Ketcyian, S. J. FACSM; Goldstein, S.; Bravner, C. A.; Kacaoka, T.; Fedel, F.; Levine, T. B. Author Information
We examined whether an increase in stroke volume (SV) contributes to the increase in cardiac output that occurs when cardiac transplant patients (CT) exercise between 50% and 75% of maximum. Upright arm and leg exercise was performed by 13 CT and 10 normal controls. Cardiac output (CO2 rebreathing), expired air, and catecholamine measures were obtained at rest and at 50% and 75% of maximum. From rest to 50% of maximum both normals and CT increased heart rate (HR) and SV during arm and leg exercise. In normals, HR (arm = +17 +/- 2 min-1; leg = +21 +/- 3 min-1) was increased further at 75% of maximum but not SV (arm = 3 +/- 4 ml; leg = +2 +/- 8 ml). In CT, further increases in both HR (arm = +9 +/- 1 min-1; leg = +13 +/- 1 min-1) and SV (arm = +12 +/- 5 ml; leg = +12 +/- 3 ml) were observed at 75% of maximum. During leg exercise plasma norepinephrine was increased more in CT than in normals. Between 50% and 75% of maximum, an increase in SV is a more important mechanism for increasing cardiac output during upright arm and leg exercise in CT than in normals.
A group of orthotopic heart transplant (OHT, n = 28) and heart surgery (n = 19) patients, with similar ejection fractions and left ventricular end-diastolic pressures, were exercised to symptom-limited maximum to describe differences in cardiovascular and gas exchange responses. Testing was performed at a mean of 3 and 6 mo after surgery, respectively (P less than 0.05). OHT patients have a greater resting systolic and diastolic blood pressure (P less than 0.01) and a significantly greater (P less than 0.01) heart rate (HR) at rest in the supine and standing positions and during minutes 2 through 7 of supine recovery. Peak treadmill time was significantly less (P less than 0.01) in OHT patients. No significant differences were found for systolic blood pressure (SBP) during recovery, peak HR, ventilation, relative O2 uptake (VO2), body weight, ventilatory equivalents for O2 and CO2, O2 pulse, and HR-SBP product (peak HR x peak SBP). Peak pulse pressure, heart rate reserve, total VO2, and absolute VO2 at ventilatory threshold were significantly lower (P less than 0.01) in the OHT patients. We concluded that 1) complete cardiac decentralization is evident, 2) the significantly reduced VO2 at ventilatory threshold should be considered when activities of daily living are prescribed, and 3) SBP response is more appropriate than HR for assessing recovery of the decentralized heart after maximal exercise.
Schairer, J.; Keteylan, S. FACSH; Fedel, F.; Ehrman, J.; Shaw, T.; Alam, M.; Stein, P. Author Information
Keteyian, S. FACSM; Harks, C. R.C.; Fedel, F.; Kataoka, T.; Ehrman, J.; Ramirez, R.; Levine, T. B.; Levine, A. B. Author Information
This investigation examines the hypothesis that athletes increase stroke volume with submaximal exercise through an augmentation of left ventricular (LV) end-diastolic volume and a reduction of LV end-systolic volume, whereas sedentary adults only increase stroke volume modestly, because LV end-diastolic volume does not increase. Upright bicycle exercise was performed by 17 endurancetrained male athletes and 15 sedentary men. Mmode echocardiograms were obtained during submaximal exercise at predetermined heart rates. Athletes, at a heart rate of 130 beats/min, increased their stroke volume 67% from 72 ± 18 ml to 120 ± 26 ml (p < 0.001). This resulted from an increase of LV end-diastolic volume from 119 ±23 to 152 ± 28 ml (p < 0.001) and a reduction in LV end-systolic volume from 46 ± 14 to 31 ± 9 ml (p < 0.001). Sedentary men at the same heart rate increased stroke volume 22% from 63 ± 15 to 77 ± 21 ml (p < 0.05). LV end-diastolic volume did not change (96 ± 20 vs 97 ± 28 ml) (p = not significant), but LV end-systolic volume decreased (33 ± 11 vs 20 ± 9 ml) (p < 0.001). In conclusion, athletes increased cardiac output through a more prominent augmentation of stroke volume than sedentary subjects at submaximal exercise. This was accomplished through an augmentation of LV end-diastolic volume. This may have a conserving effect on myocardial oxygen consumption at these levels of exercise.
To determine the response to exercise of the left ventricle of endurance-trained athletes, 6 elite (world class) cyclists were compared to 6 untrained healthy control subjects. In athletes the stroke volume increased with exercise. In untrained volunteers the stroke volume did not change with exercise. This difference of the response of the stroke volume to exercise reflected a difference of the left ventricular end-diastolic volume. In athletes the left ventricular end-diastolic volume tended to increase. In control subjects the end-diastolic volume decreased. In conclusion, athletes increased cardiac output by increasing stroke volume and heart rate, whereas control subjects increased their cardiac output only by increasing their heart rate.
Orthotopic heart transplantation (OHT) represents an effective alternative for individuals with end-stage heart disease. The current literature reports only the responses of OHT patients to greater than or equal to 4 mo of exercise training (ET) and frequently lacks adequate controls. Most programs currently treating OHT patients usually provide 6-12 wk of ET. This study describes the effects of a 10-wk supervised ET program in 12 male OHT patients and 5 other male OHT patients who served as a comparison group. Graded exercise tests were performed before and after ET. After ET, maximal O2 consumption was significantly greater for the ET group than the comparison group (P less than 0.05) and the mean increase in peak heart rate was 18 +/- 4 and 6 +/- 4 (SE) min-1 for ET and comparison groups, respectively (P less than 0.05). Maximal ventilation was also significantly greater for the ET group at after ET, while resting heart rate and blood pressure and peak blood pressure, O2 pulse, respiratory rate, and ventilatory equivalents for O2 and CO2 were not significantly changed. We conclude that after OHT a 10-wk ET program improves maximal O2 consumption and, by improving peak heart rate, improves O2 delivery.
Fedel, F.; Ketoyian, S.; Eheman, J.; Marks, C.; Goslin, B.; Elder, R.; Connolly, A.; Fachnie, D.; Lovine, B.; O'Nell, M. Author Information
Elder, R.; Keteyian, S.; Ehrman, J.; Marks, C.; Connolly, A.; Fachnie, D.; Levine, B.; Fedel, F. Author Information