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Acute & Chronic Endocrine
Responses to Exercise Induced Disruptions in
Abstract: The importance of nutrition following training-induced homeostatic disruption can be traced to our most ancient of writings. Esau, the first born of Isaac, in what is estimated to be 1800 B.C. appears to have had incredible genetics. His training sessions, however, were not found in the gym, but rather in the field as he hunted the most ferocious of beasts. So vital was the post-workout meal to the father of the Edomites that he sold his birthright to his brother Jacob for it! And Jacob sod pottage:
and Esau came from the field, and he was faint: And Esau said to Jacob, Feed me,
I pray thee, with that same red pottage; for I am faint: therefore was his name
called Edom. And Jacob said, Sell me this day thy birthright. And Esau said,
Behold, I am at the point to die: and what profit shall this birthright do to
me? And Jacob said, Swear to me this day; and he sware unto him: and he sold his
birthright unto Jacob. Then Jacob gave Esau bread and pottage of lentiles; and
he did eat and drink, and rose up, and went his way: thus Esau despised his
birthright. Genesis 25:19-34 It is astonishing to note that, until today, such a protocol has not been matched (though even now, after thousands of years of advancement, some still hold to the unscientific, wholly unsupported practice of consuming fructose, fat, and fiber upon cessation of training).
But what of
pre-workout historical nutrition? The variety of diets has ranged from the
extreme to the sensible. On the former end, ancient Romans and Grecians would
eat the heart of a lion to obtain its courage, while on the latter it is said
that Charmis of Sparta would consume figs before a training bout. It appears
that even as late as the 1936 Olympic Games that many of the worlds top
nutritionists had not nailed home the most accurate of methods for pre-workout
prep. In one German publication, Schenk describes the athletic diet for those
competing in Berlin:
Historically,
I believe men such as Galen (born AD
129, , Pergamum, Mysia, Anatolia died AD 216
) who studied the homeostatic displacement following the onset of exercise were
a major key to our current scientific breakthroughs. He stated the following: “To me it does not seem that all movement is exercise, but only when it is vigorous. But since vigor is relative, the same movement might be exercise for one and not for another. The criterion of vigorousness is change of respiration; those movements, which do not alter the respiration, are not called exercise. But if anyone is compelled by any movement to breathe more or less or faster, that movement becomes exercise for him (13).” What Galen noted is of unspeakable importance. You see, the respiratory response, which was discussed, can and indeed is positively correlated to the field of exercise endocrinology. That is, at certain rates of one’s V02 max, we can predict aspects of hormonal output, such as levels of both the catabolic hormone cortisol, and the anabolic peptide insulin. Antoine Laurent Lavoisier (1743-1794), undoubtedly one of the greatest scientists, was the first man we know of to quantitatively measure oxygen consumption during training.
In 1780, Lavoisier in 10 hours collected 3 grams of carobonic acid from a guinea pig breathing oxygen. In a further experiment, the subject was placed in a confined space with ice surrounding it. The outside of the space was walled off with ice so as to ensure the environment stayed the same temperature. However, the inner wall of frozen H20 melted due to the animal’s heat expenditure. From this Antoine concluded:
From an exercise physiology standpoint, Lavoisier noted the drastic changes in heat production in varying states of stressful environments. " The quantity of oxygen absorbed by a resting man at a temperature of 26 degrees C is 1200 pounces de France (approximately 24 liters). The quantity of oxygen required at a temperature of 12 degrees C rises to 1400 pounces. During the digestion of food the quantity of oxygen amounts to from 1800 to 1900 pounces. During exercise 4000 pounces and over may be the quantity of oxygen absorbed. "
I have always
found his methods of experimentation fascinating. You can glean much from this
work. For example, it is important to realize that the digestion of food is an
extremely complex process, which requires additional energy expenditure as well
as the release of specified chemical agents, which can either enhance or detract
from your training session. The question therefore arises, when and what should
one consume before, during, and after a workout? Should it be simplified
nutrition, or complex? Is there a difference between what we consume 30 minutes
before training, and 30 minutes into training? To understand such principles,
you have no further to look then the complexities of maintaining equilibrium
while under the gun (or rack).
