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Endothelial function response to different modes of acute and chronic exercise in both health and diseased populations

Kirk, Richard James Thompson


Richard James Thompson Kirk


Leigh A. Madden

Rebecca V. Vince


Endothelial microparticles (EMP) offer an insight into the state of the endothelium and are known to be elevated in diseases characterised by endothelial dysfunction (ED) (Horstman et al., 2004; Vince et al., 2009a). EMP have also been shown to increase after exercise/endothelial stress in healthy individuals (Sossdorf et al., 2011; Vince et al, 2009) but this area remains relatively novel.

The purpose of the first experiment was to quantify the effects of an acute bout of strenuous exercise on the circulating levels of EMP and to assess if this effect is different after the ingestion of an extensively researched ergogenic aid (sodium bicarbonate, NaHCO3). Seven physically active and apparently healthy males volunteered to perform 10 x 15 second (s) cycle sprints after the ingestion of either 0.03⁻¹ NaHCO₃ or 0.045⁻¹ of a placebo (sodium chloride, NaCl) in capsules. The ingestion of NaHCO₃ induced a pre exercise alkalosis as evidenced by a significantly altered resting acid base status, but had no influence on levels of EMP in healthy males. As a result, the data was combined for the two experimental groups, and the exercise produced a significantly increased level of CD105+ MP (MP; microparticles) at 90 minutes (min) and 180 min when compared with resting levels (p = 0.010, p = 0.043 respectively). The observed peak value at 90 min was also significantly greater compared to immediately post exercise (p = 0.019). CD106+ MP also increased significantly to 90 min from immediately post exercise (p = 0.020) and this was still greater at 180 min compared to post exercise (p = 0.015). It was concluded that exercise of this nature was sufficient to elicit ED, although the endothelium shows signs of endothelial repair within a matter of hours (hr). Also, it appears that pre exercise alkalosis has no effect on the attenuation of EMP quantity.

Additional work was completed to verify the novel finding that CD105+ MP and CD106+ MP appear markers of endothelial function (EF), and to further examine the quantification of EMP, this time in healthy females. There was also an additional blood draw in order to assess where the maximum level of endothelial stress was occurring post exercise. In the second experiment, 10 healthy females completed the identical repeated sprints protocol as the first experiment, this time without the ingestion of NaHCO₃. CD105+ MP were increased 90 min post exercise compared to immediately after exercise (p = 0.042). There was again a decline in both markers from 90 min to 180 min, although this was not significant. Furthermore, with the addition of a blood draw at 45 min post exercise, it was suggested that EMP levels appear to be rising between 45 min and 90 min post exercise, speculating this is the time point of greatest endothelial damage. Finally, shear stress was suggested as a key reason behind the increase in endothelial damage as a result of exercise, as indicated by significant changes in variables such as heart rate (HR) and systolic blood pressure (SBP).

The third experiment employed a longer 90 min interval cycling protocol with the purpose of quantifying EF over a greater period of time, allowing investigation into whether the markers of EF were altered in the same way as the previous two experiments. It was also an aim to further assess the possible influence of shear stress factors on ED. Fourteen healthy males completed 90 min of high intensity aerobic exercise, and there were several changes in both CD105+ MP and CD106+ MP. CD105+ MP rose significantly from rest to an observed peak at 90 min (p = 0.019). Both of these markers indicated a significant restoration of the endothelium as indicated by a fall from peak values during recovery to 180 min post exercise (CD105+ MP, p = 0.009; CD106+ MP, p = 0.022). This experiment concluded that the endothelium is greatly affected by highly intense exercise over a prolonged period of time, but is recovered fully in a time period of 3 hr. The effects of shear stress again appear to be largely influential, but future work must now be conducted in order to build on the findings from this research and examine shear stress closely during exercise and its relationship with EMP quantification.

It was the aim of the next experiment to investigate two separate methods of assessing EF (EMP and EndoPAT-2000), this time in a group of sedentary, but otherwise healthy individuals, in order to monitor the changes as a result of an acute bout of moderate intensity acute exercise. There were no significant differences found in EF as a result of exercise. This was indicated by no significant changes in CD105+ MP concentrations from pre to post exercise (p = 0.84) or pre to 60 min post exercise (p = 0.612). CD106+ MP concentrations showed a decrease from resting values (2513 CD106+ MP per μl platelet free plasma; PFP) to immediately post exercise (1368 CD106+ MP per μl PFP, p = 0.09), and again at 60 min post exercise (1293 CD106+ MP per μl PFP, p = 0.073) compared to resting values. Additionally, EndoPAT scores were unaffected by exercise, with values of reactive hyperaemia index (RHI) changing from rest (2.43) to post exercise (2.57), but this was not significant (p = 0.35). Correlations were carried out in order to determine and comparisons that may have existed between EMP and EndoPAT score using RHI. Although there was a slight trend for the higher numbers of CD105+ MP to correlate with the lower scores of RHI (r = 0.327) this was not significant (p = 0.171). CD106+ MP showed no correlations with RHI (r = -0.087, p = 0.717). This chapter suggested that exercise was not strenuous enough to see any significant changes in EF, and EMP continue to appear efficient markers of EF in a population of sedentary, healthy individuals.

The final experimental chapter investigated the effects of a supervised 8 week moderate intensity exercise programme on women with polycystic ovary syndrome (PCOS) and control women free from any known disease. The aim was to assess if this type of exercise could improve EF in this population, and if there was a relationship with EMP (CD105+ MP and CD106+ MP) to other factors, such as body composition and cardiorespiratory fitness. EF was improved from baseline values to post exercise programme, with CD105+ MP concentrations reducing from 2113 CD105+ MP per μl PFP to 424 CD105+ MP per μl PFP (p = 0.025). Furthermore, control women showed no significant change from pre to post exercise programme in CD105+ MP (p = 0.25), or CD106+ MP (p = 0.99). Further analysis was performed to look for any associations with the changes in EMP compared to body composition changes as a result of exercise, but no significant correlations existed. This study concluded that supervised, moderate intensity exercise independent of substantial weight loss was enough to elicit an00 improvement in EF in women with PCOS compared to healthy control women. Additionally, EMP concentrations appear to be able to effectively map changes in EF across a long period of time in diseased states, adding to the notion that EMP may account for EF. Future work must now build on these findings from this research and examine this response in a larger cohort involving PCOS women with varied phenotypes and body composition.


Kirk, R. J. T. (2014). Endothelial function response to different modes of acute and chronic exercise in both health and diseased populations. (Thesis). University of Hull. Retrieved from

Thesis Type Thesis
Deposit Date Aug 7, 2018
Publicly Available Date Feb 23, 2023
Keywords Sports science
Public URL
Additional Information Department of Sport, Health and Exercise Science, The University of Hull
Award Date Sep 1, 2014


Thesis (3.2 Mb)

Copyright Statement
© 2014 Kirk, Richard James Thompson. All rights reserved. No part of this publication may be reproduced without the written permission of the copyright holder.

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