Second wind

Metabolic switching When non-aerobic glycogen metabolism is insufficient to meet energy demands, physiologic mechanisms utilize alternative sources of energy such as fatty acids and proteins via aerobic respiration. Second-wind phenomena in metabolic disorders such as McArdle's disease are attributed to this metabolic switch and the same or a similar phenomenon may occur in healthy individuals (see symptoms of McArdle's disease). Lactic acid Muscular exercise as well as other cellular functions requires oxygen to produce ATP and properly function. This normal function is called aerobic metabolism and does not produce lactic acid if enough oxygen is present. During heavy exercise such as long distance running or any demanding exercise, the body's need for oxygen to produce energy is higher than the oxygen supplied in the blood from respiration. Anaerobic metabolism to some degree then takes place in the muscle and this less ideal energy production produces lactic acid as a waste metabolite. If the oxygen supply is not soon restored, this may lead to accumulation of lactic acid. This is the case even without exercise in people with respiratory disease, challenged circulation of blood to parts of the body or any other situation when oxygen cannot be supplied to the tissues involved. Some people's bodies may take more time than others to be able to balance the amount of oxygen they need to counteract the lactic acid. This theory of the second wind posits that, by pushing past the point of pain and exhaustion, runners may give their systems enough time to warm up and begin to use the oxygen to its fullest potential. For this reason, well-conditioned Olympic-level runners do not generally experience a second wind (or they experience it much sooner) because their bodies are trained to perform properly from the start of the race. Endorphins Endorphins are credited as the cause of the feeling of euphoria and wellbeing found in many forms of exercise, so proponents of this theory believe that the second wind is caused by their early release. Many of these proponents feel that the second wind is very closely related to—or even interchangeable with—the runner's high. == Pathology ==

A second wind phenomenon is also seen in some medical conditions, such as McArdle disease (GSD-V) and Phosphoglucomutase deficiency (PGM1-CDG/CDG1T/GSD-XIV). Unlike non-affected individuals that have to do long-distance running to deplete their muscle glycogen, in GSD-V individuals their muscle glycogen is unavailable, so second wind is achieved after 6–10 minutes of light to moderate aerobic activity (such as walking without an incline). 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. Oxidative phosphorylation by free fatty acids is more easily achievable for light to moderate aerobic activity (below the aerobic threshold), as high-intensity (fast-paced) aerobic activity relies more on muscle glycogen due to its high ATP consumption. Oxidative phosphorylation by free fatty acids is not achievable with isometric and other anaerobic activity (such as lifting weights), as contracted muscles restrict blood flow (leaving oxygen and blood borne fuels unable to be delivered to muscle cells adequately for oxidative phosphorylation). A "third wind" phenomenon is also seen in GSD-V individuals, where after approximately 2 hours, they see a further improvement of symptoms as the body becomes even more fat adapted. 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. 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. For McArdle disease (GSD-V), regular aerobic exercise utilizing "second wind" to enable the muscles to become aerobically conditioned, as well as anaerobic exercise (strength training) that follows the activity adaptations so as not to cause muscle injury, helps to improve exercise intolerance symptoms and maintain overall health. Regardless of whether the patient experiences symptoms of muscle pain, muscle fatigue, or cramping, the phenomenon of second wind having been achieved is demonstrable by the sign of an increased heart rate dropping while maintaining the same speed on the treadmill. For the regularly active patients, it took more strenuous exercise (very brisk walking/jogging or bicycling) for them to experience both the typical symptoms and relief thereof, along with the sign of an increased heart rate dropping, demonstrating second wind. That said, patients with McArdle disease typically experience symptoms of exercise intolerance before the age of 10 years, Tarui disease (GSD-VII) patients do not experience the "second wind" phenomenon; instead are said to be "out-of-wind". However, they can achieve sub-maximal benefit from lipid metabolism of free fatty acids during aerobic activity following a warm-up. == See also ==