scholarly journals Effect of Endurance Exercise Training on Left Ventricular Size and Remodeling in Older Adults With Hypertension

2000 ◽  
Vol 55 (4) ◽  
pp. M245-M251 ◽  
Author(s):  
M. J. Turner ◽  
R. J. Spina ◽  
W. M. Kohrt ◽  
A. A. Ehsani
Keyword(s):  
Older Adults ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Left Ventricular ◽  
Ventricular Size ◽  
Left Ventricular Size ◽  
Endurance Exercise Training

Controlled Endurance Exercise Training and VO 2max Changes in Older Adults: A Meta‐Analysis

2005 ◽  
Vol 8 (4) ◽  
pp. 217-225 ◽  
Author(s):  
Guoyuan Huang ◽  
Cheryl A. Gibson ◽  
Zung V. Tran ◽  
Wayne H. Osness
Keyword(s):  
Older Adults ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Meta Analysis ◽  
Endurance Exercise Training

The impact of endurance exercise training on left ventricular systolic mechanics

2008 ◽  
Vol 295 (3) ◽  
pp. H1109-H1116 ◽  
Author(s):  
Aaron L. Baggish ◽  
Kibar Yared ◽  
Francis Wang ◽  
Rory B. Weiner ◽  
Adolph M. Hutter ◽  
...  
Keyword(s):  
Exercise Training ◽  
Ejection Fraction ◽  
Endurance Exercise ◽  
Systolic Function ◽  
Radial Strain ◽  
Left Ventricular ◽  
Functional Changes ◽  
Endurance Exercise Training ◽  
Lv Systolic Function ◽  
The Impact

Although exercise training-induced changes in left ventricular (LV) structure are well characterized, adaptive functional changes are incompletely understood. Detailed echocardiographic assessment of LV systolic function was performed on 20 competitive rowers (10 males and 10 females) before and after endurance exercise training (EET; 90 days, 10.7 ± 1.1 h/wk). Structural changes included LV dilation (end-diastolic volume = 128 ± 25 vs. 144 ± 28 ml, P < 0.001), right ventricular (RV) dilation (end-diastolic area = 2,850 ± 550 vs. 3,260 ± 530 mm2, P < 0.001), and LV hypertrophy (mass = 227 ± 51 vs. 256 ± 56 g, P < 0.001). Although LV ejection fraction was unchanged (62 ± 3% vs. 60 ± 3%, P = not significant), all direct measures of LV systolic function were altered. Peak systolic tissue velocities increased significantly (basal lateral S′Δ = 0.9 ± 0.6 cm/s, P = 0.004; and basal septal S′Δ = 0.8 ± 0.4 cm/s, P = 0.008). Radial strain increased similarly in all segments, whereas longitudinal strain increased with a base-to-apex gradient. In contrast, circumferential strain (CS) increased in the LV free wall but decreased in regions adjacent to the RV. Reductions in septal CS correlated strongly with changes in RV structure (ΔRV end-diastolic area vs. ΔLV septal CS; r2 = 0.898, P < 0.001) and function (Δpeak RV systolic velocity vs. ΔLV septal CS, r2 = 0.697, P < 0.001). EET leads to significant changes in LV systolic function with regional heterogeneity that may be secondary to concomitant RV adaptation. These changes are not detected by conventional measurements such as ejection fraction.

scholarly journals Response to Endurance Exercise Training in Older Adults with Heart Failure with Preserved or Reduced Ejection Fraction

2017 ◽  
Vol 65 (8) ◽  
pp. 1698-1704 ◽  
Author(s):  
Ambarish Pandey ◽  
Dalane W. Kitzman ◽  
Peter Brubaker ◽  
Mark J. Haykowsky ◽  
Timothy Morgan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Older Adults ◽  
Exercise Training ◽  
Ejection Fraction ◽  
Endurance Exercise ◽  
Reduced Ejection Fraction ◽  
Endurance Exercise Training

Effect of Controlled Endurance Exercise Training on VO2max Changes in Older Adults

2004 ◽  
Vol 36 (Supplement) ◽  
pp. S142
Author(s):  
Guoyuan Huang ◽  
Cheryl A. Gibson ◽  
Zung Vu Tran ◽  
Wayne H. Osness
Keyword(s):  
Older Adults ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Endurance Exercise Training

scholarly journals Upward resetting of the vascular sympathetic baroreflex in middle-aged male runners

