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11. 6. 2012.

Fatigue and its causes

What exactly is the meaning of the term fatique during exercise? Sensations of fatique are markedly different when a person is exercising to exhaustion in events lasting 45 to 60s, such as the 400m run, than during prolonged exhaustive muscular effort, such as marathon running. Therefore it is not surprising that the causes of fatique to describe decrements in muscular performance with continued effort accompanied by general sensations of tiredness. An alternative definition is the inability to maintain the required power output to continue muscular work at a given intensity. To distinquish fatique from muscle weakness or damage, one can think of fatique as being reversible by rest.
Ask most exercisers what causes fatique during exercise, and the most common answer involves two words: lactic acid. Not only is this common misconception an oversimplification, but there is mounting evidence that lactic acid may actually have beneficial effects on exercise performance!

Fatique is an extremely complex phenomenon. Most efforts to describe underlying causes and sites of fatique have focused on:

  • Energy delivery( ATP-PCr, anaerobic glycolysis, and oxidation);
  • Accumulation of metabolic by-products, such as lactate and H+;
  • Failure of the muscle fiber’s contractile mechanism;
  • Alterations in the nervous system.



The first three causes occur within the muscle itself and are often referred to as peripheral fatique. Changes in the nervous system may cause central fatique. None of these alone can explain all aspects of fatique, and several causes may act synergistically to cause fatique. Fatique is rarely caused by a single factor but typically by multiple factors acting at multiple sites. Mechanisms of fatique depend on the type and intensity of the exercise, the fiber type of the involved muscles, the subject’s training status, and even his or her diet. Many questions about fatique remain unanswered, especially about cellular sites of fatique within the muscle fibers themselves.



Energy systems and fatique



The energy systems are an obvious area to explore when one is considering possible causes of fatique. When we are well fatiqued, we often express this by saying:” I have no energy.” But this use of term energy is far removed from its psychological meaning.



PCr depletion



Recall that PCr depletion is used under anaerobic conditions, such as short-term high-intensity effort, to rebuild ATP as it is used and thus maintain ATP stores within the muscle. Biopsy studies of human thigh muscles have shown that during repeated maximal contractions, fatique coincidences with PCr depletion. Although ATP is directly responsible for the energy used during such activities, it is depleted less rapidly than PCr during muscular effort because ATP is being produced by other systems. But as PCr is depleted, the ability to quickly replace the spent ATP is seriously hindered. Use of ATP continues, but the ATP-PCr system is less able to replace it. Thus, ATP levels also decrease. At exhaustion, both ATP and PCr may be depleted. It now appears that Pi, which increases during intense short-term exercise because of the breakdown of PCr, is a potential cause of fatique in this type of exercise.

To delay fatique, the athlete must control the rate of effort through proper pacing to ensure that PCr and ATP are not prematurely exhausted. This holds true even in endurance-type events. If the beginning pace is too rapid, available ATP and PCr concentrations will quickly decrease, leading to early fatique and an inability to maintain the pace in the event’s final stages. Training and experience allow the athlete to judge the optimal pace that permits the most efficient use of ATP and PCr for the entire event.



Glycogen depletion



Muscle ATP concentrations are also maintained by the aerobic and anaerobic breakdown of muscle glycogen. In events lasting longer than a few seconds, muscle glycogen becomes the primary energy source for ATP synthesis. Unfortunately, glycogen reserves are limited and are depleted quickly. Since the muscle biopsy technique was first established, studies have shown a correlation between muscle glycogen depletion and fatique during prolonged exercise.

As with PCr use, the rate of muscle glycogen depletion is controlled by the intensity of the activity. Increasing the intensity results in a disproportionate decrease in muscle glycogen. During sprint running, for example, muscle glycogen may be used 35 to 40 times faster than during walking. Muscle glycogen can be a limiting factor even during mild effort. The muscle depends on a constant supply of glycogen to meet the high energy demands of exercise.

