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: 3.98). 05/2000; 32(4):756-63. DOI: 10.1097/00005768-200004000-00007
Source: PubMed


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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Available from: Lawrence L Spriet, Apr 09, 2015
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    • "s not the case in light of the unchanged _ VO 2 response . Alternatively , the tendency for a lower content and maximal activity of muscle oxidative enzymes ( CS and COX - 4 ) after the HIT period may have reduced the mitochondrial utili - zation of the produced pyruvate ( Brooks 2000 ) , thereby enhancing the lactate production catalyzed by LDH ( Spriet et al . 2000 ) . It is , however , unclear , why such changes did not occur in the first phase ( 0 – 3 min ) of INT ( Fig . 6B ) . Nevertheless , it appears that the anaero - bic energy flux during the last phase ( 3 – 6 min ) of INT was higher after the intervention period , and thus , total energy turnover , as pulmonary VO 2 was unaltered ."
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    ABSTRACT: The present study examined if high intensity training (HIT) could increase the expression of oxidative enzymes in fast-twitch muscle fibers causing a faster oxygen uptake (V˙O2) response during intense (INT), but not moderate (MOD), exercise and reduce the V˙O2 slow component and muscle metabolic perturbation during INT. Pulmonary V˙O2 kinetics was determined in eight trained male cyclists (V˙O2-max: 59 ± 4 (means ± SD) mL min(-1) kg(-1)) during MOD (205 ± 12 W ~65% V˙O2-max) and INT (286 ± 17 W ~85% V˙O2-max) exercise before and after a 7-week HIT period (30-sec sprints and 4-min intervals) with a 50% reduction in volume. Both before and after HIT the content in fast-twitch fibers of CS (P < 0.05) and COX-4 (P < 0.01) was lower, whereas PFK was higher (P < 0.001) than in slow-twitch fibers. Content of CS, COX-4, and PFK in homogenate and fast-twitch fibers was unchanged with HIT. Maximal activity (μmol g DW(-1) min(-1)) of CS (56 ± 8 post-HIT vs. 59 ± 10 pre-HIT), HAD (27 ± 6 vs. 29 ± 3) and PFK (340 ± 69 vs. 318 ± 105) and the capillary to fiber ratio (2.30 ± 0.16 vs. 2.38 ± 0.20) was unaltered following HIT. V˙O2 kinetics was unchanged with HIT and the speed of the primary response did not differ between MOD and INT. Muscle creatine phosphate was lower (42 ± 15 vs. 66 ± 17 mmol kg DW(-1)) and muscle lactate was higher (40 ± 18 vs. 14 ± 5 mmol kg DW(-1)) at 6 min of INT (P < 0.05) after compared to before HIT. A period of intensified training with a volume reduction did not increase the content of oxidative enzymes in fast-twitch fibers, and did not change V˙O2 kinetics. © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
    07/2015; 3(7). DOI:10.14814/phy2.12428
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    • "Measuring LDH levels can be helpful in monitoring treatment for cancer. Noncancerous conditions that can raise LDH levels include heart failure, hypothyroidism, anemia, and lung or liver disease [25]. Tissue breakdown releases LDH, and therefore LDH can be measured as a surrogate for tissue breakdown, e.g. "

    09/2014; 2(4):77-84. DOI:10.12691/ajmsm-2-4-3
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    • "Classical anaerobic field tests include the step-running test, or the measure of maximal La production during one all-out sprint over an established distance (eg, 80, 100 or 200 m).58 59 However, a more specific approach for anaerobic testing consists in the measurement of repeated sprint ability (RSA).60–62 "
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