In nonelite swimmers conducting an intermittent sprint protocol (Six 50m sprints every two minutes), supplementation of a creatine loading period was able to reduce the decrement in speed during the third sprint (2% decrement rather than a 5% decrement) but not the sixth sprint. There were no changes in plasma lactate or other biomarkers of fatigue. When examining a single 50m sprint in amateur swimmers, a creatine loading period is able to reduce the time to complete the sprint by 4.6%, while it had no benefit for the 100m sprint. When the loading phase was followed by three weeks maintenance in youth, there was no apparent benefit to sprint performance (50m sprint with five minutes rest followed by a 100m freestyle) despite benefits to a swim bench test (30s sprints with a five minute break in between).
Athletic performance. Creatine seems to help improve rowing performance, jumping height, and soccer performance in athletes. But the effect of creatine on sprinting, cycling, or swimming performance varies. The mixed results may relate to the small sizes of the studies, the differences in creatine doses, and differences in test used to measure performance. Creatine does not seem to improve serving ability in tennis players.
There is a genetic condition known as gyrate atrophy of the choroid and retina, which is associated with a high level of Ornithine in the blood and a relative decrease in Arginine, which causes a relative creatine deficiency due to L-arginine being required to make creatine and because high ornithine can suppress creatine synthesis (AGAT) in the glial cells of the retina. This condition can be attenuated by either reducting ornithine in the diet or by supplementing creatine, which is, in this instance, therapeutic.
I’m glad you found some good information from this article. For any of these supplements, I would suggest talking to your doctor and pharmacist. I would suggest thinking about why you are interested in taking testosterone. Are you looking to increase muscle size? Bulk up? Knowing your fitness goals will help you determine which products are appropriate for you.
One pilot study using 150mg/kg creatine monohydrate for a five day loading phase followed by maintenance (60mg/kg) for the remainder of the five weeks noted that supplementation was associated with fewer muscle symptoms and complaints alongside improved muscular function, yet a later trial trying to replicate the obsevations using 150mg/kg daily for five weeks noted the opposite, that creatine supplementation exacerbated symptoms.
Discomfort can arise from other factors. Individuals who perform large numbers of repetitions, sets, and exercises for each muscle group may experience a burning sensation in their muscles. These individuals may also experience a swelling sensation in their muscles from increased blood flow (the "pump"). True muscle fatigue is experienced as a marked and uncontrollable loss of strength in a muscle, arising from the nervous system (motor unit) rather than from the muscle fibers themselves. Extreme neural fatigue can be experienced as temporary muscle failure. Some weight training programs, such as Metabolic Resistance Training, actively seek temporary muscle failure; evidence to support this type of training is mixed at best. Irrespective of their program, however, most athletes engaged in high-intensity weight training will experience muscle failure during their regimens.
Cyclocreatine (1-carboxymethyl-2-iminoimidazolidine) is a synthetic analogue of creatine in a cyclic form. It serves as a substrate for the creatine kinase enzyme system, acting as a creatine mimetic. Cyclocreatine may compete with creatine in the CK enzyme system to transfer phosphate groups to ADP, as coincubation of both can reduce cyclocreatine’s anti-motility effects on some cancer cells.
In regard to the blood brain barrier (BBB), which is a tightly woven mesh of non-fenestrated microcapillary endothelial cells (MCECs) that prevents passive diffusion of many water-soluble or large compounds into the brain, creatine can be taken into the brain via the SLC6A8 transporter. In contrast, the creatine precursor (guanidinoacetate, or GAA) only appears to enter this transporter during creatine deficiency. More creatine is taken up than effluxed, and more GAA is effluxed rather than taken up, suggesting that creatine utilization in the brain from blood-borne sources is the major source of neural creatine. However, “capable of passage” differs from “unregulated passage” and creatine appears to have tightly regulated entry into the brain in vivo. After injecting rats with a large dose of creatine, creatine levels increased and plateaued at 70uM above baseline levels. These baseline levels are about 10mM, so this equates to an 0.7% increase when superloaded. These kinetics may be a reason for the relative lack of neural effects of creatine supplementation in creatine sufficient populations.