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Exercise and Type 2 Diabetes: New Prescription For An Old Problem

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ByCrossFitSeptember 1, 2019

In this short, accessible 2012 review, Stephen Bird and John Hawley argue interval training (HIT or HIIT) is an effective intervention for preventing and treating Type 2 diabetes.

In healthy individuals, blood glucose levels are tightly controlled to around 5 mM through the actions of insulin and glucagon. The former hormone lowers blood glucose levels by encouraging certain tissues to take up glucose from the blood; the latter raises blood glucose levels by increasing the release of glucose from the liver into the blood. Insulin resistance, and later diabetes, develops when the body is no longer able to regulate blood glucose, and specifically, when insulin is unable to reduce blood glucose levels effectively.

Skeletal muscle is a major mediator of insulin response. When insulin acts to lower blood glucose, 80% of the glucose removed from the blood is transported into the skeletal muscle (compared to only 3-4% into fat tissue). As a result, when skeletal muscle becomes insulin resistant — that is, when insulin fails to stimulate sufficient glucose uptake by the skeletal muscle — the body as a whole struggles to bring glucose levels back down, which can lead to the development of diabetes.

Bird and Hawley summarize evidence indicating exercise maintains or improves skeletal muscle insulin sensitivity and as a result reduces risk of insulin resistance and diabetes. Exercise increases skeletal muscle insulin activity in the obese, while sedentary behavior decreases it. The ability of the muscle to take up and burn fuel (i.e., skeletal muscle oxidative capacity) is a strong predictor of whole-body insulin resistance. Unfortunately, despite this consistent evidence and widespread recommendations to increase activity levels among those who have or are at higher risk of having diabetes, patient compliance with exercise regimens remains low.

The most commonly cited barrier to exercise compliance is time. Thus, Bird and Hawley analyze whether shorter, more intense exercise like that delivered through interval training has similar benefits to the moderate-intensity, prolonged exercise most commonly prescribed. While the overall data set related to HIT in diabetics was small, short-term studies consistently indicated HIT improved cardiorespiratory fitness as much, if not more than, prolonged exercise. The data also suggest HIT rapidly and durably improved glycemic control in diabetic subjects (i.e., it reduced both 24-hour blood glucose levels and the number of high-glucose spikes/excursions).

This led Bird and Hawley to conclude the existing evidence base collectively suggests HIT is likely to have significant efficacy in preventing diabetes in those at high risk and managing blood glucose levels in those who already have the condition. They advocate for long-term studies testing interventions using HIT for diabetes prevention and the management of comorbidities such as heart disease in diabetic populations.


References

  1. See “The effect of insulin on the disposal of intravenous glucose. Results from indirect calorimetry and hepatic and femoral venous catheterization,” “Effects of insulin on peripheral and splanchnic glucose metabolism in noninsulin-dependent (type II) diabetes mellitus,” “The glucose uptake of human adipose tissue in obesity,” and “Effect of insulin on the distribution and disposition of glucose in man.”
  2. See “Exercise as a therapeutic intervention for the prevention and treatment of insulin resistance,” “What’s new since Hippocrates? Preventing type 2 diabetes by physical exercise and diet,” “Exercise training-induced improvements in insulin action,” and “Waging war on modern chronic diseases: Primary prevention through exercise biology.”
  3. See “Muscle oxidative capacity is a better predictor of insulin sensitivity than lipid status” and “Dissociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with type 2 diabetes.”

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