REF-807 · Nummela et al., 1992 · Journal of Sports Sciences, Vol. · Paper · PubMed

Changes in force production, blood lactate and EMG activity in the 400-m sprint

Blimited evidenceMeasured on trained to highly trained athletesWritten before October 2026, being re-checked

Six male sprinters ran 100-, 200-, 300- and 400-m sprints at the velocity of their 400 m, with integrated EMG, stride characteristics, blood lactate and drop jumps (with EMG) at rest and after each sprint. Over the 400 m, running velocity and stride length fell and contact time rose; the rise in contact time was greatest immediately after the 100 and 300 m.

Peak lactate rose and the rate of lactate accumulation fell with distance. Drop-jump height was lower after the 300 m and the 400 m than at rest and correlated negatively with peak lactate (r = -0.77). EMG and the EMG:velocity ratio rose with distance.

The authors conclude that leg force production began to fall in the first quarter, the loss was compensated for until about 200-300 m, and after that speed dropped; fatigue was mainly within skeletal muscle rather than the central nervous system.

Participants

Six male sprinters ("trained athletes"). Age and performance level are not given in the abstract.

Protocol

Experimental sprints of 100, 200, 300 and 400 m, each run at the velocity of the athlete's 400 m.
Integrated EMG (iEMG) and stride characteristics during running.
Blood lactate (BLa) after each sprint.
Drop jumps with EMG at rest and after each sprint (height of rise of the centre of mass).

Key Results

During the 400 m, running velocity (P < 0.001) and stride length (P < 0.05) decreased and contact time increased (P < 0.01); the increase in contact time was greatest immediately after the 100 and 300 m runs.
Peak BLa increased and the rate of BLa accumulation decreased with running distance (P < 0.001).
Drop-jump rise of the centre of mass was smaller after the 300 m (P < 0.05) and the 400 m (P < 0.01) than at rest, and correlated negatively with peak BLa (r = -0.77, P < 0.001).
EMG and the EMG:running velocity ratio increased with running distance.
Authors' conclusion: force generation had already begun to decrease in the first quarter of the 400 m; it was compensated for until about 200-300 m, after which speed dropped. Fatigue in the 400 m among trained athletes is mainly due to processes within skeletal muscle rather than the central nervous system.

Practical Application

"Why does the last 100 m of a 400 m fall apart?" — in six trained male sprinters running 100-400 m at 400 m race speed, leg force was already falling in the first quarter, more muscle activation (EMG) covered the loss until about 200-300 m, and then speed dropped; drop-jump height fell with rising lactate (r = -0.77), and the fatigue was mainly in the muscle, not the brain.
Expect the fade to start late but the fatigue to start early: the runner is compensating long before the speed drops.
Inference, not tested here: because the limit sat within the muscle and tracked lactate, 400 m special-endurance work that trains the muscle to keep producing force at high lactate is the logical target; this study tested no training.
Not from this paper; the base's own practice: special endurance goes on top of speed work, not instead of it (SYNTH-59).

Limitations

Six male sprinters; small and men only.
Separate sprints of 100-400 m at 400 m velocity stand in for one continuous race; each distance was a new effort.
Surface EMG and drop jumps are indirect markers of neural drive and muscle force.
Written from the abstract and record metadata only (full text not read).
How this entry was checked and changed
Why this level

small within-subject study, n=6