M. Gleeson et al., EFFECT OF EXERCISE-INDUCED MUSCLE DAMAGE ON THE BLOOD LACTATE RESPONSE TO INCREMENTAL EXERCISE IN HUMANS, European journal of applied physiology and occupational physiology, 77(3), 1998, pp. 292-295
Eccentric muscle actions are known to induce temporary muscle damage,
delayed onset muscle soreness (DOMS) and muscle weakness that may pers
ist for several days. The purpose of the present study was to determin
e whether DOMS-inducing exercise affects blood lactate responses to su
bsequent incremental dynamic exercise. Physiological and metabolic res
ponses to a standardised incremental exercise task were measured two d
ays after the performance of an eccentric exercise bout or in a contro
l (no prior exercise) condition. Ten healthy recreationally active sub
jects (9 male, 1 female), aged 20 (SD 1) years performed repeated ecce
ntric muscle actions during 40 min of bench stepping (knee high step;
15 steps.min(-1)). Two days after the eccentric exercise, while the su
bjects experienced DOMS, they cycled on a basket loaded cycle ergomete
r at a starting work rate of 150 W, with increments of 50 W every 2 mi
n until fatigue. The order of the preceding treatments (eccentric exer
cise or control) was randomised and the treatments were carried out 2
weeks apart. Two days after the eccentric exercise, all subjects repor
ted leg muscle soreness and exhibited elevated levels of plasma creati
ne kinase activity (P < 0.05). Endurance time and peak (V) over dot O-
2 during cycling were unaffected by the prior eccentric exercise. Minu
te volume, respiratory exchange ratio and heart rate responses were si
milar but venous blood lactate concentration was higher (P < 0.05) dur
ing cycling after eccentric exercise compared with the control conditi
on. Peak blood lactate concentration, observed at 2 min post-exercise
was also higher [12.6 (SD 1.4) vs 10.9 SD (1.3) mM; P < 0.01]. The hig
her blood lactate concentration during cycling exercise after prior ec
centric exercise may be attributable to an increased rate of glycogeno
lysis possibly arising from an increased recruitment of Type II muscle
fibres. It follows that determination of lactate thresholds for the p
urpose of fitness assessment in subjects experiencing DOMS is not appr
opriate.