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"Diabetes is estimated to cause around 5% of all deaths globally each year and this number is likely to increase by more than 50% in the next 10 years without urgent action."
Given the above statement, it is quite clear that more attention must be focused on preventative and management strategies to contend with this very prevalent disease.
Type 2 accounts for ~90% of all diabetes (WHO, 2010) and as evidence shows (McArdle et al., 1996) this type of diabetes is heavily associated with factors susceptible to change, i.e. diet, exercise patterns etc.
The following paper will explain the pathophysiology of type II diabetes and examine through the review of empirical evidence, the role exercise plays relative to a therapeutic diabetes intervention and also the specific mechanisms it can affect change in, in order to enhance the manageability of the disease.
Diabetes Mellitus is the name given to a collective group of metabolic disorders which has become common worldwide. Caused by various genetic and environmental factors, this group of disorders are all characterised by the shared characteristic of hyperglycemia (Fauci et al., 2008).
Type II describes the most common and increasing form. Occurring more frequently with age, it is related to insulin resistance and deficiency (Lebovitz et al., 1999). The genotypic description of Type II refers to a wide variety of genotypes which can range from maturity onset diabetes of youth (MODY) to polygenic metabolic disturbances (classic type II diabetes) (Lebovitz et al., 1999) however, it is always preceded by abnormal glucose homeostasis (Fauci et al., 2008).
There are two main hypotheses around the origins of type II diabetes. The polygenic theory speculates that it is a consequence of a thrifty genotype from ancient times which is now causing obesity, insulin resistance and type II diabetes (Neel., 1962). The opposing view is that these unwanted variables are as a result of fetal malnutrition (Barker et al., 1993).
Whatever the cause, type II diabetes is a disease which has long term ramifications on the body's organ systems (McArdle et al., 1996). On the other hand, if detected and treated early, the risk of developing diabetes related complications such as stroke, heart attack, eye and foot diseases and kidney failure is reduced (Fauci et al., 2008).
As part of this treatment, the relevance of exercise as a therapeutic intervention for type II diabetes has been well established (Thomas et al., 2007; Sigal et al., 2006; Fritz et al., 2006). However lack of compliance and adherence to an exercise regimen generally restricts the long term clinical benefits of such interventions (Praet et al., 2008). Nevertheless, despite these benefits, specific cardiovascular risks are associated with diabetes and exercise (McCully et al., 2002; Wilmore et al, 2001) as well as certain diabetic populations being at increased risk compared with others (Elhendy et al., 2001). Therefore, careful screening of long-term complications of diabetes is essential for diabetics before beginning any exercise programme (A.D.A., 2002; Gregg et al., 2002).
Although the causes of type II diabetes differ on an individual basis, there are frequent behavioural commonalities which are controllable such as smoking, excess body weight, poor diet and low levels of physical activity (Fauci et al., 2008). All these factors increase risk of developing type II diabetes (RCPI., 2010). There are also uncontrollable factors which increase the risk of developing the disease such as age, genetics and gender (Scheen, 2003)
According to Fauci et al. 2008, the main functional changes which characterise type II diabetes include insulin resistance, impaired insulin secretion, abnormal lipid metabolism and excessive hepatic glucose production and as I will continue to explain regular exercise can positively affect these processes.
Each of these factors is a consequence of a defect in a related area which causes a complex chain reaction. For example, Î² cell defect leads to insulin resistance, which impairs insulin secretion which in turn has negative effects on lipid metabolism (Fauci et al., 2008).
Abnormal glucose homeostasis or Impaired glucose tolerance (IGT) as it is commonly referred to (for which the specific levels for each category are outlined in Fig. 2) always precede diabetes. IGT is characterised by elevated postprandial glucose levels.
The progression to overt type II diabetes requires both insulin resistance and impaired insulin secretion which disrupts the communication between beta cells and target tissue (Scheen et al., 2003).
Exercise is well documented as improving glucose and lipid metabolism and also reduces insulin resistance (Harding et al., 2001).
Insulin resistance is an impairment of normal glucose uptake by muscle and/or restraint in glucose production in the liver (Walker et al., 1997).
When insulin resistance is present, target tissue is unaffected by insulin and so it cannot fulfil its role as a mediator of "facilitated diffusion", the process whereby it combines with a glucose carrier and is transported into cells (McArdle et al., 1996). Thus insulin resistance results in increased plasma glucose levels. Most research supports that insulin resistance precedes insulin secretion defects (Fauci et al., 2008). Insulin resistance can contribute to facilitated increased body fat (McArdle et al., 1996).
Impaired Insulin Secretion:
Since insulin resistance and secretion are closely linked (Fauci et al., 2008; Sigal et al., 2006) through a feedback loop, when one is defected, the other reacts accordingly. Diabetes only develops after the defect with insulin secretion occurs (Surampudi et al., 2009).
Insulin secretion is regulated by blood glucose levels detected by the pancreatic Î² cells (Fauci et al., 2008). In the early stages of type II diabetes however, despite insulin resistance IGT remains near normal because Î² cells compensate and increase insulin production (known as compensatory hyperinsulinemia) (Fauci et al., 2008).
Eventually however, the deficiency in secretion becomes insufficient. The exact reasons for this are not yet known but according to Fauci (Fauci et al., 2008) a second genetic defect is assumed to be responsible which leads to beta cell failure.