We need to
magnify that last concept further while continuing on the ever-present theme of
homeostasis. When doing so, it becomes so much clearer why the heart rate
increases while training, how blood vessels dilate, and so much more! Now, take
a look at a term known as a regulated variable. An RV can change due to
external stimuli, but cannot exude its narrow limit before deleterious
occurrences arise. One example of this is blood acidity levels. The Limit of
pH is 7.35 to 7.45. A pH below 7.35 is known as acidosis. The body must be
extremely precise in its regulation. Indeed, if the level of acidity falls to
just 6.8 for even a moment, the cost is your life ( 14 )! During high-intensity
training, the participant’s need for oxygen increases. Aerobic Cellular
Respiration can be defined as follows: This increase in acidity is dealt with immediately with a complex buffering system which permeates blood plasma. Think of this as your first line of defense. A second line is quite noticeable. You see, chemoreceptors are found all throughout the body. Chemoreceptors identify the chemical composition of a fluid. Such receptors found away from the brain’s center of respiratory control are known as peripheral chemoreceptors. They can communicate with the brain by secreting their own chemical messenger to specialized, electrically active messenger cells known as neurons, which then relay the message to the mother system, or control center, known as the medulla or brain stem. If C02 levels rise, then the medulla gives the command to increase the rate at which you exhale (your rate of respiration). One experiment to test how sensitive the body is to C02 is to hyperventilate, and then to see how long you can hold your breath (note: do not do this while in water to win a contest! It’s not a game to play with). Then compare this to how long you could hold your breath without hyperventilation. The former lowered overall C02 levels, which therefore lowered the stimuli for the need to breathe. The kidneys also control acidity through an extremely complex process which serves to pump H+ ions out for disposal at an increased rate. There are numerous regulatory variables in the body, and exercise pushes our ability to maintain them to the highest of degrees! Two systems are ultimately responsible for the maintenance of your internal environment. These are the endocrine and nervous systems. Again, our focus today is on the former. Cardio respiratory System / Thermo Balance during Exercise
The
following, describes how the body’s CR system responds to training. I do this
to clarify what actions the endocrine system supports.
3. Diversion of vital resources to supply high energy needs. Accomplished by lowering the diameter of blood vessels in lower energy regions such as the digestive tract, while simultaneously increasing the diameter of vessels surrounding the working musculature. Note this has the effect of increasing resistance to the former, while decreasing resistance of blood flow to the latter. A nice analogy can be used by comparing your body to the Enterprise on Star Trek. When the ship is under attack, power is diverted to weaponry and shields; so too is blood flow diverted to working musculature, as well as to the increased oxygen demand placed on the lungs. 4. Lavoisier noted a heat increase in consumption of food, as well as with exercise. If the body is not able to control a heat influx, then various malfunctions such as heat stroke will occur. For more on this, see Venom’s article on fluid intake. He addresses thermoregulation in depth, including concepts such as the basal metabolic rate and exercise induced thermogenesis. For now, realize that the body controls your temperature by directing blood to or away from the skin, as well as the control of sweat glands. What does the endocrine system have to do with this? As you will see, the catecholeamines epinephrine and nor-epinephrine reinforce the sympathetic nervous system in each of the above processes. Metabolic System
1.
To make fuel readily available for the synthesis of ATP, which itself is needed
for contractile activity. Accomplished by stimulating the catabolism of
glycogen to glucose, as well as the mobilization of fatty acids. Moreover, the
mobilization of amino acids for a process known as gluconeogenesis (the creation
of glucose from a non glucose substance) is stimulated. Metabolic hormones include: insulin, glucagon, cortisol, growth hormone, t-3, as well as the catecholamines. Note: The field of study which deals with energy transference is known as bioenergetics and will be covered like never before right here on ABC in the near future!
Fluid
Regulation Chemical Communication under the Microscope
A chemical messenger is a ligand, which itself is defined as a “molecule which can bind reversibly to a protein (14). It is fascinating to note that the word hormone has its roots in the Greek language, in which case it can be properly translated: “to arouse activity (15).” At a time it was believed that hormones were purely synthesized by one organ and then subsequently transported via the circulatory system to eventually affect a different tissue. Daryl K. Granner states that this original description is too restrictive, because hormones can act on adjacent cells (i.e. paracrine action) and on the cell in which they were synthesized (i.e. autocrine action without entering circulation) (15). We can therefore say that a hormone is a chemical messenger which is secreted (a process of release) and that acts on a target cell, that is, a cell which contains specific receptor sites which have an affinity, can bind to, interact, or recognize that which was secreted. So efficient is this God-designed system that it has the capacity to link over 75 trillion cells with incredible precision!
Basic
Classes of Hormones These synthesizing factories are extremely complex, and studies show that they adapt wonderfully to damaged regions. Indeed, Stephen Welle and A. Chesley et al. showed that ribosomes actually increase their regional specificity in response to areas being degraded by exercise (7, 40), that is, the cellular machinery responsible for protein synthesis increases the rate at which it synthesizes proteins in the areas which need attention. In fact, Dr. Horne and colleagues stated their results indicate that “increased association of ribosomes with the myofibrils occurs during muscular hypertrophy (18).” In
regards to hormonally influenced changes in optimal recovery, Kramer and some of
the worlds top scientists assert that: “Clearly, heavy-resistance exercise
disrupts or damages certain muscle fibers that later must undergo a remodeling
repair process. Dietary nutrients, hormones, and growth factors interact to
regulate this remodeling of skeletal muscle proteins….
to enhance the development of muscular strength and size with heavy-resistance
training, optimal conditions for recovery from the individual
exercise training sessions are necessary.
