Introduction
The purpose of this paper was to review Lactate production
and training adaptations involved in surpamaximal exercise stimuli.
Lactate
production
One of the major misconceptions in exercise
science is that there exists both an aerobic and anaerobic form of
glycolysis. When pyruvate is the end product of the energy pathway,
glycolysis is said to be aerobic. Further, when lactic acid is the end
product, the process is said to be anaerobic. The attribution of these two
forms is often credited to the presence or lack of oxygen. In reality
glycolysis is by its very nature an anaerobic process, and a lack of 02 is
seldom the cause of lactate formation. Brooks (2000) summarizes the
process as follows: 1. Performance of high intensity exercise at high
altitude (low 02 concentration) situations results in little lactate
accumulation. 2. Lower blood lactate levels do not indicate that lactic
acid is not being produced, but rather that its production rate is
balanced with its clearance rate. 3. Lactic Acid is always produced even
at rest.
From these points, Brooks (2000) suggests that the scientific community
implement new terminology for glycolysis. The term anaerobic glycolysis
would be changed to fast glycolysis, while aerobic would be changed to
slow glycolysis. The implications are that the faster glycolysis takes
place, the more rapid the accumulation of lactic acid will be. Reasons
are as follows:
1. There is a finite amount of NAD in the muscle cell. NAD serves to
accept electrons (become reduced) along with two hydrogens. These are then
deposited to the electron transport chain, or to pyruvate itself. When NAD
is reduced to NADH + H+, another molecule known as 3 phosphoglyceraldehyde
is subsequently oxidized (loses its electrons). This is known as a coupled
reaction. Glycolysis produces two ATPs from substrate level
phosphorylation when glucose is the substrate, and 3 when glycogen is the
substrate. However, there are a finite number of the NAD+ co enzymes in
the cell. The oxidation of 3 phosphoglyceralehyde must continue if
glycolysis itself is to continue. The ratio of NADH + H+ to NAD+ is known
as Redox Potential, and is maintained by pyruvate and or acceptance of
electrons at the ETC. Consequently, pyruvate is known as a hydrogen sink.
As discussed in the energy continuum, glycolysis is far more powerful than
oxidative energy production, and is stimulated by muscular contraction
itself. The more rapid the contractions, the faster the pathway will run,
outside of fatigue mechanisms.
2. The speed of a reaction is directly correlated to the catalytic rate
of the enzyme controlling the process. Lactate Dehydrogenase is the
rate-limiting enzyme, which transfers two hydrogens to pyruvate to form
Lactic Acid. Its rate of catalytic activity is faster than each of the
glycolytic enzymes. Further it also operates at a higher rate than
Pyruvate Dehydrogenase. The latter enzyme converts pyruvate to Acetyl Co
enzyme A, which enters the aerobic pathways. Therefore any increase in
NADH + H+ and pyruvate will inevitably increase the formation of Lactate.
From this it can be seen why Brooks suggests the terms fast and slow
glycolysis.
3. Glycogen phosphorylase is the enzyme responsible for the catabolism of
glycogen, which is the stored form of glucose. Muscular contraction is
activated by a series of neurological events. First, movement is initiated
in the motor cortex. The efferent motor pathways arise out of the motor
cortex and have connections with every motor unit in the body. Neurons
arising out of this region are meters in length, and are known as upper
motor neurons. These connect with lower motor neurons. A lower motor
neuron and the muscle fibers it innervates are a motor unit. Electrical
pulses travel from upper to lower motor neurons and activate musculature
by transferring pulses to the membrane of the muscle cell, which then
spreads inside of the cell by a series of structures known as t-tubules. A
flow of ions then enters the cell and stimulates an organelle known as the
sarcoplasmic reticulum to release Ca++. This Ca++ acts as a key for
muscular contraction. Consequently, it also activates the enzyme glycogen
phosphorylase. Because the rate of catalytic activity is related to
substrate concentration, the catabolism of glycogen increases the rate at
which glycolysis runs, which inevitably results in greater lactic acid
production.
4. Lactate is cleared by being transformed to pyruvate in the
mitochondria. Slow twitch muscle fibers have a greater supply of
mitochondria, and a greater ability to take up lactic acid into those
mitochondria. The motor program, defined as the spatial and temporal
elements available to the user prior to the initiation of movement,
provides the pulses responsible for that movement and will activate more
fast twitch motor units as force production increases. These have a lesser
ability to clear the lactate produced, which will therefore enhance
lactate build up.
5. The sympathetic nervous system is activated by increased movement, and
in turn releases the fast acting hormones norepinephrine and epinephrine.
