hot object and pulls away before even realizing the object was hot. This reflex
also dictates that when a distal joint is flexed, the more proximal joints are also
flexed. For example, if the ankle is dorsiflexed during the recovery phase of a
sprint cycle, the hip will also flex, swinging the thigh forward. However, if the
ankle continues to extend after toe-off, the hip will continue to extend resulting
in back sided running mechanics.

The Crossed Extension Reflex. The crossed extension reflex goes hand-in-hand
with the flexion reflex. If one steps on a sharp object, they quickly lift their foot
(flexion reflex), but simultaneously they extend their opposite leg so that they
don’t fall. For example, in a jump, as the free leg is swung in hip flexion a more
forceful hip extension of the support leg is created for takeoff.

The Stumble Reflex. The stumble reflex is seen when balance is deteriorating,
and results in a reaching for the ground to regain stability. This results in
technical disruptions resulting from hastened grounding, the shifting of body
segments, or stiffening.
o
Reflex Routing. Reflexes travel to the spinal cord, and directly back to the muscle for
quick response. However, the signals also travel to the brain for necessary adaptation of
movement. For example, if the ankle suffers an inversion sprain, the muscle spindles
and Golgi tendon organs of that area are likely damaged, sending mixed signals to the
brain. When these sensors are dysfunctional it’s impossible for reflexes to operate
properly. If the brain starts receiving signals from one area that don’t synchronize, the
brain will modulate the reflex from that joint by inhibiting, or turning it off; causing
deafferentation of the sensory neuron from the joint. As discussed earlier, treatment
must be directed at correcting not only the tissue damage from the injury but also the
dysfunctioning joint receptors of the foot and ankle whether through chiropractic
manipulation, manual muscle therapies, mobilization techniques, or through other
proprioceptive therapies.
o
Application of Knowledge. Understanding the various reflexes allows us to modify our
coaching/teaching to take advantage of the way the human body is wired. No matter
how hard you or the athlete tries, they will not be able to correct the reflex you see as
bad technique without correcting the imbalance that triggered the reflex. Until the
source of the instability is fixed the athlete will be unable to complete a proper second
phase.
o
Rehabilitation Considerations. This also helps us to understand the necessity of various
therapies. Since all reflexes pass through the spinal cord chiropractic becomes
invaluable to correct subluxations whether central or peripheral so that the reflexes
continue to operate properly. I mentioned the example of the iliopsoas earlier, which
may be addressed by any of a host of soft tissue therapies. If you don’t have access to
therapists for whatever reason, you can still address these issues through general
strength circuits, medicine ball routines, weight training, and so on.
Cellular Anatomy

Cellular Anatomy. Cells are the basic building blocks of life. Cells join together to form tissues,
tissues make up organs, organs work together in systems, and systems form the organism. In
this section, we’ll primarily be looking at the energy systems, but we’ll start at the beginning
with the cell, its components, and their functions.

The Cell. Cells come in all shapes and sizes to perform various functions, but most all share the
same basic properties. Outside the cell is water-based interstial fluid, and inside the cell is
cytosol, also a water-based gelatinous fluid. Since the internal and external environments are
water based, the biphospholipid membrane with hydrophilic phosphorous tails making up the
center of the membrane and the hydrophobic lipid heads being the interior and exterior
surfaces of the membrane provides a barrier to control the flow of various substances to and
from the cell.
o
Integrins. Mounted in the membrane are a series of proteins called Integrins that serve
as gates and pumps to channel or push substances to or from the cell.
o
The Cell Membrane. The cell membrane although extremely thin has an enormous
voltage across it, amounting to some millions of volts per meter. The molecules in a
liquid crystal with that voltage across it should vibrate strongly and emit signals.
Molecular systems must produce giant coherent or laser like oscillations that will move
about within the organism and be radiated into the environment

Coherence. Coherence is a connectedness or a consistency in the system. We
refer to people’s speech or thought as coherent if the parts fit together well,
and incoherent if the ideas don’t make sense as a whole.

Coherent Vibrations. It’s predicted that these signals have important roles in
the regulations that lead to unity of function: wholeness in the organism.
Coherent vibrations recognize no boundaries: at the surface of a molecule, cell,
or organism.

Amplification. Cell membranes seem to act as powerful amplifiers, boosting
minute electromagnetic fields as the first step in a series of long-range quantum
processes.
o
The Nucleus. Within the cell are a series of organelles. The nucleus holds our
deoxyribonucleic acid (DNA) and serves as the brain of the cell controlling the cellular
functions through genetic expression by protein transcription.

