Diabetes is characterized by elevated blood glucose stemming from defects in insulin secretion, insulin action (sensitivity) or both. Individuals with a family history of diabetes, sedentary lifestyle and obesity are at particularly high risk for developing type 2 diabetes. Approximately 90 percent of all cases are type 2.
Obesity and type 2 diabetes are so inextricably linked that the term “diabesity” has begun to appear in the medical literature. It is widely accepted that as body fat levels increase, so does the relative risk of developing insulin resistance. If left unchecked, a “pre-diabetic” with mild insulin resistance will likely evolve to full blown type 2 diabetes. Early diagnosis is critical for effective management and reduced risk of long term complications.
While many fitness professionals are satisfied with the mere knowledge that this obesity-diabetes link exists, it is crucial to understand the mechanisms that explain why obesity interferes with the insulin signaling cascade and ways in which physical activity mitigates the onset of diabetes or improves long term health outcomes in those already diagnosed with the disease.
Current Theories of Insulin Resistance
Excess body fat, or more specifically intramuscular triglyceride (IMTG), is “associated” with type 2 diabetes. However, it is not accurate to say that a cause and effect relationship between obesity and diabetes exists. For example, trained athletes also exhibit a higher IMTG content but remain insulin sensitive with normal glucose uptake. This paradox suggests that there are other mechanisms operating at the myocellular level, which may explain why an obese person becomes insensitive to insulin action. There are three key factors likely responsible for impaired insulin action:
- Disruption of insulin-dependent insulin signaling pathways at the level of the muscle
- Disuse of the insulin-independent pathways, which are easily activated by muscle contraction
- Secretion of adipocytokines, substances secreted from deep fat around the organs (belly fat), that are strongly associated with insulin resistance and a variety of related chronic health problems
These three points will be explained in greater detail below.
Insulin-dependent pathways (insulin required)
The insulin-dependent pathways for glucose uptake are extremely intricate. Our scientific understanding of how disruptions in these pathways lead to insulin resistance is still under investigation. In very simple terms, think of the insulin-dependent signaling pathway as a lock and key. The muscle insulin receptor is like a lock and the insulin is the key that opens the muscle to allow for glucose uptake. In the case of insulin resistance and type 2 diabetes, it is theorized that intramuscular triglyceride (or associated lipid metabolites like ceramide and diacylglycerol) interferes with the normal action of these receptors1, thus leading to a “backing up” and accumulation of blood sugar. For a comprehensive discussion on insulin signaling pathways, please refer to a review by Le Roith and Zick2.
Insulin-independent pathway (no insulin required)
While we often associate glucose uptake with efficient insulin action, the body (in its infinite wisdom!) has alternative pathways to circumvent the need for insulin. The body contains a variety of glucose transporters across different tissues. Muscle tissue contains a high concentration of the fourth type of glucose transporter, aptly abbreviated GLUT4. GLUT4 transport is activated with muscle contraction and can function without the need for insulin3. The good news is that your insulin resistant clients can put these transporters to use just by getting up off the couch and putting one foot in front of the other. Even low level activity can lead to significant improvements in glucose uptake.
Visceral obesity and adipocytokines (a metabolically active organ)
It is fascinating that a mere 10 to 15 years ago, we thought all fat was simply a reservoir for storage of excess energy. However, advances in obesity research now underscore the relevance of fat’s anatomic location. Deep fat within the abdominal cavity (i.e., visceral adiposity) is now viewed in the medical literature as a metabolically active organ4. We now recognize that visceral adipose tissue secretes very potent substances into the blood called adipocytokines, which are strongly linked to a variety of negative health effects such as insulin resistance (diabetes), inflammation (coronary artery disease) and vasoconstriction (high blood pressure) among others4.
Exercise and Improvements in Insulin Sensitivity
Numerous randomized controlled trials support the role of exercise in improving a variety of health outcomes in people with type 2 diabetes5-17. Results from these investigations were critically evaluated and aggregated in a recent meta-analytic review by Thomas et al18. In order to isolate the effects of exercise, all included reports entailed strict exercise protocols without additional dietary, pharmacological or psychological interventions. Based on these data, exercise has been shown to improve glycemic control5-17, increase insulin sensitivity12,15, increase lean body mass5, decrease visceral and subcutaneous fat6,12, decrease triglycerides11-14, 17,19 and improve maximal oxygen uptake12,19.
