Recommend reading:
The Anatomy of A Muscle
Take Fat Burning To A Whole New Level!!
The Window of Opportunity
Dextrose, Maltodextrin, and Sodium an In Depth Analysis
Endocrine Insanity Part III
Metabolic Primer Part I
Photo Explanation: Vitamin C
crystals, dark field with homemade patch stop and blue filter, courtesy Ian
Walker, UK.
Introductory Statements
Skeletal muscle is seldom
considered a primary target of oxidative stress. Moreover, these
tissues have proven to be distinctively designed to
withstand stresses of countless sorts. During severe hypertrophy-inducing
exercise, they are exposed to levels of mechanical and metabolic
insult that would fatally injure or kill most other cell varieties.
Oxygen (O2) is
a universal electron acceptor that allows aerobic organisms to use
energy stored in foodstuffs, such as carbohydrates, fats, and protein
(24).
The sweeping incremental
changes in O2 metabolism that occur in the body during intense
exercise are nothing short of mind-boggling.
Like a high-precision
motor, O2 flux through the mitochondria can increase 100
times when going from rest to maximum exercise in highly trained
oxidative muscle fibers (40).
Free Radicals
A Free
Radical is defined as any chemical species that possesses an unpaired
electron or odd number of electrons.
Free
radicals survive in a state of thermodynamic volatility. They are highly
reactive and search to combine with another molecule to pair off its solitary
electron. These radicals can be formed by several mechanisms (8):
-
Electron transfer,
-
Heterolytic fission,
-
and Homolytic fission.
There are 3
important steps in free radical reactions (25).
The initial
step is chain initiation, in which a free radical is formed, usually by
homolytic fission. The second step, chain propagation, occupies a reaction where
a free radical is consumed but a new free radical is produced to continue the
chain. As the reaction proceeds, many radicals are present at once. The final
step is when a chain termination reaction occurs when two free radicals combine,
thus pairing off each other's lone electron.
Mechanisms
for Free Radical Production include (8):
1. Mitochondria: Most free radical
generation within the cell occurs by electron transfer reactions.
2. Inflammation.
Not all free radical formation in biological systems is accidental. Catalysis
caused by some enzymes is the result of their use of a free radical at the
active site in response to inflammation (25).
3.
Ischemia Reperfusion.
All the previously mentioned mechanisms for free radical production can be
related back to ischemia-reperfusion injury. Ischemia, from whatever cause,
results in a decrease in oxygen and substrate availability. The lack of
adenosine triphosphate (ATP), due to the inability of anaerobic means to
maintain pace with energy demands, results in damaging effects (25).
Methods in which Free Radicals
Instigate Tissue Damage
The reaction
of free radicals with cell membranes is one of the actions that lead to tissue
damage.
During
resistance exercise, ischemia reperfusion (the
restoration of blood flow to an organ or tissue that has had its blood supply
cut off) occurs within the active muscles, possibly
even to a higher degree than within other organs. Muscles undertaking strong
concentric and eccentric actions are open to experience brief hypoxic
conditions. Intense muscle actions temporarily decrease blood flow and thus
oxygen availability, whereas with muscle relaxation there is oxygen reperfusion.
Furthermore, membrane disruption has also occurred, identified by a leakage of
intra-muscular enzymes into the blood, such as creatine kinase.
It is also likely that the
trauma to muscle cells during high-intensity exercise results in the activation
of inflammatory intermediaries. These mediators act through phagocytic- and
endothelial-mast cell pathways of free radical creation (48).
These mechanisms indicate that anaerobic
training could result in free radical production beyond what has been measured
with aerobic exercise. From the abovementioned mechanisms, the active muscle
site in hypertrophy training may result in a significant increase in the
production of free radicals either during or after exercise. Consequently, it is
possible that a resistance exercise protocol will result in quantifiable
increases in lipid peroxidation. A previously proposed mechanism of free radical
production during exercise, particularly resistance exercise, is an
ischemia-reperfusion environment at the muscle site (38).
One study looked specifically at this
concept using repetitive static muscle contractions. A knee extension exercise
was used with a 10-second exertion phase and a 10-second resting phase protocol
at 30% of maximal voluntary contraction force (39).
