Ventilation and cardiac output subside gradually following cessation o
f exercise, which is commonly linked to the slow wash-out of materials
from the recovering muscles. The effect of hindering the removal of t
he metabolic products of heavy cycle exercise on the kinetics of venti
lation and gas exchange was studied in 5 subjects by occluding the fem
oral circulation with cuffs during the first 2 min of recovery (15 tes
ts). Fifteen undisturbed recoveries served as controls. Compared to sp
ontaneous recovery, circulatory obstruction induced an immediate (from
the first breath) decrease in minute ventilation (V(E)), while end-ti
dal CO2 (PET(CO2)) as well as lactate and K+ in venous blood at forear
m did not change significantly. A ventilatory deficit of 27 +/- 9 L wa
s observed from the 2 min of occlusion. Following cuff deflation, VE r
ose 2-3 breaths after PET(CO2) began to increase in every subject. The
mechanisms of the normocapnic reduction of VE during occlusion, as we
ll as the rise of ventilation following cuff release, are still unclea
r. However, these results argue against any significant role for hyper
pnea-inducing intramuscular chemoreception, or point to muscular perfu
sion as a prerequisite of such a mechanism to operate.