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Titolo:
CONTRIBUTION OF THE RESPIRATORY MUSCLES TO THE LACTIC-ACIDOSIS OF HEAVY EXERCISE IN COPD
Autore:
ENGELEN MPKJ; CASABURI R; RUCKER R; CARITHERS E;
Indirizzi:
UNIV CALIF LOS ANGELES,HARBOR MED CTR,DEPT MED,DIV RESP & CRIT CARE PHYSIOL & MED,BOX 24 TORRANCE CA 90509 UNIV CALIF LOS ANGELES,HARBOR MED CTR,DEPT MED,DIV RESP & CRIT CARE PHYSIOL & MED TORRANCE CA 90509
Titolo Testata:
Chest
fascicolo: 5, volume: 108, anno: 1995,
pagine: 1246 - 1251
SICI:
0012-3692(1995)108:5<1246:COTRMT>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD LACTATE; VENOUS-BLOOD; ALKALOSIS; ARTERIAL; DISEASE;
Keywords:
COPD; LACTIC ACIDOSIS; RESPIRATORY MUSCLES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
23
Recensione:
Indirizzi per estratti:
Citazione:
M.P.K.J. Engelen et al., "CONTRIBUTION OF THE RESPIRATORY MUSCLES TO THE LACTIC-ACIDOSIS OF HEAVY EXERCISE IN COPD", Chest, 108(5), 1995, pp. 1246-1251

Abstract

Patients with COPD usually are limited in their exercise tolerance bya limited ventilatory capacity, Lactic acidosis induced by exercise increases the stress on the ventilatory system due to CO2 generated by bicarbonate buffering and hydrogen ion stimulation. Patients with COPDare often observed to increase blood lactate levels at low levels of exercise. We wished to determine whether patients with COPD who experience lactic acidosis do so because of respiratory muscle production oflactate. Eight patients with moderate to severe COPD (FEV(1)=43.5+/-11.6% predicted) and 5 healthy subjects performed 10 min of moderate constant work rate exercise either breathing spontaneously or volitionally increasing their ventilation for 5 min to approximate the peak minute ventilation seen during incremental exercise, During volitional increased ventilation, 3% CO2 was added to the inspirate to prevent alkalosis and hypocapnia. In neither the healthy subjects nor the COPD group was the end-exercise lactate level significantly higher during volitional ventilation increase than during spontaneous ventilation. Further, in the COPD patients, the blood lactate levels during volitional ventilation increase were much lower than during maximal exercise (averaging 2.4 vs 5.3 mmol/L) despite similar ventilation levels (averaging 50 and 53 L/min). We conclude that it is unlikely that the respiratorymuscles have an important influence on the blood lactate level elevation seen during maximal exercise in COPD patients.

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Documento generato il 06/07/20 alle ore 08:13:02