The Nuclear Envelope. The nucleus has its own double layer membrane called
the nuclear envelope which is impermeable to most molecules so there are
nuclear pores to allow the passage of certain very small molecules and ions.
Larger proteins require active transport by carrier proteins; which serves to
protect the integrity of our DNA.

The Nucleoskeleton. Connected to the interior of the nuclear envelope is the
nuclear lamina which is continuous with the nucleoskeleton, similar to the
cytoskeleton of the cell. Both provide structure and mechanical support to the
nucleus, but also regulate important cellular events such as DNA replication and
cell division.

The Nucleolus. Within the nucleus is the nucleolus, possessing proteins and
nucleic acids for the transcription and assembly of Ribosomal RNA (rRNA).
o
The Mitochondria. In the cytoplasm are mitochondria, the power house of the cell,
generating the majority of ATP for cellular activities. Mitochondria are self-replicating,
possessing their own genome separate from that of the cell.
o
The Endoplasmic Reticulum. The endoplasmic reticulum (ER) directs and transports
certain molecules for modification to their destination.

Rough ER. Rough endoplasmic reticulum has ribosomes on its surface where
mRNA translation occurs to build proteins.

Smooth ER. The smooth endoplasmic reticulum is important for lipid synthesis
and as a calcium reservoir.
o
The Golgi Apparatus. The Golgi apparatus primarily modifies molecules received from
the rough ER, and serves as the central delivery system and a location of protein
processing, packaging, and transport, much like a post-office.
o
Lysosomes & Peroxisomes. Lysosomes and peroxisomes serve as the garbage disposals;
dense with digestive enzymes to break down proteins, nucleic acids, and
polysaccharides; they digest then join membranes with the cell’s exterior to excrete the
molecules.
o
The Centrosome. The centrosome produces microtubules, key components of the
cytoskeleton.
o
The Cytoskeleton. The cytoskeleton is a network of proteins traditionally thought to
provide structure to the cell, but more recent research indicates that the cytoskeleton
likely serves as a vast communication system, and is frequently referred to as the
nervous system of the cell; possessing the ability to process electromechanical,
electrochemical, and electrooptical signals. In fact, cellular architecture regulates
metabolic processes and not the other way around.
o
Continuity of the Living Matrix. Every time a cell moves or changes shape specific
vibrations (phonons) travel throughout the nuclear and cytoplasmic matrix into the
extracellular matrix.15 Muscle contraction also produce sound vibrations throughout the
body. Although some cells secrete molecules that diffuse to other cells and act upon
them, there is a much faster means of communication provided by the continuity and
vibratory character of the living matrix.
Cellular Physiology

Energy Systems. There are different pathways and substrates that can be used to provide
energy to muscles cells for contractions (producing movement). The energy system(s) used for
an athletic endeavor depend on the duration and intensity of the event. The three energy
systems are the ATP-CP (Phospagen) System, the Anaerobic System, and the Aerobic System.
The ATP-CP System provides energy for the shortest most intense activities, such as the field
events. The anaerobic or glycolytic system is the predominate system for activities lasting less
than 2 minutes, such as sprinting events up to the 400m. The aerobic system is the predominate
system used in activities of longer duration and more of a factor in mid distance and distance
running events. For speed power athletes the most important systems are the ATP-CP and
Glycolytic systems. All three energy pathways will be described in more detail below.

Adenosine Triphosphate. ATP is the basic unit of energy on which the body operates. As a
phosphate breaks off of ATP, making it adenosine diphosphate (ADP) and inorganic phosphate
(Pi), energy is released for metabolic reactions to take place. In muscle, there is a very limited
store of ATP; only enough to last for about three seconds of maximal exertion. The benefit of
having low stores of ATP is that the body is keenly sensitive to changes of ATP concentration, as
any small utilization changes the level markedly, stimulating processes that produce ATP.
Interestingly enough, intramuscular ATP levels hardly drop at all during maximal exercise, and
never drop below 50% of resting concentrations. It is hypothesized that an accumulation of Pi is
a major cause of fatigue as a mechanism of protecting the body from depleting ATP and
becoming locked in rigor.

ATP Production. There are three means through which ATP is produced and rejuvenated: the
Phosphagen system, Glycolysis, and Oxidative phosphorylation. What one must realize is that all
three energy systems are active all of the time, but provide different contributions based on the
intensity and duration of effort.

