Central Nervous System(CNS) Fatigue

brainThe realization that strength and power are mainly of neural origin was a breakthrough point in exercise physiology. What coaches and physiotherapists knew by experience for the last forty years is still a matter of debate in purely scientific circles. This is because the central nervous system is still an elusive, complicated largely uncharted area of the mammalian physiology. We do know bits and pieces of information that can be put together to form merely a coherent image that allows us to understand the etiology behind training, adaptation, fatigue and overtraining.

Anatomy of a nerve cell.

A nerve cell is the most advanced and delicate part of an organism. Their physiology and mechanism of action is interpreted by the synaptic theory which was a turning point in medical science.

A nerve cell is formed by four main parts. The dendrite, the soma, the axon and the axon terminal. In the central nervous system the dendrites are connected to the axon terminals of surrounding nerve cells which forms a neuronal grid, eventually some axons will leave the brain area and feed the periphery. The nerve cells are essentially electrochemical plants. They receive chemical information in the form of neurotransmitters, turn that into electric current, which travels through the axon and reaches the axon terminal which in term turns it back into neurotransmitters.

Essentially two (or more) nerve cells do not actually touch, they are close enough for neurotransmitters to travel fast and efficiently from one to another, this is because the body must somehow regulate the neural activity, that regulation is achieved through inhibition of neurotransmitters (though some nerve cells do communicate directly through voltage differentials). The area between two nerve cells is called the synaptic cleft; the area inside the axon terminal is called pre synaptic and the area in the dendrite post synaptic.

The pre synaptic area has two main mechanisms; it has voltage gate ion channels on the surface and within it has several “docking areas” called synaptic vesicles that contain neurotransmitters. When the action potential reaches the axon terminal it causes the voltage gate ion channels to open up allowing calcium ions to rush into the pre synaptic area and fuse with the synaptic vesicles which release their neurotransmitters. The neurotransmitters pass the cell membrane into the synaptic cleft and bind to the receptors found in the postsynaptic area. Causing another action potential, that will travel through the axon and reach the axon terminal etc. That being said it must be made clear that nerve cells have a certain threshold of voltage differential that excites them and also a specific time of response, thus it is not possible to excite a nerve cell with to small a stimulus or by very fast successive stimuli. For example, the feeling of pain cannot be initiated by a light touch, nor be transmitted by very fast blows to the same area, only the first will be felt, if the second is right after the first the nerve cell won’t be able to transmit the message. In muscle contraction the above procedure is heavily regulated, small electric impendence, in nerve cells and properly trained CNS can make muscle contractions more powerful. The total limit of muscle contractile frequency is the tetanic limit, where the muscle cramps.

When a neurotransmitter is released and accomplishes its purpose it returns to the synaptic cleft, there if left unattended it will bind with the post synaptic receptor again causing another action potential; this is regulated in two ways, either through a mechanism called neurotransmitter re uptake which is essentially a set of carrier proteins that carry the neurotransmitter into the pre synaptic vesicle or by degradation of the neurotransmitter by enzymes. This modulation ensures that the nerve cells elicit and receive the same level of excitement by action potentials each time, i.e. to avoid receptor degradation which could lead to impairment of the neuron.

From the brain to the neuromuscular junction.

Simply put, every conscious movement of the human body originates in the brain. A series of complex electrochemical reactions both cognitive and automatic causes the desired muscle to contract. This does not happen always in a direct and coherent way, a lot of muscles are involved even in the simplest of movements, either as agonists, antagonists or stabilizers receiving and transmitting electrical signals that are used to coordinate, propriosence and eventually apply force.

The movement is initially “formed” in the motor cortex, the part of the brain that is responsible for conscious movement. The motor cortex is divided in two part, the primary motor cortex that is responsible for the creation of the electrical impulses that will execute the movement and the secondary motor cortices which must interpret and utilize optical information regarding the movement, the proprioceptive activation or inactivation of the proximal-trunk muscles of the body and finally the planning of complex kinetic patterns that involve a large number of delicate movements.

