Hitting the wall

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Statue of the "Tired Man" (Megfaradt ember in Hungarian), referring to the poem of Attila Jozsef. The statue is the work of Jozsef Somogyi. Statue of the Tired Man.JPG
Statue of the "Tired Man" (Megfáradt ember in Hungarian), referring to the poem of Attila József. The statue is the work of József Somogyi.

In endurance sports such as road cycling and long-distance running, hitting the wall or the bonk is a condition of sudden fatigue and loss of energy which is caused by the depletion of glycogen stores in the liver and muscles. Milder instances can be remedied by brief rest and the ingestion of food or drinks containing carbohydrates. Otherwise, it can remedied by attaining second wind by either resting for approximately 10 minutes or by slowing down considerably and increasing speed slowly over a period of 10 minutes. Ten minutes is approximately the time that it takes for free fatty acids to sufficiently produce ATP in response to increased demand. [1]

Contents

During a marathon, for instance, runners typically hit the wall around kilometer 30 (mile 20). [2] The condition can usually be avoided by ensuring that glycogen levels are high when the exercise begins, maintaining glucose levels during exercise by eating or drinking carbohydrate-rich substances, or by reducing exercise intensity.

Skeletal muscle relies predominantly on glycogenolysis for the first few minutes as it transitions from rest to activity, as well as throughout high-intensity aerobic activity and all anaerobic activity. [3] The lack of glycogen causes a low ATP reservoir within the exercising muscle cells. Until second wind is achieved (increased ATP production primarily from free fatty acids), the symptoms of a low ATP reservoir in exercising muscle due to depleted glycogen include: muscle fatigue, muscle cramping, muscle pain (myalgia), inappropriate rapid heart rate response to exercise (tachycardia), breathlessness (dyspnea) or rapid breathing (tachypnea), exaggerated cardiorespiratory response to exercise (tachycardia & dyspnea/tachypnea). [3] The heart tries to compensate for the energy shortage by increasing heart rate to maximize delivery of oxygen and blood borne fuels to the muscle cells for oxidative phosphorylation. [3]

Without muscle glycogen, it is important to get into second wind without going too fast, too soon nor trying to push through the pain. Going too fast, too soon encourages protein metabolism over fat metabolism, and the muscle pain in this circumstance is a result of muscle damage due to a severely low ATP reservoir. [4] [5]

Protein metabolism occurs through amino acid degradation which converts amino acids into pyruvate, the breakdown of protein to maintain the amino acid pool, the myokinase (adenylate kinase) reaction and purine nucleotide cycle. [6] Amino acids are vital to the purine nucleotide cycle as they are precursors for purines, nucleotides, and nucleosides; as well as branch-chained amino acids are converted into glutamate and aspartate for use in the cycle (see Aspartate and glutamate synthesis ). Severe breakdown of muscle leads to rhabdomyolysis and myoglobinuria. Excessive use of the myokinase reaction and purine nucleotide cycle leads to myogenic hyperuricemia. [7]

In muscle glycogenoses (muscle GSDs), an inborn error of carbohydrate metabolism impairs either the formation or utilization of muscle glycogen. As such, those with muscle glycogenoses do not need to do prolonged exercise to experience hitting the wall. Instead, signs of exercise intolerance, such as an inappropriate rapid heart rate response to exercise, are experienced from the beginning of activity. [4] [5]

Etymology, usage, and synonyms

The term bonk for fatigue is presumably derived from the original meaning "to hit", and dates back at least half a century. Its earliest citation in the Oxford English Dictionary is a 1952 article in the Daily Mail. [8]

The term is used colloquially as a noun ("hitting the bonk") and as a verb ("to bonk halfway through the race"). The condition is also known to long-distance (marathon) runners, who usually refer to it as "hitting the wall". The British may refer to it as "hunger knock," while "hunger bonk" was used by South African cyclists in the 1960s.

It can also be referred to as "blowing up" [9] or a "weak attack".

In other languages

In German, hitting the wall is known as "der Mann mit dem Hammer" ("the man with the hammer"); the phenomenon is thus likened to a man with the hammer coming after the athlete, catching up, and eventually hitting the athlete, causing a sudden drop in performance.

In French, marathoners in particular use "frapper le mur (du marathon)", literally hitting the (marathon) wall, just like in English. One may also hear "avoir un coup de barre" (getting smacked by a bar), which means experiencing sudden, incredible fatigue. This expression is used in a wider set of contexts.

Mechanisms

Athletes engaged in exercise over a long period of time produce energy via two mechanisms, both facilitated by oxygen:

How much energy comes from either source depends on the intensity of the exercise. During intense exercise that approaches one's VO2 max, most of the energy comes from glycogen.

A typical untrained individual on an average diet is able to store about 380 grams of glycogen, or 1500 kcal, in the body, though much of that amount is spread throughout the muscular system and may not be available for any specific type of exercise. [10] Intense cycling or running can easily consume 600–800 or more kcal per hour. Unless glycogen stores are replenished during exercise, glycogen stores in such an individual will be depleted after less than 2 hours of continuous cycling [11] or 15 miles (24 km) of running. Training and carbohydrate loading can raise these reserves as high as 880 g (3600 kcal), correspondingly raising the potential for uninterrupted exercise.

