Essay One:
Q: What is
the Histological Background Linking Optimal Post-Workout Research to
Enhanced Recovery?
A: J. W. Conn documented the glycemic
response to isoglucogenic quantities of protein and carbohydrate in 1936.
In the late 1960s, research confirmed that carbohydrate (CHO)
ingestion after intense exercise acts to promote the restoration
of muscle glycogen (1).
Also during this time, research-oriented experiments
for the post-workout “window” were catalogued (21, 22).
Throughout the 1960s and early ‘70s, Floyd began
studying the insulinotropic effect of intravenous amino acid
administration.
Cocktails of several amino acid samples lead to
quantifiable increases in plasma insulin (7-12, 15).
 Additionally,
during these experiments Floyd observed a synergistic effect
when glucose was administered intravenously with these various
amino acid groupings.
In later studies, Floyd investigated the combined
effect of intravenous glucose administrations with the blending
of various amino acids and found that arginine-leucine and
arginine-phenylalanine resulted in the strongest increase in
plasma insulin concentrations (13,14).
More recently, numerous combinations of
amino acids were investigated, and it was shown that, when coupled
together with glucose, the mixtures resulted in large increases
in plasma insulin concentrations.
Several in vitro studies using incubated ß-cells
of the pancreas showed strong insulinotropic effects of arginine,
leucine, phenylalanine, and leucine in combination with glutamine
(2, 3, 16, 17, 18, 23, 24, 25, 26, 28).
Described later by Nuttall in the 1980s, the
synergistic kindling properties of the combined consumption of
carbohydrates and protein on plasma insulin concentrations were
tested (19, 20).
These studies helped confirm that liquid carbohydrate
(CHO) ingestion after intense exercise promotes rapid restoration
of muscle glycogen (1, 4, 5, 6).
Teresa A.
Hillier, David A. Fryburg, Linda A. Jahn, and Eugene J. Barrett (27)
recently
confirmed in vivo that insulin increases protein synthesis.
Moreover, the ideology of carbohydrate consumption in
conjunction with post-training can be traced back to the ancient Greeks
and ancient Hebrews (See:
Acute & Chronic Endocrine Responses to Exercise Induced Disruptions in
Homeostasis Part One - Exercise Endocrinology Principles and
Catecholamines).
Subsequent to these earlier reports, considerable
amounts of research have been built upon these findings and have been
conducted addressing the nutritional concerns of muscle and how
various diets impact muscle metabolism and performance post-exercise.
In rare instances, unscientific and illogical claims
are attributed to liquid and/or high GI carbohydrate utilization
post-workout.
One such dismissal is reduction of this protocol to
nothing more than a tactic of supplement companies in an effort to make
money. This is not only scientifically invalid, but furthermore a faulty
argument.
In logical circles such attacks are called
ad hominems,
and are highly fallacious.
Ad hominems present no real logical argument
whatsoever to the topic at hand, but rather attempts to discredit the
argument by attacking the person or the person’s circumstances, rather
than dealing with the opposing evidence or argument.
In layman’s terms, this is referred to as, “Killing
the Messenger”.
Supplement companies did not invent the usage of high
GI carbohydrates post-workout; they marketed the investigations of
legitimate research.
See:
The Window of Opportunity
References for essay one:
1.Bergstrom, J, and Hultman E. Muscle glycogen
synthesis after exercise: an enhancing factor localized to the muscle
cells in man. Nature 210: 309-310, 1966)
2.Blachier F, Mourtada A, Sener A, Malaisse WJ.
Stimulus-secretion coupling of arginine-induced insulin release. Uptake of
metabolized and nonmetabolized cationic amino acids by pancreatic islets.
Endocrinology 1989;124:134–41.
3.Blachier F, Leclercq Meyer V, Marchand J, et al.
Stimulus-secretion coupling of arginine-induced insulin release.
Functional response of islets to L-arginine and L-ornithine. Biochim
Biophys Acta 1989; 1013:144–51.
4.Costill, DL. CHO for exercise dietary
demands for optimal performance. Int J Sports Med 1: 1-18, 1988.
5.Costill, DL, Craig B, Fink WJ, and Katz A. Muscle and liver glycogen
restoration after oral glucose and fructose feedings in rats. In:
Biochemistry of Exercise, edited by Knuttgen HG, Vogel JA, and
Poortmans J.. Boston, MA: Human Kinetics, 1983, p. 281-285.
6.Costill, DL, Pearson DR, and Fink WJ. Impaired muscle glycogen storage
after muscle biopsy. J Appl Physiol 64: 2245-2248, 1988)
7. Floyd JC Jr, Fajans SS, Conn JW, Knopf RF, Rull J.
Stimulation of insulin secretion by amino acids. J Clin Invest
1966;45:1487–502.
8.Floyd JC Jr, Fajans SS, Knopf RF, Conn JW. Evidence
that insulin release is the mechanism for experimentally induced leucine
hypoglycemia in man. J Clin Invest 1963;42:1714–9.
