Dissociation Between Structural and Functional Changes in Arterial Stiffness After High Intensity Endurance Training in Sedentary Middle-Aged Adults: 2760 Board #75 May 29, 2

Increased arterial stiffness resulting from sedentary aging has been implicated as a marker for atherosclerosis, as well as a strong predictor for future cardiovascular disease. Arterial stiffness also increases afterload and may restrain exercise-induced increases in cardiac output. In sedentary seniors aged > 65 yrs, we have demonstrated that there is little structural plasticity of either the heart or large blood vessels despite a year of training, though stroke volume may nevertheless increase by functional (probably endothelial) mechanisms. Whether initiating training earlier in life may be better able to alter arterial structure is unknown. PURPOSE: To investigate the effect of a progressive, high-intensity endurance exercise program in improving central pulse wave velocity (cPWV) and peak cardiac output (Qc) in middle-aged adults. METHODS: 41 sedentary, healthy middle-aged adults (19 males; 52 ± 5 yrs) were recruited and randomized to one of two study groups, Exercise (EX; n=21) or non-exercise Control (CON; n=20); EX completed a 9-month progressive phase of a 24-month exercise prescription. At baseline and month 10 of training, all subjects underwent cPWV analysis [SphygmoCor tonometry] and maximal exercise testing, in which VO2max [Douglas Bags] and peak Qc [C2H2 rebreathing] were measured during incremental treadmill exercise. RESULTS: CON participants had no change in cPWV (719 ± 122 to 754 ± 117cm/s, p=0.148) or peak Qc (14.35 ± 3.75 to 14.95 ± 3.73L/min, p=0.228). EX also had no change in cPWV (716 ± 136 to 716 ± 94cm/s, p=1.000), yet increased peak Qc substantially (14.77 ± 3.06 to 16.05 ± 3.29L/min, p=0.016) entirely due to an increased peak SV (86.6 ± 20.1 to 93.5 ± 20.3mL, p=0.02). There was a modest association between cPWV change and peak Qc change in EX (R2=0.2194, p=0.032), but none in CON. CONCLUSION: 9 months of progressive, high-intensity training improved peak Qc without a measureable change in arterial stiffness. Thus, training allowed an augmented exercise stroke volume, due either to changes in ventricular compliance or v-a coupling, without evidence of meaningful changes in arterial structure. Whether such training can prevent (if not reverse) age-associated deterioration in arterial stiffness remains to be determined.