Glucagon is also secreted. These stimulate the catabolism of glycogen,
which increases the rate of glycolysis.
Lactic Acid
Clearance
Lactate clearance is important for numerous reasons, which are intimately
related to the dissipation of hydrogen ions. Venom (2003, Active Recovery)
explains the following mechanisms by which pH levels affect performance:
Problems with Lactic acid occur when the amount of free hydrogen ions (H+)
surpasses your bodies buffering systems, effectively decreasing normal pH
levels (acidity levels; the lower the pH is, the more acidic your blood
becomes). When this occurs, the athlete will begin to feel pain, and
suffer a decrease in athletic performance.
This pain is caused by an accumulation of hydrogen ions
that stimulate pain nerves located in the muscle [14]. Performance decline
is induced by both metabolic and muscular fatigue.
Metabolically, a decreased pH causes the inactivation of
several enzymes [15], membrane nutrient transport mechanism inefficiencies
[15], and energy decreased accessibility. To elaborate on energy
deficiencies; glycogen catabolism is slowed by the inactivation of the
enzyme glycogen phosphorylase, and lactic acid inhibits the recruitment of
fatty acids, minimizing there utilization. Due to these effects,
carbohydrates are used at a heightened rate, and PC catabolism is
increased, which inhibits ATP regeneration. All of these factors
ultimately lead to reduction in the production of ATP. Thus, decreased
performance [1, 9,15].
Concerning muscular exhaustion, lactic acid promotes the
restrain of the actomyosin ATPase, which breaks down ATP so it can provide
energy for your body. In addition, H+ interferes with calcium uptake that
is essential for muscular contractions. Increased lactate may also
interfere with cross bridging [16]. These factors lead to a decline in
both the force and velocity of muscular contractions.
Lactic acid is mainly removed by oxidation and gluconeogenesis (Brooks et
al., 2000). One of the critical issues of lactic acid clearance
mechanisms concerns a family of structures known as monocarboxylate
transporters (MCTs). They are also referred to as Lactate shuttles. Lactic
acid travels from producing cells to consuming cells through MCTs (Brooks
et al., 2000; Brooks 2000). Intracellular MCTs are able to transport
lactate produced in the cytosol to the mitochondria for oxidation.
Oxidation occurs by transferring hydrogens to NAD, which then enters the
ETC, while the pyruvate is converted to Acetyl Co-A. Further, extacellular
MCTs are able to transport lactate between tissues. In this way lactate
can move from fast glycolytic fibers to slow oxidative fibers, or reach
the blood stream where the substrate can be oxidized by the heart
(Gladden, 2000).
Slow oxidative fibers as well as the heart have a greater concentration of
mitochondria. Further, the mitochondria contain MCT I proteins. These are
specialized at transporting lactate from the cytosol into the mitochondria
for oxidation or consumption. Fast twitch muscle fibers contain a higher
concentration of MCT 4 proteins, which are concentrated on the sarcolema
of the muscle cell, and are specialized to transport lactate to oxidative
muscle cells, or to the blood stream itself. Once in the blood stream,
lactate can circulate to the liver or the heart. Interestingly enough, the
heart uses lactate as its main fuel sources during exercise. Because fast
twitch fibers do not contain a high density of mitochondria, they
facilitate the storage of glycogen from lactate in a reversible action, in
which the lactate is used to synthesize glucose (called gluconeogenesis).
This occurs with some of the lactate that does not diffuse out of the cell
after exercise has ceased. Lactate that travels to the liver is converted
to glucose, and then can be released by the bloodstream and used by
working musculature. This process is known as the Cori Cycle.
Training
Adaptations
Training adaptations will be viewed as specific to imposed demands placed
on participants. Henry (1950) proposed the specificity hypothesis,
suggesting that the attributes that underlie an activity are specific to
that activity and not transferable (task-specific). Sawyer et al. (2002)
suggests that an attribute is the underlying capacity within an
individual, which allows for the expression of skill (these are presently
viewed as genetically predisposed and typically unaffected by practice).
The statistical evidence highly supports these concepts (Sawyer et al.,
2002).
It
is important to understand that greater transfer, even at the level of
energy systems, will be realized when training is specific to the
criterion task. For example, riding the stationary bike will produce
cardiovascular adaptations, but they will not enhance the extraction of
the extra oxygen delivered when training the upper extremities (known as
arterial venous difference). Maximum oxygen uptake by an organ is
described by Fick’s principle. Fick’s principle states that the amount of
oxygen utilized by a tissue is defined as the product of blood traveling
to that tissue and the extraction of the oxygen delivered. Therefore,
adaptations from a physiological level occur centrally, peripherally, and
at the cellular level itself. These adaptations occur through increased
and specific capillarization, increased mitochondria number, as well as
specific enzymatic activity.
