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Heat stress does not modify lactate exchange and removal abilities during recovery from short exercise.

Arterial and femoral venous lactate concentrations were measured before, during, and after short intermittent exercise (55-118% of maximal O2 consumption) in thermoneutral (N, 25 degrees C, 10.5 Torr) and hot (H, 45 degrees C, 17.5 Torr) conditions. The thermal load induced significantly higher heart rate and rectal temperature in H relative to N. All the arterial lactate (La) recovery curves were fitted to an equation containing two exponential time functions of the form La(t) = La(0) + A1a(1 - e-gamma 1at) + A2a(1 - e-gamma 2at) where the velocity constants gamma 1a and gamma 2a are the body's overall ability to exchange and remove lactate after exercise, respectively, and t is time. There was no significant difference in these constants, regardless of thermal conditions. The arterial lactate concentration at the end of exercise, the peak lactate concentration during recovery, the amplitudes A1a and A2a of the biexponential function, and the arteriofemoral venous lactate concentration difference during recovery were not significantly different in H relative to N. However, measured and computed arterial lactate concentrations during recovery, especially at the end of the tests, were higher in H (P < 0.04). The more elevated lactate concentrations in H at rest at the end of recovery denote a higher basal lactate production, and they were not due to muscle hypoxia.