9. Floyd JC Jr, Fajans SS, Conn JW, Thiffault C,
Knopf RF, Guntsche E. Secretion of insulin induced by amino acids and
glucose in diabetes mellitus. J Clin Endocrinol Metab 1968;28:266–76.
10.Floyd JC Jr, Fajans SS, Pek S, Thiffault CA, Knopf
RF, Conn JW. Synergistic effect of essential amino acids and glucose upon
insulin secretion in man. Diabetes 1970;19:109–15.
11.Floyd JC Jr, Fajans SS, Pek S, Thiffault CA, Knopf
RF, Conn JW. Synergistic effect of certain amino acid pairs upon insulin
secretion in man. Diabetes 1970;19:102–8.
12.Fajans SS, Knopf RF, Floyd JC Jr, Power L, Conn
JW. The experimental induction in man of sensitivity to leucine
hypoglycemia. J Clin Invest 1962;42:216–29.
13.Floyd JC Jr, Fajans SS, Pek S, Thiffault CA, Knopf
RF, Conn JW. Synergistic effect of essential amino acids and glucose upon
insulin secretion in man. Diabetes 1970;19:109–15.
14.Floyd JC Jr, Fajans SS, Pek S, Thiffault CA, Knopf
RF, Conn JW. Synergistic effect of certain amino acid pairs upon insulin
secretion in man. Diabetes 1970;19:102–8.
15.Fajans SS, Knopf RF, Floyd JC Jr, Power L, Conn
JW. The experimental induction in man of sensitivity to leucine
hypoglycemia. J Clin Invest 1962;42:216–29.
16.Hutton JC, Sener A, Malaisse WJ. Interaction of
branched chain amino acids and keto acids upon pancreatic islet metabolism
and insulin secretion. J Biol Chem 1980;255:7340–6.
17.Malaisse WJ, Plasman PO, Blachier F, Herchuelz
A, Sener A. Stimulus-secretion coupling of arginine-induced insulin
release: significance of changes in extracellular and intracellular pH.
Cell Biochem Funct 1991;9:1–7.
18.Malaisse Lagae F, Brisson GR, Malaisse WJ. The
stimulus-secretion coupling of glucose-induced insulin release. VI.
Analogy between the insulinotropic mechanisms of sugars and amino acids.
Horm Metab Res 1971;3:374–8.
19.Nuttall FQ, Gannon MC, Wald JL, Ahmed M: Plasma
glucose and insulin profiles it normal subjects ingesting diets of varying
carbohydrate, fat, and protein content J Am Coll Nutr 4:437-450, 1985
20.Nuttall FQ, Mooradian AD, Gannon MC
Billington C, Krezowski P: Effect of protein ingestion on the glucose and
insulin response to a standardized oraglucose load. Diabetes Care
7:465-470, 1984
21.Pallotta JA, Kennedy PJ: Response of plasma
insulin and growth hormone to carbohydrate and protein feeding. Metabolism
17:901-908, 1968
22.Rabinowitz D, Merimee TJ, Maffezzoli R, Burgess
JA: Patterns of hormonal release after glucose, protein, and glucose plus
protein. Lancet 2:454-456, 1966
23.Sener A, Malaisse WJ. L-Leucine and a
nonmetabolized analogue activate pancreatic islet glutamate dehydrogenase.
Nature 1980; 288:187–9.
24.Sener A, Hutton JC, Malaisse WJ. The
stimulus-secretion coupling of amino acid-induced insulin release.
Synergistic effects of L-glutamine and 2-keto acids upon insulin
secretion. Biochim Biophys Acta 1981;677:32–8.
25.Sener A, Malaisse WJ. The stimulus-secretion
coupling of amino acid-induced insulin release: insulinotropic action of
branched-chain amino acids at physiological concentrations of glucose and
glutamine. Eur J Clin Invest 1981;11:455–60.
26.Sener A, Blachier F, Rasschaert J,
Mourtada A, Malaisse Lagae F, Malaisse WJ. Stimulus-secretion coupling of
arginine-induced insulin release: comparison with lysine-induced insulin
secretion. Endocrinology 1989;124:2558–67.
27. Teresa A. Hillier,
David A. Fryburg, Linda A. Jahn, and Eugene J. Barrett. Extreme
hyperinsulinemia unmasks insulin's effect to stimulate protein synthesis
in human forearm. Am. J. Physiol. 274 (Endocrinol. Metab. 37):
E1067-E1074, 1998
28.Varnier M, Leese GP, Thompson J, Rennie
MJ. Stimulatory effect of glutamine on glycogen accumulation in human
skeletal muscle. Am J Physiol 1995;269:E309–15
Essay Two:
Q: What are
the properties of glycogen? And why are these properties so vital post
workout?
A:
 Glycogen
is a polysaccharide, (C6H10O5)n
that is the main form of carbohydrate storage in animals and humans and
occurs primarily in the liver and muscle tissue. It is readily converted
to glucose as needed by the body to satisfy its energy needs (21), such as
during intense training.