The current scientific
evidence advocates that free radical production within the body depends on
exercise intensity, whether one is referring to aerobic or anaerobic exercise. A
body building protocol must provide a considerable disturbance to the
physiological state of the body. This includes significant ischemia-reperfusion
conditions and muscle damage (38).
Free Radicals and Muscle Injury
It has been
theorized that the membrane disruption that transpires with high-intensity
resistance exercise is largely due to the mechanical loads placed on the muscle.
This would result in disarray in the muscle's structural integrity.
However, a
fascinating study by Kraemer et al. (26) indicated that some mechanism is
continuing to cause damage even after the actual exercise bout is completed.
The study
compared a group performing a resistance training protocol using
5-repetition-maximum sets (5-RM set using resistance in which only 5 repetitions
can be completed) with 1 minute of rest between sets (5/1) and a group
performing the same exercises except with 10-RM sets and a 1-minute rest period
between sets (10/1).
This study
reported that the 10/1 group had a significantly higher creatine kinase
response! This group was subjected to lighter loads but had greater muscle
membrane disruption despite the fact that total work load was equivalent.
Corresponding studies also have shown that creatine kinase responses often peak
between two to four days after eccentric exercise protocols (34, 15, 9).
Mechanisms
outside motorized force may be accountable for muscle membrane disruption after
high-intensity exercise. The number of circulating neutrophils has been shown to
continually increase for several hours after exercise (7).
(“Neutrophils,
which are also known as polymorphonuclear leukocytes (PMN), represent 50 to 60%
of the total circulating leukocytes and constitute the ''first line of defense''
against infectious agents or ''nonself'' substances that penetrate the body's
physical barriers. Once an inflammatory response is initiated, neutrophils are
the first cells to be recruited to sites of infection or injury. Their targets
include bacteria, fungi, protozoa, viruses, virally infected cells and tumor
cells.
Two types of free radicals are produced by neutrophils, macrophages,
endothelial and other cells. The first type is represented by reactive oxygen
intermediates which are formed in neutrophils by the activity of NADPH oxidase,
the enzyme of the respiratory burst. The second type includes reactive nitrogen
intermediates, the first member of them, nitric oxide being produced by nitric
oxide synthase.”
Academic
Electronic Press. 1995.)
The current
research suggests free radical formation, by the above described pathways, plays
a role in continuing the amount of muscle membrane disruption after exercise.
Additionally, malfunctioning mitochondria, due to intra-muscular increases in
calcium, could resume free radical production after exercise ceases (38).
In
Summary:
-
Free radicals are very unstable,
-
React quickly with other compounds, doing cell and body damage,
-
Once produced they multiply unless neutralized by anti-oxidants (or other free
radical scavengers).
Anti-Oxidants
An antioxidant has been
defined as "any substance that, when present at low concentrations compared
to those of an oxidizable substrate (e.g., proteins, lipids, carbohydrates and
nucleic acids), significantly delays or prevents oxidation of that substrate".
(22)
The definition proposed by
the Panel on Dietary Antioxidants and Related Compounds of the Food and
Nutrition Board is that "a dietary antioxidant is a substance in foods that
significantly decreases the adverse effects of reactive oxygen species, reactive
nitrogen species, or both on normal physiological function in humans". (38)
The Core Anti-oxidants
Vitamin E
There are
several non-enzymatic anti-oxidant materials in the body that can be easily
supplemented. The most focused on and significant is vitamin E
(alpha-tocopherol).
It has been shown that this lipid-soluble vitamin is an effective antioxidant
within the cell membrane. (5)
The capacity
of vitamin E to prevent oxidation of unsaturated fatty acids is understood to be
its primary function in the body. The absence of vitamin E results in the
abnormal structure and function of cellular organelles and the cell membrane
itself. (23)
Vitamin E status in rats
has been highly correlated with the susceptibility of that animal to damage from
muscle contractions (27). In addition, studies have shown the protective effect
of oral vitamin E supplementation (47).
Experiments looking at the
effects of vitamin E supplementation on muscle damage have involved muscle
contraction (14). Vitamin E wields its foremost effect by the oxidation of free
radicals. The mechanisms of ischemia-reperfusion injury have been the basis for
which the damaging effects of free radical formation may be seen. Studies have
shown vitamin E supplementation as an efficient means of reducing
exercise-induced muscle damage due to free radical formation (35).
