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.
Using too much weight, too soon; always start lower than your expected ability and work your way up that first workout. If your form suffers, you are swinging the weight, or using momentum, this indicates you may be using too much weight. Greater momentum increases the potential for injury and reduces the effectiveness to the muscle group being targeted.
Bodybuilders have THE BEST mind to muscle connection of any resistance-training athletes. Ask a seasoned bodybuilder to flex their lats or their rhomboids or their hamstrings and they will do it with ease. Ask other strength athletes and you will see them struggle and although they may tense up the target muscle they will also tense up about 15 other surrounding muscles. This is because strength athletes train MOVEMENTS. They don’t care about targeting their lats. They just want to do the most pull ups. They don’t worry about feeling their quads. They just want to squat maximum weight. Although this is an expected and positive thing for the most part, there are real benefits to being able to isolate and target muscles.
One study on 27 otherwise healthy men supplementing creatine (0.3g/kg loading for a week, 0.05g/kg thereafter for 8 weeks) with a thrice weekly exercise regiment noted that alongside greater increase in lean mass and power relative to placebo at 4 and 8 weeks, myostatin in serum decreased to a greater extent with creatine (around 17% at 8 weeks, derived from graph) than it did with placebo (approximately 7%). Increases in GASP-1, a serum protein that inhibits the actions of myostatin by directly binding to it, were not different between groups.
Without supplementation, approximately 14.6mmol (2g) of creatinine, creatine’s urinary metabolite, is lost on a daily basis in a standard 70kg male ages 20-39. The value is slightly lower in females and the elderly due to a presence of less muscle mass. This amount is considered necessary to obtain in either food or supplemental form to avoid creatine deficiency. Requirements may be increased in people with higher than normal lean mass. Creatine excretion rates on a daily basis are correlated with muscle mass, and the value of 2g a day is derived from the aforementioned male population with about 120g creatine storage capacity. Specifically, the rate of daily creatine losses is about 1.6%-1.7%, and mean losses for women are approximately 80% that of men due to less average lean mass. For weight-matched elderly men (70kg, 70-79 years of age) the rate of loss of 7.8mmol/day, or about half (53%) that of younger men.
Based on the limited data on performance and safety, some authors have not identified any conclusions and do not recommend its consumption in regards to creatine supplementation in children and adolescents [52,54]. Conversely, according to the view of the ISSN , younger athletes should consider a creatine supplement under certain conditions: puberty is past and he/she is involved in serious competitive training; the athlete is eating a well-balanced caloric adequate diet; he/she as well as the parents approve and understand the truth concerning the effects of creatine supplementation; supplement protocols are supervised by qualified professionals; recommended doses must not be exceeded; quality supplements are administered.
In a pilot study on youth with cystic fibrosis, supplementation of creatine at 12g for a week and 6g for eleven weeks afterward was associated with a time-dependent increase in maximal isometric strength reaching 14.3%, which was maintained after 12-24 weeks of supplement cessation (18.2% higher than baseline). This study noted that more patients reported an increase in wellbeing (9 subjects, 50%) rather than a decrease (3, 17%) or nothing (6, 33%) and that there was no influence on chest or lung symptoms.
Activation of NMDA receptors is known to stimulate Na+,K+-ATPase activity secondary to calcineurin, which which has been confirmed with creatine in hippocampal cells (0.1-1mM trended, but 10mM was significant). This is blocked by NMDA antagonists. This increase in Na+,K+-ATPase activity is also attenauted with activation of either PKC or PKA, which are antagonistic with calcineurin.
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.