When the movement is formed in the assigned pathways of the motor cortex it travels through specialized nerve cells called motor neurons, these originate in the brain and going through the spinal cord reach the muscles. There are two kinds of motor neurons, alpha efferent motor neurons and gamma efferent motor neurons, the former are responsible for innervating muscle fibers, the latter are connected within the muscle spindles, a proprioceptive mechanism that senses the stretch of a muscle.

The initial electrochemical reaction (called action potential) travels through the motor nerve axon, reaching a place called the neuromuscular junction; there it opens the voltage dependant calcium channels, enabling Ca2+ ions to travel from the extra cellular fluid into the motor neuron. The Ca2+ ions trigger a procedure called the “excitation contraction coupling” that in term releases the neurotransmitter acetylcholine into the synaptic cleft. Acetylcholine travels the synaptic cleft and binds to the nicotinic receptors found in the motor end plate. The receptors are also based on the movement of electrolytes, when excited by acetylcholine they allow sodium and potassium ions to travel in and out of the muscle cytosol causing an electrical differential on the end plate called end plate potential. This electrical differential spreads in the across the surface of the muscle fibers releasing calcium which finally initiates the muscle contraction.

This procedure is repeated as many time as needed (and possible) to create the desired movement. The excitatory effect of the neurotransmitter acetylcholine is inhibited by an enzyme called acetylcholinesterase. The body can regulate this by increasing the production of the enzyme peripherally or by decreasing the motor cortex ability to cause the release of acetylcholine in the first place. This is where the neural fatigue lies. The need for faster degradation of acetylcholine through enzymes can’t be localized but is systemic, ergo, all acetylcholine utilized in muscular movement must be degraded with an increased rate. That goes for smooth muscles too which are responsible for very primal procedures of the body. It is obvious that a total peripheral shutdown will result in death.

It is much safer to inhibit the initial reaction being formed in the CNS.

Clinical depression and overtraining.

Just like every other mechanism in the body, neural fatigue has a negative feedback loop. When the body is overstressed peripherally, the CNS inhibits its excitatory procedures causing a state of fatigue and recovery. The above procedure can be initiated for various reasons. Chronic stress and anxiety caused by a heavy psychological stimulus like the loss of a loved one, a chronic and persistent exposure to stressful environments like work, the use of certain medications and chemical compounds like anti depressants and CNS stimulants and finally the repeated overexposure to intense training. All those things have in common a continual over physiological release of adrenaline and noradrenalin, acetylcholine, dopamine, certain serotonin variables, corticosteroids and underproduction of GABA and serotonin.

When the body is chronically exposed to that kind of stimulation it will eventually engage the negative feedback loop to protect it self from total exhaustion and initiate healing. That procedure is more commonly known in psychiatry as depression. Depression is essentially a defense mechanism, and just like fever can be good for the body. If left unattended, or for various reasons “pushed through” it can become dangerous. Overtraining is very closely related to depression. Depression and overtraining are characterized by the underproduction, underutilization and efficient reuptake of excitatory neurotransmitters, and the overproduction of inhibitory neurotransmitters. The main neurotransmitter affected is dopamine which is involved in the pleasure, kinetic, motivation and reward pathways of the brain. This accompanied by reduction in serotonin utilization ends in a generalized feeling of dysphoria, lack of energy, motivation, power production, loss of pleasure, apathy and even pathological thought procedures (i.e. thoughts of escape or suicide).

