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We combined tracer and arteriovenous (a-v) balance techniques to evaluate the effects of exercise and endurance training on leg triacylglyceride turnover as assessed by glycerol exchange. Measurements on an exercising leg were taken to be a surrogate for working skeletal muscle. Eight men completed 9 wk of endurance training [5 days/wk, 1 h/day, 75% peak oxygen consumption ([[??].sub.2peak])], with leg glycerol turnover determined during two pretraining trials [45 and 65% [[??].sub.2peak] (45% Pre and 65% Pre, respectively)] and two posttraining trials [65% of pretraining [[??].sub.2peak] (ABT) and 65% of posttraining [[??].sub.2peak] (RLT)] using [[sup.2][H.sub.5]]glycerol infusion, femoral a-v sampling, and measurement of leg blood flow. Endurance training increased [[??].sub.2peak] by 15% (45.2 [+ or -] 1.2 to 52.0 [+ or -] 1.8 ml x [kg.sup.-1] x [min.sup.-1], P < 0.05). At rest, there was tracer-measured leg glycerol uptake (41 [+ or -] 8 and 52 [+ or -] 15 [micro]mol/min for pre- and posttraining, respectively) even in the presence of small, but significant, net leg glycerol release (-68 [+ or -] 19 and -50 [+ or -] 13 [micro]mol/min, respectively; P < 0.05 vs. zero). Furthermore, while there was no significant net leg glycerol exchange during any of the exercise bouts, there was substantial tracer-measured leg glycerol turnover during exercise (i.e., simultaneous leg muscle uptake and leg release) (uptake, release: 45% Pre, 194 [+ or -] 41, 214 [+ or -] 33; 65% Pre, 217 [+ or -] 79, 201 [+ or -] 84; ABT, 275 [+ or -] 76, 312 [+ or -] 87; RLT, 282 [+ or -] 83, 424 [+ or -] 75 [micro]mol/min; all P < 0.05 vs. corresponding rest). Leg glycerol turnover was unaffected by exercise intensity or endurance training. In summary, simultaneous leg glycerol uptake and release (indicative of leg triacylglyceride turnover) occurs despite small or negligible net leg glycerol exchange, and furthermore, leg glycerol turnover can be substantially augmented during exercise. exercise; crossover concept; stable isotopes; lipid metabolism

To evaluate the contribution of working muscle to whole body lipid oxidation, we examined the effects of exercise intensity and endurance training (9 wk, 5 days/wk, 1 h, 75% [Vo.sub.2peak]) on whole body and leg free fatty acid (FFA) kinetics in eight male subjects (26 [+ or -] 1 yr, means [+ or -] SE). Two pretraining trials [45 and 65% [Vo.sub.2max] (45UT, 65UT)] and two posttraining trials [65% of pretraining [Vo.sub.2peak] (ABT), and 65% of posttraining [Vo.sub.2peak] (RLT)] were performed using [1-[sup.13]C] palmitate infusion and femoral arteriovenous sampling. Training increased [Vo.sub.2peak] ak by 15% (45.2 [+ or -] 1.2 to 52.0 [+ or ] 1.8 ml * [kg.sup.-1] * [min.sup.-1], P < 0.05). Muscle FFA fractional extraction was lower during exercise (EX) compared with rest regardless of workload or training status [approximately equal to] 20 vs. 48%, P < 0.05). Two-leg net FFA balance increased from net release at rest ([approximately equal to]-36 [micro]mol/min) to net uptake during EX for 45UT (179 [+ or -] 75), ABT (236 [+ or -] 63), and RLT (136 [+ or -] 110) (P < 0.05), but not 65UT (51 [+ or -] 127). Leg FFA tracer measured uptake was higher during EX than rest for all trials and greater during posttraining in RLT (716 [+ or -] 173 [micro]mol/min) compared with pretraining (45UT 450 [+ or -] 80, 65UT 461 [+ or -] 72, P < 0.05). Leg muscle lipid oxidation increased with training in ABT (730 [+ or -] 163 [micro]mol/min) vs. 65UT (187 [+ or -] 94, P < 0.05). Leg muscle lipid oxidation represented ~62 and 30% of whole body lipid oxidation at lower and higher relative intensities, respectively. In summary, training can increase working muscle tracer measured FFA uptake and lipid oxidation for a given power output, but both before and after training the association between whole body and leg lipid metabolism is reduced as exercise intensity increases. crossover concept; free fatty acids; substrate partitioning; exercise; regional metabolism