To enhance the progress of muscular strength and size with
heavy-resistance body building programs, optimal conditions for recovery
from training sessions are imperative, primarily glycogen
re-synthesis (22).
Recovery occupies the coordinated operation of multiple
physiological processes that are heavily influenced by the
accessibility and actions of exclusive hormones and nutrients
(16, 17).
Both qualitative and quantitative modifications in skeletal
muscle contractile proteins are all supported and signaled by a
horde of systematic -trophic influences from hormones to
nutrient availability (18, 19).
Markedly, concentric and eccentric contractions disrupt or damage
certain muscle fibers that must undertake a remodeling restoration
process. Dietary nutrients, hormones, and growth factors
interact to regulate this remodeling of skeletal muscle
proteins (5).
One primal factor associated with muscular fatigue
is depletion of muscle glycogen (1).
These stores must be replaced rapidly during the
post-workout initial recovery phase in order for performance to be
reproducible in a subsequent exercise bout(s).
Glycogen synthesis may be restricted by blood glucose
concentration, glucose transport, and the activity of the
enzymes involved in the pathway, particularly glycogen synthase (10).
Body building training programs provide conditions within skeletal
muscle to support the rapid synthesis of glycogen.
Glycogen synthase action is inversely relative to glycogen
intensity (23); as a result of the glycogen-depleted state post-training,
skeletal muscle (24) and hepatic glycogen synthase activity are
raised (13).
Basal glucose transport within skeletal muscle occurs via
GLUT-4 (A powerhouse effect of insulin is the stimulation of glucose
transport via the translocation of the insulin responsive glucose
transporter, GLUT4, to the plasma membrane) (14).
Nevertheless, the ability of skeletal muscle to
take up glucose is relative, due to adjustments in the GLUT-4
content of the sarcolemal membrane.
 Image
1. Atrophic muscle fibers.
The sarcolemal membranes of these two
atrophic fibers have a wavy appearance. Courtesy: Department of Pathology;
Virginia Commonwealth University;
There are hypothesized to be one or more intracellular pools
of GLUT-4 proteins, which are translocated to the sarcolema in
response to both increased insulin concentration (20) and prior
exercise (9); these effects are additive (6).
 In the
post-workout period, therefore, muscle membrane permeability to
glucose is high, thus favoring the accretion of glycogen
replacement. However, if rapid carbohydrate distribution is not provided
during recovery, glycogen synthesis will be limited
because the rate of endogenous glucose production from gluconeogenic
precursors such as alanine and glycerol is inadequate to support
maximal rates of glycogen synthesis (15).
The ingestion of high GI carbohydrates increases glycogen synthesis in
two ways.
The first (12) is increased substrate availability through
the increased blood glucose concentration, which results in an
increased glucose uptake due to mass action.
Moreover, the resultant increase in systemic insulin
concentration stimulates the translocation of GLUT-4
transporters from an intracellular pool to the sarcolemal
membrane (7).
The hormone insulin is also a powerful activator of glycogen
synthase and inhibitor of glycogen phosphorylase (2).
The effectiveness of a specific carbohydrate in encouraging
resynthesis of the carbohydrate stores is reliant on the
insulin and glucose response to the carbohydrate load (4).
This is directly linked to gastric emptying and intestinal
absorption rates. It is also associated with the insulinogenic potential
of the carbohydrate, as indicated by the glycemic index (GI) of
a carbohydrate.
The development of glycogen synthesis relies upon the
accessibility of glycogenic substrate (8) and the activity of
the enzymes implicated in glycogen synthesis. These include
hexokinase and glycogen synthase.
Prior exercise
enhances skeletal muscle glucose transport (3) because of the
translocation of GLUT-4 transporters from an intracellular pool
to the sarcolemal membrane.
The inclination
for skeletal muscle to extort blood glucose will thus be
increased, and the glucose will tend to be directed toward
glycogen synthesis because glycogen synthase is activated
during recovery due to the low intramuscular glycogen
concentration (23).
These conditions
favoring the resynthesis of
glycogen can be exploited (8) by the provision of a quality
carbohydrate source.
The consequential
amplification in glucose availability and the insulin response
to the glucose load would tend to stimulate (7) a further
increase in the GLUT-4 content of the sarcolemal membrane.
Research has
demonstrated (11) that there is a direct correlation between
the rate of glycogen storage during recovery and total muscle
GLUT-4 protein content.
On a side note,
observational and empirical evidence makes it plainly obvious that the
endocrinal state of the body builder post-workout is nothing like that of
a sedentary individual.
 A
red herring argument is an attempt to offer evidence to support one
proposition by arguing for a different one entirely, or dodging the main
argument by going off on a tangent.
Oftentimes
opponents of high GI carbohydrate supplementation post-workout will point
to the dangers of excess insulin-spiking and glucose intake; however, this
is a red herring argument. This claim is like comparing apples to
oranges.
The physiological
state of that of a sedentary individual and that of a body builder during
the post-workout scenario are polar opposites. Comparing the two states in
such a manner is faulty logic.
