Poster Presentation ESA-SRB-ANZBMS 2024 in conjunction with ENSA

The effects of acute and chronic high intensity exercise on lipocalin-2 in middle-aged and older adults (#345)

Carlie Bauer 1 2 , Marc Sim 3 4 , Patrice Jones 1 , Rhiannon Healy 1 , Cassandra Smith 3 4 , Elizabeth Byrnes 5 , Joshua R Lewis 3 4 6 , 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. Nutrition & Health Innovation Research Institute, Edith Cowan University, Perth, WA, Australia
  4. Medical School, University of Western Australia, Perth, WA, Australia
  5. PathWest, Sir Charles Gairdner Hospital, Perth, WA, Australia
  6. Biomedical School, University of Western Australia, Perth, WA, Australia

Lipocalin-2 (LCN2) is a hormone involved in bone-muscle-fat crosstalk and is produced by multiple cell types such as osteoblasts, adipocytes and renal tubular cells. Increased LCN2 is implicated in satiety control, poor energy regulation and increased cardio-metabolic risk. Exercise is a known intervention to improve cardio-metabolic health LCN2 is implicated in this relationship is not clear. We tested the hypothesis that acute and chronic high intensity exercise will reduce LCN2 in middle-aged and older adults.

33 middle-aged and older adults free of major disease participated (45 – 84 years, median BMI 26.21 (23.14, 30.09) kg/m2). All participants completed acute high intensity interval exercise (HIIE) on a cycle ergometer (4 x 4 mins at 90-95% heart rate reserve) and were then randomised to 4 weeks HIIE training or control. Blood and urine was collected at baseline and immediately, 1 h and 3 h post-acute exercise, and 4 weeks post-intervention. LCN2 was analysed using a monoclonal immunoassay. Linear mixed modelling was used to assess change in LCN2 with acute exercise. Linear regression was used to assess whether change in LCN2 was associated with exercise training following the 4 week intervention.

A main effect for time was detected in the acute HIIE model (p < 0.001). Circulating serum LCN2 levels increased significantly immediately post-HIIE compared to baseline (p <0.001). LCN2 levels returned to baseline levels 60 and 180 minutes post-HIIE (p>0.05). 4 weeks of HIIE training had no significant effect on serum and urinary LCN2 levels (p = 0.175 and p = 0.215 respectively).

Acute HIIE, but not exercise training, transiently increased circulating LCN2 levels in middle-aged and older adults. Whether the transient increase in LCN2 is related to post-exercise satiety and is beneficial, detrimental or has no effect on cardio-metabolic health should be explored further.