Effect of exercise training on left ventricular performance in older women free of cardiopulmonary disease

Robert J. Spina, Takeshi Ogawa, Tom R. Miller, Wendy M. Kohrt, Ali A. Ehsani

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52 Scopus citations


Endurance exercise training increases aerobic exercise capacity (maximal oxygen consumption rate [V̇O2max]) and attenuates the age-related decline in left ventricular (LV) function during exercise in older men. To determine whether similar adaptations occur in older women, 10 subjects (aged 63 ± 4 years mean ± SE) were studied before and after 9 to 12 months of endurance exercise training. They exercised 3.85 ± 0.06 days/week at 81 ± 0.3% of maximal heart rate. LV function at rest and during supine exercise was assessed by radionuclide ventriculography. V̇O2max was increased by 21% (from 1.40 ± 0.1 to 1.7 ± 0.1 liter/min; p < 0.001) in response to training. Maximal heart rate and systolic blood pressure during treadmill exercise were unchanged (161 ± 5 beats/min before vs 164 ± 3 beats/min after; p = NS, and 208 ± 7 mm Hg before vs 214 ± 8 mm Hg after; p = NS, respectively) after training. LV ejection fraction at rest (70.4 ± 2% before vs 70 ± 1% after) and during peak exercise (78.6 ± 2% before vs 79.3 ± 2% after) did not change in response to training. Furthermore, the increases in ejection fraction from rest to exercise were similar before and after training (change: 8.8 ± 1 vs 9.1 ± 1%). Stroke volume and cardiac output at peak exercise also did not change in response to training. Exercise training did not induce LV enlargement as evidenced by absence of an increase in LV end-diastolic volume (rest: 117 ± 6 vs 108 ± 9 ml, p = NS; exercise 124 ± 7 ml before vs 123 ± 9 ml after; p = NS). End-systolic volume (rest: 33 ± 2 ml before vs 33 ± 2 ml after, p = NS; exercise: 28 ± 3 ml before vs 25 ± 2 ml after, p = NS), and systolic blood pressure-end systolic volume relation did not change. The results indicate that endurance exercise training improves V̇O2max in older women primarily by means of peripheral adaptations without inducing LV enlargement or enhancement of LV systolic function.

Original languageEnglish
Pages (from-to)99-104
Number of pages6
JournalThe American journal of cardiology
Issue number1
StatePublished - Jan 1 1993


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