Therefore if a participant seeks to increase mitochondrial density, and
therefore enhance the arterial venous difference, they will need to train
the upper extremities in an aerobic fashion.
Further, it is important to also understand that these adaptations are
also specific to the actual task itself. Riding a bike while standing will
activate the motor neuronal pool, as well as various other musculatures,
in a different manner than riding a bike while seated will. Moreover,
running on a horizontal surface will activate musculature in a different
pattern than running on an incline. It is for this reason that coaches
will benefit by training their athletes for the event that they will have
to face. If a cross-country team is used to running horizontal, and then
are faced with running on an incline type of hilly surface, they will be
seriously under matched. Therefore, the following recommendations and
adaptations will be heightened when done specific to the task. This factor
should be assumed throughout the remainder of the paper.
Energy System
Specificity
The overload principle
will have to be applied in order to achieve adaptations in energy system
pathways. The energy-time-continuum should be used in this case.
A Lactic Anaerobic
Metabolism
The A Lactic or
phosphagen system is best stressed at 10-30 seconds. It clearly dominates
at 10 seconds, however. Further it is important to realize that ATP-PC
stores are fully recovered by 2 minutes, while the half-life is 30
seconds. Therefore, participants can train 10-30 seconds on, with 30
seconds of rest, and still recover half of their CP stores. At 1 minute
these stores will have recovered to a greater extent. The theory is to
continually stress the ATP-PC system, while not allowing full recovery so
as to force a change in its total capacity.
Lactic Anaerobic
Metabolism
This system dominates
from 30 seconds to 2 ˝ to 3 minutes. In order to change its capacity the
athlete will want to train within this range. However, unlike the A Lactic
system, the half-life for the LA system is much longer, ranging from 15-20
minutes in duration. Therefore, a one to three minute rest between sets
would be prudent, as this would allow for full recovery of CP stores to
assist maximizing workload. The system will again be stressed to both
increase its ability to clear lactic acid, and also to increase glycogen
storage capacity. For example, Macdougall et al. (1979) showed that 10
weeks of heavy external resistance training increased concentrations of
muscle creatine by 39%, Creatine Phosphate by 22%, and ATP by 18%.
Adaptations will occur when a specific workload is able to be handled
without as much homeostatic disruption, or an even greater work load is
able to be handled. When this occurs a further overload should be placed
on the body.
Overload can come in the form of a greater intensity, increased volume, or
increased frequency, and each should be utilized. However, intensity
appears to be the factor that causes the greatest regression in the
individual when lowered. That is, both frequency and volume are vital when
overloading the system, but intensity appears to be more important when
maintaining that adaptation (Mujika and Padilla 2000 Part I, Mujika and
Padilla 2000 Part II).
Anaerobic Training
Adaptations in Specific Enzymes and Receptors
It
appears that enzymatic activity is enhanced more than enzymatic
concentration in terms of adaptations involved in anaerobic training.
MacDougall et al. (1999) investigated the effect of intense interval
training on glycolytic enzyme activity. Participants consisted of 12
healthy males, with an average age of 22 + / - 2 years. The apparatus
consisted of a bicycle ergometer. Training consisted of the Wingate
protocol with 2-4 minutes of rest between sets, three days a week, for 7
total weeks. The effect of 7 weeks of intense cycling on glycolytic enzyme
activity resulted in an increase in activity in hexokinase, and in
phosphofructokinase. The effect of training on cycling performance found
significant increases in peak power output, total work over
30 s, and  O2
max. The implications are that high intensity specific training can
increase glycolytic enzymes, and that the enzymatic activity is highly
correlated to peak power output, and total work. Further, these results in
glycolytic enzyme activity do not appear to be prevalent in endurance
training (Holloszy, 1976).
The adaptations seen were in Hexokinase and phosphofructokinase.
Hexokinase is an important rate-limiting enzyme in glycolysis, and serves
to phosphorylate glucose and prepare it for extraction of energy. Further,
Phosphofructokinase is the most important rate-limiting enzyme in
glycolysis. As its activity increases, glycolysis increases.
In
another interesting study, Costill et al. (1979) investigated the effect
of 7 weeks of isokinetic strength training on muscle enzyme activities.
Two experimental conditions were implemented. In the first, one of the
participants’ legs was trained using 10 repeated 6-s maximal work bouts.