This self inhibition happens with several methods, and depends on the reason it caused it in the first place as well as the time of exposure. For example cocaine inhibits the production of DAT a dopamine transporter protein resulting in an inability of clearance of dopamine from the synaptic cleft. The body initially reacts by overproducing DAT to reach homeostasis, when cocaine stops being administered the overabundance of DAT will clear dopamine more than was needed causing a depressed, fatigued state which most cocaine users refer to as “crash”. It will take several hours for the body to reach its previous state. If there is a chronic administration of cocaine the overproduction of DAT will not suffice because it will be continually inhibited by the drug. Thus, the body will react in a more permanent manner; it will reduce the post synaptic receptor density. There will be dopamine, but no where to bind to. It will, eventually, re normalize after discontinuing the drug use, but the manufacture of dopamine receptors is much more difficult so instead of a few hours it will take days, or even weeks. It is assumed that heavy abuse can cause permanent reduction in post synaptic receptor density causing the user inability to receive pleasure from anything else besides cocaine itself. This procedure is called long term depression.

Exercise causes a similar effect. The overproduction of dopamine (of which main metabolites are adrenaline and noradrenalin) that is involved in voluntary movements will eventually cause a self inhibition to protect peripheral tissue. The muscle trauma, and pain of exercise cause the production of natural painkillers endorphins which are sedatives. This as well as peripheral nutrient depletion and muscle acidosis cause the acute fatigue felt from exercise. More specifically, most power athletes can tell you that while low intensity high volume exercise such as tempo runs is tough and feels tiring you can recover from it very fast, within a few hours. On the other hand, high intensity exercise (short sprints, maximal weight lifts etc.) feels easy due to sparing the muscles from acidosis but can be exceptionally difficult to recover from. The exhaustion after high intensity exercise starts to set in 1-3 hours later, peaking after 6-8 and it takes the body more or less 48 hours to reach its previous state, and for exceptionally intense bouts of exercise (say a personal record at the 100m sprint, or in an Olympic lift) it can take up to ten days.

After high intensity exercise the feeling can be described as muscle tremors, fatigue, inability to perform high intensity movements even though there can be the mental will to do so, increased muscle tone, lethargy and in extreme cases even fever. This has very little to do with the actual ability of the muscles or the peripheral nervous system to perform, it is as previously said the reaction of the body to prevent excessive peripheral fatigue and to recover from the micro trauma caused by exercise. If the athlete pushes through this state either by using shear will of force or using stimulants and other ergogenic substances to mask the problem it will eventually cause long term depression, i.e. a more permanent CNS inhibition which is quite similar to depression. The symptoms of a severely over trained athlete are loss of performance, coordination, motivation to train and take care of himself, fatigue, muscle tremors and eventually proper depression. It is reported that severe overtraining can take months to be overcome. Most experienced coaches can gauge this by observing initially the form of exercise of the athlete, and later on by changes in personality and mental state. It should be noted that if an athlete actually reaches overtraining, any exercise of high intensity will just make it worse, and should be immediately ceased in order for the recovery process to begin.

The whole effect is obviously not limited to dopamine, or even all of the catecholamine family. Truth be told, the understanding of depression and brain neuronal plasticity is poorly understood and highly controversial. Pharmaceutical companies have been advertising SSRI’s (selective serotonin re uptake inhibitors – a class of drug commonly used in the treatment of depression) as the absolute cure for depression, dysphoria or simply bad mood while most neurophysiatrists claim that serotonin deficiency is not a factor (or may be one of many factors) that is involved in depression. Acetylcholine is also a CNS neurotransmitter heavily involved in learning and mood patterns, with excitatory effects in the CNS. What we do know is the final effect and the vague reasons for it, but the precise mechanisms are unknown.

Avoiding neural fatigue.

