By William C. Haas III, MD, MBA

Integrative Medicine Fellow, Department of Family and Community Medicine, University of Arizona, Tucson

Dr. Haas reports no financial relationships relevant to this field of study.

SYNOPSIS: High-intensity intermittent training improves cardiac structure and function in addition to reducing liver and visceral fat mass among non-insulin dependent type 2 diabetics.

SOURCE: Cassidy S, et al. High intensity intermittent exercise improves cardiac structure and function and reduces liver fat in patients with type 2 diabetes: A randomized controlled trial. Diabetologia 2015; [Epub ahead of print].

Summary Points

  • High-intensity intermittent training (HIIT) is a form of exercise interspersing brief periods of vigorous exercise with periods of rest.
  • HIIT improves cardiac structure and function in patients with type 2 diabetes.
  • HIIT reduces liver fat and visceral adiposity.

Type 2 diabetes mellitus (T2DM) affects multiple organ systems within the body. The cardiovascular system is especially prone to damage as a result of elevated blood glucose levels. In fact, cardiac disease remains the leading cause of morbidity and mortality in patients with T2DM.1

Lifestyle modifications, including exercise, are among the foundational treatment strategies for both T2DM and heart disease. Traditionally, recommendations have centered on moderate levels of continuous aerobic exercise totaling 150 minutes per week. Recently, other exercise methods have generated attention, particularly high-intensity intermittent training (HIIT). HIIT involves brief intervals of vigorous activity interspersed with periods of low activity or rest. Variations of HIIT have been well studied in athletes with demonstrated improvements in cardiac function, carbohydrate and fat utilization, as well as mitochondrial efficiency.2-4 On the other hand, less is known about the effect of HIIT on individuals with chronic disease.

Given that patients with T2DM have been shown to exhibit changes in left ventricular structure and function without overt cardiac disease, researchers in the United Kingdom set out to determine the cardiac benefits of HIIT on a small group of type 2 diabetics. Using advanced magnetic resonance imaging (MRI) techniques, researchers evaluated cardiac structure and function as well as regional fat deposition in response to HIIT.

Twenty-eight type 2 diabetics managed with diet and metformin were randomized to a HIIT intervention (n = 14) or a control group (n = 14). More than 200 patients were excluded during initial screening based on the presence of overt cardiac disease, regular participation in exercise (> 60 min per week), contraindication to exercise stress testing, or use of a beta-blocker medication. The HIIT group performed three structured exercise sessions per week for 12 weeks. Each session consisted of five intervals of “very hard” cycling with a pedal cadence > 80 revolutions/minute; “very hard” was defined at 16-17 out of 20 on the Borg Rating of Perceived Exertion (RPE) scale. Intervals lasted 2 minutes during the first week and were extended by 10 seconds per week, reaching a final duration of 3 minutes and 50 seconds by the end of the study. Regardless of the duration, intervals were flanked by a 5-minute warm-up and a 3-minute cool-down with a 3-minute recovery period. The initial session was supervised and subsequent sessions were audio guided using voice-recorded instructions. Both the HIIT and control groups were instructed to continue their normal diabetic care without changing medication, physical activity, diet, or body weight.

The variables measured for both groups included cardiac structure and function, liver and visceral fat, body composition, and glycemic control. Measurements were taken at baseline and again after the 12-week intervention. Cardiac variables (left ventricular wall mass, end-diastolic blood volume, systolic function) were evaluated using advanced MRI scanning technology and validated modeling algorithms. Similar technology was used to measure liver and visceral fat mass. Body composition was also measured using air displacement plethysmography. Glycemic control was evaluated using a fasting oral glucose tolerance test along with insulin resistance and beta-cell function calculations using HOMA2 and area under the glucose curve.

Twenty-three of the original 28 participants completed the study with no difference between the groups at baseline. Two patients in the control group declined to undergo MRI scanning and one patient cited time constraints. In the HIIT group, two patients withdrew for unrelated medical problems. No patients were excluded from analysis due to failed compliance with the treatment protocol, and no changes were noted in general daily activity levels during the intervention for either group.

With regards to cardiac structure and function, several key variables improved in the HIIT group and were statistically different from the control group. Among HIIT participants, left ventricular wall mass increased by 12% (P = 0.02) without a corresponding change in myocardial wall thickness. This increased ventricular mass among HIIT participants was accompanied by improvements in their ejection fraction percentage (65.8 ± 8% pre-HIIT vs 70.0 ± 6% post-HIIT; P = 0.02). HIIT also improved end-diastolic volume, which increased by 4 mL (P = 0.01), as well as early diastolic filling rate by 51 mL/s (P = 0.01).

