Oral Presentation ESA-SRB-ANZOS 2025 in conjunction with ENSA

The effects of acute and chronic exercise on lipocalin-2 in middle-aged and older adults (128663)

Carlie Bauer 1 2 , Marc Sim 3 4 , Cassandra Smith 3 4 , Rhiannon Healy 1 , Andrew Garnham 1 , Navabeh Zare 1 , Elizabeth Byrnes 5 , Mary Woessner 1 , Joshua Lewis 3 4 , Itamar Levinger 1 2
  1. Institute for Health and Sport, Victoria University, Footscray, Victoria, Australia
  2. Australian Institute for Musculoskeletal Science (AIMSS), Victoria University, University of Melbourne and Western Health, Melbourne, Victoria, Australia
  3. Medical School, University of Western Australia, Perth, WA, Australia
  4. Nutrition & Health Innovation Research Institute, Edith Cowan University, Joondalup, Western Australia, Australia
  5. PathWest, Sir Charles Gairdner Hospital, Perth, WA, Australia

Lipocalin-2 (LCN2) is a mechanoresponsive hormone involved in bone-muscle-fat crosstalk. Chronically elevated circulating LCN2 levels are implicated in poor energy regulation, increased cardiometabolic disease risk and poor physical function. Exercise is known to improve the aforementioned factors, but whether LCN2 is implicated in this relationship is not clear. We examined the effect of acute and chronic exercise on serum LCN2 levels and whether this relates to glucose regulation, body composition and physical function.

Thirty-three middle-aged and older adults (45 – 84 years, 72.73% female, median BMI 26.21kg/m2) completed a single acute high intensity interval exercise session (HIIE) (4 x 4 mins at 90 – 95% Heart Rate Reserve). Participants were then randomised to four weeks of high intensity interval training (HIIT) or control in a parallel groups design. LCN2, insulin, glucose and homeostatic model assessment for insulin resistance (HOMA-IR) were analysed in serum at baseline and immediately, 1 h and 3 h post-HIIE, and four weeks post-intervention. Urinary LCN2 was assessed pre and post four weeks of HIIT at rest. Linear mixed-modelling was used to assess change in LCN2 post-acute and chronic exercise.

A main effect for time for serum LCN2, insulin, glucose and HOMA-IR was detected after acute HIIE (p < 0.001). Circulating serum LCN2 levels increased significantly immediately post-HIIE compared to baseline (p < 0.001) and returned to levels similar to baseline by 60 and 180min post-HIIE. Four weeks of HIIT improved VO2peak yet had no significant effect on urinary and serum LCN2 levels or physical function.

Acute HIIE, but not four weeks of HIIT, transiently increased circulating LCN2 and improved insulin sensitivity in middle-aged and older adults. Whether the transient increase in LCN2 is related to post-exercise appetite suppression and long-term glucose regulation following exercise training should be explored further.