Some level of fatigue is to be expected from training, it is after all needed to maintain a proper slightly sub maximal level of training intensity, but it should be so low that it does not interfere with proper form and obviously lifestyle. The first line of defense is maintaining an adequate level of exposure to intensity. Even though it is always better to err on the under training side, in which case there is slow, or not optimal progress, instead of actually detraining if overtraining sets in. A strange fact is that inexperienced athletes cannot cause enough CNS fatigue through training to be over trained, while all exercise is on the upper limits of their CNS capability (but not potential) and it feels tiring they can recover from it fast, and perform in the same level almost continually even though they cannot sustain a large volume of training due to mechanical and energy reasons. In layman terms, someone who sprints the 100m in 13sec can do it every day for weeks; someone who sprints the 100m at 10sec can do it once in ten days, perhaps even less. As progression and adaptation occurs the athlete’s ability to perform a larger volume of exercise increases as well as his ability to excite his nervous system more. An interesting fact is that this cannot happen continually after some point, the athlete becomes so strong that he can cause harm to himself and the training volume should be reduced to compensate for the increase in intensity. This is a very common error for coaches that believe the quantity of training increases linearly with training age. After some point, the athlete ceases to progress which some coaches try to correct by increasing training volume which actually makes the problem worse, or rely on drugs to keep progressing which will eventually cause injury.

When the proper volume exercise is estimated there are several indirect ways to increase recovery and subsequently the quality and quantity of training. Conjugate training systems, where a state of slight fatigue is intentionally reached in mesocycles in order to be overcompensated during a deloading period have become exceptionally popular. Most if not all coaches follow some form of this even if it is merely the few days of tapering before a meet.

Contrast showers have been proven to be a very good (and cheap) way of recovery. A contrast shower is interchanging exposure to cold and hot water. Most commonly 1 minute of cold is followed by three minutes of hot for a total of three times. The prepuce here is the flushing vasolidating action that the heat contrast cause which speeds up the metabolism and removes training byproducts. For whatever reason it also helps with neural recovery, though the exact process is unknown, it is empirically undisputed.

Massage, sauna, proper nutrition, supplementation with vitamins and minerals also help with proper and efficient recovery, though they are not as available to armature athletes as contrast showers. They are invaluable and extensively studied tools of recovery for elite athletes that follow complex and perfectly timed programs of physiotherapy, nutrition and supplementation.

The use of stimulants, ergogenics, nootropics, and neuroprotectants.

Stimulants have been widely used in power sports as a pre competition performance booster and training aid. Even though they are banned from officials the search for a new unknown stimulant is everlasting. At this point most CNS stimulants cannot be used prior to competition because they can be easily detected. Cocaine, amphetamines (and their family), caffeine, β2 agonists, ephedrine are all banned. Thus there has been a shift of the usage of those compounds as training aids. Two major dangers underlie such use besides the obvious health risks. Stimulants (especially dopaminergic stimulants) mask the effects of exhaustion which can lead to severe overtraining over time. The second danger is the fact that stimulants if not dosed correctly can actually hinder performance by disturbing the motor unit firing patterns and causing antagonist muscles to counteract agonists. Stimulant use should always be monitored by medical personnel, regulated, be dosed at the low side and only if needed for plateau breakthroughs or especially important training sessions.

Ergogenics, such as anabolic androgenic steroids, are also in profound use among athletes. Their effects are largely undisputed but great care must be taken because most AAS (especially those that are heavily androgenic) can cause a dramatic increase in intensity, so much so that the recovery ability of the CNS cant keep up with it. There is a believe that during AAS administration an increase in training volume is mandatory, this is quite false, while there is an increased recovery ability this is countered by the shear intensity increase. Training with AAS should be exactly the same (if not more careful for experienced athletes) as without them. Several other compounds have been used, like insulin and EPO but these have little relevance with CNS recovery.

Neuroprotectants are a bold and relatively new area in chemically enhanced training. Human growth hormone, Insulin like growth factor, Nerve growth factors, inosin, L-dope and various nootropics medications such as piracetam are used to aid not only with recovery (which by all accounts is impressive) but also to aid in the learning of new skills. Certain reprecautions must be taken with the use of such compounds given the limited clinical experience there is with them. Definite protocols and methods of administration are still unknown. Experience and medical supervision are required given the fact that very few coaches and athletes will give out their secretes.




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