As such, the design of this study should allow for the results to be more generalizable to the find more habitual consumption of bottled water than would results from a laboratory controlled study. Influence on Acid-Base Balance When compared with the consumption of the placebo bottled water,
habitual consumption of AK water in the present study was associated with Mocetinostat nmr an increase in both urine (Table 7) and blood (Figure 3) pH while measures of both daily PA (Table 4) and dietary composition remained stabile. Previous research by Welch et al. [11] demonstrated that urinary pH from 24-hour collection samples could function as an effective surrogate marker for changes in acid-base balance when evaluating differences in dietary intake. König et al [10] used this information as a premise for determining that consumption of a mineral-rich supplement significantly increased both urine (5.94 to 6.57) and blood pH (7.40 to BMS202 7.41). Similarly, Berardi et al. [9] showed that urinary pH increased from 6.07 to 6.21 and 6.27
following one and two weeks of ingestion, respectively, of a plant-based supplement. The observations from these studies [9, 10] are consistent with the changes in urine (6.23 to 7.07) and blood pH (7.52 to 7.69) observed by the present study for the Experimental group. Thus, the habitual consumption of AK water under free-living conditions had a similar influence on urinary and blood pH as has been shown to occur with nutrition supplements specifically designed to impact the body’s acid-base balance. The above observations, however, are not without limitations as the onset and magnitude of the urine alkalization within the Experimental group was influenced by daily PA, SRWC, and computed dietary PRAL (Table 9). Specifically, urine pH tended to increase sooner within the treatment period and to a higher pH level for those who habitually engaged in more physical activity, self-reported drinking more AK water, (-)-p-Bromotetramisole Oxalate as well as those who regularly reported higher nutritionally-induced acid loads (Table 9). Thus, the actual impact of consuming the AK water’s mineral-based alkalizing
agents on urine pH may be dose dependent. This observation would certainly explain the differences in urinary pH between “”low”" and “”high”" levels of AK water consumption and daily PA, but a study that precisely controls AK water intake is needed to support the speculation of a dose-response relationship. It is interesting to note that the blood pH values reported for this study are somewhat higher than the 7.35-7.45 range typically ascribed as the ideal range for blood pH. It is likely that the measurement procedures used (i.e., fingertip samples collected in heparinized capillary tubes and refrigerator stored for 6-10 hrs) allowed the samples to slightly increase pH prior to the actual measurement of pH.