HIIT back at diabetes
Research that furthers our understanding of the health benefits of high-intensity interval training (HIIT) was presented at the 58th EASD Annual Meeting. Lisa Buckingham reports.
HIIT is increasingly coming under the spotlight as an effective tool in the fight against diabetes and obesity. As part of an Exercise Your Tissues into Shape session at September’s EASD conference, Dr Rodrigo Mancilla, postdoctoral researcher at Maastricht University, presented recent research on the topic.
Setting the scene, he began with what we know. Obesity is mainly expressed by an excess of fat accumulation in the adipose tissue. It is also associated with other metabolic dysfunctions, such as insulin resistance, which is mainly expressed in the skeletal muscle, as well as with ectopic fat accumulation in peripheral tissues, such as the liver, and with a decrease in skeletal muscle mitochondrial function and content.
He explained that there are two main glucose-disposal pathways in skeletal muscle: non-oxidative glucose disposal (NOGD), which refers to the storage of glucose in the form of glycogen, and oxidative glucose disposal, which refers to the oxidation of glucose via mitochondrial respiration.
When individuals are exposed to insulin stimulation, he said, there is an increase in the glucose-disposal rate in obese and type 2 diabetes patients, which is mainly explained by reduced NOGD. Therefore, they hypothesise that targeting the NOGD pathway in skeletal muscle is crucial to improving insulin sensitivity in insulin-resistant people.
He covered previous research looking at the effects of conventional exercise training on skeletal muscle insulin sensitivity in type 2 diabetes patients, with exercise such as weights and cycling three times a week over 12 weeks. They found a significant improvement in peripheral insulin sensitivity in type 2 diabetes patients but it did not reach the levels seen in the obese normal glycaemic control group.
Interestingly, he said, they found a restoration of insulin-stimulated oxidative glucose disposal in the type 2 diabetes patients to the levels of the obese normal glycaemic control group. However, they didn’t find any significant effect of training on the insulin-stimulated NOGD in the type 2 diabetes patients. They believe this was due to the moderate intensity of this conventional type of exercise training.
This led them to think that they needed to come up with exercise modalities that target the NOGD pathway in order to improve and restore insulin sensitivity in insulin-resistant individuals.
Targeting metabolically compromised individuals
High-intensity interval training (HIIT) consists of short bouts of exercise performed at a high intensity interspersed with short periods of rest. Dr Mancilla explained that it prompts skeletal muscle glycogen utilisation as the main energy source, leading to a significant reduction in muscle glycogen content post-exercise. In the recovery period, muscle glycogen is re-synthesised to basal levels.
This led to their research question: does HIIT improve skeletal muscle NOGD in obese, metabolically compromised individuals? They recruited 25 males and females with obesity or overweight who were sedentary but without type 2 diabetes. They were randomised into two groups: both exercised three times per week for 12 weeks with one minute of stationary cycling at 80-90% of maximum power output, followed by two minutes resting, repeated 10 times. Group 1 consumed water within 30 minutes post-exercise; group 2 consumed a carbohydrate-rich drink.
By taking a range of metabolic measurements, they found that HIIT significantly improves insulin-stimulated plasma glucose disposal in both groups. Subsequently, they measured effects of HIIT on insulin-stimulated NOGD and found that it significantly improves NOGD upon insulin effects in both groups, which was in line with their hypothesis.
They also found that HIIT robustly increases the glycogen synthesis capacity in skeletal muscle as well as significantly improving skeletal muscle oxidative capacity in vivo and mitochondrial content.
When measuring the effect of HIIT on intrahepatic fat content, preliminary data suggests that HIIT has no effect on this. However, it does suggest that HIIT alters intrahepatic fat composition, with a significant increase in polyunsaturated fatty acids (PUFAs) content in both training groups, but no significant effects on monounsaturated and saturated fatty acids.
In conclusion, Dr Mancilla said that 12 weeks of HIIT:
- Significantly improves the insulin-stimulated NOGD in obese adults, which co-exists with an increase in skeletal muscle glycogen content and improved skeletal muscle glycogen synthesis capacity
- Improves peripheral insulin sensitivity in obese adults
- Enhances the skeletal muscle oxidative capacity and increases the mitochondrial content
- Alters the intrahepatic lipid composition
- These changes were observed regardless of the consumption of glucose post-exercise and without changes in body weight and body composition
Watch out for the next module in our Lifestyle intervention course, due to launch in 2023, which will be looking at the role of exercise in diabetes prevention and management.
Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.