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High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients
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 (O2max) 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
Figures
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Citation: Madsen SM, Thorup AC, Overgaard K, Jeppesen PB (2015) High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients. PLoS ONE 10(8): e0133286. doi:10.1371/journal.pone.0133286
Editor: Raffaella Buzzetti, University, ITALY
Received: February 3, 2015; Accepted: June 19, 2015; Published: August 10, 2015
Copyright: © 2015 Madsen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Data Availability: All relevant data are within the paper and its Supporting Information files.
Funding: This work was supported by Accu Trend, Denmark and Department of Clinical Medicine, Aarhus University. Roche Diagnostics has kindly supported the study by giving glucometers (Accu Trend). Neither Roche Diagnostics nor Department of Clinical Medicine, Aarhus University had any role in study design, data collection and analysis, decision to publish or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
Introduction
Type 2 diabetes (T2D) can be defined as a bihormonal metabolic disorder characterised by insufficient insulin secretion and abnormal glucagon secretion [1]. According to International Diabetes Federation, estimated worldwide prevalence of diabetes was 382 million people in 2013 with a projection of 592 million people suffering from diabetes in 2030. It is well established that physical activity per se improves glucose homeostasis [2–4], a cornerstone of regulating overall glycaemic control among T2D patients. As of 2013, it is recommended that T2D patients should perform at least 150 minutes per week of moderate-intensity aerobic exercise corresponding to 50–70% of maximal heart frequency [5,6]. Since Bjorntorp and co-workers established the importance of regular moderate to strenuous exercise to increase insulin sensitivity among T2D patients [7], considerable molecular and metabolic research has demonstrated pivotal (patho)physiological linkages between health-related benefits of physical activity and T2D. Though physical exercise is advocated in the treatment of T2D, existing strategies face huge challenges, including the lack of adherence, motivation and time to follow these guidelines [6].
Recently, more focus has addressed the health beneficial effects of different high intensity interval training (HIIT) regimens to T2D. Novel findings here include reduced hyperglycaemia following 2 weeks of HIIT on cycle ergometer [8,9], ameliorated insulin action and upregulated skeletal muscle metabolic capacity after walking intervals [10] and improved pancreatic β-cell function [11]–pivotal physiological phenomena in the attempt to regulate whole body metabolism in T2D patients. These health beneficial effects seem to be independent of changes in body weight in moderate intensity training regimens [12–14], and glycaemic control may be even more improved by intensities above recommended guidelines [15,16]. There seems to be accumulating evidence that HIIT induces increased overall fat loss and abdominal fat mass loss as opposed to traditional continuous endurance training [17]. The cardiovascular adaptations that appear with HIIT are comparable, or even sometimes superior as opposed to traditional continuous endurance training [18–20]. However, in the T2D population, research in long-term training-induced changes of both glycaemic control and the pancreatic homeostasis is sparse and further detailed knowledge on this topic is needed to evaluate the true clinical effect of training.
In inactive individuals diagnosed with T2D and age- and BMI-matched normal glucose tolerant subjects, we therefore tested the effects of 8 weeks of low volume HIIT on 1) Glycaemic control (fasting plasma glucose concentration, 2-hour oral glucose tolerance test (OGTT) response, area under curve (AUC) and glycosylated haemoglobin (HbA1C)), 2) pancreatic homeostasis (OGTT-derived surrogate markers) and 3) total fat and abdominal fat mass.