Recovery involves the coordinated
functioning of several physiological processes that are heavily
influenced by the availability and actions of specific hormones
and nutrients (52).
“ Note the aspect which I bolded. These
scientists stated that a large part of whether or not you recover is the
availability of various hormones. I would add that the availability of other
hormones, such as those which linger following an insufficient( strawberries and
cream ) post-workout
refill, can enhance unneeded catabolic processes. The opposite of what you
want! In some target cells, the hormone receptor G protein complex of events activates calcium channels (ion channels). This activation increases the flow of extracellular calcium ions into the cells. Calcium can also be released from intracellular reserves – calcium already stored inside of the cell. Calcium then binds to, and activates a regulatory protein called calmodulin. Calmodulin, now activated by calcium ions, in turn activates protein kinases, which catalyze the phosphorylation of some inactive proteins into their active forms. As with cAMP, these effects also result in the immense amplification of the original hormonal signal. Some peptide hormones, such as insulin, also bind to membrane receptors. But their action does not involve G proteins or secondary messengers. Instead, the receptor has an intracellular domain that can act as an enzyme. This enzyme is called tyrosine kinase. The hormone, binding to the membrane receptor, activates this receptor enzyme resulting in a variety of signaling systems not involving second messengers. Growth hormone acts in a similar manner. Quick Question: Why would calcium channels cause such a rapid response in the cell? Answer below. The above two paragraphs cannot be understated! In fact, in this post-workout series, you will find that we can actually mimic hormones such as insulin through differing pathways; furthermore, these pathways can act synergistically with insulin to enhance glucose uptake and glycogen restoration. It is for this reason that an understanding of this vital system is a must for all serious athletes. Your understanding of bodily mechanisms and what they control will have a direct correlation to your ability to manipulate those mechanisms for the optimization of anabolism. Answer: The body uses calcium as a messenger for several functions. For example, it is the key to muscular contraction. It is regulated by a process known as primary active transport. Literal pumps are found on the cell membrane that pump calcium against their concentration gradient into the EFC and out of the ICF. Also note that Joe discussed that calcium can also be released from intracellular reserves. These reserves are known as smooth endoplasmic reticulum, and in a muscle cell they are denoted the “sarcoplasmic reticulum ( 50 ).” Binding sites in the cell are specific for Ca++, and by controlling their release you can efficiently control cellular actions. From a more direct standpoint, calcium concentration inside the cell is only 100-200 nanoMoles, whereas in the extra cellular fluid it is approximately 1.2 milliMoles. Put in clearer terms, the ECF has a concentration of 5, 000 to 10, 000 fold above the ICF (15)! Calcium is also charged, which means that it can be used to conduct an electrical current rapidly. The rapid influx is of course due to its concentration gradient, and electrical gradient. The intracellular environment is negative relative to the ECF. Thus, calcium will fly faster into the cell than a bullet out of gun! We will cover calcium mediated hormonal stimuli even further in a very near issue.
Endocrine
Stimuli (2) Our second option concerned hormonal activation. When a hormone stimulates the release of another hormone, it is called a trophic hormone. The hypothalamus is infamous for this very aspect of its function. It releases growth hormone releasing hormone, which stimulates the secretion of GH from the anterior pituitary, as well as a vast number of other releasing factors. (3) Humeral activation is associated with fluids in the body, in particular the blood. Nutrients carried in by the blood affect hormonal secretion here. For example, aldosterone is responsible for the secretion of potassium (it secretes it for elimination from the body). There is a condition known as HyperKalemia in which K+ levels rise to a level above normal concentrations. The results can actually lead to death! An increase in aldosterone increases secretion of K+, and therefore an increase in K+ leads to an increase in aldosterone secretion. Walcott et al. states that, "increases of plasma potassium directly stimulate aldosterone secretion. This effect of potassium on aldosterone serves as a protective mechanism against the development of hyperkalemia (51)." Conversely, when sodium is in excess, aldosterone and renin are suppressed (41). This is because aldosterone acts to retain sodium. Higher levels of this electrolyte would lower the need for higher concentrations of this hormone. Dr. Rasmussen and colleagues increased the sodium intake of eight individuals. They found that, "Significant natriuresis occurred within 1 h (48)." Natriuresis is defined as a high level of sodium excretion by the body. Why did this occur? Check it out: "A 6-fold increase was found during the last hour of infusion as plasma renin activity, angiotensin II (ANGII) and aldosterone decreased markedly. Sodium excretion continued to increase after NaLoading." In essence, the endocrine system works through a “closed loop feedback mechanism.” It can be summarized as follows (19): · Organ X secretes a trophic hormone, which stimulates organ Y to secrete a specific hormone, which in turn inhibits the release of the trophic hormone from Organ X. · Nutrient X decreases, Gland Y is stimulated to secrete a chemical substance which stimulates the release of stored X. Nutrient X increases, and inhibits secretion from Gland Y. Of course the process goes through endless combinations, and numerous hormones regulate these processes, but the above is a general idea of what a closed loop feedback mechanism is. As you will see, other actions such as agonistic/antagonistic relationships also play a major role.
