Training theory in the middle-distance events requires knowledge of biological adaptations and the work stimuli needed to achieve improvement of the body’s physiological functions. Much of this physiological knowledge is at the tissue level and involves understanding changes to the muscle fibers as they interact with neighboring fibers in organs that are called muscles.
Through running, the muscular work done against a progressively challenging overload leads to increases in muscle mass and cross-sectional area, and is referred to as hypertrophy. But why does a muscle cell grow and how does it grow? Although it has been an intense topic of research, scientists still do not fully understand the picture of how muscle adapts to gradually overloading stimuli.
Muscular hypertrophy is an increase in muscle mass and cross-sectional area. The increase in dimension is due to an increase in the size (not length) of individual muscle fibers. Muscle fibers are another name for any muscle cell. Not more fibers, just bigger fibers is the result of training. Both cardiac (heart) and skeletal (striated) muscle adapt to regular, increasing work loads that exceed the pre-existing capacity of the muscle fiber.
With cardiac muscle, the heart becomes more effective at pumping blood out of its chambers, (resource: heartrate training) whereas skeletal muscle becomes more efficient at transmitting forces through tendons and their attachments to bones of the skeleton. Both types of adaptations are necessary to improve middle-distance running performance.
Skeletal muscle has two basic functions in the activity of running; contraction to cause body movement, and to provide stability for body posture. Each skeletal muscle must be able to contract with different levels of tension to perform these functions. Progressive overload through increases in running intensity is a means of applying varying and intermittent levels of stress to skeletal muscle, thus making it adapt by generating comparable amounts of tension. The muscle is able to adapt by increasing the size and amount of contractile proteins, which comprise the myofibrils within each muscle fiber. This leads to an increase in the size of the individual muscle fibers and their consequent force production as the runner pushes off of the surface.
Understanding the physiology of skeletal muscle hypertrophy involves the role and interaction of satellite cells, immune system reactions, and growth factor proteins.
Satellite cells in the muscle are special muscle fibers that function to facilitate growth, maintenance, and repair of damaged skeletal (not cardiac) muscle tissue. These cells are termed satellite cells because they are located on the outer surface of the muscle fiber, in between the sarcolemma and basal lamina (uppermost layer of the basement membrane) of the muscle fiber. Satellite cells have one nucleus, which constitutes most of the cell volume. Usually these cells are dormant, but they become activated when the muscle fiber receives any form of trauma, damage, or injury, such as from running training overload.
The satellite cells then proliferate or multiply, and the daughter cells are drawn to the damaged muscle site. They then fuse to the existing muscle fiber, donating their nuclei to the fiber, which helps to regenerate the muscle fiber. It is important to emphasize the point that this process is not creating more skeletal muscle fibers, but increasing the size and number of contractile proteins (actin and myosin) within the muscle fiber (Photograph 1).
Photograph 1. The symmetry of the actin and myosin filaments on the left photograph before an intense interval session and the damage to the filament symmetry on the right photograph following the training session as seen through muscle biopsy studies.
The number of satellite cells present within a muscle depends on the type of muscle. Type I or slow-twitch oxidative fibers, tend to have a five to six times greater satellite cell content than Type II (fast-twitch fibers), due to an increased blood and capillary supply. This may be due to the fact that Type 1 muscle fibers are used with greatest frequency, and thus more satellite cells may be required for ongoing minor injuries to muscle.
Training in the middle-distance events causes trauma to skeletal muscle on a regular basis. The immune system responds with a complex sequence of immune reactions leading to inflammation. The purpose of the inflammation response is to contain and repair the damage, and to clean up the injured area of waste products. (Related: Dealing with Common Running Injuries.)
The immune system causes a sequence of events in response to the injury of the skeletal muscle. Macrophages, which are involved in phagocytosis (a process by which certain cells engulf and destroy microorganisms and cellular debris) of the damaged cells, move to the injury site and secrete cytokines, growth factors, and other substances.
Cytokines are proteins which serve as the directors of the immune system. They are responsible for cell-to-cell communication. Cytokines stimulate the arrival of lymphocytes, neutrophils, monocytes, and other healer type cells to the injury site to repair the injured tissue. This could take days to occur depending on the strength of the training stimuli.
The three important cytokines relevant to muscle damage from intense middle-distance training are: Interleukin-1 (IL-1), Interleukin-6 (IL-6), and tumor necrosis factor (TNF). These cytokines produce most of the inflammatory response, which is the reason they are called the “inflammatory or pro-inflammatory cytokines”. They are responsible for protein breakdown, removal of damaged muscle cells, and an increased production of prostaglandins (hormone-like substances that help to control the inflammation).