Methodology
Subjects
Subjects were recruited through local newspaper advertisements and evening sessions at Centre for Clinical Research, Vendsyssel Hospital, Aalborg University, where the study was carried out. 10 T2D patients and 13 age, height and weight matched control (CON) individuals were eligible for the study (see flow chart, Fig 1). All individuals answered a medical questionnaire to evaluate their individual lifestyles (history of genetic T2D, physical activity, smoking habits, alcohol consumption and diet). T2D inclusion criteria were: 2-hour end point OGTT ≥ 11.1 mmol·l-1, BMI < 40 kg·m-2, both genders and < 65 of age. Exclusion criteria were: diabetes duration < 1 year, BMI < 25 kg·m-2, moderate intensity exercise > 1 hour per week, use of exogenous insulin, evidence of liver, renal, cardiopulmonary, neuromuscular and/or psychological disease, other debilitating diseases or contraindicating physical activity [21]. Furthermore, there were two eligibility tests during the visits: 1) if markers or analytes as given below in detail did not fulfil criteria ranges, subjects were excluded and 2) if there were any perturbations during the heart cycle electrocardiogram (ECG) of both resting and working myocardium, subjects were excluded. All ten T2D patients were under treatment with oral antidiabetic agents, either with metformin (N = 8) or glimepiride (N = 2). Additionally, lipid-reducing agents (N = 9), anti-hypertensive agents (N = 8), glucagon-like peptide-1 (GLP-1) receptor agent (N = 1) and glucagon-like peptide-1 (GLP-1) inhibitor agent (N = 3) were taken on a daily basis. All subjects continued their medication throughout the study.
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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.
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The study was approved by the Ethics committee of Central and North Denmark Region (M-2013-56-13) and implemented in accordance with the guidelines of Declaration of Helsinki. The study was registered at http://www.ClinicalTrials.gov. (NCT02333734). Written informed consent was obtained from all participants prior enrolment to the study.
Participants were carefully instructed to continue their individual eating habits and to maintain a eucaloric diet [22].
Experimental overview
Baseline post intervention outcomes were assessed over three test days in the week before and in the week following the HIIT program. On Mondays, Wednesdays and Fridays in week 1–8, participants conducted HIIT. An outline of the experimental time schedule appears in Fig 2.
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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.
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Study design
Day 1 –oral glucose tolerance test.
All participants underwent an OGTT before (week 0) and again after the HIIT intervention (week 9). All subjects abstained from performing any strenuous physical activity for 2–3 days prior to both OGTTs to avoid the effects of acute exercise. The participants came into the clinic after a 12-hour overnight fast. Before the initiation of the OGTT, a fasting urine sample was collected from each participant and was immediately frozen and stored at -80°C. This was followed by an assessment of body weight (TANITA, BWB-800), height (only at week 0) and waist circumference in duplicate at the level of the umbilicus conducted by a trained person. Then fasting capillary blood glucose was conducted and analysed in duplicate using an OneTouch glucose monitoring apparatus (Precision Xceed MediSense, Abbott Laboratories A/S, Denmark).
Afterwards, a cannula (Beckton, Dickinson & Company, Franklin Lakes, NJ, USA) was carefully placed into an antecubital vein followed by infusion of saline solution to control and maintain clean access. Fasting venous blood samples were taken to the times -15, -10 and 0 minutes before a glucose load of 75 g anhydrous glucose dissolved in water was given. At the first (-15 min) fasting venous blood sample, 4 blood samples were taken to screen the coagulation (II, VII, X and INR), liver (ASAT and ALAT), cell (leucocytes, erythrocytes and thrombocytes), kidney (albumin and creatinine), inflammatory (CRP) and hormonal (TSH) status to preclude any underlying disease. At same time point (-15 min), additional 3 blood samples were taken to determine overall inflammation, lipids and HbA1C. At all time points (-15, -10 and 0 min), a blood sample was collected to analyse glucose, insulin and glucagon. Following the glucose load ingestion, venous blood samples were taken after 15, 30, 60 and 120 minutes and were assayed for glucose, insulin and glucagon concentrations. ~10 g of saline solution was flushed through the vein after each collected blood sample. Each blood sample was transferred to either 2.7 ml EDTA (Beckton, Dickinson & Company, Franklin Lakes, NJ, USA) or lithium heparin (Beckton, Dickinson & Company, Franklin Lakes, NJ, USA) evacuated tubes, briefly stored on ice (
Biochemical analyses.
