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Endothelial function following glucose ingestion in adults with prediabetes: Role of exercise intensity
Author(s) -
Malin Steven K.,
Rynders Corey A.,
Weltman Judy Y.,
Jackson Roberts L.,
Barrett Eugene J.,
Weltman Arthur
Publication year - 2016
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21522
Subject(s) - medicine , prediabetes , brachial artery , endocrinology , oxidative stress , ingestion , lactate threshold , aerobic exercise , exercise intensity , biomarker , diabetes mellitus , type 2 diabetes , heart rate , blood pressure , blood lactate , biochemistry , chemistry
Objective To determine whether high intensity exercise (HIE) would improve endothelial function more than an isocaloric bout of moderate intensity exercise (MIE) following glucose ingestion in adults with prediabetes. Methods Twelve subjects with prediabetes completed all three conditions: time‐course matched control and isocaloric exercise (∼200 kcal) at moderate (MIE; at lactate threshold) and high intensity (HIE; 75% of difference between lactate threshold and VO 2 peak). Brachial artery flow‐mediated dilation (FMD) was measured before exercise (baseline), within 30 min postexercise, and 1 and 2 hr following a 75 g oral glucose tolerance test (OGTT). Plasma F2‐isoprostanes were also assessed during the protocol (i.e., baseline to 2 hr OGTT) as a biomarker of oxidative stress. Results MIE reduced postexercise F2‐isoprostanes AUC compared with time‐course matched control and HIE. Although exercise had no statistical effect on FMD postexercise or during the OGTT, elevations in FMD AUC after MIE and HIE were associated with reduced postexercise F2‐isoprostanes AUC . Conclusions Exercise at either intensity had no effect on FMD immediately postexercise following glucose administration. However, individuals with reduced oxidative stress responses to exercise had greater exercise‐induced improvement in FMD. Further work is required to identify the mechanism by which exercise alters oxidative stress to enhance endothelial function.