title: Training does not protect against exhaustive exercise-induced lactate transport capacity alterations.
abstract: The effects of endurance training on lactate transport capacity remain controversial. This study examined whether endurance training 1) alters lactate transport capacity, 2) can protect against exhaustive exercise-induced lactate transport alteration, and 3) can modify heart and oxidative muscle monocarboxylate transporter 1 (MCT1) content. Forty male Wistar rats were divided 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 familiarized with the exercise task for 5 min/day. Before being killed, E and TE rats underwent exhaustive exercise (25 m/min, 10% grade), which lasted 80 and 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 presented 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, despite the metabolic adaptations typically observed after endurance training, we also noted increased lipid peroxidation byproducts after exhaustive exercise. We concluded that 1) endurance training does not alter lactate transport capacity, 2) exhaustive exercise-induced lactate transport alteration is not prevented by training despite increased MCT1 content, and 3) exercise-induced oxidative stress may enhance the passive diffusion responsible for the apparent loss of saturation properties, possibly masking lactate transport regulation.
authors.affiliation: Laboratoire de Physiologie des Interactions, Service Central de Physiologie Clinique, Hôpital Arnaud de Villeneuve, 34295 Montpellier, France. physio34@aol.com
authors.forename: N
authors.initials: N
authors.lastname: Eydoux
authors.forename: G
authors.initials: G
authors.lastname: Py
authors.forename: K
authors.initials: K
authors.lastname: Lambert
authors.forename: H
authors.initials: H
authors.lastname: Dubouchaud
authors.forename: C
authors.initials: C
authors.lastname: Préfaut
authors.forename: J
authors.initials: J
authors.lastname: Mercier
mesh_terms: D000818:Animals; D001692:Biological Transport; D001835:Body Weight; D002352:Carrier Proteins / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D019344:Lactic Acid / Q000097:blood / Q000378:metabolism*; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D027501:Monocarboxylic Acid Transporters; D018482:Muscle, Skeletal / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D010805:Physical Conditioning, Animal; D010807:Physical Endurance / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012508:Sarcolemma / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D027501:Monocarboxylic Acid Transporters; D019344:Lactic Acid; D008315:Malondialdehyde; D006003:Glycogen