Ryan Perkins

BMI‐matched normal‐ (NGT, n = 10, 41 ± 4y, 35.6 ± 3.0 kg/m 2 ) and abnormal‐glucose‐tolerant (AGT, n = 16, 51 ± 3y, 34.3 ± 1.5 kg/m 2 ) participants were evaluated for body composition, metabolic health (oral glucose tolerance test [OGTT]), and VO 2 max. Participants also completed a treadmill walking test at 65% VO 2 max for 30 min. Total sRAGE, esRAGE, sTLR2, and sTLR4 were assessed via ELISA, and cRAGE was calculated. AGT exhibited greater ( p < 0.05) body fat % (+24%), fasting plasma glucose (+37%), OGTT AUC (+59%), and HOMA‐IR (+55%) and lower ( p < 0.05) VO 2 max (−24%). sTLR2 was 33% lower in AGT than NGT (main effect, p = 0.034). However, sTLR2 did not change ( p > 0.05) following AE. sTLR4 tended to be 36% lower in AGT than NGT (main effect, p = 0.096) and did not change following AE ( p > 0.05). Total sRAGE and isoforms were similar ( p > 0.05) between groups and did not change following AE ( p > 0.05). sTLR2 was correlated with ( p < 0.05) basal BG ( r = −0.505) and OGTT AUC ( r = −0.687). sTLR4 was correlated with basal BG ( p < 0.10, r = −0.374) and OGTT AUC ( p < 0.05, r = −0.402). Linear regressions were predictive of sTLRs in the basal state (sTLR2: R 2 = 0.641, p = 0.01; sTLR4: R 2 = 0.566, p = 0.037) and after acute exercise state (sTLR2: R 2 = 0.681, p = 0.004, sTLR4: R 2 = 0.568, p = 0.036).These findings show circulating sTLR profiles are disrupted in AGT and acute AE minimally modulates their levels.