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The kinetics of lactate production and removal during whole-body exercise

DOI: 10.1186/1742-4682-9-7

Keywords: Aerobic power, Anaerobic power, Blood lactate, Cross-country skiing, Muscle lactate, pH

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Abstract:

The simulated and experimental data differed less than 0.5 mmol/L both during steady state and varying sub-maximal intensities. However, the simulation model for lactate removal after high exercise intensities seems to require further examination.Overall, the simulation models of lactate production and removal provide useful insight into the parameters that affect blood lactate response, and specifically how blood lactate concentration during practical training and testing in dynamical situations should be interpreted.The metabolic power in humans is based on the production and consumption of adenosine triphosphate (ATP). Despite the approximately 100-fold increase in ATP utilization from rest to maximal-intensity exercise, the energetic demands of the muscles are usually satisfied without depleting the intracellular ATP e.g., [1-3]. In this connection, three sources for ATP synthesis are available; First, ATP can be produced aerobically in the mitochondria by oxidative phosphorylation. Second, ATP can be produced by anaerobic synthesis due to glycolysis or glycogenolysis. Finally, ATP can be produced by phosphocreatine (PCr) break down to Creatine (Cr) (i.e., ADP + PCr gives ATP + Cr in the Creatine Kinease (CK) reaction) e.g., [1-3].The rate of oxygen (O2) consumption can be set to the sum of 1) a constant rate (resting O2 consumption), 2) a rate due to unloaded body movements and 3) a rate proportional to the aerobic energy used to perform work. For moderate constant work rates, the aerobic power increases towards a steady state condition. The concept of maximal lactate steady state (MLSS), that is the highest intensity where a steady state lactate can be obtained, has been regarded as important for endurance performance e.g., [4-6]. For exercise intensities above MLSS, associated with sustained acidosis, a slow component delays the attainment of a steady state value and causes O2 uptake to increase to values greater than those predicted from aerobic steady state

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