Key result
Committed lifelong exercise attenuated the age-related reduction in left ventricular systolic longitudinal strain observed in sedentary seniors.
Why the study?
Does lifelong exercise preserve left ventricular longitudinal systolic function compared to sedentary aging?
Cross-Sectional (n=73)
Does lifelong exercise preserve left ventricular longitudinal systolic function compared to sedentary aging?
Committed lifelong exercise attenuates the age-related reduction in left ventricular systolic longitudinal strain, primarily by preserving LV diastolic filling.
Answers are grounded in this paper and cite their sources.
May support lifelong exercise for LV preservation in aging; hypothesis-generating and requires prospective trials before practice change.
PURPOSE: The current study examined whether age-related changes in left ventricular (LV) longitudinal systolic function is an adaptation to a more sedentary lifestyle and can be preserved by lifelong exercise training. METHODS: A cross-sectional examination of 18 sedentary young (37 ± 6 yr), 29 sedentary seniors (71 ± 5 yr, 0-3 exercise sessions per week), and 26 seniors (68 ± 5 yr) who had performed a committed level (four to seven exercise sessions per week) of lifelong (>25 yr) exercise. Invasive right heart catheterization (pulmonary capillary wedge pressure) and noninvasive measures of LV function were collected at the following conditions: 1) supine rest, 2) during LV unloading (lower body negative pressure), and 3) LV loading (saline infusion). Ejection fraction and preload-recruitable stroke work (PRSW) were used to describe global LV systolic function, while peak systolic tissue velocity and longitudinal strain (LS) indicate LV longitudinal systolic function. To adjust LS for aging and training-related differences in LV preload and afterload, LV end-diastolic volume and end-systolic pressure (ESP) were included as covariates in ANCOVA models. RESULTS: Ejection fraction and PRSW were unaffected by aging or lifelong exercise (P = 0.22, P = 0.08, respectively). Peak systolic tissue velocities decreased with aging (P < 0.001) and sedentary seniors had a smaller LS compared with young (P = 0.023) and lifelong exercisers (P = 0.046). Preload-recruitable stroke work, ESP as a covariate did not alter group differences; however, LV end-diastolic volume eliminated group differences between senior groups. Longitudinal strain was preload dependent (P < 0.001), which was independent of aging and lifelong exercise. CONCLUSIONS: Sedentary aging leads to a reduction in systolic LS, which is attenuated by committed lifelong exercise due to improved LV diastolic filling.
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Howden et al. (2017) conducted a cross-sectional in Sedentary aging (n=73). Committed lifelong exercise vs. Sedentary aging was evaluated on Left ventricular longitudinal systolic function (longitudinal strain and peak systolic tissue velocity) (p=0.046). Committed lifelong exercise attenuated the age-related reduction in left ventricular systolic longitudinal strain observed in sedentary seniors.
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