Vitamin A
Often there is confusion over
how to identify vitamin A because of the varying forms that exist in nature.
Vitamin A is a retinol and is
related to but different from retinoids and carotenoids. Beta carotene, which is
commonly mistaken as a vitamin A equivalent, is actually two retinols with the
alcohol groups removed. It is classified as a carotenoid (6). Beta carotene has
been identified as a possible antioxidant because of its ability to scavenge
singlet oxygen. On demand beta carotene can be broken down into two retinol
equivalents (RE) if other sources of vitamin A are not available. This mechanism
is how beta carotene has been identified as a vitamin A precursor (32). Much
less work has been done with vitamin A compared with vitamin E and C as a
protective antioxidant in relation to exercise (38).
Vitamin C
Vitamin C
or L-ascorbic acid has been implicated as an
important water-soluble antioxidant in biological fluids.
The meticulous role of
vitamin C literally reaches to every cell of the body. This vitamin plays many
vital roles including immune system functioning, connective tissue repair, and
is a vital ingredient of
collagen (16).
For the purposes of this journal, focus will be upon its protection from free
radical damage.
Vitamin C readily
scavenges reactive oxygen and nitrogen species, such as superoxide and
hydroperoxyl radicals, aqueous peroxyl radicals, singlet oxygen, ozone,
peroxynitrite, nitrogen dioxide, nitroxide radicals, and hypochlorous acid, thus
effectively protecting other substrates from oxidative damage (19).
Compounding Evidence of Research
Numerous studies have
shown the effectiveness of antioxidant, in particular Vitamin C, supplementation
for the athlete in combating Free Radical Damage, and also enhancing the
hormonal effects of the post-exercise scenario.
Alessio HM, Goldfarb AH,
and Cao G (1) concluded:
“Vitamin C (ascorbic acid) was
supplemented (1 g/day) for 1 day and 2 weeks in the same subjects…It was
concluded that exercise-induced oxidative stress was highest when subjects did
not supplement with vitamin C compared to either 1 day or 2 weeks of vitamin C
supplementation.”
In 2000,
Evans WJ (18) found:
Vitamin C and, especially, vitamin
E are shown to decrease the exercise-induced increase in the rate of lipid
peroxidation. No ergogenic effects of either vitamin C or E have been shown.
Vitamin E was shown to significantly increase circulating neutrophils in older,
but not younger, subjects performing eccentric exercise that causes an increase
in skeletal muscle damage. In addition to its effect in augmenting the
neutrophil response to eccentric exercise, vitamin E causes a greater increase
in circulating creatine kinase activity, perhaps indicating increased skeletal
muscle repair. Increased vitamin E intake has been associated with enhanced
glucose tolerance and insulin action as well as improved lipoprotein status.
Ghosh MK, Chattopadhyay
DJ, and Chatterjee IB (19) have shown
the powerful effect of vitamin C to a healthy diet. This can be directly
correlated to the sport of body building:
The observations substantiate the
previous in vitro findings that ascorbate specifically prevents oxidative
degradation of microsomal membranes. The results indicate that vitamin C may
exert a powerful protection against degenerative diseases associated with
oxidative damage and play a critical role in wellness and health maintenance.
The observations made by
Maxwell SR, Jakeman P, Thomason H, Leguen C , Thorpe GH (37)
have shown the clear benefit of supplementing with anti-oxidants for body
building specific training styles.
It is concluded that plasma
antioxidant capacity rises in response to one hour of eccentric exercise and
that the contribution of individual antioxidants to this change can be
influenced by vitamin supplementation.
In a 2001 study (43)
Peters EM, Anderson R, Nieman DC, Fickl H, and Jogessar V. reveled
the effects Vitamin C can have on stress hormones.
The study demonstrates an
attenuation, albeit transient, of both the adrenal stress hormone and
anti-inflammatory polypeptide response to prolonged exercise in runners who
supplemented with 1500 mg vitamin C per day when compared to < or = 500 mg per
day.
Sastre J, Asensi M, Gasco
E, Pallardo FV, Ferrero JA, Furukawa T, and Vina J
showed the preventive power of antioxidant administration in a 1999 experiment
(49).
Thus, both in rats and humans,
exhaustive physical exercise causes a change in glutathione redox status in
blood. We have also found that antioxidant administration, i.e., oral vitamin C,
N-acetyl-L-cysteine, or glutathione, is effective in preventing oxidation of the
blood glutathione pool after physical exercise in rats.
