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
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.