For superior glycogen synthesis post-workout,
JHR recommends a mixed solution of
Dextrose and Maltodextrin carbohydrate sources. See:
Dextrose, Maltodextrin, and Sodium an In Depth Analysis
References for essay two:
1.Bergstrom, J, and Hultman E. A study of
glycogen metabolism during exercise in man. Scand J Clin Lab Invest 19:
218-228, 1967
2.Cohen, P. Muscle glycogen synthase.
Enzymes 17: 461-497, 1986.
3.Douen, AG, Ramlal T, Rastogi S, Bilan PJ,
Cartee GD, Vranic M, Holloszy JO, and Klip A. Exercise induces recruitment
of the "insulin-responsive" glucose transporter. J Biol Chem 124:
13427-13430, 1990.
4.Doyle, JA, Sherman WM, and Strauss RL.
Effects of eccentric and concentric exercise on muscle glycogen
replenishment. J Appl Physiol 74: 1848-1855, 1993
5.Florini, J. R. Hormonal control of muscle
cell growth. J. Anim. Sci. 61: 21-37, 1985
6.Gao, J, Ren J, and Holloszy JO. Additive
effect of contractions and insulin on Glut-4 translocation into the
sarcolemma. J Appl Physiol 77: 1597-1601, 1994
7.Goodyear, LJ, Hirshman MF, Napoli R,
Calles J, Markuns JF, Ljungqvist O, and Horton ES. Glucose ingestion
causes Glut 4 translocation in human skeletal muscle. Diabetes 45:
1051-1056, 1996
8.J. L. Bowtell1,
K. Gelly1, M. L. Jackman1, A. Patel1, M.
Simeoni2, and M. J. Rennie1.
Effect of different carbohydrate drinks on
whole body carbohydrate storage after exhaustive exercise. J Appl Physiol
Vol. 88, Issue 5, 1529-1536, May 2000
9.Kristiansen, S, Hargreaves M, and Richter
EA. Progressive increase in human sarcolemmal vesicles during moderate
exercise. Am J Physiol Endocrinol Metab 272: E385-E389, 1997
10.Luc JC van
Loon, Wim HM Saris, Margriet Kruijshoop and Anton JM Wagenmakers .Maximizing
postexercise muscle glycogen synthesis: carbohydrate supplementation and
the application of amino acid or protein hydrolysate mixtures.American
Journal of Clinical Nutrition, Vol. 72, No. 1, 106-111, July 2000
11.McCoy, M, Proietto J, and Hargreaves M.
Skeletal muscle GLUT-4 and post-exercise muscle glycogen storage in
humans. J Appl Physiol 80: 411-415, 1996
12.Nesher, R, Karl SE, and Kipnis DM.
Dissociation of effects of insulin and contraction on glucose transport in
rat epitrochlearis muscle. Am J Physiol Cell Physiol 249: C226-C232, 1985
13.Niewoehner, CB, and Nuttall FQ. Glycogen
concentration and regulation of synthase activity in rat liver in vivo.
Arch Biochem Biophys 318: 271-278, 1995
14.Robinson LJ, Pang S,
Harris DS, Heuser J, James DE.
Translocation of the
glucose transporter (GLUT4) to the cell surface in permeabilized 3T3-L1
adipocytes: effects of ATP insulin, and GTP gamma S and localization of
GLUT4 to clathrin lattices. J Cell Biol. 1992 Jun; 117(6): 1181-96
15.Satabin, P, Bois-Joyeux B, Chanez M,
Guezennec CY, and Peret J. Post-exercise glycogen resynthesis in trained
high-protein or high-fat-fed rats after glucose feeding. Eur J Appl
Physiol 58: 591-595, 1989
16.Staron, R. S., D. L. Karapondo, W. J.
Kraemer, A. C. Fry, S. E. Gordon, J. E. Falkel, F. C. Hagerman, and R. S.
Hikida. Skeletal muscle adaptations during the early phase of
heavy-resistance training in men and women. J. Appl. Physiol. 76:
1247-1255, 1994
17.Symons, D. J., and I. Jacobs.
High-intensity exercise performance is not impaired by low intramuscular
glycogen. Med. Sci. Sports Exerc. 21: 550-557, 1989
18.Tarnopolsky, M. A., S. A. Atkinson, J. D.
MacDougall, A. Chesley, S. Philips, and H. P. Schwarcz. Evaluation of
protein requirements for trained strength athletes. J. Appl. Physiol. 73:
1986-1995, 1992
19.Thissen, J. P., J. M. Ketelslegers, and
L. E. Underwood. Nutritional regulation of the insulin-like growth
factors. Endocr. Rev. 15: 80-101, 1994
20.Watkins, SC, Frederickson A, Theriault R,
Korytkowski M, Turner DS, and Kelley DE. Insulin-stimulated GLUT4
translocation in human skeletal muscle: a quantitative confocal
microscopical assessment. Histochem J 29: 91-96, 1997
21.Webster's Revised Unabridged Dictionary, 1996, 1998 MICRA, Inc.