The second condition consisted of repeated 30-s maximal knee extension
exercise. The effect of various maximal work bout conditions on
enzymatic activity, found that the 30-second condition produced a
significant increase in glycolytic enzymes, while the 6-second condition
found no significant increase in glycolytic enzymes. The suggestion is
that training the glyolytic pathway is time continuum specific.
Cadefau et al. (1990) investigated the effects of 8 months of a specific
and controlled sprint training program on three groups of young athletes
(two groups of males and one of females). Glycogen content and the
activities of the enzymes of glycogen metabolism (glycogen synthase and
glycogen phosphorylase), glycolysis (phosphofructokinase, pyruvate kinase)
were measured. The effect of 8 months of sprint training resulted
increased glycogen content, and increased activities of glycogen synthase,
glycogen phosphorylase, phosphofructokinase, pyruvate kinase.
Glycogen synthase is the rate-limiting enzyme involved in the storage of
glycogen. As its activity increases, so too does the participant’s ability
to store glycogen. Glycogen is the preferred fuel of glycolysis. Moreover,
an increase in substrate availability would also directly increase
catalytic rate due to concentration and availability of binding.
Glycogen Phosphorylase is the enzyme responsible for introducing glycogen
into the glycolytic process. As the activity of GP increases, so too does
the activity of the pathway itself. It is highly correlated to
bodybuilding type activities.
Pyruvate Kinase is important because it is responsible for substrate level
phosphorylation of ATP. In this step a phosphate is removed from
phosphoenolpyruvate to ADP, in turn producing Pryuvate and ATP.
Adaptations to
Lactate Accumulation
As
with other enzymes, various species of Lactate Dehydrogenase (LDH) exist.
The enzyme is of course responsible for the production of lactate from
pyruvate. Comparison of LDH found in the myocardium (heart musculature)
and skeletal muscle results in the cardiac LDH having a lower affinity for
pyruvate than skeletal musculature. In a review of the effect of endurance
training on enzymatic activity Abernethy et al. (1990) found that skeletal
muscle could acquire the cardiac form of LDH through training. Therefore
pyruvate would be more likely to enter into the Krebs cycle directly. This
would tend to decrease lactate build up during exercise.
Pyruvate dehydrogenase is the rate-limiting enzyme for pyruvate entry into
the Krebs cycle. Its activity therefore affects the oxidation of pyruvate,
as well as lactate accumulation (Heigenhauser and Parolin, 1999). The
catalytic rate of lactate dehydrogenase is much higher than pyruvate
dehydrogenase. It follows that an increase in pyruvate will ultimately
lead to an increase in lactate accumulation. It is for this reason that
higher work loads facilitate the build up of LA. However, endurance
training may enhance the activity of Pyruvate dehydrogenase. It would
therefore accept more pyruvate, which would lower overall lactate levels,
especially at submaximal exercise intensities (Heigenhauser and Parolin,
1999).
Interestingly enough, high intensity and endurance training lowers
epinephrine and nor epinephrine levels at absolute workloads. These
sympathetic messengers speed the rate of glycogenolysis. If lower, then
not as much lactate will build up, and training can last longer. However,
this is for absolute and submaximal relative workloads. When training
maximally, sympathetic hormones will actually increase (Wilson, 2004).
Other avenues for management of lactate occur at the Monocarboxylate level
(MCT). For example, mitochondria increase preferentially to more
endurance than weight training (Brooks, 2000). More mitochondria would
afford a greater supply of MCT proteins, just by sheer concentration of
this organelle itself, leading to increased oxidation of lactate. Such an
adaptation would be beneficial for recovery between high intensity sets,
but may not enhance performance directly during those sets. MCT 1 proteins
may increase in concentration as well overall (Brooks, 2000). This would
facilitate lactate removal. At maximal workloads, lactate levels are
actually higher in the trained individual, for reasons such as increased
sympathetic activity as mentioned, as well as greater glycogen storage and
catalytic activity. Yet, these greater levels of lactate can be tolerated.
Galbo (1983) suggests that this is due to psychological aspects of
training, in that the athlete is more prepared mentally for higher levels
of lactate than the untrained.
