We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate]a) during continuous exercise by decreasing net lactate release (L˙) and appearance rates (Ra) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O2consumption (V˙o 2 peak)] and after training [65% pretrainingV˙o 2 peak, same absolute workload (ABT), and 65% posttrainingV˙o 2 peak, same relative intensity (RLT)]. Nine men (27.4 ± 2.0 yr) trained for 9 wk on a cycle ergometer, 5 times/wk at 75%V˙o 2 peak. Compared with the 65%V˙o 2 peakpretraining condition (4.75 ± 0.4 mM), [lactate]a decreased at ABT (41%) and RLT (21%) (P < 0.05). L˙ decreased at ABT but not at RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. MCR was unchanged at ABT but increased at RLT. We conclude that1) active skeletal muscle is not solely responsible for elevated [lactate]a; and2) training increases leg lactate clearance, decreases whole body and leg lactate production at a given moderate-intensity power output, and increases both whole body and leg lactate clearance at a high relative power output.

  • lactate shuttle
  • exertion
  • glycogen
  • glucose
  • stable isotopes


  • Address for reprint requests and other correspondence: G. A. Brooks, Exercise Physiology Laboratory, Dept. of Integrative Biology, 5101 Valley Life Sciences Bldg., Univ. of California, Berkeley, Berkeley, CA 94720-3140 (E-mail: gbrooks{at}socrates.berkeley.edu).

  • This work was supported by National Institutes of Health Grants AR-42906 and DK-19577.

  • The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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