Adaptations in fat and carbohydrates metabolism after a prolonged endurance training program were examined using stable isotope tracers of glucose ([6,6-2H2]glucose), glycerol ([2H5]glycerol), and palmitate ([2H2]palmitate). Active, but untrained, males exercised on a cycle for 2 h/day [60% pretraining peak O2 consumption (VO2peak) = 44.3 +/- 2.4 ml.kg-1.min-1] for a total of 31 days. Three cycle tests (90 min at 60% pretraining VO2peak) were administered before training (PRE) and after 5 (5D) and 31 (31D) days of training. Exercise increased the rate of glucose production (Ra) and utilization (Rd) as well as the rate of lipolysis (glycerol Ra) and free fatty acid turnover (FFARa/Rd). At 5D, training induced a 10% (P < 0.05) increase in total fat oxidation because of an increase in intramuscular triglyceride oxidation (+63%, P < 0.05) and a decreased glycogen oxidation (-16%, P < 0.05). At 31D, total fat oxidation during exercise increased a further 58% (P < 0.01). The pattern of fat utilization during exercise at 31D showed a reduced reliance on plasma FFA oxidation (FFA Rd) and a greater dependence on oxidation of intramuscular triglyceride, which increased more than twofold (P < 0.001). In addition, glucose Ra and Rd were reduced at all time points during exercise at 31D compared with PRE and 5D. We conclude that long-term training induces a progressive increase in fat utilization mediated by a greater oxidation of fats from intramuscular sources and a reduction in glucose oxidation. Initial changes are present as early as 5D and occur before increases in muscle maximal mitochondrial enzyme activity.

To investigate the hypothesis that respiratory gas exchange and, in particular, the O(2) consumption (VO(2)) response to exercise is altered after a 21-day expedition to 6,194 m, five male climbers (age 28.2 +/- 2 yr; weight 76.9 +/- 4.3 kg; means +/- SE) performed a progressive and prolonged two-step cycle test both before and 3-4 days after return to sea level. During both exercise tests, a depression (P < 0.05) in VO(2) (l/min) and an increase (P < 0.05) in minute ventilation (VE BTPS; l/min) and respiratory exchange ratio were observed after the expedition. These changes occurred in the absence of changes in CO(2) production (l/min). During steady-state submaximal exercise, net efficiency, calculated from the rates of the mechanical power output to the energy expended (VO(2)) above that measured at rest, increased (P < 0.05) from 25.9 +/- 1.6 to 31. 3 +/- 1.3% at the lighter power output and from 24.4 +/- 1.3 to 29.5 +/- 1.5% at the heavy power output. These changes were accompanied by a 4.5% reduction (P < 0.05) in peak VO(2) (3.99 +/- 0.17 vs. 3.81 +/- 0.18 l/min). After the expedition, an increase (P < 0.05) in hemoglobin concentration (15.0 +/- 0.49 vs. 15.8 +/- 0.41 g/100 ml) was found. It is concluded that, because resting VO(2) was unchanged, net efficiency is enhanced during submaximal exercise after a mountaineering expedition when the exercise is performed soon after return to sea level conditions.

To investigate the effects of a single session of prolonged cycle exercise [60% peak O2 uptake (VO2 peak) for 5-6 h] on metabolic adaptations in working vastus lateralis muscle, nine untrained males (peak O2 uptake = 47.2 +/- 1.1 ml x kg(-1) x min(-1), means +/- SE) were examined before (Pre) and at 2 (Post-2), 4 (Post-4), and 6 (Post-6) days after the training session. On the basis of 15 min of cycle exercise at 59% VO2 peak, it was found that training reduced (P < 0.05) exercise muscle lactate (mM) at Post-2 (6.65 +/- 0.69), Post-4 (7.74 +/- 0.63), and Post-6 (7.78 +/- 1.2) compared with Pre (10.9 +/- 1.3). No effect of training was observed on exercise ATP, phosphocreatine, and glycogen levels. After the single session of training, plasma volumes were elevated (P < 0.05) at Post-2 (6.7 +/- 1.7%), Post-4 (5.86 +/- 1.9), and Post-6 (5.13 +/- 2.5). The single exercise session also resulted in elevations (P < 0.05) in the monocarboxylate transporters MCT1 and MCT4 throughout the 6 days after exercise. Although epinephrine and norepinephrine both increased with exercise, only norepinephrine was reduced (P < 0.05) with training and only at Post-4. These results indicate that regulation of cellular lactate levels occurs rapidly and independently of other metabolic adaptations. It is proposed that increases in MCT and plasma volume are at least partly involved in the lower muscle lactate content observed after the training session by increasing lactate membrane transport and removal, respectively.

A short-term training model previously shown to result in a tighter metabolic control in working muscle in the absence of an increase in mitochondrial potential was used to examine changes in lactate turnover. Lactate flux was studied before and after 10 days of cycle training [2 h/day at 59% maximal oxygen consumption (VO2max)] in untrained men [VO2max = 45.5 +/- 2.4 (SE) ml.kg-1.min-1). A primed constant infusion of L-[1-13C]lactate was used to examine lactate kinetics during a prolonged exercise protocol (90 min at 59% VO2max). Rate of appearance of lactate increased with exercise (P < 0.01), both pretraining (rest = 30.3 +/- 4.9 ml.kg-1.min-1, exercise = 115 +/- 14 ml.kg-1.min-1) and posttraining (rest = 28.4 +/- 4.7 ml.kg-1.min-1, exercise = 112 +/- 13 ml.kg-1.min-1). Despite a lower blood lactate concentration (P < 0.05) during exercise after training, there was no difference in the rate of appearance of lactate. Training increased (P < 0.05) the metabolic clearance rate of lactate during exercise from 36.8 +/- 4.8 to 51.4 +/- 6.8 ml.kg-1.min-1. These findings indicate that at least part of the lower exercising blood lactate observed after training is due to an increase in metabolic clearance rate. In addition, the lower intramuscular lactate levels suggest a decreased recruitment of glycolysis particularly early in exercise.