Abnormal Lipid Metabolism:
In short, high BMI levels are closely linked with type II diabetes and dyslipidemia is another concern for this population (Fauci et al., 2008). This is because obesity and genetic factors makes one more likely to develop diabetes. High lipid mass levels especially central and visceral adiposity are major contributors in types II diabetes (Banerji et al, 1997; Lemiuez, 1996) and are thought to be part of a pathogenic process. Features of dyslipidemia include low HDL and elevated triglyceride levels (Fauci et al., 2008) which both increase CVD risk. Adipose tissue can secrete various molecules that may interfere with glucose metabolism and insulin sensitivity such as leptin, tumour, necrosis factor (TNF)-Î±, resistin adiponectin (Greenberg et al., 2002).
Evidence also shows that in genetically susceptible individuals, body weight gain is one of the most powerful predictors for diabetes (Li et al., 2003).
Excessive Hepatic Glucose:
It is caused by low levels of insulin in a fasting state promoting hepatic gluconeogenesis and glycogenolysis (Fauci et al., 2008). Upon secretion into the portal venous system, ~50% of insulin is degraded by the liver (Fauci et al., 2008). Exercise may exaggerate these mechanisms and cause hypo- or hyper-glycemia by increased hepatic glucose production or induce increased sensitivity (Turgan et al., 1996; Riddell et al., 2008).
Below is Fig. 1: conclusions from various studies in relation to the characteristics of type II diabetes.
Impaired Insulin Secretion
Abnormal Lipid Metabolism
Excessive Hepatic Glucose
Fauci et al., 2008
Exercise can delay or even prevent its onset & type II diabetes in individuals at increased risk
Progressive, due to Î² cell defects. However aerobic exercise can positively affect this by increasing insulin sensitivity.
Increased exercise as well as other lifestyle changes are advised as therapy to type II diabetics
Insulin resistance is also a key contributor to this which results in hypergycemia, which exercise can positively affect
McArdle et al., 1996
Exercise increases insulin sensitivity and so contributes to better glucose homeostasis
Alpha and beta cells positively influenced by prolonged exercise
Increased fat mass leads to increased FFA's which contributes to this
FFA's promote this & impair Î² cell function. Exercise can positively effect this by effecting insulin sensitivity
Boule et al., 2001
Aerobic exercise training
decreases hepatic & muscle insulin resistance
Amylin deposits may contribute to defect & eventually Î² cell failure follows
Weight loss not needed to induce beneficial glycemic control through exercise
Failure of hyperinsulinemia to suppress gluconeogenesis due to Insulin resistance in the liver
As evidence shows in Fig 2. (Below) regular exercise greatly decreases the chances of developing type II diabetes (McArdle et al., 1996).
Fig 2: Adapted from McArdle et al., 1996 (pg. 376)
A single bout of acute exercise causes an abrupt decrease on glucose plasma levels. This improvement with both high and low intensity exercise may persist for up to several days (McArdle et al., 1996). The long term improvement of glycemic control from regular exercise is most likely due the reoccurring benefits of each acute session rather than a chronic change in function (McArdle et al., 1996).
Much like any, the benefits of exercise as an intervention, are more enhanced the earlier intervention occurs. Research has documented that when exercise is performed regularly in type II diabetes patients; there are still enormous benefits (Thomas et al., 2007). The table below (adapted from Fauci et al., 2008), shows that regression through the various stages of type II diabetes is possible.
Type of Diabetes
Normal Glucose Tolerance
Impaired fasting glucose or
Impaired glucose tolerance (IGT)
Not Insulin Insulin
Insulin required required
Requiring for for
Other specific types
Fig. 3: Spectrum of glucose homeostasis & diabetes mellitus adapted from Fauci et al., 2008 (pg. 2275)
Fig. 3 shows the spectrum from normal glucose tolerance to diabetes. Arrows indicate the direction individual's transverse from the stages of normal to impaired glucose tolerance to overt diabetes. Some types of diabetes may not require insulin for survival hence the dotted line. As the table shows, glucose tolerance in some types of diabetes may be bi-directional. Type II Diabetes is such a type. Type II diabetes allows for regression from the overt stage to IGT with weight loss and from the IGT stage back to normal (Fauci et al., 2008).
Given this knowledge, exercise clearly has a pivotal role to play in maintaining healthy levels of body composition which can help maintain positive or delay more negative results.
Reflection & Conclusion
Upon review of the research, exercise quite clearly exerts many positive effects as a therapeutic interventional strategy in type II diabetes sufferers (Li et al., 2003; Thomas et al., 2007). Interestingly however, such interventions must be tailored to sufficient type, intensity and duration (Hiatt et al., 1991). Also, it should be noted that studies have showed exercise along with diet have yielded better therapeutic results on diabetes than diet alone (Li et al., 2003).
Boule et al., 2001 also speculates that a greater decrease in cardiovascular complications might be anticipated with exercise than with insulin or sulfonylureas in the UKPDS, since unlike these medications, exercise is associated with other cardioprotective benefit. The WHO estimates that in the year 2030, over 360 million people worldwide will have diabetes. In order to decrease this incidence and provide management and therapeutic interventions for these individuals, exercise must be considered as an integral part of diabetes intervention.