Journal of Applied Physiology, Vol 74, Issue 3 1248-1255, Copyright © 1993 by American Physiological Society
Heat stress does not modify lactate exchange and removal abilities during recovery from short exercise
S. Oyono-Enguelle, A. Heitz, J. Marbach, C. Ott, A. Pape and H. Freund
Groupe de Recherche Activites Physiques et Sportives, Strasbourg, France.
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.