Muscle glycogen is used more rapidly during the first few minutes of exercise than in the later stages, as seen in figure below. The illustration shows the change in muscle glycogen content in the subject’s gastrocnemius(calf) muscle during the test. Although the subject ran the test at a steady pace, the rate of muscle glycogen metabolized from the gastrocnemius was greatest during the first 75 min.




The subject also reported his perceived exertion(how difficult his effort seemed to be) at various times during the test. He felt only moderately stressed early in the run, when his glycogen stores were still high, even though he was using glycogen at a high rate. He did not perceive severe fatique until his muscle glycogen levels were nearly depleted. Thus, the sensation of fatique in long-term exercise conincides with a decreased concentration of muscle glycogen, but not with its rate of depletion. Marathon runners commonly refer to the sudden onset of fatique that they experience at 29 to 35 km(18-22 mi) as “hitting the wall”. At least part of this sensation can be attributed to muscle glycogen depletion.



Glycogen depletion in different fiber types



Muscle fibers are recruited and deplete their energy reserves in selected patterns. The individual fibers most frequently recruited during exercise may become depleted of glycogen. This reduces the number of fibers capable of producing the muscular force needed for exercise.

This glycogen depletion is illustrated in the figure below, which shows a micrograph of muscle fibers taken from a runner after a 30km(18.6 miles) run. Figure a has been stained to differentiate type I and type II fibers. One of the type II fibers is circled. Figure b shows a second sample from the same muscle, stained to show glycogen. The redder(darker) the stain, the more glycogen is present. Before the run, all fibers were full of glycogen and appeared red(not depicted). In figure b(after the run), the lighter type I fibers are almost completely depleted of glycogen. This suggests that type I fibers are used more heavily during endurance exercise that requires only moderate force development, such as the 30km run.




The pattern of glycogen depletion from type I and type II fibers depends on the exercise intensity. Recall that type I fibers are the first fibers to be recruited during light exercise. As muscle tension requirements increase, type IIa fibers are added to the workforce. In exercise approaching maximal intensities, the type IIx fibers are added to the pool of recruited fibers.



Depletion in different muscle groups



In addition to selectively depleting glycogen from type I or type II fibers, exercise may place unusually heavy demands on select muscle groups. In one study, subjects ran on a treadmill positioned for uphill, downhill, and level running for 2h at 70% of VO2max. Figure below compares the resultant glycogen depletion in three muscles of the lower extremity: the vastus lateralis(knee extensor), the gastrocnemius(ankle extensor), and the soleus(another knee extensor).




The results show that whether one runs uphill, downhill, or on a level surface, the gastrocnemius uses more glycogen than does the vastus lateralis or the soleus. This suggests that the ankle extensor muscles are more likely to become depleted during distance running than are the thigh muscles, isolating the site of fatique to the lower leg muscles.



Glycogen depletion and blood glucose



Muscle glycogen alone cannot provide enough carbohydrate for exercise lasting several hours. Glucose delivered by the blood to the muscles contributes a lot of energy during endurance exercise. The liver breaks down its stored glycogen to provide a constant supply of blood glucose. In the early stages of exercise, energy production requires relatively little blood glucose; but in later stages of an endurance event, blood glucose may make a large contribution. To keep pace with the muscles’ glucose uptake, the liver mus break down increasingly more glycogen as exercise duration increases.

Liver glycogen stores are limited, and the liver cannot produce glucose rapidly from other substrates. Consequently, blood glucose levels can decrease when muscle uptake exceeds the liver’s glucose output. Unable to obtain sufficient glucose from the blood, the muscles must rely more heavily on their glycogen reserves, accelerating muscle glycogen depletion and leading to earlier exhaustion. On the other hand, most studies have shown no effect of carbohydrate ingestion on net muscle glycogen utilization during prolonged, strenuous exercise.

Not surprisingly, endurance performances improve when the muscle glycogen supply is elevated before the start of activity. Glycogen depletion and hypoglycemia(low blood sugar) limit performance in activities lasting longer than 60 to 90 min.