All analytic processes were conducted according to the manufacturer’s instructions. Plasma glucose content (unit: mmol·l-1) was determined applying an enzymatic reference method (Roche Diagnostics, Switzerland) on a Cobas c111 system. Plasma insulin concentrations (unit: pmol·l-1) were measured with an enzyme-linked immunosorbent assay (ELISA) (Dako, Glostrup, Denmark) and plasma glucagon concentrations (unit: pg·ml-1) were determined by a radioimmunoassay (RIA) kit (EMD Millipore Corporation, Billerica, MA, USA). Glycosylated haemoglobin (HbA1C) was determined applying high-performance liquid chromatography (HPLC) on the TOSOH G8 (Tosoh Bioscience, Tokyo, Japan). Health status markers, fasting total cholesterol (TC), high-density lipoprotein (HDL) and triglyceride (TG) were determined using the immunonephelometry procedure (Siemens, Erlangen, Germany) on the Vista Dimension 1500 system. Low-density lipoprotein (LDL) was estimated by using the Friedewald equation. Except for glucose, all samples were analysed in duplicate.
Day 2 –aerobic testing and blood pressure.
On a separate day, subjects performed an incremental exercise test on a cycling ergometer (Monark 928 E, Varberg, Sweden) to determine maximal pulmonary oxygen uptake (O2max). The exercise protocol began with a warm-up phase of 8 minutes at a workload of 80–100 W, inducing a working heart frequency of ~65% of the estimated maximal heart rate (Polar 625X, Kempele, Finland). A facemask was fitted covering mouth and nose. The mask was instrumented with a flowmeter and a sampling tube allowing for continuous breath-by-breath measurement of ventilation volume and expired O2 and CO2 concentrations. These data were used for calculation of O2 values (Oxycon Pro, Jaeger Gmbh, Hoechberg, Germany). After careful instruction, each subject performed the O2max test with a workload that was increased by 15 W·min-1. During the last minutes of the test, the subjects were vigorously encouraged to continue until exhaustion, and the achievement of O2max was established by standard criteria in all tests [23]. The gas analyzers and the flow were calibrated prior to each test. Individual power output used for the HIIT intervention was taken as the power output eliciting ~90% of maximal heart rate during the O2max test. The test was repeated in week 9 after the completion of the HIIT intervention.
Subjects had their resting and post-work heart function controlled by 12-lead electrocardiogram (ECG) (Mortara ELI 150, Milwaukee, WI, USA). There were no signs of ischemia or arrhythmias during rest or after the O2max test as controlled by a physician.
Prior to each O2max test, blood pressure (Microlife BP A100 Plus, Widnau, Switzerland) was registered in a supine position in a quiet room at ambient temperature. The cuff was placed around the participant’s left arm and inflated every 10 minutes (0–30 minutes). Systolic (BPs) and diastolic (BPs) were registered followed by measurement of mean arterial pressure (BPm), i.e. BPd+⅓×(BPs-BPd). The lowest values were used for comparison. There was no or little (
Day 3.
On a separate day (week 0), a whole body dual x-ray absorptiometry (DXA) scan (XR-800 Swissray, Cooper, Surgical, USA) was conducted at Frederikshavn Hospital. Additionally, abdominal and femoral regions were assessed for fat mass and lean mass. Another DXA scan (week 9) was conducted after the completion of the HIIT intervention for comparison. A trained radiographer performed all scans.
High intensity interval training program
Subjects conducted supervised HIIT on a cycling ergometer (Kettler Axiom, Germany) three times per week over 8 weeks (every Monday, Wednesday and Friday) in three groups of five and two groups of four. During the entire intervention, a physiotherapist supervised the subjects to control that they adhered to and completed their individual power output obtained from their O2max test. Halfway through the intervention subjects had their power output increased by ~5% for the remaining period in order to maintain a sufficient relative intensity despite neural and muscular adaptations. Each training session consisted of a 5-minute warm-up (eliciting ~65% of HRmax) followed by 10×1 minute intervals each interspersed by 1 minute of recovery [9,24]. Cadence during the HIIT was ~70 RPM. During recovery, the participants were allowed to either rest or pedal with a minimum of resistance. The session was completed by a cool-down period of 5 minutes. Total time commitment was ~30 minutes per HIIT session. During each training session, the heart rate was registered from the cycling ergometer with additional reporting of rating of perceived exertion (Borg Scale). During the intervention, participants were only allowed to exercise during the HIIT sessions. However, we allowed easy gardening, walking and other daily activities.
