Anaerobic Threshold: Does it Exist? (or blood lactate inflection point?) Wasserman et al. (1973) proposed that muscle became hypoxic at higher intensities and thus produce ATP and lactate anaerobically as well as VE Challenges to Wasserman theory –McArdle's syndrome patients lack phosphorylase still demonstrate VT –does muscle become hypoxic? –are there other factors that explain the sudden increase in blood La?
Muscle intracellular PO 2 and net lactate release. Note that PO 2 remains above critical mitochondrial O 2 tension (1 torr). Relationship between mitochondrial VO 2 and PO 2. Critical mitochondrial PO 2 is around 1.0 torr. Mitochondrial PO 2 during exercise
Motor Unit Recruitment Pattern -- Size Principle
Influence of exercise intensity on rate of blood La clearance during recovery
Metabolic Fate of Lactate During exercise: –~¾ oxidized by heart, liver, and ST fibers During recovery: –oxidized by heart, ST fibers, and liver (1 fate) –converted to glycogen –incorporated into amino acids –La metabolism depends on metabolic state
Fate of lactate under three conditions 4 hr after injection. Note that oxidation is the 1 pathway of removal.
Effect of Altitude on La Response At altitude: blood [La] is higher at same absolute workloads muscle blood flow similar at same absolute workloads La threshold occurs at same relative intensity EPI threshold occurs earlier at altitude Lactate paradox – peak [La] is less under hypoxic conditions than at normoxia
Determining lactate turnover during exercise: tracer methodology use naturally occurring isotopes – 13 C and 2 H isotopes most commonly used pulse injection tracer technique –isotopically-labeled La added to blood in single bolus –concentration measurements taken over time –rate of concentration decline represents turnover rate
Continuous-infusion tracer techniques Continuous-infusion technique –isotopically-labeled La added at increasing rate until equilibrium point is reached La appearance = La removal Primed continuous-infusion technique –priming bolus of isotopically-labeled La added initially speeds time to reach equilibrium –remaining isotopically-labeled La added at continuous, constant rate –[isotope] depends on rate of infusion and volume of distribution (estimated)
Primed continuous-infusion technique (used by Stanley et al. and MacRae et al.) turnover rate = appearance - disappearance Ra dependent on: –volume of distribution –arterial [La] Rd = Ra minus arterial [La] metabolic clearance rate (MCR) = Rd / [La] –calculates La clearance rate relative to arterial [La] –increasing MCR indicates Rd is dependent upon [La]
Read one of the following articles for next Tuesday Holden, S.-MacRae, S.C. Dennis, A.N. Bosch, and T.D. Noakes. Effects of training on lactate production and removal during progressive exercise in humans. J. Appl. Physiol. 72: 1649-1656, 1992. Stanley, W.C., E.W. Gertz, J.A. Wisneski, D.L. Morris, R. Neese, and G.A. Brooks. Systemic lactate turnover during graded exercise in man. Am. J. Physiol. 249 (Endocrinol. Metab. 12): E595-E602, 1985.
Lactate response to graded exercise (Stanley et al., JAP, 1985) Ra and Rd exponentially related to VO 2 linear relationship between arterial [La] and Ra curvilinear relationship between arterial [La] and Rd
Effects of exercise intensity on rate of lactate appearance and removal
Rates of blood lactate appearance (Ra) and disappearance (Rd) during graded exercise before and after training MacRae et al., JAP, 1992
Training adaptations to lactate kinetics (MacRae et al., JAP, 1992) submaximal Ra by training peak Ra similar regardless of training status at same relative intensities, Ra was at 60% Rd by training peak Rd at same relative intensities, Rd was similar at 60% MCR at higher exercise intensity and with training
Effect of training on blood lactate response 65% pre-training 65% post-training – same relative workload 45% post-training – same absolute workload 45% pre-training