This study assessed whether the elevated sensitivity of ventilation to hypoxia during exercise is accounted for by an elevation of esophageal temperature (Tes). Eleven males volunteered for two exercise sessions on an underwater, headout cycle ergometer at a steady-state rate of oxygen consumption (V O 2) of ϳ0.87 l/min (SD 0.07). In one exercise session, 31.5°C (SD 1.4) water held Tes at a normothermic level of ϳ37.1°C, and in the other exercise session, water at 38.2°C (SD 0.1) maintained a hyperthermic Tes of ϳ38.5°C. After a 30-min rest and 20-min warm-up, exercising participants inhaled air for 10 min [Euoxia 1 (E1)], an isocapnic hypoxic gas mixture with 12% O2 in N2 (H1) for the next 10 min and air again [Euoxia 2 (E2)] for the last 10 min. A significant increase in V E during all hyperthermia conditions (0.01Ͻ P Ͻ 0.048) was evident; however, during hyperthermic hypoxia, there was a disproportionate and significant (P ϭ 0.017) increase in V E relative to normothermic hypoxia. This was the main explanation for a significant esophageal temperature and gas type interaction (P ϭ 0.012) for V E. Significant effects of hyperthermia, isocapnic hypoxia, and their positive interaction remained evident after removing the influence of V O2 on V E. Serum lactate and potassium concentrations, as well as hemoglobin oxygen saturation, were each not significantly different between normothermic and hyperthermic-hypoxic conditions. In conclusion, the elevated sensitivity of exercise ventilation to hypoxia during exertion appears to be modulated by elevations in esophageal temperature, potentially because of a temperature-mediated stimulation of the peripheral chemoreceptors. oxygen consumption; isocapnia; hyperpnea; chemosensitivity; immersion THERE HAVE BEEN SEVERAL PROPOSED mechanisms for the hyperpnea that occurs during exercise (16,25,37). A neurogenic hypothesis (16) implicates core temperature as a central mediating stimulus in the control of pulmonary ventilation during both actively and passively induced hyperthermia (2, 37). It suggests that increases in core temperature could increase pulmonary ventilation by several mechanisms. One proposed mechanism suggests an increase in core temperature is associated with an increase in carbon dioxide sensitivity (30), while another suggests a direct physical effect of increased temperature in the respiratory control center and the peripheral chemoreceptors (5). The increased sensitivity to carbon dioxide (CO 2 ) appears to be evident during exercise (35), and during postexercise hyperthermia (28). Another hypothesis suggests a direct effect of an increase in core temperature causing a change in the equilibrium constants of the CO 2 buffer system, resulting in a diminished capacity to buffer CO 2 by body fluids (32). Pulmonary ventilation is then elevated after hydrogen ion (H ϩ ) concentration is increased in the regions of the central respiratory centers in the medulla oblongata.Hypoxia is another well-established modulator of pulmonary ventilation. Low inspired O 2 parti...

We devise a method for automatically detecting treatment relationships using lexico-syntactic patterns and its application to medical-oriented patent retrieval. This process for detecting treatment relationships involves finding lexico-syntactic patterns that are highly indicative of treatment relationships and also producing classification rules for those patterns.This treatment relationship detection process is then used in a system to find treatment relationships based on a user query in a medical patent source. The query will consist of terms that the user wants to find in the subject or object of a treatment relationship. This is of great interest to both patent examiners and patent applicants as they search for prior art. Through the use of classification rules, this system was able to achieve a precision of 85.81% on a set of 20 test queries.

[Purpose]Postprandial lipemia (PPL) contributesto the development of atherosclerosis. In females, repeated 8-second bouts of interval sprinting exercise reduced PPL, however, the effect of 8-second bouts of interval sprinting on PPL of overweight males is undetermined. Thus, the effect of 8-secondsof interval sprinting for 20 min, the night before ingestion of a high-fat meal (HFM), on plasma triacylglycerol(TG) levelswas examined.[Methods]Ten overweight males acted as participants (BMI = 26±3.0kg/m2, age 22 ± 2.5 years). A crossover design was employed withinterval sprinting and a noexercise condition separated by 7days. Participants consumed a milkshake (high-fat meal;HFM = 4170 kJ/993 Kcal) the morning after an overnight fast, followed by 4 hourly blood samples. Participants performedone bout of interval sprinting (8seconds sprinting at 110-115rpm, 12seconds active recovery at ~60rpm for 20 minutes) the evening before the consumption of the HFM.[Results]Postprandial TG was 22.5% lower in the interval sprinting compared to the noexercise condition when comparing the change in total area under the curve (ΔAUCT): ISE(7.15±1.90mmolL-1h-1) versus noexercise (9.22±3.44mmolL-1h-1), p=.014. The correlation between fasting TG levels in the noexercise condition and total reduction in AUCT between the conditions was significant (r=.87, p=.001).[Conclusion]One 20-min bout of interval sprinting,the night before consumption of a HFM,significantly attenuated the PPL response of sedentary males.

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