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Randomized Controlled Trial
. 2015 Aug 10;10(8):e0133286.
doi: 10.1371/journal.pone.0133286. eCollection 2015.

High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients

Affiliations
Randomized Controlled Trial

High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients

Søren Møller Madsen et al. PLoS One. .

Abstract

Physical activity improves the regulation of glucose homeostasis in both type 2 diabetes (T2D) patients and healthy individuals, but the effect on pancreatic β cell function is unknown. We investigated glycaemic control, pancreatic function and total fat mass before and after 8 weeks of low volume high intensity interval training (HIIT) on cycle ergometer in T2D patients and matched healthy control individuals. Study design/method: Elderly (56 yrs±2), non-active T2D patients (n = 10) and matched (52 yrs±2) healthy controls (CON) (n = 13) exercised 3 times (10×60 sec. HIIT) a week over an 8 week period on a cycle ergometer. Participants underwent a 2-hour oral glucose tolerance test (OGTT). On a separate day, resting blood pressure measurement was conducted followed by an incremental maximal oxygen uptake (VO2max) cycle ergometer test. Finally, a whole body dual X-ray absorptiometry (DXA) was performed. After 8 weeks of training, the same measurements were performed. Results: in the T2D-group, glycaemic control as determined by average fasting venous glucose concentration (p = 0.01), end point 2-hour OGTT (p = 0.04) and glycosylated haemoglobin (p = 0.04) were significantly reduced. Pancreatic homeostasis as determined by homeostatic model assessment of insulin resistance (HOMA-IR) and HOMA β cell function (HOMA-%β) were both significantly ameliorated (p = 0.03 and p = 0.03, respectively). Whole body insulin sensitivity as determined by the disposition index (DI) was significantly increased (p = 0.03). During OGTT, the glucose continuum was significantly reduced at -15 (p = 0.03), 30 (p = 0.03) and 120 min (p = 0.03) and at -10 (p = 0.003) and 0 min (p = 0.003) with an additional improvement (p = 0.03) of its 1st phase (30 min) area under curve (AUC). Significant abdominal fat mass losses were seen in both groups (T2D: p = 0.004 and CON: p = 0.02) corresponding to a percentage change of -17.84%±5.02 and -9.66%±3.07, respectively. Conclusion: these results demonstrate that HIIT improves overall glycaemic control and pancreatic β cell function in T2D patients. Additionally, both groups experienced abdominal fat mass losses. These findings demonstrate that HIIT is a health beneficial exercise strategy in T2D patients.

Trial registration: ClinicalTrials.gov NCT02333734 http://clinicaltrials.gov/ct2/show/NCT02333734.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Flow chart.
1 T2D patient was excluded due to impossible insertion of catheter, and the last T2D patient dropped out of the study immediately after the initiation of HIIT. 5 matched controls were excluded due low BMI.
Fig 2
Fig 2. Study overview of the experiment prior to and after the HIIT intervention.
On a separate day, a urine sample, oral glucose tolerance test (OGTT), weight and height measurements were conducted. On another day: resting blood pressure measurement in supine position and 12-lead electrocardiogram (ECG) prior and after measurement of maximal oxygen consumption on bicycle ergometer. On the last experimental day, a whole body dual energy X-ray absorptiometry (DXA) was performed. These measurements were followed by 8 weeks of HIIT. Finally, laboratory measurements were repeated.
Fig 3
Fig 3. The development of glycaemic control prior to and after the HIIT intervention.
In the CON-group, there were no statistical effects (p>0.05) observed on average fasting venous glucose concentration (A), HbA1C (B) or postprandial glucose concentration 2 hours after OGTT (C). However, following 8 weeks of low volume HIIT, statistical significant reductions were detected on average fasting venous glucose concentration (A), HbA1C (B) and postprandial glucose concentration 2 hours after OGTT (C) in the T2D-group (all denoted by †).
Fig 4
Fig 4. The development of HOMA-IR.
Following 8 weeks of HIIT, the HOMA-IR in the CON-group remained unchanged (p>0.05), whereas HOMA-IR was significantly reduced p = 0.035 in the T2D-group (as denoted by †).
Fig 5
Fig 5. The development of HOMA-%β.
Following 8 weeks of HIIT, the HOMA-%β in the CON-group remained unchanged (p>0.05), whereas HOMA-%β was significantly reduced p = 0.026 in the T2D-group (as denoted by †).
Fig 6
Fig 6. The development of ISIcomposite (A), Insulin secretion (B) and DI (C).
Following 8 weeks of HIIT, ISIcomposite, Insulin secretion and DI remained unchanged (p>0.05) in the CON-group. In the T2D-group, pancreatic β-cell function as determined by DI was significantly elevated (p = 0.03) (denoted by †). In both groups, neither ISIcomposite nor insulin secretion was significantly reduced (p>0.05).
Fig 7
Fig 7. Insulin sensitivity (abscissa axis) and insulin secretion (y-axis) among controls (A) and among T2D diabetes patients (B).
Small dots represent values prior HIIT intervention, whereas big dots represent values after HIIT intervention. Each colour represents one individual.
Fig 8
Fig 8. Hyperbola fitting of insulinogenic index and composite insulin sensitivity index.
These differences between before and after HIIT can be seen from both the CON-group (A and B) and the T2D-group (C and D).
Fig 9
Fig 9. Plasma glucose levels and total AUC before and after the HIIT intervention in the CON- and T2D-group.
Following 8 weeks of HIIT, the plasma glucose levels were not significantly reduced (p>0.05 at all time points) in the CON-group (A). Total AUC in the CON-group were not significantly reduced (p>0.05) (A). In the T2D-group (B), plasma glucose concentrations were significantly lowered at time points -15 min (p = 0.03 as denoted by †), -10 min (p = 0.003 as denoted by ‡), 0 min (p = 0.003 as denoted by ‡), 30 min (p = 0.03 as denoted by †) and 120 min (p = 0.03 as denoted by †). AUC was not statistically changed (p = 0.0982) (B).
Fig 10
Fig 10. 1st phase AUC after 30 minutes of the plasma glucose concentration.
Following 8 weeks of HIIT, the CON-group had unaltered (p>0.05) 1st phase AUC of plasma glucose concentration, whereas the T2D-group had reduced p = 0.03 its 1st phase plasma glucose concentration (as indicated by †).
Fig 11
Fig 11. Plasma insulin levels before and after the HIIT intervention.
Following 8 weeks of HIIT, the fasting insulin levels were not significantly changed in the CON-group (A) and T2D-group (B) (p>0.05 at all time points). AUC in the CON-group (A) and T2D-group (B) were not significantly reduced (p>0.05).
Fig 12
Fig 12. Plasma glucagon levels before and after the HIIT intervention.
Following 8 weeks of HIIT, the fasting glucagon levels were not significantly changed in any group (p>0.05 at all time points). Additionally, AUC in the both groups was not significantly changed (p>0.05).
Fig 13
Fig 13. Percentage change in abdominal fat mass (A) and waist circumference (B) after 8 weeks HIIT intervention.
The CON-group lowered its abdominal fat mass significantly (p = 0.02 as denoted by †) by -9.66±3.07% and the T2D-group by -17.84±5.02% (p = 0.004 as denoted by ‡). Waist circumference changed significantly in both groups by -4.04±1.20% (p = 0.006 as denoted by ‡) in the CON-group and by -5.74±2.05% (p = 0.02 as denoted by †) in the T2D-group.

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