22.William J. Kraemer, Jeff S. Volek, Jill A. Bush,
Margot Putukian, and Wayne J. Sebastianelli.
Hormonal responses to
consecutive days of heavy-resistance exercise with or without nutritional
supplementation
J Appl Physiol, Oct 1998; 85: 1544 - 1555.
23.Yan, Z, Spencer MK, and Katz A. Effect of
low glycogen on glycogen synthase in human muscle during and after
exercise. Acta Physiol Scand 145: 345-352, 1992
24,Yan, Z, Spencer MK, Bechtel PJ, and Katz
A. Regulation of glycogen synthase in human muscle during isometric
contraction and recovery. Acta Physiol Scand 147: 77-83, 1993
Essay Three:
Q: Of what
significance are the timing of carbohydrate consumption and the window of
opportunity?
A: The timing and digestion of post-exercise
carbohydrates is imperative for two reasons.
·
Glycogen replacement.
·
Translates the body’s hormonal state from catabolic to anabolic
(Muscle protein synthesis, cortisol suppression, shuttling of nutrients
into the muscles. The amplified cellular sensitivity to insulin
post-exercise provides for the express delivery and intra-cellular
transport of glucose and creatine).
Muscle glycogen is an indispensable fuel source for body building
training regimens. Glycogen is broken down and used during
exercise as energy for muscle contraction.
This energy is moderated by the
Glycogen-Lactic Acid System, which is profoundly employed in body
building training curriculums. The energy source drawn from during this
stage of work is glycogen.
The process begins by converting glycogen
into glucose, which then metabolizes to ATP, known as anaerobic
metabolism. Interference with ATP production, by means of lactic acid and
depleted stores of glycogen, causes eventual fatigue in the muscle if the
intensity is maintained (See: (
Muscle Fibers Part One and
Eight Weeks To A Freakier Tibialis.)
Degradation of stored glycogen, known as
glycogenolysis, occurs through the feat
of glycogen phosphorylase.
The purpose of phosphorylase is to phosphorolytically
eliminate single glucose residues from a-(1,4)-linkages within the
glycogen molecules.
Moreover, the glycogen-lactic acid system is responsible for the
concept known as “time-under-tension (TUT),” which is an invaluable tool
in the quest for enhanced hypertrophy.
“Why Moderate Reps Stimulate Optimal
Hypertrophy”-
Excerpt from
Physiological Aspects of Bodybuilding Part I:
As an overview of
the concepts I have covered, studies have shown that moderate repetition
sets are best for improving hypertrophy in fast twitch fibers and high
repetition sets are best for increasing hypertrophy in slower twitch
fibers. There are several reasons why. The first is that one to 5 rep
maximums based sets will most likely cause you to fail due to nervous
system signaling problems before a strong enough stimulus to muscle growth
can be induced (1, 2). Secondly moderate rep sets (6-12 and even 15 reps,
for example) take full advantage of our body's recruiting system. The
nervous system will recruit lower threshold fibers firstly and as the set
intensifies it will enlist more and more high threshold fibers. By the
end of a set all available muscle cells have been brought into play (3).
Thirdly the release of anabolic hormones is highest after these types of
sets (4, 5, 6, 7, 8) (look for detailed articles on how to manipulate
natural hormone release in the near future in our anatomy section!).
This is of
obvious benefit! After all, why do you think anabolic steroids are so
successful? They are simply inject-able hormones! The more you have
circulating in your body, the greater your muscle gains will be, and no
one will argue this point! Interestingly enough, many elite trainers,
doctors and professors have theorized that lactic acid production can be
very conducive to the release of anabolic hormones such as testosterone
and growth hormone (3, 4, 5)! Lactic acid is a by product of the G-L-A
System (6). This is the energy system that is used most heavily
during 30-90 seconds of work. Power lifting type movements are dependent
on the creatine phosphate system which is used for extremely low rep, high
percentage (of your maximum strength) sets. The PC system does not result
in lactic acid production. This is just another reason to use supersets,
strips, and other techniques that produce this effect.
Sets that use the
Glycogen-Lactic Acid system (30-90 seconds, shocking methods or 6-15 reps)
prime the pump (create extreme pumps). There are many benefits to this in
regards to hypertrophy. One is to super hydrate your myofibrils (9)(see
anatomy of a muscle fiber for detailed explanation of myofibrils)! A
pump is caused by the collapsing of veins. As you know from the anatomy
of a muscle, veins take blood out and arteries bring blood to the
muscles. Even though the veins begin to fail, the arteries continue to
bring blood to the muscles! This build up of fluid causes a flow of blood
to go back into the
muscle which in turn causes
the pump! What does more fluid in the muscle
cells equal? Hydration correct!? Surely you have heard of the numerous
benefits of super hydration! Several studies have shown that it literally
inhibits protein breakdown and stimulates protein synthesis (growth!) (10,
11, 12). Again, low repetition sets (especially 1-3 rep ranges) do not
provide enough time to produce a significant pump. Blood is also
responsible for the precious nutrients needed for growth or the rebuilding
process of muscle tissue! Finally time under tension has been a proven
factor in stimulating optimal growth (13)! The longer actin and myosin
filaments interact with each other to produce contraction the greater the
damage to the muscle tissue will be. It’s apparent that this time is
extremely short in low rep sets. Therefore you need to recruit and expose
the muscle fiber to enough time under tension to optimally grow!”