Effects

In one study of five male subjects, "reduction in preexercise muscle glycogen from 59.1 to 17.1 µmol × g−1 (n = 3) was associated with a 14% reduction in maximum power output but no change in maximum O2 intake; at any given power output O2 intake, heart rate, and ventilation (VE) were significantly higher, CO2 output (VCO2) was similar, and the respiratory exchange ratio was lower during glycogen depletion compared with control." [12]

Avoidance

There are several approaches to prevent glycogen depletion:

See also

Related Research Articles

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Adenosine monophosphate (AMP), also known as 5'-adenylic acid, is a nucleotide. AMP consists of a phosphate group, the sugar ribose, and the nucleobase adenine. It is an ester of phosphoric acid and the nucleoside adenosine. As a substituent it takes the form of the prefix adenylyl-.

<span class="mw-page-title-main">Adenosine monophosphate deaminase deficiency type 1</span> Medical condition

Adenosine monophosphate deaminase deficiency type 1 or AMPD1, is a human metabolic disorder in which the body consistently lacks the enzyme AMP deaminase, in sufficient quantities. This may result in exercise intolerance, muscle pain and muscle cramping. The disease was formerly known as myoadenylate deaminase deficiency (MADD).

<span class="mw-page-title-main">Glycogen storage disease type V</span> Human disease caused by deficiency of a muscle enzyme

Glycogen storage disease type V, also known as McArdle's disease, is a metabolic disorder, one of the metabolic myopathies, more specifically a muscle glycogen storage disease, caused by a deficiency of myophosphorylase. Its incidence is reported as one in 100,000, roughly the same as glycogen storage disease type I.

<span class="mw-page-title-main">Glycogen storage disease</span> Medical condition

A glycogen storage disease is a metabolic disorder caused by a deficiency of an enzyme or transport protein affecting glycogen synthesis, glycogen breakdown, or glucose breakdown, typically in muscles and/or liver cells.

<span class="mw-page-title-main">Glycogen</span> Glucose polymer used as energy store in animals

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<span class="mw-page-title-main">Exercise physiology</span>

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<span class="mw-page-title-main">Hyperuricemia</span> Medical condition

Hyperuricaemia or hyperuricemia is an abnormally high level of uric acid in the blood. In the pH conditions of body fluid, uric acid exists largely as urate, the ion form. Serum uric acid concentrations greater than 6 mg/dL for females, 7 mg/dL for men, and 5.5 mg/dL for youth are defined as hyperuricemia. The amount of urate in the body depends on the balance between the amount of purines eaten in food, the amount of urate synthesised within the body, and the amount of urate that is excreted in urine or through the gastrointestinal tract. Hyperuricemia may be the result of increased production of uric acid, decreased excretion of uric acid, or both increased production and reduced excretion.

<span class="mw-page-title-main">Phosphoglucomutase</span> Metabolic enzyme

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Starvation response in animals is a set of adaptive biochemical and physiological changes, triggered by lack of food or extreme weight loss, in which the body seeks to conserve energy by reducing metabolic rate and/or non-resting energy expenditure to prolong survival and preserve body fat and lean mass.

<span class="mw-page-title-main">Myophosphorylase</span> Muscle enzyme involved in glycogen breakdown

Myophosphorylase or glycogen phosphorylase, muscle associated (PYGM) is the muscle isoform of the enzyme glycogen phosphorylase and is encoded by the PYGM gene. This enzyme helps break down glycogen into glucose-1-phosphate, so it can be used within the muscle cell. Mutations in this gene are associated with McArdle disease, a glycogen storage disease of muscle.

<span class="mw-page-title-main">Bioenergetic systems</span> Metabolic processes for energy production

Bioenergetic systems are metabolic processes that relate to the flow of energy in living organisms. Those processes convert energy into adenosine triphosphate (ATP), which is the form suitable for muscular activity. There are two main forms of synthesis of ATP: aerobic, which uses oxygen from the bloodstream, and anaerobic, which does not. Bioenergetics is the field of biology that studies bioenergetic systems.

Second wind is a phenomenon in endurance sports, such as marathons or road running, whereby an athlete who is out of breath and too tired to continue, finds the strength to press on at top performance with less exertion. The feeling may be similar to that of a "runner's high", the most obvious difference being that the runner's high occurs after the race is over. In muscle glycogenoses, an inborn error of carbohydrate metabolism impairs either the formation or utilization of muscle glycogen. As such, those with muscle glycogenoses do not need to do prolonged exercise to experience "hitting the wall". Instead, signs of exercise intolerance, such as an inappropriate rapid heart rate response to exercise, are experienced from the beginning of an activity, and some muscle GSDs can achieve second wind within about 10 minutes from the beginning of the aerobic activity, such as walking. (See below in pathology).

<span class="mw-page-title-main">Inborn errors of carbohydrate metabolism</span> Medical condition

Inborn errors of carbohydrate metabolism are inborn error of metabolism that affect the catabolism and anabolism of carbohydrates.

<span class="mw-page-title-main">Metabolic myopathy</span> Type of myopathies

Metabolic myopathies are myopathies that result from defects in biochemical metabolism that primarily affect muscle. They are generally genetic defects that interfere with muscle's ability to create energy, causing a low ATP reservoir within the muscle cell.

<span class="mw-page-title-main">Purine nucleotide cycle</span>

The Purine Nucleotide Cycle is a metabolic pathway in protein metabolism requiring the amino acids aspartate and glutamate. The cycle is used to regulate the levels of adenine nucleotides, in which ammonia and fumarate are generated. AMP converts into IMP and the byproduct ammonia. IMP converts to S-AMP (adenylosuccinate), which then converts to AMP and the byproduct fumarate. The fumarate goes on to produce ATP (energy) via oxidative phosphorylation as it enters the Krebs cycle and then the electron transport chain. Lowenstein first described this pathway and outlined its importance in processes including amino acid catabolism and regulation of flux through glycolysis and the Krebs cycle.

References

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