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Lactate threshold is an important reference point when setting training intensities for endurance athletes. Ventilatory threshold has been used as a noninvasive estimate of lactate threshold, but appears to underestimate training intensity for many athletes. This study evaluated whether data obtained during a noninvasive, maximal exercise test could be used to predict lactate threshold. Maximal oxygen consumption (55+/-2 ml O(2) x kg(-1) x min(-1)) and heart rate at the ventilatory threshold (V-slope method) were determined for 19 cyclists (10 men, 9 women, 35+/-2 years). Cyclists also performed a lactate threshold test, consisting of 8 min stages at power outputs below, at, and above the ventilatory threshold. Heart rate associated with the lactate threshold was determined using the Dmax method. The correlation coefficient between heart rates at the ventilatory and lactate thresholds was 0.67, indicating 45% shared variance. The best fitting model to predict heart rate at the lactate threshold included heart rate at the ventilatory threshold, gender, body weight, and an interaction between gender and body weight. Using this model, R(2) was 0.70. Thus, heart rate at the ventilatory threshold may be adjusted to more accurately predict a heart rate that corresponds to the lactate threshold for recreational cyclists.

Plasma triglyceride concentrations were shown to be higher in hypertensive (153±2 mm Hg) male Dahl salt-sensitive rats than in control Sprague-Dawley rats (122 ±2 mm Hg). These differences in triglyceride concentrations were seen when blood was drawn at 9 AM from unfasted animals (229±27 versus 111±8 mg/dL), at 1 PM after a 4-hour fast (186±13 versus 88±4 mg/dL), or at 9 AM after a 13-hour fast (151±6 versus 90±6 mg/dL), all p<0.001. Total triglyceride secretion was also compared in groups of rats by determining the increment in plasma triglyceride concentration for 2 hours after blocking triglyceride removal from plasma by injecting Triton. Studies performed at 1 PM and 9 AM, after the 4-and 13-hour fast, demonstrated that total triglyceride secretion was greater (p<0.05) in Dahl rats only when studied at 1 PM. Direct estimates of hepatic triglyceride secretion at 1 PM also demonstrated a significant (p<0.02) increase in secretion rate by perfused livers from Dahl rats, due in part to their increased liver size. In addition, removal of prelabeled very low density lipoprotein-triglyceride in the intact rat was significantly (p<0.05) decreased in Dahl rats. Lipoprotein lipase activity measured in skeletal muscle, heart, and adipose tissue was also significantly decreased at 9 AM and 1 PM (after 0 and 4 hours of fasting) in tissue from Dahl rats. These data confirm that Dahl rats have higher plasma triglyceride concentrations than Sprague-Dawley rats. Since both total and hepatic triglyceride secretion were somewhat greater in Dahl rats, in association with a decrease in both removal of very low density lipoprotein from plasma and decreased muscle and adipose tissue lipoprotein lipase activity, it seems likely that hypertriglyceridemia in Dahl rats results from a combination of increased triglyceride secretion and decreased triglyceride removal. 1 Since hypertriglyceridemia has also been noted in patients with hypertension, 23 as well as in two other models of rodent hypertension, 45 it seemed possible that an increased understanding of the cause of hypertriglyceridemia in a rodent model of hypertension would provide useful information relevant to the change in lipoprotein metabolism seen in patients with high blood pressure. As a first step in this process, we initiated a series of studies to define the mechanism of hypertriglyceridemia in Dahl S rats. Increased plasma very low density lipoprotein-TG (VLDL-TG) concentration in Dahl S rats may be due to increased hepatic VLDL-TG secretion, decreased VLDL-TG removal, or both, with the latter process dependent on the activity of lipoprotein lipase (LPL). 6 We determined TG secretion in both the intact

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