 Body builders
are focused on lifting progressively heavier weights under longer time
under tensions.
Therefore, storehouses rich in glycogen should be of the highest
importance (aside from glycogen depleting stages) in order to make full
use of the G-L-A system. These storehouses are depleted after a workout,
and need to begin to be replaced as soon as possible for maximum usage of
the G-L-A for subsequent training bouts.
Power output and muscle mass recruited determine
glucose disposal (39).
 Once
glycogen stores are depleted, the capacity to perform exercise
at full potential is lost or severely limited. Glycogen depletion has a
direct impact on decreasing the levels of maximum intensity that can be
dispersed during training (1, 5, 12, 15, 19, 21).
Image One. Rough Endoplasmic Reticulum,
Mitochondria and Glycogen. Photo
Courtesy: CSLUB.
The results of
K. M. Zawadzki, B. B. Yaspelkis 3rd and
J. L. Ivy experiments showed (29),
“that post-exercise muscle glycogen storage can be
enhanced with a carbohydrate-protein supplement as a result of the
interaction of carbohydrate and protein on insulin secretion.”
Supplementation at the adequate phase to begin replacing lost glycogen
is crucial.
For maximal anabolic potential, research shows macronutrient ratios
should consist of a liquid solution containing both carbohydrates and
protein.
Delaying the ingestion of a carbohydrate supplement
post-exercise will result in a reduced rate of muscle glycogen
storage (20).
Inferior post-workout recipes that slow gastric emptying or dull
insulin release can enhance this delaying effect.
Due to the damage of muscle proteins and the distraction of
amino acids and energy away from the actions of protein synthesis
during exercise, there is a resulting need for improved
post-exercise protein repair and synthesis.
Therefore, the appropriate readiness, and therefore, timing of nutrient
intake is necessary to achieve positive net muscle protein
balance.
It has been confirmed through research that fast-acting post-exercise
ingestion of a nutrient supplement enhances accretion of whole
body protein, suggesting a common mechanism of exercise-induced
insulin action (14).
Muscle protein
synthesis is stimulated in the recovery period after resistance exercise
(7, 10).
However, the net protein balance (the difference between muscle
protein synthesis and protein breakdown) generally remains negative
in the recovery period after resistance exercise in the absence
of nutrient intake; this causes the muscle to be in a catabolic, or
muscle wasting, state (7, 32, 33, 35).
Recently, Elisabet Børsheim,
Melanie G. Cree, Kevin D. Tipton, Tabatha A. Elliott, Asle Aarsland, and
Robert R. Wolfe (16) tested this concept utilizing
100 g of carbohydrates (Maltodextrin) post-workout.
They concluded:
In conclusion, the
principal finding of this study was that intake of 100 g of
carbohydrates (Maltodextrin) after resistance exercise improved
muscle net protein balance, but the improvement was only minor
compared with the reported effect of intake of amino acids.
We conclude that intake of carbohydrates alone after resistance
exercise will modestly improve the anabolic effect of exercise.
However, amino acid intake is necessary for a maximal response.
During their research they concluded that carbohydrates and amino acids
coupled together provided the most ideal anabolic circumstances.
In 2000, Rasmussen, BB, Tipton KD, Miller SL, Wolf SE, and Wolfe RR
(37) showed that muscle protein synthesis was increased 3.5-fold when
only a small amount (6 g) of a mixture of essential amino acids
(EAAs) was given along with 35 g of carbohydrate after resistance
exercise.
Clearly the combination of protein and carbohydrates post-workout is
vital to both muscle protein and glycogen synthesis. As mentioned earlier,
there is a synergistic effect between amino acids and carbohydrates.
Fusion of glycogen and protein
is essential for skeletal muscle recovery from the catabolic events of
exercise (20).
In recent years, different methods of increasing the muscle
glycogen stores post-workout have been extensively investigated.
Research studies addressing this question have focused on:
·
The timing (20, 22, 26, 27, 28, 30)
·
Frequency (15)
·
Amount of supplementation (8, 21-23, 25)
·
As well as type of supplement to ingest (9, 34, 38, 41, 44).
It has been well-established that the
timing of carbohydrate intake after exercise significantly
influences post-exercise carbohydrate homeostasis and recovery (20, 40).
The research confirms that rapid digestion and
assimilation of carbohydrates will produce the most favorable
circumstances.
In the attempt to act upon this early window, the next logical
conclusion to the post-workout theory would be to consume nutritional
sources that act upon rapid gastric emptying to enhance these early
periods of post-workout recovery (muscle protein and glycogen synthesis).
