NW Spine - Library

© 1999

By subscribing to this publication and becoming affiliated with the International Association of Resistance Trainers (I.A.R.T.), you have already taken the first measures toward becoming a revolutionary in the fitness industry, one of a new breed of intellectual resistance enthusiasts who aspires to reach the apex of knowledge in the field of anaerobic exercise science. For those of us who are not content simply to know that something happens, but instead have an insatiable desire to understand the causality, this article is for you.

To my knowledge, the subject of genetic regulation of training-induced muscle hypertrophy has never been addressed in depth in any physical culture magazine nor in the publication of another certification organization. Nor has it appeared in any exercise physiology textbook I've read. Therefore, the subject of what determines genetic potential is a completely nebulous concept to most exercise physiologists and personal trainers.

Suppose a personal training client asked you, "Given that I train with high intensity and rest sufficiently, exactly why is my muscle growth much slower now than it was when I first began weight training?" Would you be able to give a satisfactory answer? After thoroughly reading and understanding this article, you will again be setting yourself apart from the rest of the pack by recognizing that genetic regulation of training-induced muscle hypertrophy is not some mysterious occurrence, but rather a biological phenomenon with a variety of mitigating influences.

The I.A.R.T. recognizes the importance of genetic factors in strength training and body building, and discusses several of them at length in the I.A.R.T. Reference Manual (8). In his book Heavy Duty (11) and also on the Heavy Duty/I.A.R.T. web site, Mike Mentzer wrote this regarding genetics and muscular development:
"Within the human genome (full complement of chromosomes), there are coded instructions that regulate the rate and degree of response to intense exercise. I am not referring here to genes that control the traits discussed above [including sex, skeletal structure, muscle belly length, and muscle fiber density], but those whose specific task it is to temporarily shut off the process of growth that occurs in response to single bouts of intense exercise, and then permanently once individual potential has been fully actualized. These regulatory traits, like many genetic traits, are expressed across a broad continuum, which helps explain why there exists such a wide range of variation with regard to individual response to intense exercise."

While most individuals familiar with resistance training recognize that progress tapers off as one becomes more fully developed, yielding a curvilinear graph of time versus growth (figure 1), the physiological mechanism that governs what we refer to as "genetic potential" remains a mystery to most. The purpose of this article is to introduce the reader to molecular genetics as it relates to how muscular growth occurs and what defines its upper limits.

The vast majority of protein synthesis in nearly all body cells is under the direction of the double-membrane-bound nucleus, the largest organelle within a cell. The exceptions to nuclear sovereignty are mature human red blood cells, which have no nucleus (3,13) and the organelle known as the mitochondrion, or "power house," which is found in great numbers in most cells and which contains instructions to manufacture some proteins independently of the nucleus (7,10,13,15). Muscle cells, also called muscle fibers, myofibers, and myocytes, each contain several nuclei along their length. Interestingly, the nuclei lie along the outside of the muscle cell just beneath the cell membrane to prevent the nuclei from obstructing the path of the contractile filaments (actin and myosin) as they slide past one another during muscular movement (10).

It should be noted that an important function of the nucleus is that it contains the blueprint for cell replication, or mitosis (12). However, mature myocytes are postmitotic (7). That is to say, they can't divide to increase their numbers. Additionally, gametes, or sex cells, do not engage in mitosis but rather another kind of cell division called meiosis (5). (Hey, I managed to find a way to cram muscle and sex into this article; maybe this will broaden our appeal.)

Inside the nucleus are the 23 pairs of chromosomes. All of the cells in your body, with the exception of gametes (sperm or ova) (15) and mature red blood cells have identical chromosomes. What makes the difference between a brain cell and a muscle cell, for example, is not that cell's particular genetic material, but rather what genetic material is permitted to be expressed.

Chromosomes have specific regions called genes, which are arranged in linear fashion (14). It is estimated that among the 23 pairs of chromosomes, there may be 100,000 genes, or about 3,000 to 4,000 genes per chromosome (2). Genes are the basic unit of heredity, and a single gene contains the information, or instructions, for making one polypeptide (14). So, when we refer to genetic expression, we're really talking about what peptides (up to 4050 amino acids linked together) (6) or proteins (generally over 50 amino acids linked together) (6) are being produced. These peptide or protein products may serve as hormones, enzymes, or as structural materials based upon the amino acids present, which help determine the folding pattern and function of the protein (2).

Muscles mainly increase their size by an increase of the number of myofilaments, which increases the size and number of myofibrils within myofibers (9, 10, 12) (figure 2). When a muscle's growth slows, the cellular basis is that not enough contractile muscle protein is accruing at a sufficient rate to result in a net increase in the number of myofibrils, which are mainly comprised of the myofilament proteins actin and myosin. The concept of rate should be understood, because growth, or accretion, is about the struggle between two opposing forces, namely synthesis and degradation. For example, an increase in synthesis does not necessarily guarantee accretion if the synthesis reactions must compete with a concurrent increase in degradation. Such may be the case with many overtrained resistance trainees who may stimulate muscle protein synthesis but are awash in a flood of protein degradation. In this instance, the enhanced synthesis is masked by the enhanced degradation. On the other hand, an accretion of muscle can occur even without an increase in synthesis if degradation is decreased enough to allow synthesis to prevail.