Tauler P, Aguilo A,
Fuentespina E, Tur JA, and Pons A. demonstrated
that “diet supplementation with vitamin E, vitamin C and beta-carotene cocktail
enhances basal neutrophil antioxidant enzymes in athletes, (51)” and thus
concluded the connotation of antioxidant supplementation:
Exercise increases oxygen
consumption and causes a disturbance of intracellular pro-oxidant-antioxidant
homeostasis… Plasma vitamin E, beta-carotene and vitamin C concentrations in the
antioxidant-supplemented group were approximately 1.6, 10, and 1.2 times higher
respectively than those of the placebo group. The antioxidant-supplemented group
presented a significantly higher glutathione versus glutathione disulfide ratio
in neutrophils (about 20%) than the placebo one. Antioxidant supplementation
enhances the antioxidant enzyme activity of superoxide dismutase and catalase in
neutrophils.
An exciting 2001 analysis
(44) presented by Peters EM, Anderson R, Theron AJ. uncovered:
These observations provide evidence
that supplementation with vitamin C may blunt the adaptive mobilization of this
vitamin from the adrenals during exercise-induced oxidative stress and may be
associated with an enhancement of the acute phase protein response and
attenuation of the exercise-induced increase in serum cortisol.
The above
report reveals that Vitamin C can actually weaken the exercise-induced increase
in cortisol, while increasing the sensitive post-workout protein response!
Course of Exercise Induced
Oxidative Stress (EIOS)
In General, molecules contain pairs of
electrons that orbit their nucleus. Conversely, an electron is occasionally
"lost," which alters the molecule into a free radical (44).
In the standard process of metabolism, this
often happens to oxygen. Most of the oxygen consumed is condensed to water in
the mitochondria. However, a small fraction of oxygen intermediates (i.e., O2•-
and H2O2) are produced and escape the
electron-transport-chain (the electron transport system is a chain of electron
acceptors embedded in the inner membrane of the mitochondrion) (10).
The presence of free radicals is damaging to
the cell, predominantly to cell membranes.
What emerges as an irony is that exercise
increases the production of free radicals by virtue of an increase in oxygen
exploitation. Overall, oxygen radicals and the reactive species that they spawn
harm other species with which they come in contact. For instance,
oxygen-centered radicals have been implicated with cancer as they are believed
to aid in damaging DNA strands. Cell membranes possess polyunsaturated fatty
acids that are highly susceptible to radical assault. This process is known as
lipid peroxidation and increases permeability. As a result (44) this causes an
influx of Ca2+, a deficit of intracellular enzymes, and an advent of
lysosomal (destructive) enzymes. There are numerous antioxidant defenses (44,
38) which comprise enzymes and non-enzymatic antioxidants that restrain or react
with radicals and radical intermediates. Superoxide dismutase is the principal
security in the cell and catalyzes the subsequent reaction:
2O2•- + 2H+ ——> H2O2
+ O2
Although H2O2
itself not a radical, it has been shown to injure nucleic acids. Other
antioxidant enzymes such as catalase and glutathione peroxidase, catalyze the
decrease of H2O2. Glutathione is a foremost non-enzymatic
antioxidant and has several important functions including elimination of H2O2
and recycling of vitamin E (18).
The body has other
antioxidant defense schemes, including antioxidant vitamins. Embedded within the
various membranes (sarcoplasm and inner mitochondrial membrane) is the
lipid-soluble vitamin E (2).
Vitamin E is a
chain-breaking antioxidant which reacts rapidly with fatty acid radicals, but
must be reduced after each reaction by glutathione or vitamin C (ascorbate).
As well, glutathione
catalyzes the renewal of ascorbate. The principal role of ß-carotene (a
precursor to vitamin A) is to quench singled oxygen (O2•-) in
addition to slow down lipid peroxidation (44).
Although an abundance of studies (1, 18, 19, 43, 44, 49, 51) have shown that
antioxidant supplements can be beneficial, there are data that demonstrate no
effect of supplementation. As with all studies, controls can dictate their
relation to the conclusion, particularly with exercise. An element of these
conclusions is that many of these reviews have studied only a single vitamin
when effectiveness of supplementation may depend on the presence of all the
antioxidants.