The Cellular Response When
the concentration of a hormone increases, the cellular response increases like
so (14):
Receptor activity is influenced in great part by hormones themselves. Catecholamines Responses to Exercise
Catecholamines are ultimately derived from the amino acid tyrosine. In
catecholamine synthesis, one catecholamine serves as a precursor to the next
catecholamine in a sequence-like fashion. Joe King summarizes the synthesis of
epinephrine and nor epinephrine as follows (27): “Tyrosine > dopa > dopamine > norepinephrine > epinephrine” Note how dopamine acts as a precursor to norepinephrine, while NE subsequently becomes the precursor to epinephrine. This is called a chemical pathway. We must note that, ultimately, it is the enzymes contained within a cell that determine how long this chemical pathway will last. For example, if a cell secretes the hormone dopamine, it lacks the enzyme that catalyzes the reaction, which would morph it to NE. Dopamine is the precursor for each of the other catecholamines, and is therefore contained in all catecholamine-secreting cells (14). What is fascinating to note is that both the nervous system and endocrine system secrete epinephrine (also known as adrenaline) and norepinephrine (or noradrenaline). However, NE is the prominent neurotransmitter (chemical released from a neuron) released by sympathetic peripheral (see notes) neurons, while epinephrine is the dominant hormone secreted by chromaffin cells in the adrenal medulla (51) and plays a role in central nervous system stimulation. The adrenal glands are composed of the outer cortex, and an inner core called the medulla. The word chromaffin is a term reflecting the fact that within these cells are granules, which turn brown when treated with certain oxidizing agents for histological analysis (16). Epinephrine is known as the dominant hormone of the adrenal medulla because it accounts for 80 percent of secretion in this region, while norepinephrine accounts for 20 percent. Note: The Central Nervous system includes the brain and spinal cord; the nerves which branch off of this run to effectors: organs/cells. The sympathetic nervous system in physiological terms is known as the fight or flight system. However, in anatomical terms it is referred to as the thoracolumbar nervous system, as nerves which serve this function branch out of the thoracic and lumbar regions.
There are a few principles, which you need to understand: When at rest, most of the energy needed for muscular contraction occurs in the viscera, that is, the organs responsible for digestion. Internal organs operate off of smooth muscle, which is not under your control. 2.
The sympathetic nervous system reacts faster than the endocrine system.
Therefore, an athlete will see a quicker rise in norepinephrine than epinephrine
in response to exercise, as is explained below.
5. Both neurotransmitters/hormones (depending on whether they are secreted by neurons or the adrenal medulla respectively) have higher affinities at varying sites. However, they both can bind to the same receptors sites. The actual difference occurs in affinity for that receptor, not the response. Thus, they act as agonists for a common cause (fight or flight optimization). To understand four through five, we need to take a look at adrenergic receptors (receptors with an affinity for adrenalene/noradrenalene). During a fight or flight response, you need optimal energy for muscular contraction. This entails increasing cardiac output (again, the amount of blood pumped throughout circulation per minute), increased blood flow to skeletal muscles, and decreased blood flow to the digestive tract, as well as most other organs relative to the working muscles. This is accomplished by:
A.
