The effect of high-intensity interval training on glucose metabolism signaling in mice fed a Western diet

Abstract

Background: Western diet (WD) consumption is associated with disturbances in insulin-related signaling pathways, whereas exercise training may favorably modify several molecular components of these pathways. Objective: This study investigated the effects of high-intensity interval training (HIIT) on the abundance of insulin-signaling–related proteins in the cardiac tissue of mice fed a Western diet. Methods: Eighteen male C57BL/6J mice were initially randomized into three experimental groups (n=8/group): standard diet (Control), Western diet (WD), and WD + high-intensity interval training (WD+HIIT). Following attrition during the experimental period, six animals per group completed the protocol and were included in the final analyses (n=6/group; total n=18). The HIIT group performed a 4-week treadmill running protocol (3 sessions/week, 5° incline). Each session included: a 10-min warm-up at 6 m/min, followed by 10 × 2-min high-intensity bouts at 85–90% of Vmax (absolute speeds progressing from 19 to 22 m/min), each followed by 2-min active recovery at 50% of Vmax (absolute speeds progressing from 8 to 11 m/min), and a 5-min cool-down at 5 m/min. Maximum speed (Vmax) was determined using a graded treadmill test, where speed was increased every 2 minutes until the mouse could no longer run. After the intervention, levels of IRS1, EGR-1, p-AKT, t-AKT, and PTP1B proteins abundance were evaluated using the Western blot method. Statistical analyses were performed using one-way ANOVA followed by LSD post-hoc test. Results: HIIT training significantly increased the expression of IRS1 and p-AKT proteins (P<0.001) and significantly decreased the expression of PTP1B protein (P<0.001) compared to the WD group. Conclusion: The Western diet was associated with an unfavorable pattern of cardiac insulin-signaling proteins, characterized by increased PTP1B and reduced IRS1 and p-AKT abundance. Four weeks of HIIT partially counteracted these molecular alterations. However, because direct measures of glucose tolerance, insulin sensitivity, or glucose uptake were not performed, these findings should be interpreted as changes in cardiac insulin-signaling–related proteins rather than evidence of improved systemic glucose homeostasis.