The Alactic Acid System

o
Operation. In addition to the stored ATP being used for immediate muscular
contractions, creatine phosphate (CP), also known as phosphocreatine (PC) gives up its
phosphate releasing enough energy for that phosphate to bond with ADP regenerating
ATP.
o
The Phosphogen System. This system is also commonly referred to as the Phosphogen
system because of the involvement of phosphates in its metabolic pathways.
o
Phosphagen Duration. There are enough stored phophagens to almost exclusively serve
the first 7-8 seconds of intense effort. The ATP-PC system is the primary energy source
for up to 20 seconds of maximal effort, and is a very limited contributor from 30
seconds and beyond.
The Glycolytic (Anaerobic) System. The glycolytic system produces ATP from carbohydrate.
Glycolysis occurs in the cytoplasm and is the splitting of glucose molecules from blood sugar into
lactate or pyruvate, producing multiple ATP in the process. This is the first step in both
anaerobic and aerobic respiration.
o
Glycolysis

Process Steps. There are several enzymatic steps to glycolysis. Two ATP are
burned to fuel the process. Phosphofructokinase (PFK) is the rate limiting step in
glycolysis as many metabolic byproducts come back to inhibit PFK, slowing the
glycolytic process. High levels of Pi and a high ratio of ADP:ATP mobilize PFK to
stimulate glycolysis; and the opposite inhibit glycolysis. The effect of glycolysis is
the production of 4 ATP molecules (minus the 2 to run the process for a net of 2
ATP per glucose molecule) and 2 nicotinamide adenine dinucleotide (NADH)
molecules that move to the mitochondria to produce 4-6 more ATP through the
electron transport system. The end product of glycolysis is either pyruvic acid
that can enter the mitochondria for further processing, or pyruvate is
metabolized in the cytosol down to lactic acid. Whether the end result of
glycolysis is pyruvate or lactic acid is dependent upon relative glycolytic and
mitochondrial activities, which depends on the intensity of exercise, how fast
energy is needed, not the presence or lack of oxygen.

Anaerobic with Oxygen. Consequently, the term ‘anaerobic’ is misleading.
Oxygen is virtually always present, it’s just that ATP can be produced much
faster through glycolysis than by oxidative phosphorylation, so if the intensity
and resultant energy demand is higher than oxidative phosphorylation can
produce ATP, then glycolysis must be called upon. The term anaerobic really
refers to the fact that oxygen molecules do not play a role in the glycolytic or
Phosphagen systems.

Glycolytic Products. In both anaerobic and aerobic respiration, glycolysis results
in the production of two molecules of pyruvic acid, two molecules of ATP, and
two molecules of NADH per glucose molecule.
o
The Glycogenolysis.. Glycogenolysis adds a step to glycolysis by initially breaking down
intramuscular glycogen stores into glucose.
o
Anaerobic Respiration. In anaerobic respiration, NADH is oxidized to NAD during the
conversion of pyruvic acid to lactic acid in the cytoplasm of the cell.
o
Lactate

Lactate as Energy. Lactate is actually a useful energy source. Fast twitch muscle
fibers produce more lactic acid and have fewer mitochondria to oxidize the
lactate, so lactate is shuttled intramuscularly to slow twitch fibers that are
better equipped to oxidize it, or to the brain or heart; all of which will actually
use lactate as the preferred energy source during exercise.

Lactate Clearance. Interpretation of lactate kinetics by way of blood
concentration is then inappropriate because lactate production and disposal are
not equal.

Lactate Processing. Once shuttled to more oxidative cells lactate enters the
mitochondria for further processing through the Krebs cycle to continue
producing ATP.

Gluconeogenesis. If energy needs have reduced, lactate can be shuttled to the
liver where it can undergo gluconeogenesis restoring liver glycogen.

Lactic Acid Myths. Previously the ‘accumulation of lactic acid’ had been
considered the primary cause of peripheral fatigue; this has been found to be
untrue though.

Lactic Acid Disassociation. Almost immediately and completely, lactic acid
dissociates to a Lactate ion (La-) and a hydrogen ion (H+); accordingly, there is
almost no lactic acid in the blood.

Infusion Trials. Lactate infusion trials have reported no adverse effects of
increased La- on perceived effort or pain in the muscles or joints, and conversely
have actually shown increases in force production.

Excitability. Lactate may actually delay the onset of fatigue by maintaining the
excitability of the muscle during intensive exercise.

Anabolic Lactate. Lactate also possesses anabolic properties. Collagen synthesis
nearly doubles in lactate incubated fibroblasts.

Lactate Stimulates mRNA. Lactate also promotes an increase in procollagen
mRNA.22

Lactate Correlates with HGh. More specifically, weight training protocols that
produce high levels of lactate stimulate marked serum Growth Hormone levels.

Necessary for High Level Training. This type of endocrine support is necessary
for high level training. Being sure that recovery training is dialed in to produce
mild amounts of lactate can substantially enhance the prophylactic and
restorative effects as well as stimulating glycogen stores to supercompensate.

