Muscle is a site of lactate production and utilization with shuttling and oxidation occurring both among (Brooks, 1985) and within (Brooks, 1998) muscles. Additionally, during moderate-intensity exercise lactate turnover often exceeds that of glucose (Brooks, 1991), and lactate rate of oxidation (R ox ) can represent as much as 25 % of whole body carbohydrate (CHO) R ox (Bergman et al. 1999b). Whereas the importance of lactate as a fuel is recognized, the interactions of lactate and glucose as CHO sources for exercising muscle are relatively unexplored. Pearce & Connett (1980) demonstrated in isolated, noncontracting, rat soleus muscle that 8 mM lactate resulted in a decreased oxidation of glucose compared to no lactate. Further, a series of studies on rats Vettor et al. 1997) demonstrated that lactate infusion decreased glucose rate of disappearance (R d ) in skeletal muscle ) during a euglycaemichyperinsulinaemic clamp, and a lactate infusion during hyperglycaemia resulted in increased glucose R d with increased glycogen synthesis, but unchanged flux through glycolysis . More recently the same group (Lombardi et al. 1999) demonstrated that a 24 h lactate infusion decreased GLUT-4 mRNA and protein content, offering a possible mechanism for decreased glucose disposal in disease states with chronic elevated lactate levels. Whereas the data on resting rats are in good agreement, data in humans are less consistent.Lactate infusion in resting humans during a euglycaemichyperinsulinaemic clamp had no effect on glucose exchange across an inactive forearm (Ferrannini et al. 1993). We (Miller et al. 2002) recently demonstrated with a lactate clamp (LC) procedure that exogenous lactate infusion resulted in decreased glucose oxidation during rest after an 8-12 week training programme. We also reported decreased glucose oxidation with exogenous lactate infusion during exercise at the same absolute, but not relative, exercise intensity after training. Additionally, during exogenous lactate infusion the percentage of glucose R d oxidized decreased during rest pre-and posttraining and during exercise at the same absolute intensity
We sought to determine whether lipolysis, fatty acid (FA) mobilization, and plasma FA oxidation would remain elevated for hours following isoenergetic exercise bouts of different intensities. Ten men and eight women received a primed-continuous infusion of [1,1,2,3,3-2 H 5 ]glycerol and continuous infusion of [1-13 C]palmitate to measure glycerol and plasma FA kinetics. On Day 1 (D1), participants were studied under one of three different conditions, assigned in random order: (1) before, during and 3 h after 90 min of exercise at 45%V O 2 peak (E45), (2) before, during and 3 h after 60 min of exercise at 65%V O 2 peak (E65), and (3) in a time-matched sedentary control trial (C). For each condition, participants were studied by indirect calorimetry the following morning as well (D2). Rate of appearance (Ra) of glycerol (Ra GL ) increased above C during exercise in men and women (P < 0.05), was higher in E45 than E65 in men (P < 0.05), and was not different between exercise intensities in women. During 3 h of postexercise recovery, Ra GL remained significantly elevated in men (P < 0.05), but not women. FA Ra (Ra FA ) increased during exercise in men and women and was higher in E45 than E65 (P < 0.05), and remained elevated during 3 h of postexercise recovery in both sexes (P < 0.05), but with a greater relative increase in men than women (P < 0.05). Plasma FA oxidation (Rox) increased during exercise with no difference between intensities, and it remained elevated during 3 h of postexercise recovery in both sexes (P < 0.05). Total lipid oxidation (Lox) was elevated in both sexes (P < 0.05), but more in men during 3 h of postexercise recovery on D1 (P < 0.05) and remained elevated on D2 in men (P < 0.05), but not in women. There were no differences between E45 and E65 for postexercise energy substrate turnover or oxidation in men and women as energy expenditure of exercise (EEE) was matched between bouts. We conclude that the impact of exercise upon lipid metabolism persists into recovery, but that women depend more on lipid during exercise whereas, during recovery, lipid metabolism is accentuated to a greater extent in men.
