The purpose of this study was to determine if supplementing the diet with recommended (1.5 g/d for 28-days) or creatine equivalent loading and maintenance doses of a purported buffered form of creatine (20 g/d for 7-days and 5 g/d for 21-days) was more effective in increasing muscle creatine retention, body composition, strength, and/or anaerobic capacity than supplementing the diet with creatine monohydrate (20 g/d for 7-days and 5 g/d for 21-days). Additionally, the study was undertaken to determine whether supplementing the diet with recommended or equivalent creatine doses of a purported buffered form of creatine was associated with fewer side effects in comparison to creatine monohydrate. Results of the present study clearly show that supplementing the diet with a purported buffered form of creatine is not a more efficacious and/or a safer form of creatine to consume than creatine monohydrate.
According to product claims [28, 30], KA is “up to ten times more powerful than ordinary Creatine”. The rationale for this contention is based on experiments reported in a patent  and/or on the manufacturer’s website [28, 30] which indicates that KA has less conversion of creatine to creatinine in fluid over time compared to creatine monohydrate. This is despite the fact that studies show that creatine monohydrate is not significantly degraded to creatinine during the normal digestive process and nearly 99% of creatine monohydrate that is orally ingested is either taken up by tissue or excreted in the urine [1–3, 18, 21]. Because of this fact, an accepted method of assessing whole body creatine retention has been to subtract daily urinary creatine excretion from daily dietary intake of creatine [32, 33, 45–47]. Additionally, while it is true that generally the lower the pH and higher the temperature, the greater conversion of creatine to creatinine, studies show that this process takes several days to occur at significant levels even when creatine is exposed to low pH environments [1, 19, 48]. As described in a recent review , the degradation of creatine can be reduced or even halted by either lowering the pH to under 2.5 or increasing the pH. A very high pH results in the deprotonation of the acid group, thereby slowing down the degradation process by making it more difficult for the intramolecular cyclization of creatine to creatinine. However, a very low pH (as is the case in the stomach) results in the protonation of the amide function of the creatine molecule, thereby preventing the intramolecular cyclization of creatine to creatinine . This is the reason that the conversion of creatine to creatinine in the gastrointestinal tract has been reported to be minimal regardless of transit time [7, 18, 20]. Thus, on the surface, the KA manufacturer’s claims that creatine monohydrate is degraded to creatinine in large amounts after oral ingestion and that a “buffered” or “pH-correct” would significantly reduce this effect once consumed and thereby promote greater uptake of creatine in the muscle is inconsistent with available literature on creatine .
Results of the present study do not support claims that a large amount of creatine monohydrate was converted to creatinine during the digestive process and thereby resulted in less of an increase in muscle creatine than KA. In this regard, while serum creatinine levels increased to a greater degree in the KA-H and CrM groups that ingested larger amounts of creatine, the 0.1 - 0.2 mg/dL greater increase observed in creatinine compared to the KA-L group was well within normal limits (i.e., <1.28 ± 0.20 mg/dl) particularly for resistance-trained males. Therefore, this small change would be clinically insignificant. Additionally, a significant increase from baseline in serum creatinine was also observed in the KA-L and KA-H groups despite claims that KA completely prevents the conversion of creatine to creatinine. These findings do not support contentions that CrM is degraded to creatinine in large amounts or that KA is not converted to creatinine at all.