Vasocontriction – To constrict blood vessels surrounding a particular region,
thereby restricting blood flow. Note: The above is only a partial view of receptor-mediated actions and makes this concept easier to comprehend; however, it appears to be more complex. For example, if you are working your calves, you need vasodilatation to occur there and not in other non-working musculature. The control mechanisms for this will be described under the alpha 1 subsection. The concept of adrenergic receptors becomes more complex. Nearly 20 years after Ahlquist’s findings, a group of scientists led by Dr. Lands observed that enhanced cardiac activity and vasodilation were signaled by the binding of differing structural receptors. Thus, they denoted receptors responsible for cardiac effects as beta 1 receptors, while the latter were denoted beta 2 receptors. Such a discovery prompted Langer et al. to discover an alpha 2 receptor which was structurally distinguished from alpha one receptors in pre-synaptic nerve terminals. Simply put, this means that they are used to regulate the release of post synaptic neurons which are responsible for the release of NE. As you will see, alpha 2 receptors have fascinating properties! In fact, discoveries have changed thought patterns on these receptors, in that they have actually been found to be located in vascular smooth muscle (12). Alpha One Receptors – Cellular Actions Caused When Bound To: Alpha one receptors first bind to the extra cellular membrane. The formation of a complex (ligand to receptor) stimulates a G-protein to activate an enzyme known as phospholipase C, which in turn speeds the reaction which changes a molecule known as PIP2 (phosphatidyl inositol biphosphate) to IP3 (inositol triphosphate and DAG (diacylglycerol). IP3 goes on to initiate the release of intracellular Ca++ (calcium) stores which then initiates a specific response in the cell. DAG activates a protein kinase C, which also initiates a response in the cell. In summary:
Epinephrine + Alpha 1 receptor
à
Epinephrine-Alpha 1 receptor complex
à
Stimulation of G Protein
à
Activation of phospholipase C
à
Catalyzed reaction of PIP2 to IP3 and DAG:
Smooth muscle is found in blood vessels, as well as viscera. Consider a blood
vessel as an adaptable tube. Inside of this vessel is a lumen (hollowed out
interior), which is lined by endothelium. Endothelium is a lining tissue which
is extremely slippery, so as to discriminate against clogging. Just deep to
that is a layer of smooth muscle, whose stimulation is regulated by the calcium
calmodulin system. For an overview of how a muscle is initiated to contract, I
would suggest reading the article on the All or None
Principle. Muscular contraction, be it smooth, cardiac, or skeletal, is
dependent on Ca++ intracellular concentrations. In skeletal muscle tissue, a
structure known as the troponin-tropomyosin complex disallows myosin cross
bridges to be formed with actin binding sites. Calcium disables the T-T
complex’s disabling abilities, and cross bridges are able to form. In smooth
muscle, an enzyme known as myosin kinase initiates the phosphorylation of myosin
cross bridges (in other words, this enzyme is needed for cross bridge formation,
and thus contraction of smooth muscle). As seen above, IP3 initiates the
intracellular release of Ca++, which in turn activates calmodulin, which in turn
activates myosin kinase and ultimately smooth muscle contraction (53). It is interesting to note that alpha 2 receptors also are involved in vasoconstriction near skeletal muscle. Studies show that acidosis, hypoxia, and ischemia (natural occurrences of a working muscle) each have inhibitory affects on alpha 2 receptors, but not alpha 1 receptors (35, 36, 37, 47). Results show that the vasoconstrictive effects of E and NE are inversely
proportional to exercise intensity. That is, “that the magnitude of
vasoconstriction decreases as exercise intensity increases (22).” At high enough
intensities, alpha 1 receptors are also inhibited (22, 6). When you think about
this from a design standpoint, it makes perfect sense. Alpha 2 receptors’
ability to bind with catecholamines decreases with less intensity than alpha 1
receptors, but as the intensity increases, alpha 1 also loses its sensitivity; I
liken this to two thresholds. Thus, if several muscle groups are working, those
which have the highest metabolic needs will be accommodated accordingly, and
those which have lower but still higher than resting needs will also be
appropriately accommodated. Some have postulated that such an occurrence is due
to increased blood flow (i.e. as blood flow goes up, alpha receptors’ response
goes down). However, studies do not back this hypothesis up; in fact they,
conflict with it (6). Muscular contraction is also put forth as a postulation. G.D. Thomas and colleagues support in their study on BF by reporting that, “the
increased muscle blood flow resulting from a combination of impaired
vasconstriction and increased arterial pressure was paralleled
by increased force of gastrocnemius-plantaris muscle contraction (17).” Binding to alpha 1 receptors also has notable metabolic aspects such as
lipolysis, or the breakdown of fats. When training, fats become a valuable
resource, and their liberation into the blood stream markedly increases their
usability. In one study,
Flechtner-Mors et al. performed a study to test
alpha 1 receptor initiation, as compared to alpha 1, alpha 2, and beta receptor
binding (34). To accomplish the alpha1 increase, a1 agonist called norfenefrine
was used, whereas norepinephrine, which binds to the three sites mentioned, was
incorporated for the comparison group. Finally, an antagonist to alpha 1
receptors was included, which is known as urapidil. Thirty-eight women were
broken up into three groups and received either the a1,a2,b
agonist norepinephrine, the a1 agonist norfenefrine, and the a1
antagonist (opposes the action of catecholamine binding to the receptor site).
It was found that: One
opposition that is beginning to be seriously studied is the fact that alpha 2
receptors inhibit fat breakdown, thus opposing alpha 1 receptors. This may
serve as a check and balance system. Catecholamines are perhaps what are mainly
responsible (directly and indirectly) for fat burning while training (30). I
feel one of the more thorough studies backing a2 as an antagonist to
lipolytic activity is found in the Journal of American Physiology and was
conducted by Vladimir Stich and his fellow scientists (49). In summary, the heart is stimulated to contract when an action potential or electrical current is conducted across the gap junctions in the myocardium. NE and E increase the rate of electrical impulses, and therefore increase the rate of contraction. Note that the sympathetic nervous system is responsible for the immediate raise in heart rate. Epinephrine takes longer to be released from the adrenal medulla and must travel to the heart via the blood stream. NE is directly released to the heart, a clear example of how fast-acting fight or flight technology truly is! Increased heart rate again is directly proportional to cardiac output. More blood is circulated, oxygen is delivered at a more expedient rate, nutrients are brought to working tissue, and C02 is carried away for expulsion at a more rampant rate. It is also important to note that Beta 1 and Beta 2 receptors have positive effects on increasing the rate of lipolysis (10, 31).
