The effects of an increase in body temperature per se on the lactate and pyruvate concentrations of the arterial blood, muscle venous blood, sagittal sinus blood, and cerebrospinal fluid were determined. Paralysed anesthetized dogs with near normal arterial pH and PC0(2) values were ventilated with a 50% 0(2), 50% N(2) mixture and heated to a temperature of 42°C and maintained at this temperature for a period of 2 hours. During hyperthermia a slight increase in lactate and pyruvate was observed in the arterial blood. However, this was not statistically significant. Also a slight increase in the concentration of these substances occurred in the muscle venous blood and sagittal sinus blood. This change, however, was parallel to that observed in the arterial blood. The lactate-pyruvate ratio of the arterial blood, muscle venous blood and sagittal sinus blood did not show any significant change and thus no increase in anaerobic processes was detected during the hyperthermic period. On the other hand the cerebrospinal fluid lactate and pyruvate increased significantly throughout the hyperthermic period but maintained a constant lactate-pyruvate ratio. The results indicate that the increase of lactate and pyruvate in the cerebrospinal fluid are a result of an increased rate of aerobic glycolysis. The fact that the increases observed in the cerebrospinal fluid lactate and pyruvate were not reflected in the cerebral venous blood indicates lactate and pyruvate may have difficulty in diffusing across the blood brain barrier and cerebral venous blood is thus a poor index of cerebral lactate and pyruvate changes. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

The purpose of this study was to investigate the effects of accentuated eccentric load (AEL) resistance training and changes in work capacity, high-intensity exercise endurance (HIEE) and lactate metabolism. Seventeen recreationally trained subjects (11 males and 6 females) (mean ± SD: age = 23.2 ± 4.2 yrs, BM = 81.3 ± 22.2 kg, height = 172.1 ± 10 cm, male relative back squat (BS) [MD1] strength (1RM*BM-1) = 1.64 ± 0.32 kg*kg-1, female relative BS strength = 1.39 ± 0.32 kg*kg-1) participated in the study. Subjects completed a week of familiarization to participate in a week of pre-testing, 4 weeks of strength endurance (S-E) training (3 weeks of increasing intensity with 1 deload week) followed by a final week of post-testing. Subjects were randomly assigned into AEL and traditional (TRAD) resistance training groups, pair matched for relative strength. The AEL subjects performed 3 sets of 10 reps for all multi-joint compound movements where 5 AEL repetitions were performed within the set followed by a traditional repletion and 15 s intraset rest to reattach AEL equipment, like a cluster set (CS) protocol. Resistance training was performed 3 days a week with sprint and agility training two days a week. Maximal BS strength (1RM) and HIEE were tested pre and post training block. HIEE was tested in an incremental exercise test to failure, starting at an initial load of 40kg for 10 reps/min with 2min rest to increase load. Additionally, blood lactate concentrations (BLa) were collected at baseline before any exercise was performed, after warming up, after stage three of HIEE, immediately after the final repetition, 5- and 10- minutes post final repetition. While over time maximal strength and work capacity increased no statistical difference was observed between AEL and TRAD groups after training. Additionally, there were no statistically significant differences in the BLa at similar time points pre and post. Statistically significant correlations were found between strength (squat 1RM) and work capacity, however, strength failed to account for a majority of the variance in the observed data. [MD1]Back Squat (BS)