Post-Workout Inflammation
Muscle contraction and
shortening produces a concentric action; in contrast, when skeletal
muscle lengthens as it produces force, the result is an eccentric
muscle action. For example, lifting a weight is a concentric action,
and lowering the weight is an eccentric action. At the same power
output, the oxygen cost is lower for eccentric than for concentric
exercise, but even so, eccentric exercise is a potent cause of muscle
damage, delayed-onset muscle soreness, and increased circulating
creatine kinase activity (18).
In 1999, Goldfarb (20)
concluded that nutritional antioxidants are therapeutic in exercise-induced
muscle damage.
Several mechanisms have been
forwarded to explain the etiology of exercise-induced muscle damage.
Free-radical mediated processes appear to be an important component of the
inflammatory mediated response.
A growing quantity of
evidence indicates that free radicals play an important role as mediators of
skeletal muscle damage and inflammation after strenuous exercise (38, 44).
The literature suggests
that dietary antioxidants are able to detoxify the peroxides produced during
exercise, which could otherwise result in lipid peroxidation, and that they are
capable of scavenging peroxyl radicals, and therefore may prevent muscle damage
(38).
Endogenous antioxidant
enzymes also play a protective role in the process of lipid peroxidation.
Multiple studies (52, 10)
using both rodent and human subjects have shown significant increases of
malondialdehyde (a product of lipid peroxidation) after exercise to exhaustion,
and also favorable changes in plasma antioxidant levels and in antioxidant
enzyme activity.
In trained individuals and
trained rats, the antioxidant enzyme activity amplifies markedly. In this way,
the increased oxidative stress induced by exercise is compromised by increased
antioxidant activity, preventing lipid peroxidation (22).
Human analyses have shown
that dietary supplementation with antioxidant vitamins has note-worthy effects
on lipid peroxidation post-exercise.
Although several points of
debate still exist, the question whether antioxidant vitamins and antioxidant
enzymes engage a protective role in exercise-induced muscle damage can be
answered affirmatively (3, 6, 38).
The human studies reviewed
by Dekkers JC, van Doornen LJP, and Kemper HCG (13) designate that antioxidant
vitamin supplementation can be recommended to individuals performing recurring
heavy exercise.
Goldfarb AH (21)
studied the role of antioxidant supplementation to prevent exercise-induced
oxidative stress.
Exercise of a sufficient intensity
and duration has been shown to increase indicators of oxidative stress.
Oxidative stress has been indicated in skeletal muscle, liver, blood, and in
expired air samples as indicated by the by-products of lipid peroxidation.
Antioxidants are known to reduce oxidative-radical-induced reactions.
Jakeman P and Maxwell S (28)
studied the “Effect of antioxidant vitamin supplementation on muscle function
after eccentric exercise.”, and found:
This study investigated the effects
of antioxidant vitamin supplementation upon muscle contractile function
following eccentric exercise and was performed double blind…These data suggest
that prior vitamin C supplementation may exert a protective effect against
eccentric exercise-induced muscle damage.
A frequent retort of
performing unacquainted or high-intensity exercise is the main occurrence for
DOMS. Much like muscle damage, DOMS results primarily from eccentric exercise,
however successive eccentric bouts will diminish the DOMS response (44).
However, soreness does not
initially come about from damage to the muscle fiber. Peak soreness occurs
within 24-48 hours post-workout, while peak muscle damage is seen three days
post-training.
Although the eccentric
range of motion is the general factor to both responses, DOMS and muscle damage
are diverse physiological reactions and are caused by separate devices (3, 28).
Aside from the damage to
the actual muscle fiber, eccentric training also upsets the connective tissue
that surrounds the muscle. It is this impairment which is considered to be the
chief source of soreness (34).
As fluid travels into the
fiber the intra-muscular pressure is amplified, which is believed to stimulate
pain sensors positioned in the connective tissue. Without a doubt, increases in
intra-muscular stress correlate exceedingly with the incidence of DOMS.
Moreover, chemicals released from the inflammation development are alleged to
increase the sensitivity of the pain sensors (39, 44).
Hypertrophic/ Hyperplastic Regeneration
Subsequent to the
degeneration process, regeneration commences with the muscle precursor cell, the
myoblasts. In adults, these myoblasts are commonly referred to as satellite
cells and are found between the basement membrane, or basal lamina, and the
sarcolemma (41, 44).
