TY - JOUR
T1 - Femoral vascular occlusion and ventilation during recovery from heavy exercise
AU - Haouzi, Philippe
AU - Huszczuk, A.
AU - Porszasz, J.
AU - Chalon, B.
AU - Wasserman, K.
AU - Whipp, B. J.
PY - 1993/11
Y1 - 1993/11
N2 - Ventilation and cardiac output subside gradually following cessation of exercise, which is commonly linked to the slow wash-out of materials from the recovering muscles. The effect of hindering the removal of the metabolic products of heavy cycle exercise on the kinetics of ventilation and gas exchange was studied in 5 subjects by occluding the femoral circulation with cuffs during the first 2 min of recovery (15 tests). Fifteen undisturbed recoveries served as controls. Compared to spontaneous recovery, circulatory obstruction induced an immediated (from the first breath) decrease in minute ventilation (V̇E), while end-tidal CO2 (PetCO2) as well as lactate and K+ in venous blood at forearm did not change significantly. A ventilatory deficit of 27±9 L was observed from the 2 min of occlusion. Following cuff deflation, V̇E rose 2-3 breaths after PetCO2 began to increase in every subject. The mechanisms of the normocapnic reduction of V̇E during occlusion, as well as the rise of ventilation following cuff release, are still unclear. However, these results argue against any significant role for hyperpnea-inducing intramuscular chemoreception, or point to muscular perfusion as a prerequisite of such a mechanism to operate.
AB - Ventilation and cardiac output subside gradually following cessation of exercise, which is commonly linked to the slow wash-out of materials from the recovering muscles. The effect of hindering the removal of the metabolic products of heavy cycle exercise on the kinetics of ventilation and gas exchange was studied in 5 subjects by occluding the femoral circulation with cuffs during the first 2 min of recovery (15 tests). Fifteen undisturbed recoveries served as controls. Compared to spontaneous recovery, circulatory obstruction induced an immediated (from the first breath) decrease in minute ventilation (V̇E), while end-tidal CO2 (PetCO2) as well as lactate and K+ in venous blood at forearm did not change significantly. A ventilatory deficit of 27±9 L was observed from the 2 min of occlusion. Following cuff deflation, V̇E rose 2-3 breaths after PetCO2 began to increase in every subject. The mechanisms of the normocapnic reduction of V̇E during occlusion, as well as the rise of ventilation following cuff release, are still unclear. However, these results argue against any significant role for hyperpnea-inducing intramuscular chemoreception, or point to muscular perfusion as a prerequisite of such a mechanism to operate.
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U2 - 10.1016/0034-5687(93)90043-A
DO - 10.1016/0034-5687(93)90043-A
M3 - Article
C2 - 8272586
AN - SCOPUS:0027442273
SN - 0034-5687
VL - 94
SP - 137
EP - 150
JO - Respiration Physiology
JF - Respiration Physiology
IS - 2
ER -