The current understanding of lactate metabolism in fish is based almost entirely on interpretation of concentration measurements that cannot be used to infer changes in flux. Moreover, the transporters regulating these fluxes have never been characterized in rainbow trout. My goals were: (1) to quantify lactate fluxes in rainbow trout under normoxic resting conditions, during acute hypoxia, and exercise by continuous infusion of [U-14C] lactate; (2) to determine lactate uptake capacity of trout tissues by infusing exogenous lactate in fish rest and during graded exercise, and (3) to clone monocarboxylate transporters (MCTs) and determine the effects of exhausting exercise on their expression. Such information could prove important to understand the mechanisms underlying the classic “lactate retention” seen in trout white muscle after intense exercise. In normoxic resting fish, the rates of appearance (Ra) and disappearance (Rd) of lactate were always matched (~18 to 13 µmol kg-1 min-1), thereby maintaining a low baseline blood lactate concentration (~0.8 mM). In hypoxic fish, Ra lactate increased from baseline to 36.5 µmol kg-1 min-1, and was accompanied by an unexpected 52% increase in Rd reaching 30.3 µmol kg-1 min-1, accounting for a rise in blood lactate to 8.9 mM. In exercising fish, lactate flux was stimulated > 2.4 body lengths per second (BL s-1). As the fish reached critical swimming speed (Ucrit), Ra lactate was more stimulated (+67% to 40.4 μmol kg-1 min-1) than Rd (+41% to 34.7 μmol kg-1 min-1), causing an increase in blood lactate to 5.1mM. Fish infused with exogenous lactate stimulated Rd lactate by 300% (14 to 56 μmol kg-1 min-1) during graded exercise, whereas the Rd in resting fish increased by only 90% (21 to 40 µmol kg-1 min-1). Four MCT isoforms were partially cloned and characterized in rainbow trout: MCT1b was the most abundant in heart, and red muscle, but poorly expressed in gill and brain where MCT1a and MCT2 were prevalent. MCT4 was more expressed in the heart. Transcript levels of MCT2 (+260%; brain), MCT1a (+90%; heart) and MCT1b (+50%; heart) were stimulated by exhausting exercise. This study shows that: (i) the increase in Rd lactate plays a strategic role in reducing the lactate load imposed on the circulation. Without this response, blood lactate accumulation would double; (ii) a high capacity for lactate disposal in rainbow trout tissues is elicited by the increased blood-to-tissue lactate gradient when extra lactate is administered; and (iii) rainbow trout may be unable to release large lactate loads rapidly from white muscle after exhausting exercise (lactate retention) because they poorly express MCT4 in white muscle and fail to upregulate its expression during exercise.

The current understanding of lactate metabolism in fish is based almost entirely on interpretation of concentration measurements that cannot be used to infer changes in flux. Moreover, the transporters regulating these fluxes have never been characterized in rainbow trout. My goals were: (1) to quantify lactate fluxes in rainbow trout under normoxic resting conditions, during acute hypoxia, and exercise by continuous infusion of [U-14C] lactate; (2) to determine lactate uptake capacity of trout tissues by infusing exogenous lactate in fish rest and during graded exercise, and (3) to clone monocarboxylate transporters (MCTs) and determine the effects of exhausting exercise on their expression. Such information could prove important to understand the mechanisms underlying the classic “lactate retention” seen in trout white muscle after intense exercise. In normoxic resting fish, the rates of appearance (Ra) and disappearance (Rd) of lactate were always matched (~18 to 13 µmol kg-1 min-1), thereby maintaining a low baseline blood lactate concentration (~0.8 mM). In hypoxic fish, Ra lactate increased from baseline to 36.5 µmol kg-1 min-1, and was accompanied by an unexpected 52% increase in Rd reaching 30.3 µmol kg-1 min-1, accounting for a rise in blood lactate to 8.9 mM. In exercising fish, lactate flux was stimulated > 2.4 body lengths per second (BL s-1). As the fish reached critical swimming speed (Ucrit), Ra lactate was more stimulated (+67% to 40.4 μmol kg-1 min-1) than Rd (+41% to 34.7 μmol kg-1 min-1), causing an increase in blood lactate to 5.1mM. Fish infused with exogenous lactate stimulated Rd lactate by 300% (14 to 56 μmol kg-1 min-1) during graded exercise, whereas the Rd in resting fish increased by only 90% (21 to 40 µmol kg-1 min-1). Four MCT isoforms were partially cloned and characterized in rainbow trout: MCT1b was the most abundant in heart, and red muscle, but poorly expressed in gill and brain where MCT1a and MCT2 were prevalent. MCT4 was more expressed in the heart. Transcript levels of MCT2 (+260%; brain), MCT1a (+90%; heart) and MCT1b (+50%; heart) were stimulated by exhausting exercise. This study shows that: (i) the increase in Rd lactate plays a strategic role in reducing the lactate load imposed on the circulation. Without this response, blood lactate accumulation would double; (ii) a high capacity for lactate disposal in rainbow trout tissues is elicited by the increased blood-to-tissue lactate gradient when extra lactate is administered; and (iii) rainbow trout may be unable to release large lactate loads rapidly from white muscle after exhausting exercise (lactate retention) because they poorly express MCT4 in white muscle and fail to upregulate its expression during exercise.