That is in completely maximal workloads, however. When submaximal, lactate
levels do significantly drop, which is highly beneficial to the
bodybuilder who trains at submaximal levels during many sets for
hypertrophy reasons. Reynolds et al. (1997) investigated the effect of
resistance training on blood lactate and rate of perceived exertion to a
set of exhaustive squats. Exhaustive squats at 50 and 70 percent of 1
repetition maximum were performed before a 10-week training program. The
effect of 10 weeks of resistance training on blood lactate levels found
that the same workloads performed at pre training had significantly lower
blood lactate levels. Further, when new workloads were performed
(participants had increased their 1-RM) at 50 and 70 percent 1 RM, there
was no significant difference between pre- and post-training lactate
levels. This suggests that lower lactate levels will accumulate at greater
absolute workloads as a result of resistance training. This may reflect
the increase in the cardiac isoform mentioned by Abernathy (1990), as well
as changed mentioned previously.
Implications
Training should be specific to the activity. Specificity includes
task-specific training, especially if in a highly specialized sport, as
well as energy continuum specificity. For the bodybuilder, a number of
skills will need to be increased in capacity if success is to be achieved.
That is, differing tasks will preferentially recruit slow or fast twitch
muscle fibers. The bodybuilder will therefore benefit by training in a
range of repetition ranges. Further areas which need improvement should
be targeted with specific training regimens.
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Parolin ML., Role of pyruvate dehydrogenase in lactate production in
exercising human skeletal muscle. Adv Exp Med Biol. 1999;474:205-18.
J. Duncan
MacDougall, Audrey L. Hicks, Jay R. MacDonald, Robert S. McKelvie, Howard
J. Green, and Kelly M. Smith Muscle performance and enzymatic adaptations
to sprint interval training J Appl Physiol 84: 2138-2142, 1998;
8750-7587/98
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creatine phosphate energy shuttle--the molecular asymmetry of a "pool".
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Mujika I, Padilla
S. Detraining: loss of training-induced physiological and performance
adaptations. Part II: Long term insufficient training stimulus. Sports
Med. 2000 Sep;30(3):145-54.
Mujika I, Padilla
S. Detraining: loss of training-induced physiological and performance
adaptations. Part I: short term insufficient training stimulus. Sports
Med. 2000 Aug;30(2):79-87.
Brooks G. (2000).
Intra and extra cellular lactate shuttle. Medicine and Science in Sports
and Exercise, 32, 790-9.
Brooks G. T.
Fahley, R. White, and K. Baldwin. (2000) Human bioenergetics and its
applications. (3rd ed) California: Mayfield Publishing.
Abernethy P., R.
Thayer, and A. Taylor. (1990) Acute and chronic responses of skeletal
muscle to endurance and sprint exercise: A review. Sports Medicine 10,
365-89.
Gladden L. (2000)
Muscle as a consumer of lactate. Medicine and Science in Sports and
Exercise, 32, 764-71.
Holloszy, J. O.,
and F. W. Booth. Biochemical adaptation to endurance exercise in muscle.
Annu. Rev. Physiol. 38: 273-291, 1976
D. L. Costill, E.
F. Coyle, W. F. Fink, G. R. Lesmes and F. A. Witzmann Adaptations in
skeletal muscle following strength training Journal of Applied Physiology,
Vol 46, Issue 1 96-99, Copyright © 1979 by American Physiological Society
Cadefau J,
Casademont J, Grau JM, Fernandez J, Balaguer A, Vernet M, Cusso R, Urbano-Marquez
A. Biochemical and histochemical adaptation to sprint training in young
athletes. Acta Physiol Scand. 1990 Nov;140(3):341-51. Related Articles,
Links
Heigenhauser GJ,
Parolin ML., Role of pyruvate dehydrogenase in lactate production in
exercising human skeletal muscle. Adv Exp Med Biol. 1999;474:205-18.
J. Duncan
MacDougall, Audrey L. Hicks, Jay R. MacDonald, Robert S. McKelvie, Howard
J. Green, and Kelly M. Smith Muscle performance and enzymatic adaptations
to sprint interval training J Appl Physiol 84: 2138-2142, 1998;
8750-7587/98
Bessman SP. The
creatine phosphate energy shuttle--the molecular asymmetry of a "pool".
Anal Biochem. 1987 Mar;161(2):519-23.
Mujika I, Padilla
S. Detraining: loss of training-induced physiological and performance
adaptations. Part II: Long term insufficient training stimulus. Sports
Med. 2000 Sep;30(3):145-54.
Mujika I, Padilla
S. Detraining: loss of training-induced physiological and performance
adaptations. Part I: short term insufficient training stimulus. Sports
Med. 2000 Aug;30(2):79-87.
Sawyer, D.R., Ostarello, J.Z., Demsey, Suess, Eric A., ( 2002 )
Relationship between football playing ability and Selected performance
measures. The Journal of Strength and
Conditioning 16, 611-616
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