2019 ◽  
Vol 317 (1) ◽  
pp. H181-H189 ◽  
Author(s):  
Denis J. Wakeham ◽  
Rachel N. Lord ◽  
Jack S. Talbot ◽  
Freya M. Lodge ◽  
Bryony A. Curry ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Exercise Training ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Endurance Exercise ◽  
Left Ventricular ◽  
Middle Aged ◽  
Endurance Exercise Training ◽  
Pressure Stability ◽  
Age Category

This study focused on the influence of habitual endurance exercise training (i.e., committed runner or nonrunner) on the regulation of muscle sympathetic nerve activity (MSNA) and arterial pressure in middle-aged (50 to 63 yr, n = 23) and younger (19 to 30 yr; n = 23) normotensive men. Hemodynamic and neurophysiological assessments were performed at rest. Indices of vascular sympathetic baroreflex function were determined from the relationship between spontaneous changes in diastolic blood pressure (DBP) and MSNA. Large vessel arterial stiffness and left ventricular stroke volume also were measured. Paired comparisons were performed within each age category. Mean arterial pressure and basal MSNA bursts/min were not different between age-matched runners and nonrunners. However, MSNA bursts/100 heartbeats, an index of baroreflex regulation of MSNA (vascular sympathetic baroreflex operating point), was higher for middle-aged runners ( P = 0.006), whereas this was not different between young runners and nonrunners. The slope of the DBP-MSNA relationship (vascular sympathetic baroreflex gain) was not different between groups in either age category. Aortic pulse wave velocity was lower for runners of both age categories ( P < 0.03), although carotid β-stiffness was lower only for middle-aged runners ( P = 0.04). For runners of both age categories, stroke volume was larger, whereas heart rate was lower (both P < 0.01). In conclusion, we suggest that neural remodeling and upward setting of the vascular sympathetic baroreflex compensates for cardiovascular adaptations after many years committed to endurance exercise training, presumably to maintain arterial blood pressure stability. NEW & NOTEWORTHY Exercise training reduces muscle sympathetic burst activity in disease; this is often extrapolated to infer a similar effect in health. We demonstrate that burst frequency of middle-aged and younger men committed to endurance training is not different compared with age-matched casual exercisers. Notably, well-trained, middle-aged runners display similar arterial pressure but higher sympathetic burst occurrence than untrained peers. We suggest that homeostatic plasticity and upward setting of the vascular sympathetic baroreflex maintains arterial pressure stability following years of training.

Exercise improves impaired ventricular function and alterations of cardiac myofibrillar proteins in diabetic dyslipidemic pigs

2005 ◽  
Vol 98 (2) ◽  
pp. 461-467 ◽  
Author(s):  
F. Steven Korte ◽  
Eric A. Mokelke ◽  
Michael Sturek ◽  
Kerry S. McDonald
Keyword(s):  
Exercise Training ◽  
Expression Pattern ◽  
Endurance Exercise ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Myofibrillar Proteins ◽  
Endurance Exercise Training ◽  
Isoform Expression ◽  
Fractional Shortening

Chronic diabetes is often associated with cardiomyopathy, which may result, in part, from defects in cardiac muscle proteins. We investigated whether a 20-wk porcine model of diabetic dyslipidemia (DD) would impair in vivo myocardial function and yield alterations in cardiac myofibrillar proteins and whether endurance exercise training would improve these changes. Myocardial function was depressed in anesthetized DD pigs ( n = 12) compared with sedentary controls (C; n = 13) as evidenced by an ∼30% decrease in left ventricular fractional shortening and an ∼35% decrease in +dP/d t measured by noninvasive echocardiography and direct cardiac catheterization, respectively. This depression in myocardial function was improved with chronic exercise as treadmill-trained DD pigs (DDX) ( n = 13) had significantly greater fractional shortening and +dP/d t than DD animals. Interestingly, the isoform expression pattern of the myofibrillar regulatory protein, cardiac troponin T (cTnT), was significantly shifted from cTnT1 toward cTnT2 and cTnT3 in DD pigs. Furthermore, this change in cTnT isoform expression pattern was prevented in DDX pigs. Finally, there was a decrease in baseline levels of cAMP-dependent protein kinase-induced phosphorylation of the myofibrillar proteins troponin I and myosin-binding protein-C in DD animals. Overall, these results indicate that 20 wk of DD lead to myocardial dysfunction coincident with significant alterations in myofibrillar proteins, both of which are prevented with endurance exercise training, implying that changes in myofibrillar proteins may contribute, at least in part, to cardiac dysfunction associated with diabetic cardiomyopathy.

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