Growth factors are highly specific proteins, which include hormones (HGH) and cytokines that are involved in muscle hypertrophy. Growth factors stimulate the division and differentiation (acquisition of one or more characteristics different from the original cell) of a particular type of cell. In regard to skeletal muscle hypertrophy, growth factors of particular interest include insulin-like growth factor (IGF), fibroblast growth factor (FGF), and hepatocyte growth factor (HGF). These growth factors work in conjunction with each other to cause skeletal muscle hypertrophy. Human growth hormones are secreted naturally in the body, but injections of additional HGH into athletes motivated to cheat have become more common.
Related Article: Recovery, Regeneration and Rest
Insulin-like growth factor is a hormone that is secreted by skeletal muscle. It regulates insulin metabolism and stimulates protein synthesis. There are two forms, IGF-I, which causes proliferation and differentiation of satellite cells, and IGF-II, which is responsible for proliferation of satellite cells. In response to progressive overload resistance exercises like running, IGF-I levels are substantially elevated, resulting in skeletal muscle hypertrophy.
Fibroblast growth factor is stored in skeletal muscle. FGF has nine forms, five of which cause proliferation and differentiation of satellite cells, leading to skeletal muscle hypertrophy. The amount of FGF released by the skeletal muscle is proportional to the degree of muscle trauma or injury.
Hepatocyte growth factor is a cytokine with various different cellular functions. Specific to skeletal muscle hypertrophy, HGF activates satellite cells and may be responsible for causing satellite cells to migrate to the injured area.
The force generated by a muscle is dependent on its size and the muscle fiber type composition. Skeletal muscle fibers are classified into two major categories; slow-twitch (Type 1) and fast-twitch fibers (Type II). The difference between the two fibers can be distinguished by metabolism, contractile velocity, neuromuscular differences, glycogen stores, capillary density of the muscle, and the actual response to hypertrophy.
Type I muscle fibers, also known as slow twitch oxidative muscle fibers, are primarily responsible for maintenance of body posture and skeletal support. The soleus is an example of a predominantly slow-twitch muscle fiber. An increase in capillary density is related to Type I fibers because they are more involved in endurance activities. These fibers are able to generate tension for longer periods of time. Type I fibers require less excitation to cause a contraction, but also generate less force. They utilize fats and carbohydrates better because of the increased reliance on oxidative metabolism (the body’s complex energy system that transforms energy from the breakdown of fuels with the assistance of oxygen). Type I fibers have been shown to hypertrophy considerably due to progressive running overload.
Type II fibers can be found in muscles which require greater amounts of force production for shorter periods of time, such as the gastrocnemius and vastus lateralis. Type II fibers can be further classified as Type IIa and Type IIb muscle fibers.
Type IIa fibers, also known as fast twitch oxidative glycolytic fibers (FOG), are hybrids between Type I and IIb fibers. Type IIa fibers carry characteristics of both Type I and IIb fibers. They rely on both anaerobic and oxidative metabolism to support contraction. With resistance training as well as endurance training, Type IIb fibers convert into Type IIa fibers, causing an increase in the percentage of Type IIa fibers within a muscle. Type IIa fibers also have an increase in cross sectional area resulting in hypertrophy with resistance exercise. With disuse and atrophy, the Type IIa fibers convert back to Type IIb fibers.
Type IIb fibers are fast-twitch glycolytic fibers (FG). These fibers rely solely on anaerobic metabolism for energy for contraction, which is the reason they have high amounts of glycolytic enzymes. These fibers generate the greatest amount of force due to an increase in the size of the nerve body, axon and muscle fiber, a higher conduction velocity of alpha motor nerves, and a higher amount of excitement necessary to start an action potential. Although this fiber type is able to generate the greatest amount of force, it is also maintains tension for a shortest period of time (of all the muscle fiber types).
Type IIb fibers convert into Type IIa fibers with resistance exercise. It is believed that resistance training causes an increase in the oxidative capacity of the strength-trained muscle. Because Type IIa fibers have a greater oxidative capacity than Type IIb fibers, the change is a positive adaptation to the demands of increasing running intensity.
Training Resource: Scott Christensen’s Entire Training Model for High School Middle Distance
Muscular hypertrophy is a multi-dimensional process, with numerous factors involved. It involves a complex interaction of satellite cells, the immune system, growth factors, and hormones within the individual muscle fibers of each muscle. It is up to the middle-distance coach to prescribe the proper stimulus to elicit the most appropriate response in order to achieve the desired and on-going degree of muscular development.
Scott Christensen is the head track coach at Stillwater Area High School in Oak Park Heights, MN.