Endocrine Connections (Apr 2024)

High-intensity interval training combining rowing and cycling improves but does not restore beta-cell function in type 2 diabetes

  • Maria Houborg Petersen,
  • Jacob Volmer Stidsen,
  • Martin Eisemann de Almeida,
  • Emil Kleis Wentorf,
  • Kurt Jensen,
  • Niels Ørtenblad,
  • Kurt Højlund

DOI
https://doi.org/10.1530/EC-23-0558
Journal volume & issue
Vol. 13, no. 5
pp. 1 – 11

Abstract

Read online

Aim: We investigated whether a high-intensity interval training (HIIT) protocol could restore beta-cell function in type 2 diabetes compared with sedentary obese and lean individuals. Materials and methods: In patients with type 2 diabetes, and age-matched, glucose-tolerant obese and lean controls, we examined the effect of 8 weeks of supervised HIIT combining rowing and cycling on the acute (first-phase) and second-phase insulin responses, beta-cell function adjusted for insulin sensitivity (disposition index), and serum free fatty acid (FFA) levels using the Botnia clamp (1-h IVGTT followed by 3-h hyperinsulinemic–euglycemic clamp). Results: At baseline, patients with type 2 diabetes had reduced insulin sensitivity (~40%), acute insulin secretion (~13- fold), and disposition index (>35-fold), whereas insulin-suppressed serum FFA was higher (⁓2.5-fold) compared with controls (all P 200%) but variable improvement in the disposition index (P < 0.05). Whereas insulin sensitivity improved to the degree seen in controls at baseline, the disposition index remained markedly lower in patients with type 2 diabetes after HIIT (all P < 0.001). In controls, HIIT increased the disposition index by ~20–30% (all P < 0.05). In all groups, the second-phase insulin responses and insulin-suppressed FFA levels were reduced in response to HIIT (all P < 0.05). No group differences were seen in these HIIT-induced responses. Conclusion: HIIT combining rowing and cycling induced a large but variable increase in beta-cell function adjusted for insulin sensitivity in type 2 diabetes, but the disposition index remained severely impaired compared to controls, suggesting that this defect is less reversible in response to exercise training than insulin resistance. Trial registration: ClinicalTrials.gov (NCT03500016).

Keywords