Rebuttal from Volker Adams

With great interest I read the opposing view by Sapp and Hagberg (2018) providing evidence that an acute bout of exercise does not damage the endothelial cell layer of systemic blood vessels in healthy individuals. Nevertheless, both of us agree that regular exercise training exerts beneficial effects in healthy individuals and patients with cardiovascular diseases. This beneficial effect is mediated by an increased laminar shear stress, whereas a disturbed turbulent shear stress mediates the development of atherosclerotic lesions. This has already been demonstrated in cell culture studies exposing human umbilical vein endothelial cells to different forms of shear stress (Morawietz et al. 2000; Takabe et al. 2011).

The point of view which is less clear is what happens with the endothelial cell layer in vivo after performing a short bout of exercise with an increase of laminar shear stress. Unfortunately, the data available are controversial as obvious from the present CrossTalk. The missing clear‐cut evidence for one or the other opinion may also be due to the problem of a missing marker, clearly indicating endothelial damage. As evident from our statements, similar markers, such as circulating endothelial cells, endothelial microparticles, circulating microRNAs or secreted protein were listed, but opposing interpretations were drawn. Therefore, just relying on these markers will not resolve the debate.

Examining endothelial function by measuring flow‐mediated vasodilatation (FMD) may help to resolve this debate. Unfortunately, also by measuring the FMD before and after an acute bout of exercise the results are controversial, with some investigations reporting a reduced FMD (Gonzales et al. 2011; Llewellyn et al. 2012; Birk et al. 2013) whereas others (Harris et al. 2008; Hallmark et al. 2014) could not confirm this observation. This discrepancy is probably due to the definition of the term ‘single bout of exercise’ (maximal exercise test to running a marathon or even a 246 km run), the intensity at which this bout was performed (ranging from below 50% to 90% ${\dot{V}}_{{\mathrm{O}}_2\max }$) and the time of assessing FMD (immediately after the exercise or 2 h after finishing the test). Based on the data available and also the opinion of Sapp and Hagberg (2018), we may postulate that when the intensity is high enough (above 70% ${\dot{V}}_{{\mathrm{O}}_2\max }$) and the duration is short enough (<1 h) a biphasic response occurs, in which the endothelial function is reduced (a sign of endothelial damage) followed by a restoration of endothelial function. At the molecular level this may be triggered by a balance between reactive oxygen species and nitric oxide or other vasoconstrictive and vasodilatory substances.

Call for comments

Readers are invited to give their views on this and the accompanying CrossTalk articles in this issue by submitting a brief (250 word) comment. Comments may be submitted up to 6 weeks after publication of the article, at which point the discussion will close and the CrossTalk authors will be invited to submit a ‘LastWord’. Please email your comment, including a title and a declaration of interest, to jphysiol@physoc.org. Comments will be moderated and accepted comments will be published online only as ‘supporting information’ to the original debate articles once discussion has closed.

Additional information

Competing interests

None declared.