With regards to glycemic control, HIIT participants did not show improvement in any of the key variables after the intervention. Fasting glucose, fasting insulin, and hemoglobin A1c as well as insulin sensitivity and insulin resistance were all unchanged among HIIT participants. The same pattern was true among the control group. Interestingly, hemoglobin A1c and 2-hour glucose levels were the only variables different between the two groups after the intervention (P = 0.02).

Finally, improvements were noted with regards to visceral adiposity in addition to liver fat. Visceral adipose tissue decreased among HIIT participants (201 ± 80 cm2 to 181 ± 72 cm2, P = 0.04); however, no difference was noted between the groups. Aside from decreased visceral adiposity, HIIT elicited a 39% relative reduction in liver fat (6.9 ± 6.9% to 4.2 ± 3.6%, P < 0.05) with a significant between-group effect (P < 0.05). Researchers noted that the degree of liver fat reduction moved four patients into the normal range for liver fat. Of note, overall fat mass did not change within or between groups.

COMMENTARY

The primary focus of this study was to determine the effect of HIIT to improve cardiac structure and function in type 2 diabetics without overt cardiac disease. Based on several findings, the authors concluded that HIIT was indeed an effective strategy to reverse cardiac dysfunction. First, HIIT participants experienced increased left ventricular mass without increased myocardial wall thickness. The precise mechanism of cardiac hypertrophy is important. Unlike with exercise, pathological damage to the heart leads to an increase in both left ventricular mass and wall thickness, thereby decreasing end-diastolic blood volume, the latter being an independent predictor of cardiovascular mortality.5 Beyond improvements to cardiac structure, HIIT increased early diastolic filling rate. This changes suggests that the myocardium HIIT participants became more compliant and quicker to relax, another predictor of decreased cardiac morality.

Not only did HIIT improve cardiac parameters, it also reduced liver and visceral fat mass. Both liver and visceral fat deposition are proposed to play a key role in the underlying pathology of T2DM.6 A reduction in these fat cells should theoretically improve glucose management. Interestingly, the study did not find significant improvements in glycemic control. The authors suggested that large individual variation in liver fat changes after HIIT might have accounted for lack of improvement in glycemic control. On the other hand, both fatty liver disease and visceral adiposity have been linked to cardiovascular disease.7 The improvements in cardiac function in the present study ultimately may be attributed to reductions in liver and visceral fat.

One of the biggest drawbacks of the study was the lack of comparison between HIIT and moderate continuous exercise. Moderate continuous exercise has been extensively studied and is known to have a beneficial effect on many chronic disease states. To best determine the place for HIIT when prescribing exercise, a direct comparison between the two forms of exercise would have been helpful. Although other studies have made comparisons, few have done so with a detailed focus on cardiac structure and function.

Ultimately, the present study is one of the first to demonstrate improvements in cardiac structure and function among type 2 diabetics engaging in HIIT. Moreover, the study raises speculation about the connection between regional fat deposition and the progression or resolution of T2DM and cardiovascular disease. Despite the lack of direct comparison with moderate continuous exercise, HIIT deserves consideration for use among type 2 diabetics, especially as it offers a solution to the commonly cited limitation of “not enough time.”

REFERENCES

  1. Leon BM, Maddox TM. Diabetes and cardiovascular disease: Epidemiology, biological mechanisms, treatment recommendations and future research. World J Diabetes 2015;6:1246-1258.
  2. Slørdahl SA, et al. Atrioventricular plane displacement in untrained and trained females. Med Sci Sports Exerc 2004;36:1871-1875.
  3. Talanian JL, et al. Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women. J Appl Physiol 2007;102:1439-1447.
  4. Burgomaster KA, et al. Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. J Physiol 2008;586:151-160.
  5. Liao Y, et al. The relative effects of left ventricular hypertrophy, coronary artery disease, and ventricular dysfunction on survival among black adults. JAMA 1995;273:1592-1597.
  6. Taylor R. Type 2 diabetes: Etiology and reversibility. Diabetes Care 2013;36:1047-1055.
  7. Lim S, et al. Mechanistic link between nonalcoholic fatty liver disease and cardiometabolic disorders. Int J Cardiol 2015;201:408-414.