An enzymatic approach to lactate production in human skeletal muscle during exercise

Department of Human Biology and Nutritional Sciences, University of Guelph, Ontario, Canada.
Medicine &amp Science in Sports &amp Exercise (Impact Factor: 4.46). 05/2000; 32(4):756-63. DOI: 10.1097/00005768-200004000-00007
Source: PubMed

ABSTRACT PURPOSE: This paper examines the production of lactate in human skeletal muscle over a range of power outputs (35-250% VO2max) from an enzymatic flux point of view. The conversion of pyruvate and NADH to lactate and NAD in the cytoplasm of muscle cells is catalyzed by the near-equilibrium enzyme lactate dehydrogenase (LDH). As flux through LDH is increased by its substrates, pyruvate and NADH, the factors governing the production of these substrates will largely dictate how much lactate is produced at any exercise power output. In an attempt to understand lactate production, flux rates through the enzymes that regulate glycogenolysis/glycolysis, the transfer of cytoplasmic reducing equivalents into the mitochondria, and the various fates of pyruvate have been measured or estimated. RESULTS: At low power outputs, the rates of pyruvate and NADH production in the cytoplasm are low, and pyruvate dehydrogenase (PDH) and the shuttle system enzymes (SS) metabolize the majority of these substrates, resulting in little or no lactate production. At higher power outputs (65, 90, and 250% VO2max), the mismatch between the ATP demand and aerobic ATP provision at the onset of exercise increases as a function of intensity, resulting in increasing accumulations of the glycogenolytic/glycolytic activators (free ADP, AMP, and Pi). The resulting glycolytic flux, and NADH and pyruvate production, is progressively greater than can be handled by the SS and PDH, and lactate is produced at increasing rates. Lactate production during the onset of exercise and 10 min of sustained aerobic exercise may be a function of adjustments in the delivery of O2 to the muscles, adjustments in the activation of the aerobic ATP producing metabolic pathways and/or substantial glycogenolytic/glycolytic flux through a mass action effect.

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    ABSTRACT: Changes in body temperature and in the blood lactate concentration are typical symptoms of an organism's reaction to effort. The aim of this work was to search for a relation between the temperature of the lower extremities and the blood lactate concentration. Sixteen non-training male subjects took part in the test (average age: 22.3±1.6 years). They performed maximum-height jumps from a fully knee-bent position for one minute. Their body temperature was measured by thermographic imaging and blood lactate concentration was determined at the beginning and throughout a thirty-minute recovery. An analysis of isotherms showed a strong dependence between the temperature of the front surface (FS) and back surface (BS) of the lower extremities (r=.83, p<.05). Immediately after exercise the temperature of the lower limbs decreased on average by about 1.44°C (p<.001) and then during the recovery period rose almost to the pre-exercise value. There was a significant negative correlation (r=-.29, p<.05) between the temperature of lower limbs and the blood lactate concentration, both for FS (r=-.22, p<.05) and BS (r=-.23, p<.05). The results show that a maximum anaerobic effort is accompanied by a substantial drop of the temperature on surface of engaged muscles and the degree of the drop is proportional to the blood lactate concentration.
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    ABSTRACT: The aim of the present study was to analyse the lactate threshold (LT) changes in rats submitted to an aerobic treadmill-training programme. Twenty-five Wistar rats were divided into two groups: a sedentary control group (CG), and a trained group (TG) submitted to an aerobic training during 5 weeks. All the animals were submitted to an incremental treadmill exercise test in order to determine LT. There was an increase in the maximum running speed in the TG (from 32.25 ± 1.27 to 47.75 ± 3.13 m.min-1 - p = 0.001), and running speed at LT (from 26.21 ± 1.15 to 35.30 ± 2.24 m.min-1 - p = 0.004), a part from the reduction in blood lactate at LT. LT can be determined in rats, and aerobic training induced positive oxidative physiological adaptations in the animals.
    Brazilian Journal of Biology 05/2014; 74(2):444-449. DOI:10.1590/1519-6984.07912 · 0.68 Impact Factor
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    ABSTRACT: Lactate, the conjugate base of lactic acid occurring in aqueous biological fluids, has been derided as a “dead-end” waste product of anaerobic metabolism. Catalyzed by the near-equilibrium enzyme lactate dehydrogenase (LDH), the reduction of pyruvate to lactate is thought to serve to regenerate the NAD+ necessary for continued glycolytic flux. Reaction kinetics for LDH imply that lactate oxidation is rarely favored in the tissues of its own production. However, a substantial body of research directly contradicts any notion that LDH invariably operates unidirectionally in vivo. In the current Perspective, a model is forwarded in which the continuous formation and oxidation of lactate serves as a mitochondrial electron shuttle, whereby lactate generated in the cytosol of the cell is oxidized at the mitochondria of the same cell. From this perspective, an intracellular lactate shuttle operates much like the malate-aspartate shuttle (MAS); it is also proposed that the two shuttles are necessarily interconnected in a lactate-MAS. Among the requisite features of such a model, significant compartmentalization of LDH, much like the creatine kinase of the phosphocreatine shuttle, would facilitate net cellular lactate oxidation in a variety of cell types.
    Frontiers in Neuroscience 11/2014; 8(366). DOI:10.3389/fnins.2014.00366

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