NAR, JK, SLR and ADF were co-authors, oversaw all aspects of BX-795 clinical trial study including recruitment, data/specimen analysis, and manuscript preparation.”
“Introduction Creatine is found in small quantities within the brain, liver, kidneys, and testes, while approximately 95% of creatine stores are found in skeletal muscle [1]. Creatine or methyl guanidine acetic acid is supplied by exogenous sources such as fish and red meat and is endogenously synthesized from the amino acids arginine, glycine, and methionine

[2]. Energy is provided to the body from the hydrolysis of ATP into adenosine diphosphate (ADP) and inorganic phosphate (Pi). The phosphagen system provides a rapid resynthesis of ATP from ADP with the use of phosphocreatine (PCr) through the reversible reaction of creatine kinase [2–4]. Of the 95% of creatine stored within skeletal muscle, approximately 40% is free creatine and approximately 60% is PCr [3]. The average 70 kg person has a total creatine pool of 120–140 g. Specifically, the range of creatine in skeletal muscle is 110–160 mmol/kg dry mass [2, 1, 5]. Creatine supplementation has the ability to increase skeletal muscle stores of creatine and PCr, which could therefore increase skeletal muscle’s ability to increase ATP resynthesis from ADP. A previous study [6] employing 20 g of creatine

for 6 days showed an increase in PCr concentrations after a maximal isometric contraction during 16 and 32 seconds of recovery. Resistance training along with creatine supplementation has typically been find more shown to be more beneficial at increasing body

mass, maximal strength, and weight lifting performance compared to placebo, but responses are variable [7]. With the ergogenic benefits consistently being shown in both research settings and among the general population, creatine has become one of the most recognized Metalloexopeptidase ergogenic aids to date. Intramuscular stores of creatine are considered to be saturated at 160 mmol/kg dry mass; however, only 20% of users achieve this amount and another 20–30% do not respond to creatine supplementation at all [1]. Several hundred studies have examined creatine supplementation’s effectiveness in improving muscle performance. Approximately 70% of these studies have shown statistically significant performance improvements, with the remaining studies generally producing non-significant trends [8]. Aside from differences such as experimental design, amount and duration of creatine dosage, training status of participants, etc., the variance in response to creatine supplementation may be due to regulatory mechanisms of a sodium-chloride dependent creatine transporter. The creatine transporter is directly involved in the extracellular Selleck Crenigacestat uptake of creatine to increase the pool of metabolically active creatine in muscle [9].