Effect of eight weeks of endurance exercise training on right and left ventricular volume and mass in untrained obese subjects: a longitudinal MRI study

2008 ◽  
Vol 18 (3) ◽  
pp. 354-359 ◽  
Author(s):  
T. W. Vogelsang ◽  
B. Hanel ◽  
U. S. Kristoffersen ◽  
C. L. Petersen ◽  
J. Mehlsen ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Left Ventricular Volume ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Endurance Exercise Training ◽  
Longitudinal Mri ◽  
Obese Subjects ◽  
Mri Study

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 Endurance Exercise Training Up-Regulates Lipolytic Proteins and Reduces Triglyceride Content in Skeletal Muscle of Obese Subjects

2013 ◽  
Vol 98 (12) ◽  
pp. 4863-4871 ◽  
Author(s):  
Katie Louche ◽  
Pierre-Marie Badin ◽  
Emilie Montastier ◽  
Claire Laurens ◽  
Virginie Bourlier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Protein Expression ◽  
Endurance Exercise ◽  
Oxidative Capacity ◽  
Metabolic Effects ◽  
Gene Identification ◽  
Mrna Levels ◽  
Endurance Exercise Training ◽  
Obese Subjects

Context: Skeletal muscle lipase and intramyocellular triglyceride (IMTG) play a role in obesity-related metabolic disorders. Objectives: The aim of the present study was to investigate the impact of 8 weeks of endurance exercise training on IMTG content and lipolytic proteins in obese male subjects. Design and Volunteers: Ten obese subjects completed an 8-week supervised endurance exercise training intervention in which vastus lateralis muscle biopsy samples were collected before and after training. Main Outcome Measures: Clinical characteristics and ex vivo substrate oxidation rates were measured pre- and posttraining. Skeletal muscle lipid content and lipolytic protein expression were also investigated. Results: Our data show that exercise training reduced IMTG content by 42% (P &lt; .01) and increased skeletal muscle oxidative capacity, whereas no change in total diacylglycerol content and glucose oxidation was found. Exercise training up-regulated adipose triglyceride lipase, perilipin (PLIN) 3 protein, and PLIN5 protein contents in skeletal muscle despite no change in mRNA levels. Training also increased hormone sensitive–lipase Ser660 phosphorylation. No significant changes in comparative gene identification 58, G0/G1 switch gene 2, and PLIN2 protein and mRNA levels were observed in response to training. Interestingly, we noted a strong relationship between skeletal muscle comparative gene identification 58 and mitochondrial respiratory chain complex I protein contents at baseline (r = 0.87, P &lt; .0001). Conclusions: Endurance exercise training coordinately up-regulates fat oxidative capacity and lipolytic protein expression in skeletal muscle of obese subjects. This physiological adaptation probably favors fat oxidation and may alleviate the lipotoxic lipid pressure in skeletal muscle. Enhancement of IMTG turnover may be required for the beneficial metabolic effects of exercise in obesity.

scholarly journals Moderate Exercise Training Improves Survival and Ventricular Remodeling in an Animal Model of Left Ventricular Volume Overload

2009 ◽  
Vol 2 (5) ◽  
pp. 437-445 ◽  
Author(s):  
Dominic Lachance ◽  
Éric Plante ◽  
Andrée-Anne Bouchard-Thomassin ◽  
Serge Champetier ◽  
Élise Roussel ◽  
...  
Keyword(s):  
Animal Model ◽  
Exercise Training ◽  
Left Ventricular Volume ◽  
Ventricular Remodeling ◽  
Volume Overload ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Moderate Exercise ◽  
Moderate 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.

scholarly journals A prospective randomised longitudinal MRI study of left ventricular adaptation to endurance and resistance exercise training in humans

2011 ◽  
Vol 589 (22) ◽  
pp. 5443-5452 ◽  
Author(s):  
Angela L. Spence ◽  
Louise H. Naylor ◽  
Howard H. Carter ◽  
Christopher L. Buck ◽  
Lawrence Dembo ◽  
...  
Keyword(s):  
Exercise Training ◽  
Resistance Exercise ◽  
Left Ventricular ◽  
Resistance Exercise Training ◽  
Longitudinal Mri ◽  
Mri Study

scholarly journals Endurance exercise training attenuates natriuretic peptide release during maximal effort exercise: biochemical correlates of the “athlete’s heart”

2018 ◽  
Vol 125 (6) ◽  
pp. 1702-1709 ◽  
Author(s):  
Ankit B. Shah ◽  
Jodi Zilinski ◽  
Marcel Brown ◽  
Jennifer H. Neary ◽  
Rory B. Weiner ◽  
...  
Keyword(s):  
Exercise Training ◽  
Natriuretic Peptide ◽  
Endurance Exercise ◽  
Cardiac Remodeling ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Cardiac Wall ◽  
Endurance Exercise Training ◽  
Exercise Induced ◽  
Maximal Effort

Endurance exercise training (ET) stimulates eccentric left ventricular hypertrophy (LVH) with left atrial dilation. To date, the biochemical correlates of exercise-induced cardiac remodeling (EICR) remain incompletely understood. Collegiate male rowers ( n = 9) were studied with echocardiography and maximal-effort cardiopulmonary exercise testing (MECPET) before and after 90 days of ET intensification. Midregional proatrial natriuretic peptide (MR-proANP), NH2-terminal pro B-type natriuretic peptide (NT-proBNP), and high-sensitivity troponin T were measured at rest, peak MECPET, and 60 min post-MECPET at both study time points. Endurance exercise training resulted in eccentric LVH (LV mass = 102 ± 8 vs. 110 ± 11 g/m2, P = 0.001; relative wall thickness = 0.36 ± 0.04 vs. 0.37 ± 0.04, P = 0.103), left atrial dilation (74 ± 18 vs. 84 ± 15 ml, P < 0.001), and increased exercise capacity (peak V̇o2 = 53.0 ± 5.9 vs. 67.3 ± 8.2 ml·kg−1·min−1, P < 0.001). Left ventricular remodeling was characterized by an ~7% increase in LV wall thickness but only a 3% increase in LV chamber radius. The magnitude of natriuretic peptide release, examined as percent change from rest to peak exercise, was significantly lower for both MR-proANP (115 [95,127]% vs. 78 [59,87]%, P = 0.04) and NT-proBNP (46 [31,70]% vs. 27 [25,37]%, P = 0.02) after ET. Rowing-based ET and corollary EICR appear to result in an attenuated natriuretic peptide response to maximal effort exercise. This may occur as a function of decreased cardiac wall stress after ET as seen by disproportionally higher ventricular wall thickening compared with chamber dilation. NEW & NOTEWORTHY Using longitudinal pre- and postendurance training natriuretic peptide measurements, we demonstrate that the development of exercise-induced cardiac remodeling results in an attenuated natriuretic peptide response to acute bouts of maximal intensity exercise. Exercise-induced cardiac remodeling was associated with a disproportionally higher ventricular wall thickening compared with chamber dilation, a pattern that reduces cardiac wall stress. These observations advance our understanding of both the structural and biochemical adaptations that underlie the cardiovascular response to endurance training.

Sign in / Sign up

Export Citation Format

Share Document