 Figure
1. Gastric emptying is the
evacuation of food from the stomach into the duodenum.
In the duodenum, the last stages of digestion
occur and the earliest stages of absorption and assimilation of nutrients
begins.
The emptying rate of the contents of the stomach is determined by the
substance, volume, osmolality, and structure of the ingested meal. Liquids
empty much more quickly than solids.
The pace of gastric emptying is related to the square root of the
volume, so that a constant proportion of the gastric contents empty per
unit of time.
Moreover, stimulation of duodenal osmoreceptors with triglycerides,
fatty acids or hydrochloric acid slows gastric emptying.
Delayed gastric emptying is contrary to the ideal post-workout
scenario. The faster the muscle glycogen stores can be
replenished after exercise, the faster the recovery process and
the greater the return of performance capacity.
Backed by numerous
experiments, L. Ivy, A. L. Katz, C. L. Cutler, W. M. Sherman and E. F.
Coyle helped confirm that delaying the ingestion of a
carbohydrate supplement post-exercise will result in a reduced rate
of muscle glycogen storage (23).
These findings can also be directly correlated to reduced gastric
emptying rates (4, 11, 13, 25) that occur with carbohydrate sources such
as fibrous greens or oatmeal.
Reducing the emptying rate of the carbohydrate source would severely
delay the ingestion process, and therefore the benefits of the nutrients
for the post-workout glycogen synthesis.
Insulin has a positive effect on glycogen
resynthesis and protein synthesis (18).
This is important because insulin has been
shown to be involved in the stimulation of amino acid uptake
and incorporation of proteins after exercise (2, 17).
Teresa A.
Hillier, David A. Fryburg, Linda A. Jahn, and Eugene J. Barrett
confirmed that insulin increases protein synthesis.
In their entry, “Extreme hyperinsulinemia unmasks insulin's effect to
stimulate protein synthesis in the human forearm,” they concluded:
Insulin clearly
stimulates skeletal muscle protein synthesis in vitro. Surprisingly, this
effect has been difficult to reproduce in vivo. As in vitro
studies have typically used much higher insulin concentrations
than in vivo studies, we examined whether these concentration
differences could explain the discrepancy between in vitro and
in vivo observations.
In summary, these
results indicate that insulin at high concentrations strongly
stimulates muscle protein synthesis in the human forearm.
This effect is quite consistent with the action of insulin
described in a number of in vitro studies using similar
concentrations of insulin but distinct from what is observed with
physiological hyperinsulinemia. Therefore, much of the discrepancy
previously reported between insulin action on protein synthesis
in vivo vs. in vitro may result directly from differences in insulin
concentrations used. In addition to stimulating protein
synthesis, high-dose insulin resembles the action of IGF-I
observed previously. As IGF-I receptors can be stimulated by high
concentrations of insulin, the present results together with
findings from in vitro studies raise the possibility that some
or all of insulin's action to stimulate protein synthesis may
be mediated by pathways other than the insulin receptor.
In 1997,
B. D. Roy, M.
A. Tarnopolsky, J. D. Macdougall, J. Fowles, and K. E. Yarasheski
tested
the effects of
glucose supplement timing on protein metabolism after resistance training.
The results illustrated that the most rapid increase in muscle glycogen
post-workout was achieved by consuming foods with a high GI (6).
We
determined the effect of the timing of glucose supplementation
on fractional muscle protein synthetic rate (FSR), urinary urea
excretion, and whole body and myofibrillar protein degradation
after resistance exercise.
Their findings
revealed:
CHO supplementation
(1 g/kg) immediately and 1 h after resistance exercise
can decrease myofibrillar protein breakdown and urinary urea
excretion, resulting in a more positive body protein balance.
They fully
confirmed the importance of insulin in suppressing the increase
in muscle protein degradation rate after exercise.
Muscle growth
in adult humans
results from muscle fiber hypertrophy/plasia (31).
Hypertrophy is the result of an increased net muscle protein
balance [i.e., fractional muscle protein synthetic rate (FSR) muscle
protein degradation rate (MPD)]. Both FSR and MPD can be
stimulated by heavy-resistance exercise in humans (7, 10, 43).
However, as mentioned earlier, FSR is made null in the absence of
nutrition (7, 32, 33, 35). Delay in nutritional intake via slow-burning
sources has the same effect due to low gastric emptying rates (23).
It is also known that amino acid transport is increased
after resistance exercise. When insulin is combined with increased amino
acid delivery, FSR and WBPS (whole body protein synthesis) are both
amplified radically (3).
One methodology for delaying gastric emptying post-workout and
decreasing insulin release would be to consume foodstuffs consisting of
fat/fiber, or low GI. Such protocols may include oatmeal, peanut butter or
whipping cream.
These protocols are completely counteractive to rapid ingestion of
nutrients needed to fulfill the early post-workout recovery processes.
Insulin is released with any food, but the
macronutrient that causes its highest release is the carbohydrate (See:
Take Fat Burning To A Whole New Level!! );
the more complex and fibrous the
carbohydrate, the slower the release of insulin, and the slower the rate
of gastric emptying.