Mechanisms of fatique with glycogen depletion



It does not appear likely that glycogen depletion directly causes fatique during endurance exercise performance. Rather, the depletion of muscle glycogen may be the first step in a series of events that leads to fatique. A certain level of muscle glycogen metabolism is necessary to maintain oxidative metabolism of both carbohydrates and fats using Krebs cycle. That is, we now know that a certain rate of glycogen breakdown is needed for the optimal production of reduced nicotinamide adenine dinucleotide(NADH) and to maintain the electron transport system.

Additionally, as glycogen is depleted, exercising muscle relies more heavily on the metabolism of FFAs. To accomplish this, more FFAs must be moved into the mitochondria, and the rate of transfer may limit FFA oxidation to the point where it can no longer keep up with the need for fat oxidation.



Metabolic by-products and fatique



Various by-products of metabolism have been implicated as factors causing, or contributing to, fatique. One example is Pi, which increases during intense short-term exercise as PCr and ATP are being broken down. Additional metabolic by-products that have received the most attention in discussing fatique are heat, lactate and hydrogen ions.



Heat, muscle temperature, and fatique



Recall that energy expenditure results in a relatively large heat production, some of which is retained in the body, causing core temperature to rise. Exercise in the heat can increase the rate of carbohydrate utilization and hasten glycogen depletion, effects that may be stimulated by the increased secretion of epinephrine. It is hypothesized that high muscle temperature impair both skeletal muscle function and muscle metabolism.

The ability to continue moderate-to high-intensity cycle performance is affected by ambient temperature. Galloway and Maughan studied performance time to exhaustion of male cyclists  at four different air temperatures: 4°C(38°F), 11°C(51°F), 21°C(70°F), and 31°C(87°F). Results are shown below. Time to exhaustion was longest when subject exercised on air temperature of 11°C, but lower at colder and warmer temperatures. Fatique set in earliest at 31°C. Precooling of muscles similarly prolonged exercise, while preheating causes earlier fatique. Heat acclimation spares glycogen and reduces lactate accumulation.





Lactic acid, hydrogen ions and fatique



Recall that lactic acid is a by-product of anaerobic glycolysis. Although most people believe that lactic acid is responsible for fatique in all types of exercise, lactic acid accumulates within the muscle fiber only during relatively brief, highly intense muscular effort. Marathon runners, for example, may have near-resting lactic acid levels at the end of the race, despite their fatique. Their fatique is caused most likely by inadequate energy supply, not lactic acid.

Short sprints in running, cycling, and swimming all lead to large accumulations of lactic acid. But the presence of lactic acid should not be blamed for the feeling of fatique in itself. When not cleared, the lactic acid dissociates, converting to lactate acid causing an accumulation of hydrogen ions. This H+ accumulation causes muscle acidification, resulting in a condition known as acidosis.

Activities of short duration and high intensity, such as sprint running and sprint swimming, depend heavily on anaerobic glycolysis and produce large amounts of lactate and H+ within the muscles. Fortunately, the cells and body fluids possess buffers, such as bicarbonate(HCO3), that minimize the disrupting influence of the H+. Without these buffers, H+ would lower the pH to about 1.5, killing the cells. Because of the body’s buffering capacity, the H+ concentration remains low even during the most severe exercise, allowing muscle pH to decrease from a resting value of 7.1 to no lower than 6.6 to 6.4 at exhaustion.

However, pH changes of this magnitude adversely affect energy production and muscle contraction. An intracellular pH below 6.9 inhibits the action of phosphofructokinase, an important glycolytic enzyme, slowing the rate of glycolysis and ATP production. At a pH of 6.4, the influence of H+ stops any further glycogen breakdown, causing a rapid decrease in ATP and ultimately exhaustion. In addition, H+ may displace calcium within the fiber, interfering with the coupling of the actin-myosin cross-bridges and decreasing the muscle’s contractile force. Most researchers agree that low muscle pH is the major limiter of performance and the primary cause of fatique during maximal, all-out exercise lasting more than 20s to 30s.




