by Piotr Drabik
Coaches and athletes need to know what fatigue is to understand all issues of the training process.
The whole training process is predicated on fatigue and on recovery from it—the changes of training load, means of recovery, frequency and sequence of exercises and workouts, periodization, and nutrition. Without understanding fatigue it is not possible to understand all these issues as well as the upsides and downsides of different supplements.
Fatigue is a decreased effort capacity of a body, or part of it, resulting from exertion or excessive stimulation. There are several types of fatigue: mental (boredom), sensory (a result of intense activity of one or more of the senses), emotional (a consequence of intense emotions, observed after performance at important sports competitions, or after executing movements that demand overcoming fear), and physical (caused by muscle work). While workouts cause all types of fatigue (in various degrees) the most obvious is physical fatigue. Physical fatigue directly affects the function and structure of the musculoskeletal system and muscle fatigue is its main component.
Muscle fatigue is any reduction in force-generating capacity of the involved parts of the neuromuscular system.
For the last 150 years the nature and mechanism of fatigue were the objects of a great number of studies. Fatigue in a voluntary muscular effort is a complex phenomenon influenced by central nervous system factors and peripheral factors, such as damage to muscle cells. According to the latest scientific data, the two main factors causing muscle fatigue are mechanical damage and chemical damage to muscle cells. There is strong evidence to suggest a relationship between physicochemical damages and exercise-induced muscle soreness.
Mechanical damage is caused by mechanical stress.
Mechanical damage is most likely to occur when the vector of force acting on a muscle fiber (muscle cell) is not parallel to the long axis of this muscle fiber. This is usually the case because of the way muscle fibers are arranged in most muscles. (And indeed, hardly anyone has gotten strained or sore muscles of one’s arms, for example, by merely holding heavy weights with the arms hanging straight down. This is because in such a position the majority of muscle fibers lie parallel to the line of force and the angles of those that are not parallel are very acute.)
Mechanical stress destroys partially or completely three types of structures in the muscle cell: membranes, myofibrils, and the cytoskeleton.
Membranes (cellular membrane, mitochondrial membranes, nuclear membrane, sarcoplasmic reticulum membrane, lysosomal membrane, and more) separate various processes going on within the cell, and when the membranes are damaged the molecules mix and all cell functions are impaired.
Myofibrils are the contractile elements of muscle cells, responsible for muscle action, whether concentric, static, or eccentric. They are built of long, thin proteins that are easy to tear. When its myofibrils are destroyed, a muscle cell cannot contract.
The cytoskeleton is the internal scaffolding of the cell. Among its many functions, the cytoskeleton gives shape to the cell, and in the case of muscle cells transmits forces generated by the myofibrils. When the cytoskeleton is damaged the end effect is the same as destroying myofibrils–the cell cannot contract.
The more intense the effort, the bigger is the number of destroyed muscle cells.
Chemical damage is caused by oxidative stress—the overproduction of oxygen-derived free radicals. Oxidative stress damages all the structures of the cell as well as enzymes and nucleic acids that store and pass genetic information.
Free radicals are oxygen metabolites with unpaired electrons that are highly reactive. Examples of free radicals are superoxide and hydroxyl. Their unpaired electrons make the free radicals extremely reactive, being capable of interacting with various organic molecules-building blocks of cells–(proteins, lipids, and nucleic acids that comprise the genetic material of living cells and regulate all cell activity) and interfering with their structure and metabolism.
Though most of these radicals are inactivated by naturally occurring products of the body, a certain fraction escapes the cellular defense systems and may react with cellular components.
Exercise leads to an increase in the free radicals produced, and the following lipid peroxidation* provokes changes in all biological membranes. Their fluidity changes, thus reducing the ability to communicate with other cells. So does their integrity, which causes the dissolution of the cell.
Proteins are the most important components of all living species. They are the constituents of enzymes, receptors, and structural building blocks. All cellular proteins are endangered by free radicals, which cause cascades of changes that severely impair cellular metabolism.