(A satellite cell (blue nucleus)
adherent to a muscle fiber surface by the muscle-specific adhesion molecule, M-cadherin.
Terry Partridge, Muscle Cell Biology)
Typically they are
inactive; however, when an injury transpires, the basal lamina of the damaged
fibers releases a growth factor which kindles satellite cell proliferation
within two days after the injury (32). Within three days post-injury, satellite
cells can be observed to have crossed the sarcolemma and migrated to the site of
damage. Once at the injury site, the cells recognize each other and fuse
together into a myotube, or immature muscle fiber. Total regeneration occurs
within five days to several weeks.
Furthermore, chronic
hypertrophic/hyperplasic precise training results in a release of a growth
factor which stimulates satellite cells proliferation.
Other postulations as to how exercise
generates free radicals include (29, 30, 32, 50):
1.
Additions in epinephrine and other catecholamines that can
create oxygen radicals when they are metabolically inactive.
2.
Manufacture of lactic acid that can translate a weakly
damaging free radical (superoxide) into a powerfully damaging one
(hydroxyl).
3.
Inflammatory feedback to secondary muscle damage incurred with
excess exertion.
The structure of the body (42) encloses a
complex antioxidant defense grid that relies on dietary intake of
antioxidant vitamins and minerals and the endogenous assembly of
antioxidant compounds like glutathione.
Vitamins C, E, and beta-carotene are the
primary vitamin antioxidants (10). Along with glutathione, there are
copious amounts enzymes involved in the quenching or abstraction of free
radicals (50).
Heavy physical exercise
enhances free radical production in skeletal muscle and other tissues
(4).
Chronic exercise also
represents a form of oxidative stress (5) to the organisms and therefore
can alter the balance between pro-oxidants and antioxidants.
Because acute strenuous
exercise and chronic exercise training increase the consumption of various
antioxidants, it is conceivable that dietary supplementation of specific
antioxidants would be beneficial, both in daily supplementation and
post-exercise (38).
Daily Anti-Oxidant
Supplementation in Conjunction with Post-Workout Application
 
Although the
intention of this journal entry is to focus discussion on anti-oxidant
complementation for the anaerobic post-exercise window of opportunity,
supplementation covering the route of an entire day must be planned out to
confer ratios specifically for post-training consumption.
It has been
suggested that doses over 1,000% of the recommended daily allowance (RDA) are
not toxic for all 3 vitamins (31).
Regular
physical activity in association with dietary habits that ensure adequate
supply of a combination of appropriate antioxidants may be expected to
yield desirable results.
The Following are FRDA (Freak
Recommended Daily Allowances) based upon current research. These numbers are
allowances covering an entire day’s span.
JHR recommends these
allowances be divided throughout the day for regular supplementation, aside from
post-workout when increased anti-oxidant intake may be included to combat EIOS.
Vitamin E
Five times
the RDA for vitamin E may be necessary for prevention of free radical damage
(12).
Intense
exercise by athletes (46) may result in free radical production three times that
of sedentary individuals.
Because of
these findings, it has been stated at the Colgan Institute (11, 38) that
1,200–2,000 IU (equivalent to 800–1,350 mg of RRR-D-alpha-tocopherol or
800–1,350 TE) of vitamin E have been taken daily by athletes. This may be a
necessary dosage to counter free radical formation during exercise.
Vitamin C
Always
behind the times for athletes, the RDA for vitamin C is 60 mg. It has been
suggested (11) that this is based on an inaccurate and antiquated method for
calculating vitamin C requirements.
Dosages
given to athletes have been reported to be 2–12 grams daily. A consensus on
reviews has shown complete safety with dosages of vitamin C of 1–5 grams daily
(6, 38).
For
musculoskeletal healing, dosages of 500–1,000 mg, 2 to 4 times daily, have been
taken (6) in the form of ascorbic acid.
Beta Carotene
From current
research, the amount of beta carotene that would be necessary for it to be a
significant contributor to anti-oxidation is unclear at this point. However,
deductions can be made (38).
The RDA for
vitamin A is approximately 800–1,200 R.E. per day.
