Can HIIT benefits last? insights for diabetes management

Study reveals how metabolic benefits of high-intensity interval training differ after detraining in individuals with and without type 2 diabetes, shedding light on its long-term impacts.

Study: The role of exosomes for sustained specific cardiorespiratory and metabolic improvements in males with type 2 diabetes after detraining. Image Credit: antoniodiaz / Shutterstock.com

In a recent study published in eBioMedicine, researchers investigate whether high-intensity interval training (HIIT)-induced metabolic benefits sustain or differ between individuals with and without type 2 diabetes (T2D) after prolonged training cessation.

The benefits of HIIT for diabetes management

Moderate aerobic exercise improves mitochondrial functionality and insulin sensitivity, regardless of T2D status. Detraining, which refers to the cessation of exercise training, for four to eight weeks completely reverses these improvements in people with or without metabolic syndrome.

HIIT is a time-efficient exercise that improves insulin sensitivity and cardiorespiratory fitness in individuals at risk of, with, or without T2D. This form of exercise has been shown to increase lipolysis, citrate synthase activity, as well as mitochondrial capacity, fusion, and biogenesis.

Previously, the researchers of the current study reported that HIIT increased muscle mitochondrial capacity independent of insulin sensitivity, in addition to improving whole-body insulin sensitivity mainly in individuals with insulin resistance. Seventy-two hours after the final session of a 12-week HIIT, these effects were still evident, thus sparking scientific interest in exploring the potential sustainability of these effects for longer periods.

About the study

In the current study, researchers compare the sustainability of metabolic effects of long-term HIIT between individuals with and without T2D upon detraining. Study participants were volunteers without or with T2D who underwent a 12-week HIIT program, followed by detraining for four weeks. Non-T2D (NDM) individuals underwent an oral glucose tolerance test (OGTT) to include only those with euglycemic fasting and two-hour plasma glucose levels.

HIIT comprised four-minute high-intensity exercising at 90% of the maximal heart rate interspersed by three three-minute training intervals, in which the study participants exercised at 70% of their maximal heart rate. During detraining, participants were instructed to maintain stable body weight and reduce physical activity to pre-HIIT levels.

A hyperinsulinemic-euglycemic clamp test was performed to assess insulin sensitivity at baseline, 72 hours after the last HIIT session, and after detraining. Furthermore, an incremental exhaustive exercise test was performed on an ergometer at baseline and after the end of HIIT and detraining.

Respiratory gas exchange was monitored by open-air spirometry to determine the maximal rate of oxygen uptake (VO₂ max). All study participants underwent an OGTT at baseline, as well as after HIIT and detraining.

Magnetic resonance imaging (MRI) measured whole-body and adipose tissue volume. Proton-magnetic resonance spectroscopy (¹H-MRS) was performed to quantify liver lipid content.

Skeletal muscle tissue samples were obtained before the clamp test for high-resolution respirometry. Proteins were extracted from the skeletal muscle for western blotting.

Small extracellular vesicles (SEVs) were isolated from serum by size exclusion chromatography. SEVs were used for nanoparticle tracking analysis and mass spectrometry.

Study findings

The study included 20 males with T2D and 22 NDM males. NDM subjects were stratified as insulin-resistant (IR)-NDM and insulin-sensitive (IS)-NDM.

At baseline, T2D subjects exhibited higher subcutaneous and visceral fat, fasting insulin (FINS), glycated hemoglobin (HbA1c), serum glutamic-pyruvic transaminase (SGPT), fasting blood glucose (FBG), and plasma blood glucose (PBG) at two and three hours of OGTT than NDM subjects.

In the T2D group, HIIT-induced improvements of triglycerides (TG), non-esterified fatty acids (NEFA), SGPT, FBG, and high-density lipoprotein cholesterol (HDL-C) levels that persisted after detraining, while two-hour PBG after OGTT decreased. After detraining, NEFA, FBG, and HbA1c levels declined, whereas VO₂ max improved in the NDM group.

HIIT-induced reductions in FBG were sustained after detraining in the IR-NDM subgroup, whereas only FINS decreased in the IS-NDM subgroup. Following detraining, VO₂ max declined in IR-NDM and T2D groups; however, it was still higher than baseline in all groups.

The mitochondrial capacity of the skeletal muscle after detraining was similar to the HIIT values. The mitochondrial fission from the activation of dynamin-related protein 1 (DRP1) was significantly higher in the T2D group than the IS-NDM group at baseline. However, activated DRP1 declined after HIIT and remained unchanged after detraining in the T2D group.

Comparatively, mitochondrial fusion markers increased following HIIT and detraining in IR-NDM and T2D groups. HIIT-induced SEV release into circulation in IR-NDM and T2D groups but not in IS-NDM subjects.

The mean SEV size remained unchanged over time, except for a marginally smaller size in IR-NDM individuals post-HIIT. After detraining, SEVs increased in IR-NDM and T2D subjects and remained unchanged in IS-NDM subjects.

Enrichment analysis of the SEV proteome revealed that proteins associated with extracellular exosomes were over-represented. A total of 186 differentially abundant proteins were identified across groups, with only two proteins differing between all three groups. Moreover, 44% of these proteins lacked a predicted secretory signal peptide, thus suggesting that SEVs may represent a new mechanism for exerkine release independent of classical secretory pathways.

Conclusions

The study findings indicate that a four-week detraining period reduced HIIT-induced increases in whole-body oxidative metabolism in insulin-resistant individuals and diminished HIIT-induced increases in whole-body insulin sensitivity in T2D subjects.

Detraining did not affect improvements in glycemia, hepatic insulin sensitivity, and hepatic lipid content in insulin-resistant individuals. Furthermore, detraining stimulated mitochondrial fission in insulin-sensitive subjects and helped sustain muscle mitochondrial fusion in insulin-resistant individuals.

VO₂ max remained unchanged post-detraining only in IS-NDM subjects, although it was still higher than baseline values in all groups. The metabolic changes after detraining may be partly attributed to HIIT-stimulated SEV release and SEV protein cargo.