The potent action of exercise in improving diabetes may be explained by a number of exercise-induced physiological and biochemical changes at the level of the muscle (Table 1). Regular bouts of both structured exercise and incidental physical activity help to “resensitize” the muscle to insulin. This resensitization effect of an acute bout of exercise has been shown to last approximately 72 hours and is the justification for regular physical activity and structured exercise in pre-diabetic and diabetic clients20.
Table 1: Key exercise-induced improvements in insulin sensitivity
||Improvements in mitochondrial function and more efficient lipid (fat) transfer into the mitochondria contribute to a reduction in intramuscular triglyceride and improved insulin signaling.
|Krebs Cycle Function
||Exercise enhances the efficiency of the Krebs cycle by increasing the number and activity of key enzymes responsible for fat metabolism.
||An up regulation in capillary density helps with oxygen delivery to the muscle where it is used at the level of the mitochondria for fat oxidation.
||Exercise stimulates both the production and activity of GLUT4 transporters in the muscle. Recall these function without the need for insulin and become active with muscle contraction.
||Exercise stimulates the glycogen-storing enzymes. With regular training, the muscle “reservoir” can hold more glycogen.
||Fat loss around the abdominal region (i.e., visceral adiposity) reduces the secretion of these harmful substances into the blood and is associated with improved insulin sensitivity (and improvements in other health indices).
|Improved Pancreas and Liver Function
||Exercise causes a reduction in insulin secretion and improved liver insulin sensitivity due to improved whole body efficiency.
While a reduction in fat mass is still desirable, it is noteworthy to mention that improvements in insulin sensitivity can occur even in the absence of weight loss21. For the multitude of reasons mentioned in Table 1, we need to remind diabetic clients that exercise is potent medicine, and improvements in the condition will begin to occur even before overt changes on the scale! Here’s the evidence for your clients taking Metformin, a popularly prescribed medication for both pre-diabetic and diabetic patients. In a large scale prospective diabetes prevention trial, exercise was shown to be more effective at staving off the onset of diabetes than Metformin22.
Many fitness professionals are confused as to which exercises are appropriate for people with diabetes. You should train a diabetic client just like you would any other apparently health individual. That is, you can use all of the “weapons” in your training arsenal, provided you are observing all safety considerations. The following checklist (Table 2) will help guide you to make sure you minimize the risk of exercise-induced adverse events.
Table 2: Exercise safety precautions for type 2 diabetic clients
||Before you even let a client touch a weight, you MUST ensure they are medically stable and currently under the care of a diabetes management team (doctor, nurse, diabetes nurse educator). Get a signed consent for exercise from the medical team acknowledging that they know their patient (your client) is going to undertake exercise.
||You should always know what your client’s blood sugar is before and after an exercise session. The client should bring their own glucometer or you should have one on site. This is important for establishing a “normal” range within which the client’s blood sugar usually hovers before exercise and how much the blood sugar drops after exercise. If the client comes in with very low blood sugar or excessively high sugar, you should not allow them to exercise. Always consider the timing of both pre-exercise meals and medications, as these will influence the blood sugar readings.
|Sign and Symptom Monitoring
||Be familiar with signs and symptoms of hypo- and hyperglycemia. While type 2 diabetics frequently suffer from high blood sugar, there will be occasions where some clients will present with very low blood sugar. Many diabetic people will know their own signs and be prepared with a small snack to bring up their blood sugar. If they’re newly diagnosed and not yet well managed, they should be referred to their diabetes management team for education.
||It is advisable to keep training sessions at the same time of day on different days. This will help minimize variations in blood sugar levels, bearing in mind your client will likely be at the same post-absorptive state after breakfast or lunch. Again, always know your client’s pre-exercise blood glucose level.
||Keep the exercise intensity consistent from session to session and only make small, incremental changes over time. Radical changes in intensity may cause blood sugar levels to plummet.
|Beware of Nocturnal Hypoglycemia
||Clients exercising at night closer to bedtime need to be aware that even after the exercise session is done, their muscle enzymes remain active and will continue to pull sugar from the blood. If they go to sleep after exercise (without eating), there is the risk of nocturnal hypoglycemia and a trip to the hospital.