So, if you're not overtraining and are doing everything else correctly, precisely why do your muscles go on strike? And, more importantly, can you cross the picket line? Before addressing these important issues, we first need to review a little more about basic genetics.

At the heart of the genetic code is DNA (deoxyribonucleic acid), of which genes, and therefore chromosomes, are made. DNA exists as a double helix, like the railings of a spiral staircase or a twisted rope ladder.

Incredibly, the total DNA from the 46 chromosomes in just one human cell nucleus is approximately one meter in length (4)! Obviously, the DNA strands must be very organized to pack into a very tiny nucleus that is less than a mere 10 micrometers (1/100,000 meters) in diameter (1) (figure 3).

Each of the 46 chromosomes is made of two strands of DNA. Each single lengthy molecule of DNA is coiled around an octet aggregate of globular proteins. This coiling results in what looks like a pearl necklace. Several of these beads pack together and are held in place by a protein scaffolding that ultimately yields that familiar chromosome structure that looks like the letter X or Y under a microscope (4). So, in an X chromosome, for example, the left half is one highly organized DNA molecule, and the right half another. You can think of a chromosome as two long stretches of DNA wound up tightly with some proteins and tied together near the middle. Together, the chromosomes and all the information they contain are collectively referred to as the genome (7).

To summarize the previous section, spans of DNA make up genes, and genes make up the chromosomes that are found in the nucleus. To quote author Richard Brennan (2): "The relationship of the various elements of a cell may be thought of as follows: The nucleus of a cell is the library containing life's instructions. The chromosomes would be the bookshelves inside the library, the DNA would be individual books on each shelf, genes would be the chapters in each book..." When muscle growth tapers off in the presence of a growth stimulus and absence of overtraining or malnutrition, it is because the gene expression pattern has been altered, affecting synthesis and degradation reactions so that a net myocytic size increase does not occur.

In part two of this article (see below references), we'll explore the actual mechanisms that may regulate the production of muscular growth and just how herculean you become.

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About the Author

Dr. Greg Bradley-Popovich holds dual master's degrees in Exercise Physiology and Human Nutrition from West Virginia University as well as a doctorate in Physical Therapy from Creighton University. He is the Director of Clinical Research at Northwest Spine Management, Rehabilitation, and Sports Conditioning in Portland, Oregon.

REFERENCES
1.Alcamo, I.E. (1994). Fundamentals of Microbiology. Redwood City, CA: The Benjamin/Cummings Publishing Company, Inc.
2.Brennan, R.P. (1992). Dictionary of Scientific Literacy . New York, NY: John Wiley & Sons, Inc.
3.Chabner, D. (1991). The Language of Medicine . Philadelphia, PA: W.B. Saunders Company.
4.Champe, P.C. & Harvey, R.A. (1994). Biochemistry. Philadelphia, PA: J.B. Lippincott Company.
5.Goodman, H.D., Emmel, T.C., Graham, L.E., Slowiczek, F.M., & Shechter, Y. (1986). Biology. Orlando, FL: Harcourt Brace Jovanovich.
6.Hein, M., Best, L.R., Pattison, S., & Arena, S. (1993). College Chemistry: An introduction to General, Organic, and Biochemistry. Pacific Grove, CA: Brooks/Cole.
7.Henrickson, R.C., Kaye, G.I., & Mazurkiewicz, J.E. (1997). NMS Histology. Baltimore, MD: Williams & Wilkins.
8.Johnston, B.D. & Chokan, W. (1998). I.A.R.T. Reference Manual (6th ed.). North Bay, ON: BODYworx.
9.MacDougall, J.D. (1986). Morphological changes in human skeletal muscle following strength training and immobilization. In N.L. Jones, N. McCartney, and A.J. McComas (Eds.), Human Muscle Power (pp. 269-288). Champagne, IL: Human Kinetics.
10.McComas, A.J. (1996). Skeletal Muscle Form and Function. Champaign, IL: Human Kinetics.
11.Mentzer, M. (1993). Heavy Duty. Venice, CA: Mike Mentzer.
12.Sherwood, L. (1993). Human Physiology: From Cells to Systems. St. Paul, MN: West.
13.Taylor, E.J. (Ed.). (1988). Dorland's Illustrated Medical Dictionary (27th ed.). Philadelphia, PA: W.B. Saunders Company.
14.Weaver, R.F. & Hedrick, P.W. (1995). Basic Genetics. Dubuque, IA: Wm. C. Brown Publishers.
15.Zubay, G. (1993). Biochemistry . Dubuque, IA: Wm. C. Brown Publishers.

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