Does LV function reach a steady state during sustained exercise?

Does LV function reach a steady state during sustained exercise?

ABSTRACTS OXYHEMOGLOBIN DISSOCIATION CONTRIBUTES TO UNLOADING OXYGEN AT REST AND DURING EXERCISE IN SEVERE CHRONIC HEART FAILURE PATIENTS Mark Nemero...

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ABSTRACTS

OXYHEMOGLOBIN DISSOCIATION CONTRIBUTES TO UNLOADING OXYGEN AT REST AND DURING EXERCISE IN SEVERE CHRONIC HEART FAILURE PATIENTS Mark Nemerovski, MDI Stanley A. Rubin, MD, FACC; Harvey Brown, MD; David Mickle; H.J.C. Swan, MD, PhD, FACC, Cedars-Sinai Medical Center, Los Angeles, California

DOES LV FUNCTION REACH A STEADY STATE DURING SUSTAINED EXERCISE? Shelley Magder, MD; Joseph Hung, MD; William M. Savin,MS; Edward B. Stinson, MD, FACC; George T. Daughters II, MS; Neil B. Ingels, Jr., PhD: Edwin L. Alderman, MD, FACC, Stanford University, Stanford, CA.

ENHANCED

Exercise (Ex) studies often assume that a hemodynamic steady state is reached in 3 min. Eleven asymptomatic males 4 to 6 years post aorta-coronary bypass did supine Ex at 450 KPM/min for 3-6 min (mean 5.3). Cardiac output (CO), heart rate (HR), stroke volume (SV), ejection fraction (EF), and circumferential shortening velocity (VCF) were measured by computer assisted analysis of the motion of implanted midwall markers. HR sv EF VCF RESULTS: co circfsec beatsfmin % l/min 84,;: .61(.16) 67(10) 5.6(1.6) CONTROL 48(4) .85(.20)* 8703) Ex min 1 8.6(2.3)* 99(13)* 50(6) .94(.26)* 89(22) Ex min 3 9.8(2.2)* 112(13)* 50(7) 93(26)* 53(7)* 1.03(.28)* PEAK CO 10.9(2.7)* 118(13)* mean (SD);Ex versus CONTROL *p
Maximum oxygen transport is abnormally low in heart failure. Therefore, we studied the potential mechanisms for increased unloading of oxygen in I5 chronic heart failure pts at rest (R) and during maximum cycle ergometry (E). We measured cardiac index @I) by thermodilution, oxygen consumption (VO2) by expired air analysis, mixed venous pO2 and pH by electrodes and oxyhemoglobin saturation (S) by oximerry. Arteriovenous T=37OC) were calcu02 difference (AV-02) and P50 (pH=7.4 2 lated. (mean*D) and rose At R, CI was I.SKJ.3l/min/m slightly but significantly during E to 2.4ti.7, (pcO.01). At R, V02 was 14OK!O ml/min/m2 and rose substantially during E to 29OaO (pcO.01). At R, AV-@was 8.1*1.8 ml/100 ml and rose substantially during E to 12.5*3.4 (pcO.01). At R, mixed venous pH (MVpH) was normal (7.4Kl.05) and therefore made no contribution to enhanced oxyhemoglobin dissociation (OHD). However, P50 was increased to 29.8t3.5 torr (normal 26.9 torr, pcO.01) , accounting for 16% of peripheral 02 consumption (AV02). At E, P50 remained elevated at 30.9*5.8 torr. In addition, however, MVpH was decreased to 7.3rctO.06 (p&O5 cf. control) causing a further shift in OHD by the Bohr effect. At E, enhanced OHD also accounted for about 15% of the AV-02. After vasodilator therapy (hydralazine or minoxidil), R and E MVpH were 7.44N.03 and 7.37a.04 and P505 were 27.2*1.5 and 27.9,l.S torr respectively. We conclude that peripheral 02 consumption in the chronic heart failure patient depends in part on a shift in OHD, and is less dependent on this compensatory mechanism after vasodilator therapy.

CHANGES IN LEFT VENTRICULAR VOLUMES DURING UPRIGHT EXERCISE IN PATIENTS WITH CORONARY ARTERY DISEASE Abdulmassih S. Iskandrian, MD, FACC, A-Hamid Hakki, MD, Bernard L. Serial.MD. FACC and Sally A. Kane. RN. Cardiovascula; Instiiute, Hahnemann-Medical College and Hospital, Philadelphia, Pennsylvania. We studied 24 patients (pts) with coronary artery disease (CAD) using symptom-limited upright exercise (EX) on a bicycle ergometer. First-pass radionuclide angiograms were obtained at rest (R) and peak EX. Fifty percent of the pts had previous transmural infarctions (MI). Twelve normal men (NL) served as a control. Nine pts developed angina or ST depression during FX. The W heart rate (HR) and EX tolerance were lower in pts than normal (p < .Ol). sv (ml) LV-EF LV-EDV (ml) co (Llmin) R EX R EX R EX R W No MI 174+41 185+40 95+25 90+32 7.2+2.6*12.7+5.3 55+10*49+12 MI 229799 253798 76725 8G35 4.9?1.3*10.2T2.7 38+13 38+12 170735 92~1~12~207.5'io.9*19.8T3.9 6236 *7535 NL 15628 -

ALTERATIONS IN PLASMA LIPOPROTEIN LEVELS DURING HIGH MILEAGE RUNNING

(LV, left ventricle; EDV, end-diastolic volume measured by area-length method; SV, stroke volume; CO, cardiac output; EF, ejection fraction; *, p < .Ol, R vs EX). Six NL and 12 pts had 2 10% increase in EDV during EX. The remaining had either no change or decrease. Pts with MI had higher EDV at R and EX than NL (p < .Ol). However, there was no significant difference between R and EX-EDV (and the change in EDV during EX) in NL compared to pts (with or without MI). The SV, CO and EF were higher in NL than pts with CAD during FX (d < .Ol). We conclude: There are significant differences in the SV, CO, HR and EF between NL and pts with CAD during upright EX. However, LV dilatation is neither sensitive (50%) nor specific (50%) for CAD. Moreover, LV dilatation is not affected by the resting EF or by presence bf previous MI.

468

February 1981

The American Journal of CARDIOLOGY

Rudolph

H.

Dressendorfer,

PhD; Charles

E. Wade,

PhD;

Conrad Hornick, PhD Ezra A Amsterdam, MD, FACC Human Performance Laboratiry, Uniiersity of California' Davis and Tripler Army Medical Center. Honolulu, Hawaii. Effects of long-distance running on plasma lipoprotein levels were studied using twelve male marathon runners, mean age 40, who ran on the average of 17.3 mi/day for ten days, rested for 70 hr, then continued to run for eight more days. Body weight and percentage body fat were unchanged despite an estimated caloric intake of 4800 kcallday. Blood samples were obtained on eight mornings prior to running. No significant change in total cholesterol (C) or low density lipoprotein-C was found. Compared to control values, high density lipoprotein (HDL)-C increased 18% and triglycerides (TG) decreased 22% after one week of running, and the observed changes were inversely correlated. The 70-hr rest period disrupted this significant rise in HDL-C and fall in TG. However, with continued running HDL-C and TG returned to pre-rest period values. The findings suggest that increased HDL-C with exercise training is coupled to the mechanism which lowers plasma TG. More importantly, detraining effects on plasma HDL-C and TG may be observed within days of stopping exercise when caloric intake remains high.

Volume 47