Obesity and type 2 diabetes are partners in crime and, in tandem, can provoke a multitude of degenerative chronic diseases (i.e., vascular disease). The hallmark sign of type 2 diabetes is insulin resistance. Regular exercise training has been shown to reduce muscle insulin resistance and improve overall long term health outcomes. Diabetic, insulin resistant clients may be trained normally like any other client (weights, cardiovascular exercise, stretching, etc). However, you should observe additional safety measures to ensure blood sugar levels remain within safe limits before, during and after exercise.
- Boden, G., Ceramide: a contributor to insulin resistance or an innocent bystander? Diabetologia, 2008. 51: p. 1095-1096.
- Le Roith, D. and Y. Zick, Recent advances in our understanding of insulin action and insulin resistance. Diabetes Care, 2001. 24(3): p. 588-597.
- Wallberg-Henriksson, H., J. Rincon, and J. Zierath, Exercise in the management of non-insulin dependent diabetes mellitus. Sports Medicine, 1998. 25(1): p. 25-35.
- Kershaw, E. and J. Flier, Adipose tissue as an endocrine organ. Journal of Clinical Endocrinology and Metabolism, 2004. 89(6): p. 2548-2556.
- Baldi, J. and N. Snowling, Resistance training improves glycaemic control in obese type 2 diabetic men. International Journal of Sports Medicine, 2003. 24(6): p. 419-423.
- Cuff, D., et al., Effective exercise modality to reduce insulin resistance in women with type 2 diabetes. Diabetes Care, 2003. 26: p. 2977-2982.
- Dela, F., et al., Physical training may enhance ß-cell function in type 2 diabetes. American Journal of Physiology Endocrinology and Metabolism, 2004. 287: p. E1024-E1031.
- Dunstan, D., et al., High-intensity resistance training improves glycemic control in older patients with type 2 diabetes. Diabetes Care, 2002. 25: p. 1729-1736.
- Dunstan, D., et al., Effects of a short-term circuit weight training program on glycaemic control in NIDDM. Diabetes Research and Clinical Practice, 1998. 40: p. 53-61.
- Loimaala, A., et al., Exercise training improves baroreflex sensitivity in type 2 diabetes. Diabetes, 2003. 52(7): p. 1837-1842.
- Maiorana, A., et al., Combined aerobic and resistance exercise improves glycemic control and fitness in type 2 diabetes. Diabetes Research and Clinical Practice, 2002. 56(2): p. 115-123.
- Mourier, A., et al., Mobilization of visceral adipose tissue related to the improvement in insulin sensitivity in response to physical training in NIDDM. Diabetes Care, 1997. 20(3): p. 385-391.
- Raz, I., E. Hauser, and M. Bursztyn, Moderate exercise improves glucose metabolism in uncontrolled elderly patients with non-insulin-dependent diabetes mellitus. Israel Medical Journal, 1994. 30: p. 766-770.
- Ronnemaa, T., et al., A controlled randomized study on the effect of long-term physical exercise on the metabolic control in type 2 diabetic patients. Acta Medica Scandinavica, 1986. 220: p. 219-224.
- Tessier, D., et al., Effects of aerobic physical exercise in the elderly with type 2 diabetes mellitus. Archives of Gerontology and Geriatrics, 2000. 31: p. 121-132.
- Tsujiuchi, T., et al., The effect of Qi-Gong relaxation exercise on the control of type 2 diabetes mellitus. Diabetes Care, 2002. 25(1): p. 241-242.
- Wing, R., et al., Exercise in a behavioural weight control programme for obese patients with type 2 (non-insulin-dependent) diabetes. Diabetologia, 1988. 31: p. 902-909.
- Thomas, D., E. Elliott, and G. Naughton, Exercise for type 2 diabetes mellitus. Cochrane Database of Systematic Reviews, 2006(3): p. Art. No.: CD002968. DOI:10.1002/14651858.CD002968.pub2.
- Yeater, R., et al., Coronary risk factors in type 2 diabetes: response to low-intensity aerobic exercise. West Virginia Medical Journal, 1990. 86: p. 287-290.
- Albright, A., et al., Exercise and type 2 diabetes. Medicine and Science in Sports and Exercise, 2000. 32(7): p. 1345-1360.
- Willey, K. and M. Fiatarone-Singh, Battling insulin resistance in elderly obese people with type 2 diabetes. Diabetes Care, 2003. 26(5): p. 1580-1588.
- Diabetes Prevention Program Research Group, Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. New England Journal of Medicine, 2002. 346(6): p. 393-403.