Calculations and statistical analyses
Statistical analyses were conducted applying the STATA 13 statistical analysis system (StataCorp LP, Texas, USA), whereas the GraphPad Prism 6 statistical analysis system (GraphPad Software Inc., San Diego, CA, USA) was applied for visual presentation. In the visual presentation, mean ± S.E.M. are given. All data were tested for normality applying QQ-plots and Bland Altman Plots. After careful evaluation, all data fulfilled the criteria of being normally distributed. Student’s paired t-test was applied to test possible differences within same group before and after the HIIT intervention. Also, student’s paired t-test was applied to determine possible changes between same time points during the OGTT before (week 0) and after the HIIT intervention (week 9). AUC was calculated by the integrated trapezoid rule [25]. The insulin resistance homeostatic model assessment (HOMA-IR) was determined from fasting plasma glucose (FPG) and fasting plasma insulin (FPI) concentrations by ((FPG×FPI)/22.5). The β-cell function (HOMA-%β) was calculated by ((20×FPI)/(FPG-3.5)). Applied glucose unit: mmol·l-1, applied insulin unit: μIU·ml-1 (determined as pmol·l-1/6) [26]. Composite insulin sensitivity index (ISIcomposite) was calculated according to the formula [27]: 10.000 divided by the square root of ((FPG×FPI)×(mean FPG×mean FPI). Insulin secretion was assessed by the insulinogenic index (IGI) [28] determined from the ratio of increases of plasma insulin to glucose measured at 30 minutes expressed as: ΔI30/ΔG30, i.e. (Insulin 30 min—Insulin 0 min)/(Glucose 30 min–Glucose 0 min). The product of the ISIcomposite and the IGI, the so-called disposition index (DI), is a useful marker of pancreatic β-cell function [29]. FPG and FPI were calculated on the basis of all fasting blood samples, i.e. the mean of -15, -10 and 0 min. Applied units were the same as already given above. In all cases, p
Results
During the 8-week HIIT intervention both T2D and CON groups showed similar high training compliance (heart rate at end HIIT bout was ~90% of maximal heart rate) and there was total adherence from both groups in all 8 weeks. Except for 1 dropout, all subjects participated in the full range of the supervised 8-week HIIT sessions without exception, which highlights the feasibility of this exercise regimen.
Glycaemic control
In the CON-group, no significance was observed in either average fasting venous glucose concentration (p = 0.17), the 2-hour OGTT levels (p = 0.58) or HbA1C (p = 0.81). Among the T2D patients, significant reductions of average fasting venous glucose concentration (p = 0.01) (p = 0.0106), HbA1C (p = 0.036) and 2-hour end OGTT levels (p = 0.035) were observed (Fig 3A, 3B and 3C).
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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 †).
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OGTT-derived indices to assess pancreatic β-cell function and insulin resistance
In the CON-group, neither HOMA-IR (p = 0.63) nor HOMA-%β (p = 0.22) was significantly changed (Figs 4 and 5, respectively). However, in the T2D-group, HOMA-IR was significantly (p = 0.03) decreased (Fig 4) and HOMA-%β was significantly (p = 0.03) increased (Fig 5). Insulin secretion as determined by the insulinogenic index and ISIcomposite remained unaltered (p>0.05) in both groups (Fig 6A and 6B). Pancreatic β-cell function as determined by DI was unaltered in the CON-group (p = 0.99), but significantly improved (p = 0.03) in the T2D-group (Fig 6C).
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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 †).
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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 †).
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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).
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The hyperbolic intra-relationships between ISIcomposite and IGI are shown in Fig 7A (CON-group) and 7B (T2D-group). Additionally, the over-all best-fit lines attained by nonlinear regression analysis (logarithmic regression) between ISIcomposite and IGI are presented in Fig 8A–8D. The overall regression line between ISIcomposite and IGI among T2D patients was y = -6.642ln(x)+34.168 (R2 = 0.44) prior the HIIT intervention (Fig 8A) and y = -4.538ln(x)+25.608 (R2 = 0.42) afterwards (Fig 8B). For the CON-group, the overall regression line was y = -7.844ln(x)+52.016 (R2 = 0.31) before HIIT (Fig 8C) and y = -3.314ln(x)+29.167 (R2 = 0.10) after HIIT (Fig 8D).
