Resistance Exercise Training - one of the best things you could be doing to prevent and manage Type

The prevalence of type 2 diabetes mellitus (T2DM) is rapidly increasing, and effective strategies to manage and prevent this disease are urgently needed. T2DM is more than just a condition where you have too much sugar in the blood - it is accompanied by a host of risk factors including dyslipidaemia, hypertension, stroke and cardiovascular disease. T2DM is characterised by the body’s inability to use insulin as efficiently to remove excess glucose from the blood – as a result of becoming resistant to insulin.

I often explain this in laymen’s terms as a lock-and-key analogy. When there is excess glucose in the blood, there are cells present represented as a door with a padlock and the insulin is represented as a key. In the healthy individual the key fits well inside the padlock, where the door to the cell is opened and the excess glucose can enter the cell and be removed from the blood. In T2DM, the keys (insulin) are still being produced by the body, however they are not fitting into the padlocks as well and therefore decreasing its ability to remove the excess glucose from the blood.

If you have been diagnosed with T2DM, you may have been prescribed medication and recommended to participate in regular exercise (i.e. “try spend 20-30 minutes walking everyday"). This is because the benefits of aerobic exercise training, in reducing the risks of cardiovascular disease, including diabetes and obesity, have been well documented for decades. This aerobic type of exercise is fantastic and includes walking, jogging, bike riding etc. however, to better manage T2DM it is recommended to ensure there is a good resistance (strength training) component to your program.

Resistance exercise training appears to enhance insulin sensitivity and improve glucose tolerance. In addition, resistance training promotes health benefits through increased skeletal muscle mass and qualitative adaptations, such as enhanced glucose transport and mitochondrial oxidative capacity. These mitochondrial adaptations triggered by resistance exercise training provide evidence for this type of exercise as a feasible lifestyle recommendation to combat T2DM, a disease typically characterised by altered muscle mitochondrial function.

Furthermore, in non-diabetic individuals, skeletal muscle is responsible for approximately 80% of insulin-mediated glucose uptake in the postprandial state (the period directly following a meal). This uptake is markedly blunted in people with T2DM – and when compared to healthy lean individuals, people with T2DM experience a decreased capacity to oxidise both glucose and fat.

As the insulin resistance in an individual progresses and muscle glucose uptake becomes further impaired, the postprandial rise in plasma glucose concentration becomes excessive. This means, there is an excessive postprandial rise in plasma glucose concentration, and a longer time is required to restore normoglycemia after each meal. Eventually, however, the insulin resistance becomes so severe that the compensatory hyperinsulinemia is no longer sufficient to maintain the fasting glucose concentration at the basal level.

To summarise, all exercise is good – the best exercise is undoubtably the one that you will do. With this said, adding resistance exercise to a structured exercise routine is one of the best things you can do to help manage diabetes – or prevent diabetes. Resistance exercise can help enhance insulin sensitivity, improve glucose tolerance and increase skeletal muscle mass – which is responsible for up to 80% of insulin mediated glucose uptake in the postprandial state.

References:

1. DeFronzo RA, Tripathy D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care. 2009;32(Suppl 2):S157–63. doi: 10.2337/dc09-S302.

2. Pesta, D. H., Goncalves, R., Madiraju, A. K., Strasser, B., & Sparks, L. M. (2017). Resistance training to improve type 2 diabetes: working toward a prescription for the future. Nutrition & metabolism, 14, 24. doi:10.1186/s12986-017-0173-7