Beta 2
Receptors Hormonal Response during Exercise In order to
understand the following section, I need to reemphasize that NE is the primary
neurotransmitter of the sympathetic nervous system, whereas E is the primary
hormone of the adrenal medulla. Thus, you should expect NE to rise more rapidly
than E. The latter’s job is to elongate and enhance sympathetic effects. Also
recall that NE is also secreted by the adrenal medulla, but in lower amounts. Dr. Galba has contributed greatly to our understanding of endogenous hormone secretion in response to various exercise patterns. We will review some of his studies which are based on percentage V02 Max. Maximal Oxygen uptake is just that: the highest amount of O2 a person can consume and use to produce adenosine triphosphate aerobically during strenuous exertion. For example, there is a correlation between the Borg scale and VO2 max. At rest, which would correspond to a 1, you are using approximately 10 percent of your V02 max, moderate effort would be approximately 50 percent, fairly hard would be approximately 70 percent, while extremely hard, or a 10 in your observed exertion, would be 100 percent V02 max.
Galbo et al.
tested
graded and prolonged exercise to see what their effects were on catecholamine
concentration in the blood plasma. Graded simply means at various levels of
maximal O2 intake.
At rest and at mild oxygen consumption, epinephrine levels were at .07 (+ 0.01) ng/ml. At mild V02 the levels were at .12 (+ 0.02), and finally, at heavy, exertion levels rose to .46 (+ 0.03), which is well over 6 times resting amounts! From this we see that epinephrine levels are intensity dependent, and do not begin to rise until after 75 percent V02 max. After 75 percent, levels rise exponentially. Note that statistical significance was reached at the .0025 level (P < .0025).
From this
graph, you note a similar pattern (rest = .40, mild = .44, moderate = 1.30,
heavy = 2.22, and rest is back down to .46). The main difference is that
moderate exercise showed a markedly larger increase in NE, relatively speaking,
than E. Again, we can attribute this to the fact that the sympathetic nervous
system acts quicker than the endocrine system. The rest period lasted 15
minutes. In another study, S. F. Lewis had participants perform various
exercises, such as the arm curl, as compared to leg training. They found that, At rest E levels were at 0.05, after 40 minutes they rose to 0.12, when 60 was reached the levels rose to .24, and after 80 E rose to 0.33 ng/ml, and again fell to .07 after 15 minutes of rest. Thus, epinephrine levels appear to also be time-dependent. That is, at 75 percent V02 max, E rises positively in respect to time.
NE followed a
similar pattern. At rest they were .34, after 40 minutes they had risen to
1.20, during the 60-minute juncture 1.44 had been reached, and finally 1.51
after 80 minutes. Catecholamine Response to Resistance Training First, studies have been conducted at the 10-15 repetition range (BB rep range). If failure is reached, the response between the two protocols (10 vs. 15 repetitions) appears to be similar. Bush JA et al. tested just this scenario ( ). Purpose: “The purpose of this study was to examine the effect of dynamic resistance exercise on the response patterns of adrenal medullary neurohormones in strength-trained men.”
Protocol: A
high force vs. high power protocol was given at the same work load. For
example, 75 pounds lifted twice is the same work load as 150 lifted once. In
this case, relative work loads were given in either a 10 rep sequence, or a 15
rep sequence.
We see that
before the lift E was at .06, while after it had risen to .3, and dropped back
to base levels after 15 minutes of rest.
Further
Effects
ConclusionAs we have seen, the human body is a marvel
beyond our wildest comprehensions. It is at times like this when we need to
consider the verse (1): 6 Seek ye the LORD while he may be found,
call ye upon him while he is near: 7 Let the wicked forsake his way, and the
unrighteous man his thoughts: and let him return unto the LORD, and he will have
mercy upon him; and to our God, for he will abundantly pardon. 8 For my thoughts
are not your thoughts, neither are your ways my ways, saith the LORD. 9 For as
the heavens are higher than the earth, so are my ways higher than your ways, and
my thoughts than your thoughts. There will be a time when this option is no longer available to those who reject his offer. 2.
