The Effects of Prolonged Bouts of Exercise and Acute Ischemic Preconditioning on Cardiac Biomarker Release

Although habitual exercise can have profound beneficial effects on the cardiovascular system there is a growing evidence base to suggest that single acute bouts of endurance exercise can lead to the release of cardiac biomarkers of damage and dysfunction. Whether this cardiac biomarker release is indicative of reversible or irreversible cardiomyocyte damage is not clear. The first study in this thesis employed a new high sensitivity assay to assess cardiac troponin (hs-cTnI) as well as N terminal pro-brain natriuretic peptide (NT-proBNP) before, during and after 2 hr of treadmill exercise in young, healthy but non-athletic participants. No hs-cTnI samples were elevated above the detection limit of the assay during exercise and only one participant had a detectable hs-cTnI value post-exercise (22 ng/L). NT-proBNP levels were elevated more consistently during exercise and recovery. In the second study the repeatability of cardiac biomarker responses to 2 hr of treadmill exercise was assessed 1 and 12 weeks after an initial trial (Study 1). The same participant had an elevated hs-cTnI value post-exercise in week 0 (22ng/L) and week 1 (30 ng/L). All other participants had no detectable hs-cTn in trials in week 0 and 1. At week 12 one participant (different to the person in week 0 and 1) had elevated hs-cTnI post-exercise (25 and 38 ng/l). NT-proBNP levels rose with exercise in all trials but peaked earlier in trial 1 and demonstrated great individual variability. Study 3 and 4 investigated the role that ischemia may play in cardiac biomarker release and cardiac functional changes after endurance exercise. Ischemia was studied indirectly by employing remote ischemic preconditioning (RIPC) in a single-blind cross-over research design. In study 3 trained cyclists completed 2 one hour time trials in a controlled laboratory environment with trials preceded immediately RIPC or a SHAM protocol. Hs-cTnI values were reduced after the RIPC trial compared to the SHAM during recovery from exercise (significant main effect for trial). NT-proBNP and indices of cardiac function were not mediated by RIPC. Using the same RIPC intervention in study 4 we employed a longer exercise task (160 km cycle) in trained cyclists. We confirmed a partial attenuation of hs-cTnI appearance post-exercise following the RIPC intervention compared to the SHAM. In addition NT-proBNP was lower after the RIPC trial but RIPC did not mediate any change in cardiac function post-exercise. These data reflect the first tentative evidence that ischaemia could be implicated in post-exercise cardiac biomarker release. Although exercise can lead to cardiac biomarker appearance, and ischaemia may be implicated mechanistically, the rapid appearance and removal of these biomarkers as well as the limited impact on cardiac function still supports a reversible insult to the cardiomyocytes.

Name dc:type.qualificationname

phd_by_publication

Level dc:type.qualificationlevel

doctoral

Grantor dc:publisher.institution

Liverpool John Moores University

Year dc:date.issued

2018

Author dc:creator

• Benson, M

Contributors dc:contributor

• Professor George, K

• RC1200 Sports Medicine

DOI dc:identifier.doi

https://doi.org/10.24377/LJMU.t.00008786

OAI identifier oai:identifier

oai:researchonline.ljmu.ac.uk:8786