Metabolic fatique

Overload on muscle base can cause muscle fiber damage or metabolic fatique, like fuel exhaustion, Ca⁺⁺ outburst into the muscle or building intramuscular hydrogen ions(pH).

Usually metabolic overload mechanisms appear during extended submaximal phase or intensive repeated short exercise. Complex muscle contraction cycle is intaked by neural impulse that depolarizes surface membrane of muscle station, which result is action potential(electrocharge), which is transferred to muscle fiber later. After that there is a whole series of events where Ca⁺⁺  is connected to protein fibers(actine and myosin) which results by contractional tension.

Functional side of fatique is relation between stimulus and contraction, which results by intensity decrease of these two processes, or by sensibility decrease on activations. Changes in circulation of Ca⁺⁺  ions influents stimuli operation and contraction. Researchers came to the fact that lactic acid raise in blood and muscles affect negatively to medium or long-lasting performance and their assume is that is the word about causal connection between local muscles fatique and lactic acid accumulation. Increased acidose or lactic fatique, for which is thought to determine exhaustion point, can weaken mechanical processes included into muscle contraction in four possible ways:

1)      Accumulation of hydrogen ione influents positive energy production(ATP), by stopping phosphofructokynase(PFK), enzyme that limits the speed of aerobic glycolyse. Activities of other enzymes, like lactic dehydrogenesis(LDH), phosphorilasis and myosin-ATPase are also limited

2)      Increased acidose decreases the oxygen ability to connect haemoglobine. Moreover, to stop eventual low rate of oxygen on the muscle station, during its transport through capilars haemoglobine will release even more oxygen.

3)      Increased acidose competes with troponine for connective places, by stopping connecting of Ca⁺⁺  for troponine. Cause troponine is very important factor at muscle station contraction, its relative inactivity can explain connection between fatique and exercise. Ca⁺⁺  dropping also does that heart muscle is more sensitive than skeletal muscle, which probably explains why it has such a pressure on contractibility during acidose. Increased concentration of hydrogen ions stops Ca⁺⁺    releasing from sarcoplasmatic reticulum.

4)      Hydrogen iones accumulation creats discomfort, which can be limiting factor in psychological fatique and supercompensation.

From energy composition view, fatique appears when it comes to creatine-phosphate exhaustion in working muscle, when muscle glycogen is spared, and when carbohydrate amounts are exhausted. Obvious result is work dropping, maybe because ATP in muscle to which glycogen storage is emptied produces with lower speed than spending. Expertises show that carbohydrates are crucial for muscle ability to maintain high force. Also, endurance capacity, during longer moderate to high body activity, is related to amount of glycogen in muscle before exercise. That shows that fatique is shown as a result of muscle glycogen consumption.

At high intensity activity, but short term, energy substrates for muscle contraction are ATP and CP. Completely emptying of these sources would surely limit muscle ability to contract.

At long-lasting submaximal work free fat acids and glucose secure energy. Liver serves high amount of glucose. Limiting of free fat acids(through beta-receptors block) can increase the speed of glycogen decrease, which influents performance.

Oxidation relies on oxygen availability which in limited amount oxydates carbohydrates instead of free fat acids.  Maximal oxidation of free fat acids is though determined by the flow of free fat acids into operating muscle and aerobic training athletes status, cause aerobic training increases availability of oxygen and power of free fat acids oxidation.

Metabolic processes, like hypoxion(limited oxygen delivery into working muscle), which results by changed ion concentration amount, ATP lowering and lactic acid accumulation; can explain muscle damage. However, evidences show that it comes to bigger structural damage when muscle is the subject of repeated eccentric or concentric load. Eccentric contractions product more tension for the area of active muscle cross section, than concentric contractions. Though eccentric contractions product bigger structural loads, it has to be a lot of stress tension in repeated contractions to cause the stoppage in tension of muscle fiber. Only then it will come to rupture of muscle fibers structural components.

Model from the area of material fatique can show why is the most effective way contractions repeating. Material that is the subject of alternating excess and compression or relaxation will fail with time. Speed of exhange determines how fast material will fatique. For the most elastic materials, for fail is important the relation between stress and number of power changing cycle. So, as stress increases, number of cycles till failure decreases, We can also apply this access to muscle fibers that are constantly the subject of work that easily overtakes the power of muscle structural elements.

Heat increases muscle contractions by increasing of muscle fibers sensitivity on Ca⁺⁺   actions. That is the reason why athletes shouldn’t go without warm-up before activity. Some evidences say that heat in muscle during muscle contractions can lead to muscle damage. Eccentric muscle contractions generate more thermal energy than concentric muscle work. During concentric muscle contraction probably comes to heat increase due to decreased muscle ability to remove heat, and not due to high production heat speed inside of muscle station. Raise of intermuscular temperature explains 18% higher speed of lipids and proteins structural degradation. That happens more often with negative than with positive contractions. Speed in which contractions are made also influents heat production.

Stop of structural muscle components often leads to microtrauma. Discomfort isn’t starting in the moment, but reaches its peak in 24-72 hours. For example, pain of muscle brachioradialis is ranked with 1=normal – 10= extremely painful. Measure is done before eccentric exercise of muscle brachioradialis and then five days after exercise. Feeling that is often revived by athletes is boring dull pain combined with localized sensitivity and stiffness. These feelings are decreased inside 5-7 days after initial training. Example, this is one of variances how pain should develop – day 1- 1, day 2- 5,5, day 3- 6,4, day 4- 6,5, day 5- 4,5, day 6- 4.

During muscle work force is transferred to the bones through tendons. Fibers directly to muscle-tendon connections that form tendon tissue are oriented on wavy, but scarpy way, which leaves them vulnerable to high eccentric exercise tension. These fibers are also less elastic than muscle tissue, which is one more reason to be more accessible to injuries and localized pain.

Wavy configuration will disappear on tendon stretched 4% of its length in rest phase. 4-8 percentage of colagene fybers will slide each other once small ruptures appear inside of basic fibers. If tendon is stretched 8-10% of its length for the time of rest, consequently more fibers will be damaged. Damages appear on the weakest link of tendon. Damaged tendons can be the consequence of following conditions:

• Contraction done too fast. Explosive movement.
• Contraction done sideline.
• Tendon is under tension before load.
• Attached muscle is maximally innervated(under nerves influence). Muscle group around knee tendon is highly innervated, which makes it more reliable to injuries.
• Muscle group is stretched by outer stimulus.
• Tension is the consequence of eccentric movements.
• Tendon is weak compared to muscle.

Damaged tendons need a lot of time for regeneration. Researches say that it is due to limited blood flow in that part of muscle.

For years, lactic acid was emphasized as a factor for muscular pain. Through sophisticated chemical tests and electronic microscopes, researchers found that muscle pain is actually caused by muscle fibers damage as a consequence of Ca⁺⁺  ione in muscle station.

Fast-hitch and slow-hitch fibers are subjected to muscle damages caused by training. However, it was shown that bigger damages are in fast-hitch fibers, primarily during eccentric and maximally concentric force outgoing. Though there is no clear explanation for that difference, we can prescribe it to the contraction type, activity intensity, motor patterns of recruitment or structural differences that exist between two sets of muscle fibers.

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