“For my thoughts are not your thoughts, neither are your ways my ways” Yours in Sport, President Abcbodybuilding/Co-Editor of the Journal of HYPERplasia Research References: 1. Gods infallible, untainted, inspired word. 2. Ahlquist RP, A study of the adrenotropoc receptors. Am J Physiol 1948; 153:586 3. Arner P (1992) Adrenergic receptor function in fat cells. Am J Clin Nutr 55 (Suppl 1): 228S-236S 4. Bush JA, Kraemer WJ, Mastro AM, Triplett-McBride NT, Volek JS, Putukian M, Sebastianelli WJ, Knuttgen HG. Exercise and recovery responses of adrenal medullary neurohormones to heavy resistance exercise. Med Sci Sports Exerc. 1999 Apr;31(4):554-9. 5. Burcher, E, and Garlick D. Antagonism of vasoconstrictor responses by exercise in the gracilis muscle of the dog. J Pharmacol Exp Ther 187: 78-85, 1973
6.
Buckwalter, JB, Mueller PJ,
and Clifford PS. 7. Chesley, A., J. D. MacDougall, M. A. Tarnopolsky, S. A. Atkinson, and K. Smith. Changes in human muscle protein synthesis after resistance exercise. J. Appl. Physiol. 73: 1383-1388, 1992 8. Connolly, CC, Steiner KE, Stevenson RW, Neal DW, Williams PE, Alberti KGMM, and Cherrington AD. Regulation of glucose metabolism by norepinephrine in conscious dogs. Am J Physiol Endocrinol Metab 261: E764-E772, 1991 9. Chang An Chu, Dana K. Sindelar, Kayano Igawa, Stephanie Sherck, Doss W. Neal, Maya Emshwiller, and Alan D. Cherrington The direct effects of catecholamines on hepatic glucose production occur via 1- and 2-receptors in the dog Am J Physiol Endocrinol Metab 279: E463-E473, 2000; 0193-1849/00 10. Coppack SW, Jensen MD, Miles JM. 1994 In vivo regulation of lipolysis in humans. J Lipid Res. 35:177–193. 11. Delp MD, Laughlin MH. Regulation of skeletal muscle perfusion during exercise. Acta Physiol Scand. 1998 Mar;162(3):411-9.
12.
Drew, GM, and Whiting SB.
Evidence for two distinct types of postsynaptic 13. Green RM A translation of Galen’s Hygiene. Illinois: Charles C. Thomas Publisher, 195 14. German, William J, Stanfield, Cindy L, Principles of Human Physiology 15. Granner, K Darly Hormonal Action, Principles and Practice of Endocronology and Metabolism Second Edition. J.B. Lippincott Company, Philadlphia, 1995 16. Goldstein, David S. Physiology of the adrenal medulla and the sympathetic nervous system: Williams Textbook of Endocrinology 9th Edition 17. G. D. Thomas, J. Hansen and R. G. Victor Inhibition of alpha 2-adrenergic vasoconstriction during contraction of glycolytic, not oxidative, rat hindlimb muscle 18. Horne Z, Hesketh Increased association of ribosomes with myofibrils during the skeletal-muscle hypertrophy induced either by the beta-adrenoceptor agonist clenbuterol or by tenotomy. Biochem J 1990 Dec 15;272(3):831-3 19. Habener, Joel: Genetic Control of Hormone Formation: Williams Textbook of Endocrinology 9th Edition 20. H. Galbo, J. J. Holst and N. J. Christensen Glucagon and plasma catecholamine responses to graded and prolonged exercise in man Journal of Applied Physiology, Vol 38, Issue 1 70-76, Copyright © 1975 by American Physiological Society 21. Hartley LH, Mason JW, Hogan RP, Jones LG, Kotchen TA, Mougey EH, Wherry FE, Pennington LL, Ricketts PT. Multiple hormonal responses to prolonged exercise in relation to physical training. J Appl Physiol. 1972 Nov;33(5):607-10.
22.
John B. Buckwalter and Philip S. Clifford
23. Jeffrey S. Greiwe, Robert C. Hickner, Suresh D. Shah, Philip E. Cryer, and John O. Holloszy Norepinephrine response to exercise at the same relative intensity before and after endurance exercise training J Appl Physiol 86: 531-535, 1999 24. Kraemer WJ. Endocrine responses to resistance exercise. Med Sci Sports Exerc. 1988 Oct;20(5 Suppl):S152-7. 25. King, Joe, Endocrine Insanity Part 3 – The Journal of HYPERplasia Research. November 2003 26. Kawai, Y, Powell A, and Arinze IJ. Adrenergic receptors in human liver plasma membranes: predominance of 2- and 1-receptor subtypes. J Clin Endocrinol Metab 62: 827-832, 1986 27. King, Joe Metabolic Primer II – The Journal of HYPERplasia Research. October 2003 28. King, Joe Metabolic Primer III – The Journal of HYPERplasia Research. September 2003 29. King, Joe, Endocrine Insanity Part 2 – The Journal of HYPERplasia Research. July 2003 30. Lafontan, M., and M. Berlan. Fat cell adrenergic receptors and the control of white and brown fat cell function. J. Lipid Res. 34: 1057-1091, 1993 31. Lafontan M, Berlan M. 1993 Fat cell adrenergic receptors and the control of white and brown fat cell function. J Lipid Res. 34:1057–1091. 32. Lönnqvist F, Krief S, Strosberg AD, Nyberg B, Emorine LJ, Arner P. 1993 Evidence for a functional beta3-adrenoceptor in man. Br J Pharmacol. 110:929–936 33. Lönnqvist F, Thöme A, Nilsell K, Hoffstedt J, Arner P. 1995 A pathogenic role of visceral fat ß3-adrenoceptors in obesity. J Clin Invest. 95:1109–1116
34.
