Hitting the wall cause glycogen
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.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. 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). 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.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.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. 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.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.
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