Cardiovascular effects of 1 year of progressive and vigorous exercise training in previously sedentary individuals older than 65 years of age

Abstract

Background: Healthy but sedentary aging leads to cardiovascular stiffening, whereas life-long endurance training preserves left ventricular (LV) compliance. However, it is unknown whether exercise training started later in life can reverse the effects of sedentary behavior on the heart.

Methods and results: Twelve sedentary seniors and 12 Masters athletes were thoroughly screened for comorbidities. Subjects underwent invasive hemodynamic measurements with pulmonary artery catheterization to define Starling and LV pressure-volume curves; secondary functional outcomes included Doppler echocardiography, magnetic resonance imaging assessment of cardiac morphology, arterial stiffness (total aortic compliance and arterial elastance), and maximal exercise testing. Nine of 12 sedentary seniors (70.6±3 years; 6 male, 3 female) completed 1 year of endurance training followed by repeat measurements. Pulmonary capillary wedge pressures and LV end-diastolic volumes were measured at baseline, during decreased cardiac filling with lower-body negative pressure, and increased filling with saline infusion. LV compliance was assessed by the slope of the pressure-volume curve. Before training, Vo(2)max, LV mass, LV end-diastolic volume, and stroke volume were significantly smaller and the LV was less compliant in sedentary seniors than Masters athletes. One year of exercise training had little effect on cardiac compliance. However, it reduced arterial elastance and improved Vo(2)max by 19% (22.8±3.4 versus 27.2±4.3 mL/kg/mL; P<0.001). LV mass increased (10%, 64.5±7.9 versus 71.2±12.3 g/m(2); P=0.037) with no change in the mass-volume ratio.

Conclusions: Although 1 year of vigorous exercise training did not appear to favorably reverse cardiac stiffening in sedentary seniors, it nonetheless induced physiological LV remodeling and imparted favorable effects on arterial function and aerobic exercise capacity.

Figures

Figure 1

A, Frank Starling relationship. Systolic ventricular performance for sedentary seniors before and after exercise training and Masters athletes. Lines represent results of second linear regression analyses for sedentary seniors before (r=0.98) and after (r=0.97) training and Masters athletes (r=0.99). Note lower stroke volume index for any given PCWP in sedentary seniors before training compared with those in Masters athletes and substantially upward shift of Starling curve after training. B, Preload recruitable stroke work. Lines represent results of linear regression analyses for sedentary seniors before (r=0.98) and after (r=0.97) training and Masters athletes (r=0.99). No differences were noted in stroke work between sedentary seniors and Masters athletes before training across all loading conditions (P=0.513). However, stroke work was increased across all loading conditions in sedentary seniors after training (P=0.002).

Figure 2

Diastolic pressure volume relationships. A, Pressure-volume curves for sedentary seniors before (r=0.97) and after (r=0.98) training and Masters athletes (r=0.93). Note leftward shift and steeper slope of curve for sedentary seniors before training compared with Masters athletes, suggesting a stiffer ventricle. No significant changes in pressure-volume curves were observed after training. B, Transmural pressures (PCWP-right atrial pressure) are used instead of PCWP for sedentary seniors before (r=0.94) and after (r=0.94) training and Masters athletes (r=0.94) to minimize the effects of external constraints on LV compliance. No significant changes were observed in pressure-volume curves after training. Note that the same scale is used for both panels A and B to emphasize the very small transmural pressure gradients that actually influence LV distension.

Figure 3

Doppler measures of LV diastolic function. ▲ indicates Masters athletes; ●, sedentary subjects before training; ○, sedentary subjects after training. A, Ratio of early and late mitral inflow velocities (E/A). After exercise training, E/A ratio were increased at baseline (P=0.052) and during saline infusion (P=0.009). (B) Doppler mitral annular velocities (TDI E mean). The resting baseline TDI E mean velocities were slower after training (P<0.001). This difference was observed during saline infusion (P<0.001), but not during LBNP. C, Isovolumic relaxation time (IVRT). After training, baseline IVRT was shorter than those before training (P=0.002). This difference was present across all loading conditions (P<0.001). D, Propagation velocity of early mitral inflow (Vp). After training, Vp was increased during saline infusion, especially at maximal dose of saline infusion (P=0.003), but unaffected at baseline and during LBNP.