M.
Flechtner-Mors, C. P. Jenkinson, A. Alt, G. Adler and H. H. Ditschuneit
In Vivo
35.
McGillivray-Anderson, KM, and
Faber JE. Effect of acidosis on contraction of microvascular smooth muscle by
36.
Medgett, IC, Hicks PE, and
Langer SZ. Effect of acidosis on
37.
McGillivray-Anderson,
KM, and Faber JE. Effect of reduced blood flow on 38. Marrieb, E.: Human Anatomy (5th edition), Redwood City, Ca: Benhamin / Cummings (2001) 39. Ming-Jer Tsai, James H. Clark, William T. Schrader, Bert W. O Malley Hormones That Act as Transcription-Regulatory Factors: Williams Textbook of Endocrinology 9th Edition 40. Stephen Welle1,2, Kirti Bhatt1, and Charles A. Thornton3 Stimulation of myofibrillar synthesis by exercise is mediated by more efficient translation of mRNA. J Appl Physiol 86: 1220-1225, 1999 Departments of 1 Medicine, 2 Pharmacology and Physiology, and 3 Neurology, University of Rochester, Rochester, New York 14620 41. Singer DR, Shirley DG, Markandu ND, Miller MA, Buckley MG, Sugden AL, Sagnella GA, MacGregor GA. How important are suppression of aldosterone and stimulation of atrial natriuretic peptide secretion in the natriuretic response to an acute sodium load in man? Clin Sci (Lond). 1991 Apr;80(4):293-9. 42. Sacca, L, Morrone G, Cicala M, Corso G, and Ungaro B. Influence of epinephrine, norepinephrine, and isoproterenol on glucose homeostasis in normal man. J Clin Endocrinol Metab 50: 680-684, 43. Skoglund G, Lundquist I, Ahren B. Effects of alpha 1- and alpha 2-adrenoceptor stimulation and blockade on plasma insulin levels in the mouse. Pancreas. 1986;1(5):415-20. 44. Schimmel, RJ. Roles of alpha and beta adrenergic receptors in control of glucose oxidation in hamster epididymal adipocytes. Biochem Biophys Acta 428: 379-387, 45. Skoglund G, Lundquist I, Ahren B. Alpha 1- and alpha 2-adrenoceptor activation increases plasma glucagon levels in the mouse. Eur J Pharmacol. 1987 Nov 3;143(1):83-8. 46. S. F. Lewis, W. F. Taylor, R. M. Graham, W. A. Pettinger, J. E. Schutte and C. G. Blomqvist Cardiovascular responses to exercise as functions of absolute and relative work load. Journal of Applied Physiology, Vol 54, Issue 5 1314-1323, Copyright © 1983 by American Physiological Society
47.
Tateishi, J, and Faber JE.
Inhibition of arteriole 48. Tipton KD, Rasmussen BB, Miller SL, Wolf SE, Owens-Stovall SK, Petrini BE, Wolfe RR Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise Am J Physiol Endocrinol Metab. 2001 Aug;281(2):E197-206 49. Vladimir Stich1, Isabelle de Glisezinski2,3, Francois Crampes2,3, Hana Suljkovicova1, Jean Galitzky3,4, Daniel Riviere2,3, Jindra Hejnova1, Max Lafontan3, and Michel Berlan3,4: Activation of antilipolytic 2-adrenergic receptors by epinephrine during exercise in human adipose tissue, Am J Physiol Regul Integr Comp Physiol 277: R1076-R1083, 1999 50. Wilson, Jacob Is The All Or None Applicable To An Entire Muscle? The Journal Of HYPERplasia Research March 2003 51. Walcott C, Gould JL, Lednor AJ Effects of potassium on renin and aldosterone Arch Mal Coeur Vaiss. 1984 Apr;77 Spec No:87-91 52. William J. Kraemer3, Jeff S. Volek1, Jill A. Bush1, Margot Putukian2, and Wayne J. Sebastianelli2 Hormonal responses to consecutive days of heavy-resistance exercise with or without nutritional supplementation 53. Young, James B, Landsberg, Lewis: Catecholamines and The Adrenal Medulla : Williams Textbook of Endocrinology 9th Edition
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