Changes in blood acid–base status caused by nutrition are generally small, and the large inter-subject variation in PRAL during ND may have masked the possible effects of LPVD on acid–base balance.

Moreover, Evofosfamide research buy the large variability during ND combined with the small subject group may have made the possible influence of nutrition difficult to detect. In the present study ND, 17.6 ± 3.0% of the total energy intake (1.59 ± 0.28 g/kg) contained protein and LPVD contained 10.1 ± 0.26% (0.80 ± 0.11 g/kg) protein. The Staurosporine difference was statistically significant, but was not enough to cause changes in acid–base balance. In other studies, the difference has been greater; e.g. there are studies where the protein intakes during high- and low-protein diets have been 25.3 ± 4.1% vs. 9.4 ± 1.8%; 29 ± 4% vs. 10 ± 2% and 33 ± 6% vs. 10 ± 1% [14, 18, 19 respectively]. According to the present and other studies, and in the light of the fact that the protein intake increases the renal capacity to excrete selleck screening library acids [7], it seems that the difference in protein content of the diet must be remarkable to cause differences in acid–base status. Furthermore, the body will normally

compensate rapidly for acute changes in acid–base balance to sustain [H+ at the optimal level [5]. In the above mentioned studies [14, 18, 19], for example, pCO2 compensated the changes in venous blood pH. As is generally known, pH in body fluids is quite stable, although there are large amount of acids produced constantly in metabolism [1]. It may be that changing diet for only 4 days is not enough to shift acid–base balance to any direction so remarkably that it could be seen in venous blood samples. Since blood pH is strictly regulated,

it would be reasonable to also measure urine pH to see if acid load of the body has changed [15]. In the present study we wanted to explore if changing diet from neutral to clearly alkali-producing (instead of two extremes) affects acid–base balance and performance. SID increased by 3.1% during LPVD, which is an encouraging result, but this change was not large enough to cause a detectable change in dependent variables like H+ or HCO3 -. Moreover, SID remained at a normal level and did not rise above Phosphatidylinositol diacylglycerol-lyase 40 mmol/l, which can be considered as the lower limit of alkalosis [20]. Nonetheless, our results show that the 4-day diets we compared in this study did not cause a measurable difference in venous blood acid–base status. Oxygen consumption and fuel selection during cycling Nutrition had a statistically significant impact on O2 consumption and CO2 production during aerobic cycling. After LPVD, both O2 and CO2 were approximately 13% higher at every submaximal stage of the cycle ergometer test compared to ND. There were no differences in heart rates between the two cycling tests, so the loading for the cardiovascular system and the workload were similar during both tests.