(Toxicity
has been reported in rare instances (6) at levels of 25,000 I.U., which is
approximately 7,500 RE --7,500  g
of retinol, 9,000 g
of retinyl acetate, and 13,500 g
of retinyl palmitate)
A safe
dosage would fall somewhere between these 2 values (21). However, it is beta
carotene and not vitamin A that acts as an antioxidant, but specific values for
beta carotene are not clear.
Beta
carotene has been shown to be safe at any dose (38). Adverse effects such as
oily diarrhea have been reported, but only at absurdly high levels. The
suggested dosage of vitamin A for effective injury repair assistance is 25,000
I.U.’s or 7,500 R.E.’s, which would be approximately 45 mg per day of beta
carotene (11).
The
following is a sample supplementation outline of a bodybuilder’s regular
anti-oxidant regime:
|
Meal
One |
Multi-Vitamin |
|
Meal
Two |
Anti-Oxidant Supplement
including Vitamin C, E, and A |
|
Meal
Three |
500-1000mg Gram Vitamin C |
|
Meal
Four |
500-1000mg Gram Vitamin C |
|
Meal
Five |
Post Workout, 1-2 grams
Vitamin C, or Anti-Oxidant Supp
*
Recommended to Consume 10-20 minutes into post-workout shake |
|
Meal
Six |
500-1000mg Gram Vitamin C |
Concluding Discussion
Exercise induced oxidative
stress is a corporal reaction that needs to be counterbalanced during the body’s peak time of receptiveness to
nutrition (44).
This phase of the
physiques response to extreme physical stress can best be remedied through
appropriate post-workout supplementation.
A proper post-workout
anabolic cocktail elaborating on the shuttling effects of insulin and rapid
gastric emptying
is the
ideal atmosphere for anti-oxidant consumption in the effort to combat EIOS.
Job 22 states,
22
Accept instruction from his mouth
and lay up his words in your heart.
Psalm 19
14
May the words of my mouth and the meditation of my heart
be pleasing in your sight,
O Lord, my Rock and my Redeemer.
Psalm 119
11
I have hidden your word in my heart
that I might not sin against you.
Ezekiel 3
10
And he said to me, "Son of man, listen carefully and take to heart all the words
I speak to you.
Luke 8
15But
the seed on good soil stands for those with a noble and good heart, who hear the
word, retain it, and by persevering produce a crop.
Revelation 1
3Blessed
is the one who reads the words of this prophecy, and blessed are those who hear
it and take to heart what is written in it, because the time is near.
By constantly
supplementing with God’s Word, we can cast out the vain imaginations and
pollution put into our bodies through our flesh.
In conclusion, the adverse
effects of post-exercise free radical production can be remedied through proper
supplementation of anti-oxidants, Vitamins E, C, and A.
While the adverse effects
of the flesh can be banished through proper supplementation of God’s Word.
Adam “Old School”
Knowlden
Vice-President of Biomechanical Engineering
oldschoolabcbbing@gmail.com
Sources Cited and
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1997 Exercise-induced oxidative stress before and after vitamin C
supplementation. Int J Sport Nutr. 7(1):1-9. 23.
2. Alessio HM. Exercise-induced oxidative stress. Med Sci
Sports Exerc 1993;25:218–24.
3. Aruoma OI. Free radicals and antioxidant strategies in
sport. J Nutr Biochem 1994;5:370–81.
4. Ashton T, Rowlands CC, Jones E, et al. Electron spin
resonance spectroscopic detection of oxygen-centered radicals in human serum
following exhaustive exercise. Eur J Appl Physiol 1998;77:498–502.
5. Bjorneboe, A., B.E.A.
Bjorneboe, and C.A. Drevon. Absorption, transportation, and distribution of
vitamin E. J. Nutr. 120:233–242. 1990.
6. Bucci, L. Nutrition
Applied to Injury Rehabilitation and Sports Medicine. Boca Raton: CRC Press
Inc., 1995.
7. Cannon, J.G., R.A. Fielding,
M.A. Fiatarone, S.F. Orencole, C.A. Dinarello, and W.J. Evans. Increased
interleukin 1
in human skeletal muscle after exercise. Am. J. Physiol. 257: R.
451–R455. 1989.
8. Cheeseman, K.H., and T.F.
Slater. An introduction to free radical biochemistry. Br. Med. Bull.
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