Previous research has shown that ingestion of 20 g/d of CrM for 5–7 days can increase muscle creatine content 10-40% after 5–7 d of supplementation [1, 4–8, 10]. Prolonged low-dose ingestion of CrM (e.g., 2 – 3 g/d for 4–6 weeks) has also been reported to increase muscle creatine content in a similar manner as loading strategies [4, 7, 8]. The manufacturer of KA claims that ingesting 1.5 g of KA is equivalent to ingesting 10–15 g of CrM . If this were true, those ingesting recommended levels of KA (1.5 g/d for 28-days) should experience a similar increase in muscle creatine as those participants ingesting recommended loading (20 g/d for 7-days) and maintenance doses (5 g/d for 21-days) of CrM. Results of the present study indicated that supplementing the diet with manufacturer’s recommended levels of KA (1.5 g/d) did not increase muscle free creatine content to the same degree as loading and maintenance doses of CrM. In fact, although no overall group effect was observed among the three groups studied (p = 0.14), pairwise comparison of the mean group change from baseline in the KA-L group was 11 times less than the change observed following CrM supplementation (KA-L −1.1 ± 4.3, CrM 11.2 ± 4.3 mmol/kg DW [mean ± SEM], p = 0.053). After 28-days of supplementation, muscle free creatine content in the KA-L group was increased by 4.71 ± 27.0 mmol/kg DW compared to 22.3 ± 21.0 mmol/kg DW in the CrM group representing a 4.7 fold less effect of KA supplementation than CrM when comparing recommended levels. Consequently, results of the present study do not support claims that ingesting 1.5 grams of KA is as effective as ingesting 10–15 grams of creatine monohydrate. Even when participants ingested creatine equivalent amounts of KA and CrM (i.e., 20 g/d for 7-days and 5 g/d for 21-days), KA did not promote greater increases in muscle free creatine. In fact, while not significantly different, changes in muscle creatine in the KA-H group were more than two times less than the changes observed in the CrM group (KA-H 9.07 ± 23.2; CrM 22.3 ± 21.0 mmol/kg DW). Thus, results of the present study do not support claims that ingesting a purported buffered form of creatine is more effective in increasing muscle creatine content than creatine monohydrate.
While some may argue that since there is generally large variability in measuring muscle phosphagen levels and we were unable to obtain reliable PCr measurements, it is difficult to make a definitive conclusion about the effects of KA on muscle creatine content based on measuring muscle free content alone. However, present findings also provide no support for claims that KA supplementation is “up to ten times more powerful than ordinary Creatine.” In this regard, while time effects were observed in training adaptations, supplementing the diet with KA (at recommended or creatine equivalent loading and maintenance doses) did not promote statistically greater gains in fat free mass, 1 RM strength, or anaerobic sprint performance capacity compared to CrM. At best, one can conclude that ingesting recommended and creatine equivalent loading and maintenance amounts of KA resulted in similar training adaptations as creatine monohydrate supplementation at recommended loading and maintenance levels. However, results of the present investigation provide no evidence to support claims that KA is “the world’s most potent creatine” .
Further, results of the present investigation provided no evidence that KA is a safer form of creatine to consume at either lower recommended levels or higher creatine equivalent doses compared to normal loading and maintenance doses of creatine monohydrate. In this regard, there were no significant differences observed among groups in BIA determined total body water or serum electrolyte status. Likewise, no cramping or other side effects were reported. These findings are consistent with previous studies that have indicated that creatine supplementation does not promote dehydration and/or cramping [9, 21–26]. There were also no significant differences observed among groups in serum lipids (TCHL, HDL, TCHL:HDL ratio, TRIG) or blood glucose. Serum LDL decreased slightly in response to creatine loading in the CrM group but returned to baseline after ingesting maintenance doses of CrM suggesting these changes were transient. Additionally, no significant differences were observed among groups in markers of catabolism (BUN, BUN:CRN, AST, ALT, Total Protein, TBIL), markers of bone status (bone mineral content, ALB, GLOB, ALB:GLOB, calcium, ALK) or whole blood markers (WBC, RBC, Hematocrit, Hemoglobin, MCV, MCH, MCHC, RBCDW, platelet counts). Moreover, values remained within normal levels for active individuals. These findings are consistent with other studies that have examined the safety of creatine supplementation in active individuals [1, 3, 21, 26, 27, 38]. Consequently, present findings do not support claims that KA is a safer form of creatine to ingest than creatine monohydrate.