The Growth Process in Younger Humans (Cont'd)

That working hypothesis was developed as a means of explaining why study after study showed that exercise reduced the risk of an incredibly broad spectrum of disorders and diseases.  To the extent that the medical establishment addresses the role of exercise, it is generally considered an unusual intervention that has some beneficial effects.  To the founder, it was apparent that the right type of exercise is an absolute necessity in order to remain healthy.   


Any human who does not engage in a sufficient amount of the right type (intense) of exercise will suffer from dysfunction in every organ and system in his or her body. Intense exercise can’t guarantee that one remains healthy forever.   Other elements are also necessary.  And even if all of the necessary elements are present, one could die from diseases that are unrelated to FDS, or die in an accident.   But FDS, or the aging process, is inevitable unless one engages in a sufficient amount of intense exercise. 


That was the original working hypothesis, and it remains true today.  But further analysis into the mechanism whereby intense exercise confers health benefits led to a tantalizing possibility.  It's not the exercise itself, but the Complex X that is synthesized as a result of the exercise that activates the Growth Process.  We know that for a couple of reasons.  First, there is a study that shows that people who can’t form lactate, which is the major component of Complex X, cannot induce the secretion of human growth hormone regardless of how intensely they exercise.  Second, as will be discussed below, there is the matter of fetal growth.


The Hypothesis posits that all human growth and development occurs as the result of the Growth Process, which in turn is activated by elevated levels of Complex X in the bloodstream.  For adult humans, elevated levels of Complex X in the bloodstream typically result from intense exercise.  However, for humans, the greatest period of growth is during the fetal stage.  A fetus cannot engage in the type of intense exercise that is necessary to synthesize Complex X in adults.  The blood of the mother and the fetus never mix.  So even if the mother did engage in intense exercise, the Complex X could not pass from the mother’s bloodstream to the fetus.  So neither the mother nor the fetus can synthesize the Complex X that is necessary to induce growth and development in the fetus.


Those facts posed an apparent quandary for the Hypothesis.  The Hypothesis predicts that there must be some way in which the fetus is provided with Complex X.  These types of predictions are a measure of the power and validity of scientific theories.  That there is an interesting and unexpected answer to this quandary provides powerful validation of the Hypothesis.  Complex X is a byproduct of the metabolism of glycogen.  In adults that process occurs in the cytoplasm of muscle cells (which have stores of muscle glycogen) during intense exercise.  To the surprise of many researchers, the placenta also has stores of glycogen.  Historically, it was believed that the role of placental glycogen must be similar to that of liver glycogen – a means of storing glucose in case of emergency.   More recent thinking is that placental glycogen functions much more like muscle glycogen.  Rather than being a possible nutrition source, its sole role is to be metabolized.  The glycogen is metabolized in the placenta, and the Complex X that is produced as a result of that process enters the blood stream of the fetus and the mother.  The Complex X produced by the placenta activates and regulates the Growth Process in the fetus.


The knowledge that the Growth Process that can be activated by adults utilizes the same chemical mechanism as the Growth Process of a fetus has significant ramifications.  The Hypothesis is primarily focused on the relationship between intense exercise/Complex X/the Growth Process and FDS, or the “aging process.”  But the working hypothesis was that intense exercise is necessary for the proper development of all organs and systems in all humans of all ages.  Thus, FDS can and does afflict people of all ages.  Because it makes no sense to say that younger people are going through the aging process, the medical establishment has provided different labels for FDS when it occurs in younger people – metabolic syndrome, type 2 diabetes, etc.  But all of these disorders stem from the failure to activate the Growth Process on a regular basis. The incidence of these disorders is rising dramatically as frequent intense exercise becomes less and less common among the young.


An anecdotal observation at the other end of the spectrum also supports the Hypothesis.  Trained athletes of today (most obvious among high school and college basketball and football players) are much larger than they were a few decades ago.   In fact, elite high school athletes of today are taller and heavier than the full-grown professional athletes of the past.  The time frame is much too short for the change to be the result of genetics.  Many have attempted to ascribe the changes to improved diet.  The more likely explanation is that athletic potential is now recognized at a much younger age, and younger athletes are exposed to rigorous training regimens.  Almost none of us approach our genetic potential in terms of size or strength.  But these young athletes, who started with superior potential, are much taller and heavier than the athletes of the past because their training programs, which involve the constant activation of the Growth Process, are allowing them to come closer to achieving their genetic potential.

Intense exercise is as necessary an element of the normal evolutionary environment as is air,  food or sunlight.