MUSCLE LACTATE METABOLISM IN RECOVERY FROM INTENSE EXHAUSTIVE EXERCISE - IMPACT OF LIGHT EXERCISE

Citation
J. Bangsbo et al., MUSCLE LACTATE METABOLISM IN RECOVERY FROM INTENSE EXHAUSTIVE EXERCISE - IMPACT OF LIGHT EXERCISE, Journal of applied physiology, 77(4), 1994, pp. 1890-1895
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
77
Issue
4
Year of publication
1994
Pages
1890 - 1895
Database
ISI
SICI code
8750-7587(1994)77:4<1890:MLMIRF>2.0.ZU;2-J
Abstract
This study examined the effect of low-intensity exercise on lactate me tabolism during the first 10 min of recovery from high-intensity exerc ise. Subjects exercised (61.0 +/- 5.4 W) one leg to exhaustion (simila r to 3.5 min), and after 1 h of rest they performed the same exhaustiv e exercise with the other leg. For one leg the intense exercise was fo llowed by rest [passive (P) leg], and for the other leg the exercise w as followed by a 10-min period with low-intensity exercise at a work r ate of 10 W [active (A) leg]. The muscle lactate concentration after t he intense exercise was the same in the P and A legs, but after 10 min of recovery, the lactate concentration and the arterial blood lactate level were higher for the P leg than for the A leg (both P < 0.05). D uring the recovery, the mean blood flow was lower for the P leg than f or the A leg (P < 0.05), whereas the mean lactate efflux was not signi ficantly different. During the 10 min of recovery, lactate release acc ounted for similar to 60% of the change in muscle lactate for either l eg. The leg excess postexercise O-2 consumption during 10 min of recov ery was 440 and 750 ml for the P and A legs, respectively. The present data suggest that a lowered blood lactate level during active recover y is due to an elevated muscle lactate metabolism and is not caused by a transient higher release of lactate from the exercising muscles cou pled with greater uptake in other tissues. Furthermore, with either mo de of recovery muscle lactate does not appear to be a major substrate for glycogen synthesis and muscle glyconeogenesis seems to be a minor contributor to excess postexercise O-2 consumption.