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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.
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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).
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Plasma glucose, insulin and glucagon concentrations
Following 8 weeks of HIIT, fasting and postprandial plasma glucose concentration was unaltered (p>0.05 at all time points) in the CON-group (Fig 9A). Also the plasma glucose AUC was unaltered (p = 0.35) after HIIT in the CON-group (Fig 9A). The T2D-group had changed its glucose significantly at time points -15 min (p = 0.03), -10 min (p = 0.003), 0 min (p = 0.003), 30 min (p = 0.03) and 120 min (p = 0.03) (Fig 9B). In the T2D-group, the AUC was 1580±142.3 mmol·min·l-1 at baseline and 1447±130.0 mmol·min·l-1 post intervention, however this did not amount to a significant change (p = 0.098) (Fig 9B). In the CON-group, 1st phase plasma glucose AUC over 30 minutes was not significantly changed by the intervention effect (p = 0.36) (Fig 10). In the T2D group, however, there was a significant 1st phase glucose decrease from 289.9±25.4 mmol·min·l-1 to 265.3±23.9 mmol·min·l-1 (p = 0.03) corresponding to a change of 8±3% (Fig 10). In both groups, the insulin and glucagon concentrations and their 2-hours’ AUCs were not significantly changed (p>0.05) compared to baseline (Figs 11A, 11B and 12).
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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).
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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 †).
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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).
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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).
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Blood pressure, exercise capacity and lipid status
Following 8 weeks of HIIT, both the CON-group and the T2D-group significantly reduced their BPs (CON: p = 0.001; T2D: p = 0.0002), BPd (CON: p = 0.0009; T2D: p<0.0001) and BPm (CON: p = 0.0002; T2D: p<0.0001) (Table 1).
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Table 1. Baseline characteristics before and after 8 weeks of high intensity interval training.
Values are means ± standard error of mean (S.E.M.).
doi:10.1371/journal.pone.0133286.t001
Absolute O2max changed significantly in both groups (CON: p = 0.01; T2D: p = 0.03) with a concomitant significant increase of relative O2max (CON: p = 0.004; T2D: p = 0.002). Additionally, both groups increased absolute (CON: p<0.0001; T2D: p = 0.007) and relative (CON: p<0.0001; T2D: p = 0.002) maximal power output during incremental O2max on the final examination (Table 1). Maximal heart rate decreased during incremental O2max in both groups (CON: p = 0.01; T2D: p = 0.01) (Table 1).
No effects were demonstrated on lipid status in either group. However, in the T2D-group, post measurements of triglycerides and total cholesterol were borderline significant (p = 0.06 and 0.07) compared to baseline. HDL concentration in the CON-group was nearly significant (p = 0.06) as opposed to pre exercise values (Table 1).
Anthropometry
Abdominal fat mass changed significantly in both groups after 8 weeks of HIIT. The CON group lowered its abdominal fat mass significantly (p = 0.02) from 3.36±0.30 kg to 3.03±0.29 kg, corresponding to percentage change of -9.66±3.07% (Fig 13A). This was also confirmed with the waist circumference measurement changing significantly from 98±3 cm to 94±3 cm (p = 0.006) (Fig 13B). Among the T2D patients, abdominal fat mass was reduced significantly (p = 0.004) from 3.06±0.28 kg to 2.57±0.32 kg. This corresponded to a percentage change of -17.84±5.02% (Fig 13A). There was also a significant reduction of the waist circumference in the T2D group from 100±2 cm to 94±3 (p = 0.02) (Fig 13B). BMI was significantly reduced in both groups, thus by p = 0.0005 in the CON-group and by p = 0.003 in the T2D-group (Table 1). Lean body mass was significantly changed (p = 0.003) in the T2D-group, whereas it remained unaltered in the CON-group (p>0.05) (Table 1). Total body fat was unaltered (p>0.05) in both groups compared to baseline (Table 1).
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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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