It has been shown that exercising to exhaustion increases DNA damage in white blood cells of untrained subjects. Moderate exercise of intensities below the anaerobic threshold shows no such effects. Supplementation with the antioxidant vitamin E prevents exercise-induced DNA damage. Adaptation to exercise (being in good shape) seems to reduce free radicalassociated effects, such as DNA damage.
Many indicators of muscular damage caused by oxygen radicals are restored to normal in the after-effort recovery period. Even well-trained individuals after a bout of hard exercise display indicators of both damage and repair.
Other causes of fatigue
Apart from mechanical and chemical damages, which are the two major factors causing fatigue, there are some additional changes that contribute to muscle fatigue. They are the consequences of or a background for physicochemical damages.
Muscle performance declines during prolonged and intense activity—the force and velocity of contractions are reduced and time needed for relaxation is increased (meaning that muscles do not relax as rapidly after a contraction as they do when not fatigued). The changes in metabolites (particularly H+, Ca²+, and ATP**) lead to the observed changes in force, contraction, and relaxation.
It is generally stated that muscle H+ accumulation may contribute to fatigue during intense exercise. According to the latest research results, however, the changes in pH (an indicator of H+ concentration in a solution) may have little or no role in the loss of force production associated with muscle fatigue.
During fatigue, the sarcoplasmic reticulum (SR), an organelle which is a cellular calcium reservoir, undergoes basic changes. The Ca²+ uptake and Ca²+-ATPase activity of the SR are depressed in the fatigued muscles, thus reducing calcium reuptake by the SR and increasing the binding of calcium by calcium-binding proteins (and altering, in that way, the functions of these proteins, which impairs the cellular metabolism). These changes likely result in altered force production and energy consumption by the intact muscle.
The cellular processes contributing to fatigue may also lead to decreased force or power output due to an insufficient rate of neurotransmitter (acetylcholine) synthesis in the synapses and a reduced rate of ionic pumps function in cellular membranes of both muscle cells and nerve cells. The information about molecular changes induced by mechanical damage, chemical damage, and the other changes is sent to the brain via pain receptors and makes a person feel muscle soreness or pain.
Pain receptors are free nerve endings within the tissue that are excited by chemical, mechanical, and thermal stimuli. In health, pain informs of damage and so is a part of the body’s defense against injury. The stimuli that excite pain receptors are signals to the brain indicating damage. Substances released from damaged muscle cells include bradykinin, histamines, prostaglandins, excess potassium ions, serotonin, and proteolytic enzymes.
Apart from the cellular changes characteristic to muscle cells, fatigue seems to be connected with other important type of cells, namely neurons.
Relatively little attention has been placed on the role of the central nervous system (CNS) in fatigue during exercise. Several biological mechanisms have been proposed to explain CNS fatigue. Hypotheses have been developed related to several neurotransmitters including serotonin (5-HT—5-hydroxytryptamine), dopamine, and acetylcholine. The most prominent one involves an increase in 5-HT activity in various brain regions. Good evidence suggests that increases and decreases in brain 5-HT activity during prolonged exercise hasten and delay fatigue, respectively, and nutritional manipulations designed to reduce brain 5-HT synthesis during prolonged exercise improve endurance performance.
Other neuromodulators that may influence fatigue during exercise include cytokines and ammonia. Increases in several cytokines have been associated with reduced exercise tolerance associated with acute viral or bacterial infection. Accumulation of ammonia in the blood and brain during exercise could also negatively affect the CNS function and thus contribute to fatigue because impaired CNS function worsens coordination.
In conclusion, muscular fatigue is caused by many factors. Mechanical damage and chemical damage are the major factors, however. The role of each factor depends on the kind of exercise, individual characteristics, and external conditions.
* Lipid peroxidation may be defined as oxidative deterioration of lipids by free radical reactions.
** ATP by its very presence (in addition to its role as an energy carrier) is needed for relaxation of muscles. Without ATP, myosin crossbridges are stuck to actin and cannot move. This lack of ATP is the cause of rigor mortis.
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