Effect of exercise and fluid consumption on salivary flow and pH.

Recent claims have been made regarding the putative erosive effects of regularly ingesting low-pH beverages on the integrity of tooth enamel. The purpose of this study was to determine whether fluid consumption during exercise affects the body's defenses against enamel erosion: saliva flow and salivary pH. Males and females (n=50) exercised in the heat (26.7 degrees C, 40 % RH) for 75 min on four occasions. Within each session, subjects consumed ad-lib either water, a sports drink (Gatorade), diluted orange juice, or a homemade sports drink, with the latter three fluids all having low pH values (3.0 to 4.0). Prior to and following exercise, subjects performed a standard stimulated saliva collection procedure. Immediately following collection, saliva flow rate and pH were determined for each sample. Repeated-measures ANOVA were used to evaluate the data. Compared to pre-exercise salivary flow rates (2.6+/- 0.8 ml/min), the post-exercise rate was not different when consuming the sports drink (2.6+/- 0.9 ml/min), but decreased when water or the homemade sports drink was ingested (2.4+/- 0.9 ml/min; p<0.05). A time-by-drink interaction (p<0.05) revealed slight differences in saliva pH after exercise, depending on the beverage consumed; post-exercise saliva pH was highest for water (7.2+/- 0.2) and lowest for the homemade sports drink (7.1+/- 0.2), with the sports drink and diluted orange juice values falling in between. The results suggest that minimal changes occur in saliva pH and the rate of stimulated saliva flow with beverage consumption during exercise. Subsequent research is needed to determine whether maintenance of saliva production by drinking beverages during exercise influences the body's defenses against dental erosion via saliva production.

Gastric emptying and plasma deuterium accumulation following ingestion of water and two carbohydrate-electrolyte beverages.

The purpose of this study was to compare the gastric emptying rates (GER) of water, a 6% carbohydrate (CHO) beverage, and a 20% CHO beverage and to contrast those rates against the rate at which deuterium oxide in the drinks accumulated in plasma (DAR) following beverage ingestion. Ten subjects (8 males, 2 females) cycled at 60% VO2max for 70 min; at 13 min, the subjects ingested 400 ml of one of the beverages. The GER and DAR of water and 6% CHO were similar, while GER and DAR were both significantly slowed by ingestion of 20% CHO. Although there was a significant correlation (r = .63, p < .05) between GER and DAR, only 40% of the variation in DAR could be accounted for by variation in GER. These data support the contention that DAR is partially determined by GER, with differences in the rate of fluid absorption across the intestine and other factors accounting for the remaining variation in DAR.

Physiological and performance responses to nicotinic-acid ingestion during exercise.

The purpose of this study was to assess how selected physiological and performance responses are affected when the normal increase in plasma free fatty acid concentration during exercise is blunted by ingesting nicotinic acid. On four occasions, 10 subjects cycled at 68 +/- 1% VO2peak for 120 min followed by a timed 3.5-mile performance task. Every 15 min during exercise, subjects ingested 3.5 ml.kg LBM-1 of one of four beverages: 1) water placebo (WP), 2) WP + 280 mg nicotinic acid.l-1 (WP + NA), 3) 6% carbohydrate-electrolyte beverage (CE), and 4) CE + NA. Ingestion of nicotinic acid (WP + NA and CE + NA) blunted the rise in FFA associated with WP and CE; in fact, NA ingestion effectively prevented FFA from rising above rest values. The low FFA levels with NA feeding were associated with a 3- to 6-fold increase in concentrations of human growth hormone throughout exercise. The mean performance time for CE (10.7 min) was significantly less than for WP (12.2 min) and WP + NA (12.8 min), but did not differ from CE + NA (11.4 min). The results indicate that blunting the normal rise in FFA alters the hormonal response to exercise and reduces the capacity to perform high-intensity exercise.

Efficacy of iloprost (ZK36374) versus aspirin in preventing heparin-induced platelet activation during cardiac operations.

For patients with heparin-induced platelet activation, reexposure to heparin can result in profound thrombocytopenia, intravascular thrombosis, and hemorrhage. We compared the ability of aspirin to that of iloprost (ZK36374), an analogue of prostacyclin, in preventing heparin-induced platelet activation and thus permitting a cardiac operation in a patient with heparin-induced platelet activation. Despite abolishing thromboxane A2 synthesis, aspirin (4 mmol/L) failed to prevent either in vitro heparin-induced platelet aggregation (65.0% without versus 59% with aspirin) or carbon 14-serotonin release (81.8% without versus 59.7% with aspirin). In contrast, iloprost (0.01 mumol/L) prevented both in vitro heparin-induced platelet aggregation (65% without versus 5.0% with iloprost) and release (81.8% without versus 0% with iloprost). Consequently, a continuous infusion of iloprost was begun before administration of heparin, continued throughout cardiopulmonary bypass, and discontinued 15 minutes after administration of protamine. The whole blood platelet count (209,000/microliter) remained stable after intraoperative administration of heparin (238,000/microliter) and was 115,000/microliter after the operation. No spontaneous platelet aggregates were observed in samples of platelet-rich plasma after heparin administration, and no platelet transfusions were required. Plasma levels of platelet factor 4 rose from 27 to 725 ng/ml after heparin administration but then declined during bypass to 50 ng/ml. Beta thromboglobulin levels only rose from 92 to 496 ng/ml with administration of heparin. Fibrinopeptide A levels fell from 72 to 22 ng/ml after heparin and remained stable throughout bypass. The template bleeding time was 7.5 minutes preoperatively and 8.0 minutes postoperatively. The postoperative chest tube drainage (12 hours) was 475 ml, and platelets responded normally to adenosine diphosphate. In conclusion, iloprost but not aspirin completely prevented heparin-induced platelet activation in vitro. Furthermore, iloprost effectively prevented this syndrome clinically, which permitted a safe cardiac operation in this patient with heparin-induced platelet activation.