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High-intensity interval training combining rowing and cycling improves but does not restore beta-cell function in type 2 diabetes.
Endocrine Connections 2024 March 2
AIMS: 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<0.05). The HIIT-protocol increased insulin sensitivity in all groups (all P<0.01). In patients with type 2 diabetes, this was accompanied by a large (>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.
CONCLUSIONS: 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.
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<0.05). The HIIT-protocol increased insulin sensitivity in all groups (all P<0.01). In patients with type 2 diabetes, this was accompanied by a large (>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.
CONCLUSIONS: 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.
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