The Short and Longer Term Impact of an Iron-Distance Triathlon on Arterial Stiffness

Repetitive episodes of arterial shear stress provide a stimulus that promotes vascular adaptations through endothelium-dependent remodelling. Longer exposure to stimuli, such as during endurance exercise, may compromise the vascular system. The mechanisms are likely due to shear stress, oxidative stress and inflammatory processes having an influence on endothelial function and aortic elasticity. PURPOSE: To assess the short and longer term influence of an iron-distance triathlon on indirect measures of arterial stiffness. METHODS: Eleven athletes (TRI; age: 34.3 ± 8.7yrs; weight: 73.9 ± 10.3kg) and 10 recreational control participants (CON; age: 26.5 ± 7.1yrs, weight: 72.7 ± 5.6kg) were assessed on 4 occasions with identical time intervals. Resting heart rate (HR), carotid-femoral pulse wave velocity (PWV), augmentation index (Aix) and Aix corrected for a HR of 75 beats•min (Aix@75) were measured 7 days prior (T1) to an iron-distance triathlon. This consisted of a 3.86km swim, 180.25km cycle, and 42.2km run. Repeated measurements were obtained 12 to 18 hours post-exercise (T2), 7 days post-triathlon (T3), and 28 days post-triathlon (T4). The CON group did not participate in the triathlon. Data presented as mean ± standard deviation. RESULTS: All effects are reported as significant at p < 0.05. Average triathlon race time was 786 ± 63mins. HR, PWV, Aix and Aix@75 were not significantly different between groups at T1. A significant interaction effect for HR was found for time and group; simple main effects revealed a significant difference between TRI (56 ± 7beats•min) and CON (63 ± 13beats•min) at T2. No significant differences in HR were observed between groups at T3 or T4. PWV was significantly greater in TRI compared with CON at T2 (6.1 ± 0.4m•s-1 vs 5.5 ± 0.6m•s-1) and T3 (6.3 ± 0.7m•s-1 vs 5.6 ± 0.6m•s-1) but not at T1 (5.9 ± 0.6m•s-1 vs 5.6 ± 0.8m•s-1) or T4 (6.0 ± 0.6m•s-1 vs 5.8 ± 0.8m•s-1). No significant time or group interactions were revealed for Aix or Aix@75. CONCLUSIONS: The elevation of PWV and HR but not Aix or Aix@75 in the TRI group is likely due to the different response to shear stress and acute systemic inflammation of large and small arterial vascular beds. Importantly, all measurements were statistically similar levels at the final time point; suggesting only a short-term elevation of arterial stiffness.