Training does not protect against exhaustive exercise-induced lactate transport capacity alterations

The effects of endurance training on lactate transport capacity remain cont roversial. This study examined whether endurance training 1) alters lactate transport capacity, 2) can protect against exhaustive exercise-induced lac tate transport alteration, and 3) can modify heart and oxidative muscle mon ocarboxylate transporter 1 (MCT1) content. Forty male Wistar rats were divi ded into control (C), trained (T), exhaustively exercised (E), and trained and exercised (TE) groups. Rats in the T and TE groups ran on a treadmill ( 1 h/day, 5 days/wk at 25 m/min, 10% incline) for 5 wk; C and E were familia rized with the exercise task for 5 min/day. Before being killed, E and TE r ats underwent exhaustive exercise (25 m/min, 10% grade), which lasted 80 an d 204 min, respectively (P < 0.05). Although lactate transport measurements (zero-trans) did not differ between groups C and T, both E and TE groups p resented an apparent loss of protein saturation properties. In the trained groups, MCT1 content increased in soleus (+28% for T and +26% for TE; P < 0 .05) and heart muscle (+36% for T and +33% for TE; P < 0.05). Moreover, des pite the metabolic adaptations typically observed after endurance training, we also noted increased lipid peroxidation byproducts after exhaustive exe rcise. We concluded that 1) endurance training does not alter lactate trans port capacity, 2) exhaustive exercise-induced lactate transport alteration is not prevented by training despite increased MCT1 content, and 3) exercis e-induced oxidative stress may enhance the passive diffusion responsible fo r the apparent loss of saturation properties, possibly masking lactate tran sport regulation.