To understand the meaning of the lactate threshold (LT) and to test the hypothesis that endurance training augments lactate kinetics [i.e., rates of appearance and disposal (Ra and Rd, respectively, mg·kg(-1)·min(-1)) and metabolic clearance rate (MCR, ml·kg(-1)·min(-1))], we studied six untrained (UT) and six trained (T) subjects during 60-min exercise bouts at power outputs (PO) eliciting the LT. Trained subjects performed two additional exercise bouts at a PO 10% lower (LT-10%), one of which involved a lactate clamp (LC) to match blood lactate concentration ([lactate]b) to that achieved during the LT trial. At LT, lactate Ra was higher in T (24.1 ± 2.7) than in UT (14.6 ± 2.4; P < 0.05) subjects, but Ra was not different between UT and T when relative exercise intensities were matched (UT-LT vs. T-LT-10%, 67% Vo2max). At LT, MCR in T (62.5 ± 5.0) subjects was 34% higher than in UT (46.5 ± 7.0; P < 0.05), and a reduction in PO resulted in a significant increase in MCR by 46% (LT-10%, 91.5 ± 14.9, P < 0.05). At matched relative exercise intensities (67% Vo2max), MCR in T subjects was 97% higher than in UT (P < 0.05). During the LC trial, MCR in T subjects was 64% higher than in UT (P < 0.05), in whom %Vo2max and [lactate]b were similar. We conclude that 1) lactate MCR reaches an apex below the LT, 2) LT corresponds to a limitation in MCR, and 3) endurance training augments capacities for lactate production, disposal and clearance.
To evaluate the hypothesis that precursor supply limits gluconeogenesis (GNG) during exercise, we examined training-induced changes in glucose kinetics [rates of appearance (R a) and disappearance (Rd)], oxidation (R ox), and recycling (Rr) with an exogenous lactate infusion to 3.5-4.0 mM during rest and to pretraining 65% peak O 2 consumption (V O2 peak) levels during exercise. Control and clamped trials (LC) were performed at rest pre-(P RR, PRR-LC) and posttraining (POR, POR-LC) and during exercise pre-(P REX) and posttraining at absolute (POAB, P OAB-LC) and relative (PORL, PORL-LC) intensities. Glucose R r was not different in any rest or exercise condition. Glucose R a did not differ as a result of LC. Glucose Rox was significantly decreased with LC at P OR (0.38 Ϯ 0.03 vs. 0.56 Ϯ 0.04 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 ) and POAB (3.82 Ϯ 0.51 vs. 5.0 Ϯ 0.62 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 ). Percent glucose Rd oxidized decreased with all LC except P ORL-LC (PRR, 32%; PRR-LC, 22%; POR, 27%; P OR-LC, 20%; POAB, 95%; POAB-LC, 77%), which resulted in a significant increase in oxidation from alternative carbohydrate (CHO) sources at rest and P OAB. We conclude that 1) increased arterial [lactate] did not increase glucose R r measured during rest or exercise after training, 2) glucose disposal or production did not change with increased precursor supply, and 3) infusion of exogenous CHO in the form of lactate resulted in the decrease of glucose R ox. lactate; glucose kinetics; glucose recycling; training MAINTENANCE of blood [glucose] homeostasis requires coordination of delivery and utilization, or else hypo-or hyperglycemia results. Prolonged exercise and disease states, such as type 2 diabetes, represent situations in which glucose homeostasis is challenged. During postabsorptive rest (40) and exercise (3, 40), hepatic and renal gluconeogenesis (GNG) can increase to maintain glucose production (GP) and spare finite hepatic glycogen stores. Regular exercise training is accompanied, in part, by beneficial adaptations pertaining to glucose homeostasis (17). Donovan and Brooks (12) measured glucose recycling (R r ), an indirect measure of gluconeogenesis (GNG), and lactate incorporation into glucose and demonstrated that training increased lactate disposal and GNG in rats. Subsequently, Turcotte and Brooks (39) demonstrated that pharmacological blockade of GNG decreased run time to exhaustion and blood [glucose] during submaximal exercise in both untrained and trained rats. Together, these reports indicate that GNG capacity can increase with exercise training and that GNG is necessary to sustain blood [glucose] during exercise. Subsequent studies have demonstrated a training-induced increase in GNG in fasted rats (15) and in lactate-perfused (14) or alanine-perfused (8) livers in situ. Those reports were inconsistent with previous reports that training does not increase GNG enzyme concentrations in rats (19). Whereas there seems to be a training-induced increase in GNG capacity in rats, data on humans are less clear. The few longitudina...
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