Neuro-muscular fatique

Numerous evidences are telling us that central nervous system can be included into performance limitation in a lot bigger measure than it was thought earlier. Fatique can include various processes that are related to CNS commands or peripheral mechanisms. CNS fatique(long-term overtrainness) causes motivation falling, weakened transmission along spinae and weakened regrutation of motor neurons. Peripheral fatique(short-term overtrainness) can include weakness in the function of peripheral nerves, neuro-muscular connections, muscle fibers electrical activity or activation process inside of muscle fibers.

Peripheral fatique can be divided into two groups: high frequency fatique(electromechanic fatique) and low frequency fatique(mechanic-metabolic fatique).

The greatest fatique conditions in soccer are neural factors, ATP-CP mechanism exhaustion and lactic acidose.

Fatique	Features	Mechanisms
CNS	force or warm generated by voluntary excess lower than electric stimulation	Failure to maintain power or frequency of motor units
Peripheral	Same loss of force or heat generation caused by voluntary and stimulated contractions
a. High frequency	Selective force loss of high stimulation frequencies	Weakened neuro-muscular transmission of muscle actions potential
b. Low frequency	Selective force loss of low stimulation frequencies	Weakened irritability/ contraction

High frequency fatique is usually appeared in the sports that last less than 60 seconds or little bit more than 60 seconds. Outer force drops as a result of action potential failure(muscle membrane ability to electrolyte electric signals) along surface membrane(sarcolemma) of muscle station. Sarcolemma helps with electric signals transmission into holes on the surface of muscle station(T-tubes) and on individual actin and myosin fibers. Impossibility to spread electric signals(potentials of action) is due to potassium agglomeration in T-tubes and space between actin and myosin fibers. This fatique is shown in cold muscles, muscles that are not properly heated.

Low frequency fatique is primarily caused by station damages, specially connected to irregular contractions. Station damage leaves muscle station in the condition of chaos. Station structure damages that transmit electrosignals look like worn wires. As a consequence, electrosignals are weak.

CNS has two processes – stimulus and inhibition. Stimulus is wishful stimulating process for body activity. Inhibition is limiting process. Training changes these two processes over and over. At any stimuli CNS sends neural impuls to working muscle by ordering to make contraction and do the work. Speed, power and frequency of neural impulses are dependant of CNS condition. When controlled stimulus overcomes, neural impulses are the most effective, which is shown by good performance. When, as a fatique result, neural station is in the condition of inhibition, muscle contraction is weak and slow. So, the power of contraction and number of motor units(muscle fibers) that are directly included, are related to electric activation that is sent by CNS. Neural station working capacity cannot be maintained for long. If athlete maintains big intensity, neural station keeps the inhibition condition to protect from outer stimuli. Once when came in that condition, neural station isn’t responding in the same rate of activation. Force generated by working muscle decreases cause some neural stations decrease its warming speed a lot before the threshold value. That decreases number of included motor units.

If coach would neglect needs to change days of high intensity training with days of low intensity training, new intensive stimuli would result with exhaustion where neural station is in the inhibition stadium. While in that condition, performance is worser. Emotional problems are related to  that type of behaviour. In the end, training continuation under that amount will result with overtrainness, when athlete is completely out of form.

Fast-hitch, fast glycolitic and fast oxidative glycolitic fibers are a lot more sensitive to fatique than slow-hitch fibers. Fast-hitch fibers have huge potential for fast return of Ca⁺⁺ ion and ATP-CP related to muscle contraction and for ATP-CP production through anaerobic processes. However, slow-hitch fibers have higher aerobic potential that is shown by bigger mioglobuline and mitochondrial enzyme amount of activity. 

Few weeks	Normal amount of fatique that doesn’t stop supercompensation
2 weeks	Increased capacity of fatique tolerance. Adaptation reactions created.
1-2 weeks	Acute amount of fatique. Rest periods insufficient for compensation.
1 week	Athletes rely on motivation to win the fatique pressure.
1 week	Inhibition, improper neural activation on outer stimulus, performance starts to fall
1 week	Pressure to continue from coach, coplayers, family and competitive schedule
2 weeks	Inhibition of protection. Neural station protects from further stimuli. Performance falls. Injuries liability.
1 week	Athletes use the last sources of power and will to continue training.
2 weeks	Overtrainness. Athletes are out of form. Emotional problems. Injuries.

Skeletal muscle develops the force progressively, by activating motor units and regulating its working frequency that is progressively increased to achieve outer force. Slow-hitch muscle fibers are included according to the size of their neuro-musclular units and according to their dominant aerobic metabolism. When force demand is increased, fast oxidative glycolitic fibers become bigger, after that fast glycolitic fibers occur, and they can generate the size of force.

Fatique that inhibits muscle activity can be neutralized by adjustment strategy with the power of motor units to exchange work frequency. Muscle can more effectively keep the force under determined fatique condition. But, if lasting of continuos muscle contraction is longer, work frequency of motor units will decrease, in order to increase inhibition.

Some researches are saying that, compared to beginning of work, and maximal voluntary contraction of 30 seconds, in the end work frequency drops 80%!!!

This should warn the ones that promote theory that force can be promoted only by working every set to the exhaustion. The fact is that work frequency is dropping parallel with contraction progression, discredits theory of every exhaustion set. As the contraction progresses, fuel reserves are becoming lower and lower, which results by longer relaxation time of motor unit and decreased frequency of muscle contraction. Assume is that condition for that type of behaviour is fatique, so experts should be warned on short rest periods. Standard 2 minutes between two sets of maximal contraction are insufficient to regenerate neuro- muscular system to achieve high activation in next sets.

"Periodization, theory and methodology of training", Tudor Bompa