Individualization. One thing that is important to note here is that you must
know your athlete. A high caliber DI or post-collegiate speed/power athlete,
loaded with IIb fibers, will produce lactate and accumulate glycolytic byproducts
much more readily than a midlevel or developmental athlete. They may each
require different training constructs to get a similar stimulus.

Updated Research. One would think that even if lactate doesn’t have negative
effects, the hydrogen ions still would. Older research and most texts still
indicate that H+ ions inhibit PFK, slowing glycolysis, interfering with excitationcontraction coupling, and reducing the sensitivity of troponin for Ca2+. These
studies were conducted at temperatures well below physiological limits. These
effects are sensitive to temperature and are almost non-existent at 37o C.


Central Rather than Peripheral. Even if H+ ions don’t contribute to peripheral
fatigue, the body must still preserve homeostasis, so it is likely that as the blood
becomes more acidic, central drive is reduced. This lack of coordination can be
seen and felt at the end of a 400m or hurdle race.
o
Peripheral Causes of Fatigue. It is believed that K+, Ca2+, and Pi are the major causes of
peripheral fatigue. Na+/K+ pumps are sparse in the t-tubules so K+ will accumulate
outside the cell causing it to remain depolarized, significantly reducing force production.
o
Inorganic Phosphate. Pi accumulation from ATP and PC breakdown has also been shown
to depress muscle function by reducing Ca2+ sensitivity of the contractile proteins.
o
The Central Governor Model. The Central Governor model predicts that the brain varies
the work rate and metabolic demand by altering the motor units recruited during
exercise. Peripheral metabolites likely signal the CNS to regulate activity.
Aerobic Metabolism
o
Glycolysis. Glycolysis is also the first step in aerobic respiration. The pyruvic acid
formed by this process leaves the cell cytoplasm and enters the matrix of the
mitochondria via the monocarboxylate transporter (MCT) carrier protein. Once pyruvic
acid is in the mitochondria, the second step of aerobic metabolism begins with the
Krebs cycle.
o
The Krebs Cycle. First, carbon dioxide is enzymatically removed from each three-carbon
pyruvic acid to form the two-carbon acetic acid. It’s in the Krebs cycle that many of our
vitamins are used (e.g. coenzyme A from Pantothenic acid which is vitamin B5). The
Krebs cycle produces two NADH, one FADH, and one Guanosine Triphosphate (ATP’s
energetic equivalent).
o
Oxidative Phosphorylation. The third, and final step, in aerobic respiration is oxidative
phosphorylation. This really two processes that function together. Oxidation is a
spontaneous reaction providing the necessary energy for the endergonic
phosphorylation, the joining of Pi with ADP.
o
Substrate. NADH and FADH travel from the matrix to the cristae membrane of the
mitochondria.
o
The Electron Transport Chain. The electron transport chain (ETC) is the source of
oxidative phosphorylation. Simply described, reducing equivalents NADH and FADH
containing a high energy hydrogen and electron pair travel from the matrix to the
cristae membrane of the mitochondria where the hydrogen and electron move from
areas of electronegativity, NAD, to areas of electropositivity, oxygen. At the start of the
ETC two electrons are transferred from NADH to the NADH dehydrogenase protein that
is imbedded in the cristae membrane. Coupled with this oxidation of NADH to NAD the
H+ is pumped into the intermembrane space. The two electrons are then passed to
ubiquinone which moves the electrons to the cytochrome b-c1 complex. Each electron is
then passed to the cytochrome c protein and one H+ is pumped through the b-c1
complex as each electron is passed. Once cytochrome c passes four electrons to the
cytochrome oxidase complex they interact with eight H+ ions and two oxygen atoms to
form two molecules of water and pump four H+ ions to the intermembrane space. The
accumulation of H+ ions in the intermembrane space creates a concentration gradient
that powers ATP synthase to phosphorylate ADP + Pi into ATP.
o
Phosphorylation Stimulus. Outside the mitochondria a region of decreased pH is
created. This chemical and osmotic potential supplies the energy to phosphorylate ADP.
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
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
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
Cairns, S.P., et al. 1997. Different effects of raised potassium on membrane potential and
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
McCombas, A.J. Skeletal Muscle Form and Function. Champaign, IL: Human Kinetics, 1996.

Davydov, A.S. 1987. ‘Excitons and solitons in molecular systems’, International Review of
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
Myers, T.W. Anatomy Trains: Myofascial Meridians for Manual and Movement Therapists.
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
Staron, R.S. and Pette, D. 1990. The multiplicity of myosin light and heavy chain combinations
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
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
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
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
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
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
Miller B.F., et al. 2002. Lactate and glucose interactions during rest and exercise in men: effect
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
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
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