As seen in the figure above, reestablishing the preexercise muscle pH after an exhaustive sprint bout requires about 30 to 35 min of recovery. Even when normal pH is restored, blood and muscle lactate levels can remain quite elevated. However, experience has shown that an athlete can continue to exercise at relatively high intensities even with a muscle pH below 7.0, and a blood lactate level above 6 or 7 mmol, four to five times the resting value.

Some coaches and sport physiologists have attempted to use blood lactate measurements to gauge the intensity and volume of training needed to produce an optimal training stimulus. Such measurements provide an index of training intensity, but they might not reflect the anaerobic processes of the state of acidosis in the muscles. Because lactate and H+ are generated in the muscles, both diffuse in the body fluids and transported to other areas of the body to be metabolized. Consequently, blood lactate concentrations depend on the rates of production, diffusion, oxidation, and clearance. A variety of factors can influence these processes, so measuring blood lactate is of questionable value for fine-tuning training.



Neuromuscular fatique



Thus we have considered only factors within the muscle that might be responsible for fatique. Evidence also suggests that under some circumstances, fatique may result from an inability to activate the muscle fibers, a function of the nervous system. The neural impulse is transmitted across the neuromuscular junction to activate the fiber’s membrane, and it causes the fiber’s sarcoplasmic reticulum to release calcium. The calcium, in turn, binds with troponin to initiate muscle contraction. Two of several possible neural mechanisms that could disrupt this process and possibly contribute to fatique are described in following part.



Neural transmission



Fatique may occur at the neuromuscular junction, preventing nerve impulse transmission to the muscle fiber membrane. Studies in the early 1900s clearly established such a failure of nerve impulse transmission in fatiqued muscle. This failure may involve one or more of the following processes:

  • The release of synthesis of acetylholine(ACh), the neurotransmitter that relays the nerve impulse from the motor nerve to the muscle membrane, might be reduced;
  • Cholinesterase, the enzyme that breaks down ACh once it has relayed the impulse, might become hyperactive, preventing sufficient concentration of ACh to initiate an action potential;
  • Cholinesterase activity might become hypoactive(inhibited), allowing ACh to accumulate excessively, inhibiting relaxation;
  • The muscle fiber membrane might develop a higher threshold for stimulation by motor neurons;
  • Some substance might compete with ACh for the receptors on the muscle membrane without activating the membrane;
  • Potassium might leave the intracellular space of the contracting muscle, decreasing the membrane potential to half of its resting value.



Although most of these causes for a neuromuscular block have been associated with neuromuscular diseases(such as myasthenia gravis), they may also cause some forms of neuromuscular fatique. Some evidence suggests that fatique also may be attributable to calcium retention within the sarcoplasmic reticulum, which would decrease the calcium available for muscle contraction. In fact, depletion of PCr and lactate buildup might simply increase the rate of calcium accumulation within the sarcoplasmic reticulum. However, these theories  of fatique remain speculative.



Central nervous system



The central nervous system(CNS) also might be a site of fatique. Undoubtedly, there is some CNS involvement in most types of fatique. When a subject’s muscles appear to be nearly exhausted, verbal encouragement, shouting, playing of music, or even direct electrical stimulation of the muscle can increase the strength of muscle contraction. The precise mechanisms underlying the CNS role in causing, sensing and even overriding fatique are not fully understood.

The recruitment of muscle depends, in part, on conscious control. The stress of exhaustive exercise may lead to conscious or subconscious inhibition of the athlete’s willingness to tolerate further pain. The CNS may slow the exercise pace to a tolerable level to protect the athlete. Indeed, researchers generally agree that the perceived discomfort of fatique precedes the onset of a physiological limitation within the muscles. Unless they are highly motivated, most individuals terminate exercise before their muscles are physiologically exhausted. To achieve peak performance, athletes train to learn proper pacing and tolerance for fatique.

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