Spero Karas, MD, assistant professor of orthopaedics in the division of sports medicine at Emory University, says that testosterone, the male hormone responsible for muscle growth, maxes out between the ages of 16 and 18. It reaches a plateau during the 20s and then begins to decline. As a result, muscle building after the adolescent years can be challenging, he says.
Myotonic Dystrophy type I (DM1) is an inhereted muscular disorder caused by an expanded CTG repeat in the DMPK gene on chromosome 19q13.3 (genetic cause of the disorder[561]) resulting in muscular degeneration and myotonia. The related myopathy, Myotonic Dystrophy type II (DM2) which is also known as proximal myotonic myopathy (PROMM) is due to a CCTG repeat on 3q,[562] and is less affected by myotonia and more by muscular pain and weakness. There is no cure for either because they are genetic disorders, so current therapies are aimed at reducing side-effects. Therapies include modafinil for the somnolence[563] and perhaps creatine for the reduction in strength and functionality.[548]
In the last week leading up to a contest, bodybuilders usually decrease their consumption of water, sodium, and carbohydrates, the former two to alter how water is retained by the body and the latter to reduce glycogen in the muscle. The day before the show, water is removed from the diet, and diuretics may be introduced, while carbohydrate loading is undertaken to increase the size of the muscles through replenishment of their glycogen. The goal is to maximize leanness and increase the visibility of veins, or "vascularity". The muscular definition and vascularity are further enhanced immediately before appearing on stage by darkening the skin through tanning products and applying oils to the skin to increase shine. Some competitors will eat sugar-rich foods to increase the visibility of their veins. A final step, called "pumping", consists in performing exercises with light weights or other kinds of low resistance (for instance two athletes can "pump" each other by holding a towel and pulling in turn), just before the contest, to fill the muscles with blood and further increase their size and density.
Endogenous serum or plasma creatine concentrations in healthy adults are normally in a range of 2–12 mg/L. A single 5 g (5000 mg) oral dose in healthy adults results in a peak plasma creatine level of approximately 120 mg/L at 1–2 hours post-ingestion. Creatine has a fairly short elimination half-life, averaging just less than 3 hours, so to maintain an elevated plasma level it would be necessary to take small oral doses every 3–6 hours throughout the day. After the "loading dose" period (1–2 weeks, 12–24 g a day), it is no longer necessary to maintain a consistently high serum level of creatine. As with most supplements, each person has their own genetic "preset" amount of creatine they can hold. The rest is eliminated as waste. A typical post-loading dose is 2–5 g daily.[52][53][54]
Creatine is known to be present in the retina due to the expression of creatine kinase (CK)[466][39] and the GAMT enzyme of creatine synthesis, which is also present in the mammalian retina.[467] Creatine in the blood can be transported into the retina via the creatine transporter (confirmed in humans[468]), and inhibiting transporter activity (by depleting the medium of chloride and sodium) reduces uptake by 80%.[469] The fact that not all uptake was inhibited suggests that another transporter, such as the monocarboxylate transporter MCT12 (or SLC16A12),[470] plays a role, perhaps moreso in the lens, where its levels were comparable to that of the major creatine transporter SLC6A8.[470] 
It is known that intracellular energy depletion (assessed by a depletion of ATP) stimulates AMPK activity in order to normalize the AMP:ATP ratio,[333][334] and when activated AMPK (active in states of low cellular energy[335] and colocalizes with creatine kinase in muscle tissue[336]) appears to inhibit creatine kinase via phosphorylation (preserving phosphocreatine stores but attenuating the rate that creatine buffers ATP). While phosphocreatine technically inhibits AMPK, this does not occur in the presence of creatine at a 2:1 ratio.[334] It seems that if the ratio of phosphocreatine:creatine increases (indicative of excess cellular energy status) that AMPK activity is then attenuated, since when a cell is in a high energy status, there is less AMP to directly activate AMPK.[334][336][337]
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