We evaluated the hypothesis that net leg total FFA, LDL-C, and TG uptake and HDL-C release during moderate-intensity cycling exercise would be increased following endurance training. Eight sedentary men (26 [+ or -] 1 yr, 77.4 [+ or -] 3.7 kg) were studied in the postprandial state during. 90 min of rest and 60 min of exercise twice before (45% and 65% [Vo.sub.2 peak]) and twice after 9 wk of endurance training (55% and 65% posttraining [Vo.sub.2 peak]). Measurements across an exercising leg were taken to be a surrogate for active skeletal muscle. To determine limb lipid exchange, femoral arterial and venous blood samples drawn simultaneously at rest and during exercise were analyzed for total and individual FFA (e.g., palmitate, oleate), LDL-C, HDL-C, and TG concentrations, and limb blood flow was determined by thermodilution. The transition from rest to exercise resulted in a shift from net leg total FFA release (-44 [+ or -] 16 [micro]mol/min) to uptake (193 [+ or -] 49 [micro]mol/min) that was unaffected by either exercise intensity or endurance training. The relative net leg release and uptake of individual FFA closely resembled their relative abundances in the plasma with ~21 and 41% of net leg total FFA uptake during exercise accounted for by palmitate and oleate, respectively. Endurance training resulted in significant changes in arterial concentrations of HDL-C (49 [+ or -] 5 vs. 52 [+ or -] 5 mg/dl, pre vs. post) and LDL-C (82 [+ or -] 9 vs. 76 [+ or -] 9 mg/dl, pre vs. post), but there was no net TG or LDL-C uptake or HDL-C release across the resting or active leg before or after endurance training. In conclusion, endurance training favorably affects blood lipoprotein profiles, even in young, healthy normolipidemic men, but muscle contractions per se have little effect on net leg LDL-C, or TG uptake or HDL-C release during moderate-intensity cycling exercise. Therefore, the favorable effects of physical activity on the lipid profiles of young, healthy normolipidemic men in the postprandial state are not attributable to changes in HDL-C or LDL-C exchange across active skeletal muscle. crossover concept; cholesterol; lipid metabolism; exertion doi:10.1152/ajpendo.00020.2006

High-altitude anorexia leads to a hormonal response pattern modulated by both hypoxia and caloric restriction (CR). The purpose of this study was to compare altitude-induced neumendocrine changes with or without energy imbalance and to explore how energy sufficiency alters the endocrine acclimatization process. Twenty-six normal-weight, young men were studied for 3 wk. One group [hypocaloric group (HYPO), n = 9] stayed at sea level and consumed 40% fewer calories than required to maintain body weight. Two other groups were deployed to 4,300 meters (Pikes Peak, CO), where one group (ADQ, n = 7) was adequately fed to maintain body weight and the other [deficient group (DEF), n = 10] had calories restricted as above. HYPO experienced a typical CR-induced reduction in many hormones such as insulin, testosterone, and leptin. At altitude, fasting glucose, insulin, and epinephrine exhibited a muted rise in DEF compared with ADQ. Free thyroxine, thyroid-stimulating hormone, and norepinephrine showed similar patterns between the two altitude groups. Morning cortisol initially rose higher in DEF than ADQ at 4,300 meters, but the difference disappeared by day 5. Testosterone increased in both altitude groups acutely but declined over time in DEF only. Adiponectin and leptin did not change significantly from sea level baseline values in either altitude group regardless of energy intake. These data suggest that hypoxia tends to increase blood hormone concentrations, but anorexia suppresses elements of the endocrine response. Such suppression results in the preservation of energy stores but may sacrifice the facilitation of oxygen delivery and the use of oxygen-efficient fuels. altitude: hypoxia: hormones: energy balance; acclimatization: caloric restriction

Three weeks of caloric restriction alters protein metabolism in normal-weight young men. Am J Physiol Endocrinol Metab 289: E446-E455, 2005. First published May 3, 2005; doi:10.1152/ajpendo.00001.2005.--The effects of prolonged caloric restriction (CR) on protein kinetics in lean subjects has not been investigated previously. The purpose of this study was to test the hypotheses that 21 days of CR in lean subjects would 1) result in significant losses of lean mass despite a suppression in leucine turnover and oxidation and 2) negatively impact exercise performance. Nine young, normal-weight men [23 [+ or -] 5 y, 78.6 [+ or -] 5.7 kg, peak oxygen consumption (V[O.sub.2] peak) 45.2 [+ or -] 7.3 ml x [kg.sup.-1] x [min.sup.-1], mean [+ or -] SD] were underfed by 40% of the calories required to maintain body weight for 21 days and lost 3.8 [+ or -] 0.3 kg body wt and 2.0 [+ or -] 0.4 kg lean mass. Protein intake was kept at 1.2 g x [kg.sup.-1] x [day.sup.-1]. Leucine kinetics were measured using [alpha]-ketoisocaproic acid reciprocal pool model in the postabsorptive state during rest and 50 min of exercise (EX) at 50% of V[O.sub.2] peak. Body composition, basal metabolic rate (BMR), and exercise performance were measured throughout the intervention. At rest, leucine flux ([approximately equal to] 131 [micro]mol x [kg.sup.-1] x [h.sup.-1]) and oxidation ([R.sub.ox]; [approximately equal to] 19 [micro]mol x [kg.sup.-1] x [h.sup.-1]) did not differ pre- and post-CR. During EX, leucine flux (129 [+ or -] 6 vs. 121 [+ or -] 6) and [R.sub.ox] (54 [+ or -] 6 vs. 46 [+ or -] 8) were lower after CR than they were pre-CR. Nitrogen balance was negative throughout the intervention ([approximately equal to] 3.0g N/day), and BMR declined from 1,898 [+ or -] 262 to 1,670 [+ or -] 203 kcal/day. Aerobic performance (V[O.sub.2] peak, endurance cycling) was not impacted by CR, but arm flexion endurance decreased by 20%. In conclusion, 3 wk of caloric restriction reduced leucine flux and [R.sub.ox] during exercise in normal-weight young men. However, despite negative nitrogen balance and loss of lean mass, whole body exercise performance was well maintained in response to CR. energy intake; energy expenditure; leucine flux; exercise; nitrogen balance; lean mass