This protocol is ideal for all other meals
as the day; whether the goal is gain in mass or maintenance of mass.
However, in the case of post-training,
JHR can not stress enough what a terrible recommendation
fat/fiber during the post-workout scenario is.
Benini L, Castellani G, Brighenti F, Heaton KW, Brentegani MT,
Casiraghi MC, Sembenini C, Pellegrini N, Fioretta A, and Minniti G, et al.
(4) scientifically confirmed this conclusion:
It is known that exogenous fibre added to
liquid meals delays gastric emptying. This study therefore looked at
gastric emptying of two different solid meals in eight healthy subjects
and their blood glucose responses. The meals were exactly equivalent
except for the total dietary fibre content (high fibre 20 g, low fibre 4 g
of dietary fibre per 1000 kcal) and supplied 870 kcal (700 kcal women),
47% of which was from carbohydrates, 36% from fats, and 17% from
proteins….Total gastric emptying time was significantly reduced by fibre
removal (186.0 (15.6) v 231.7 (17.3) minutes after the low and the high
fibre meal, p < 0.05). Blood glucose was higher after the low fibre meal,
and the area under the glycaemic curve significantly greater (226 (23.1) v
160 (20.0) mmol/min/dl-1, p < 0.05). …In conclusion, fibre naturally
present in food delays gastric emptying of a solid meal, reduces the
glycemic response, and delays the return of hunger.
Moreover, there is a direct relationship
between carbohydrate absorption rate (and therefore GI) and fat content.
This is because fat acts to delay gastric emptying (13).
This makes oat fiber perhaps the worst
carbohydrate source post-workout, as it not only slows gastric emptying to
a halt, but also suppresses insulin release.
Johansen, J.N., Knudsen, K.E.B., Sandstrom,
B., and Skjoth, F (24) revealed this truth by testing various controls
such as wheat flour, oat flour, rolled oats, and oat bran for gastric
emptying rates.
Soluble fiber in
oats increases the viscosity of the stomach contents, increases water
holding capacity, and decreases the rate of gastric emptying.
Furthermore, Jenkins DJ, Josse RG, Jenkins
AL, Wolever TM, and Vuksan V (25) showed the “Implications of altering
the rate of carbohydrate absorption from the gastrointestinal tract”:
The rate of
absorption of carbohydrate from the small intestine plays a major role in
determining the metabolic effects of dietary carbohydrate. Factors which
reduce the rate of absorption include the nature of the starch and
sugars, and the presence of vegetable proteins, fats, viscous fibre,
and antinutrients, including lectins and phytates. The rate of absorption
can also be manipulated by the use of specific enzyme inhibitors and by
increasing the number and frequency of meals while holding caloric intake
constant. All these factors contribute to the creation of what may be
termed slow release or "lente carbohydrate". The slowing of small
intestinal absorption, as exemplified by increased meal frequency
("nibbling"), results in reduced postprandial insulin secretion and lower
low-density lipoprotein (LDL) cholesterol and apolipoprotein B
concentrations. A further effect of some manipulations which reduce the
rate of absorption is increased delivery of carbohydrate to the colon and
its absorption after bacterial fermentation to short-chain fatty acids (SCFA).
This study further backs the fact that fiber
and fat serve to delay gastric emptying; the complete inverse of what is
desired post-workout.
Welch IM, Bruce C, Hill SE, Read NW (42) in
their journal entry, “Duodenal and ileal lipid suppresses postprandial
blood glucose and insulin responses in man: possible implications for the
dietary management of diabetes mellitus,” inadvertently showed that
fat post-workout will delay gastric emptying and insulin release.
Infusion of lipid
into the ileum delays the transit of a meal through the stomach and small
intestine and could therefore influence the rate and degree of nutrient
absorption…Infusions of lipid into either the duodenum or the ileum
significantly reduced or abolished the immediate postprandial rises in
blood glucose and insulin and significantly delayed gastric emptying.
Blood glucose and insulin rose shortly after the lipid infusion
terminated…Intestinal lipid can thus modify the glycaemic and insulinaemic
responses to a meal, and this modulation probably explains the reduced
metabolic responses to a meal containing fat compared with a fat free
meal.
Therefore, in order to increase the rate
of absorption, fiber and fat sources should be shunned post-workout.
Aside from delaying the recovery process
post-workout, EIOS adds another negative factor to this equation.
Post-workout carbohydrate metabolism may be altered by the ingestion of
fats, as each substrate competes as an oxidative fuel source (36).
See:
Role of Anaerobic Post-Workout Antioxidant Supplementation in
Correspondence to Exercise Induced Oxidative Stress
Fat/fiber will delay the intake of nutrients, thwarting the initial,
all-encompassing recovery phase post-workout, and dampening the insulin
release associated with enhanced glycogen and protein synthesis
post-training.
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Replacing
glycogen stores rapidly as possible is the most logical conclusion for
body builders who train multiple days or follow typical body building
splits and exercise programs.