Carbohydrates provide quick energy in an anaerobic environment (high-intensity exercise), while fats provide sustained energy during periods of high oxygen availability (low-intensity exercise or rest). The breakdown of carbohydrates, fats, and ketones produces ATP (adenosine triphosphate). When cells use ATP for energy, this molecule is converted into adenosine diphosphate (ADP) and adenosine monophosphate (AMP). Creatine exists in cells to donate a phosphate group (energy) to ADP, turning this molecule back into ATP.
The neuroprotective effects of creatine appear to exist in regard to dopamine biosynthesis, and the suppression of dopamine synthesis seen with some neurological toxins appears to be partially attenuated with dietary intake of creatine. The protective effect is weak to moderate in animal research, but appears to be additive with anti-inflammatories.
Homocyteine (normal serum range of 5-14µM) is known to adversely affect motor control in genetically susceptible people when their levels exceed 500µM, which is usually associated with genetically induced deficiencies of B12. In these particular instances (assessed by rats fed homocysteine to increase serum levels to such a high level) it appears that administration of 50mg/kg creatine (injections) to these rats can protect dysfunction in muscle metabolism (pyruvate kinase activity, Krebs cycle intermediates, and muscle cell viability) induced by homocysteine.
The first open label trial on ALS failed to significantly alter lung function as assessed by FEV (when comparing the rate of decline pretreatment relative to treatment). Creatine has elsewhere failed to benefit lung function at 5g daily for months relative to control and failed to significantly attenuate the rate of lung function deterioration over 16 months at 10g daily and 5g daily over nine months.
The creatine kinase system appears to be detectable in endothelial cells. Under basal conditions, creatine itself is expressed at around 2.85+/-0.62μM (three-fold higher than HUVEC cells). When incubating the medium with 0.5mM creatine, endothelial cells can take up creatine via the creatine transporter (SLC6A8) and increase both creatine (almost doubling) and phosphocreatine (nearly 2.5-fold) concentrations.
The reasons for differences in the effect of creatine on testosterone vs. DHT across studies are not clear, but also not mutually exclusive. A measured increase in DHT could indicate that testosterone levels were increased by creatine, but rapidly converted to DHT through a homeostatic mechanism. Differences in study subject populations, methodology, or the presence and type of concurrent exercise could also be contributing factors. At any rate, the literature collectively suggests that creatine has the general ability to cause a modest increase in androgen levels in men.
Glycogen synthesis is known to respond directly and positively to cellular swelling. This was demonstrated in an earlier study, during which rat muscle cells were exposed to a hypotonic solution in vitro to induce cell swelling, which increased glycogen synthesis by 75%. In contrast, exposing these same cells to a hypertonic solution hindered glycogen synthesis by 31%. These changes were not due to alterations in glucose uptake, but are blocked by hindering the PI3K/mTOR signaling pathway. It was later noted that stress proteins of the MAPK class (p38 and JNK) as well as heat shock protein 27 (Hsp27) are activated in response to increasing osmolarity. Furthermore, activation of MAPK signaling in skeletal muscle cells is known to induce myocyte differentiation via GSK3β and MEF2 signaling, which can induce muscle cell growth.
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.
Need the motivation to push past your comfort zone and squeeze out one more push-up or bicep curl? Sure, it helps to remember that you’ll get stronger, rock more toned muscles and rev your metabolism, thanks to all that added muscle mass. But if that wasn’t enough, now comes news that all that pump-itude (yes, that’s an SNL reference) has psychological benefits, too.
Bodybuilders often split their food intake for the day into 5 to 7 meals of roughly equal nutritional content and attempt to eat at regular intervals (e.g. every 2 to 3 hours). This method can serve two purposes: to limit overindulging in the cutting phase, and to physically allow for the consumption of large volumes of food during the bulking phase. Contrary to popular belief, eating more frequently does not increase basal metabolic rate when compared to the traditional 3 meals a day. While food does have a metabolic cost to digest, absorb, and store, called the thermic effect of food, it depends on the quantity and type of food, not how the food is spread across the meals of the day. Well-controlled studies using whole-body calorimetry and doubly labeled water have demonstrated that there is no metabolic advantage to eating more frequently.
I know this goes against the recommendations you often see in stereotypical bodybuilding routines (i.e. the ones that involve having a single “chest day” or “arm day” or “shoulder day” once a week), but that’s just one of the many reasons why those types of routines suck for us natural, genetically-average people, and work best for steroid users with great genetics.