Diabetes mellitus is a metabolic disorder which is characterized by chronic hyperglycemia (WHO, 2006). This chronic hyperglycemia stems from problems with insulin secretion and insulin action which leads to disturbances in fat, protein and carbohydrate metabolism (WHO, 1999; ADA, 2011). Diabetes can be accredited with causing long-term damage, dysfunction, and failure of multiple organs: mainly the eyes (retinopathy), nerves (neuropathy), kidneys (nephropathy), heart and blood vessels (metabolic syndrome and cardiovascular disease) (ADA, 2011). Without effective treatment, it can become very severe with the possibility of death due to ketoacidosis or a non-ketotic hyperosmolar state (WHO, 1999).
There are two types of diabetes which are insulin dependent diabetes mellitus (IDDM) and insulin independent diabetes mellitus (IIDM). IDDM affects approximately 20 million people throughout the world and is caused due to an insulin secretion defect which leads to a lack of secretion by the ?-cells of the pancreas (ADA, 2001). IIDM is the most prevalent form of diabetes with it accounting for 90% of all cases of diabetes worldwide (Gonzalez et al, 2009). Impaired insulin secretion through dysfunction of ?-cells in the pancreas and impaired insulin action by means of insulin resistance can all be thought of as defects which characterize IIDM (Holt, 2004).
According to the chronic conditions hub in 2012, diabetes was the ninth leading cause of death worldwide, with it expected to be the seventh leading cause of death globally by 2030 according to the World Health Organization (WHO) in 2015. In 2000, it is estimated that 171,000,000 people were living with a type of diabetes and it was predicted by the WHO that by 2030, 366,000,000 people throughout the world would be living with the metabolic disorder (WHO, 2015).In Europe; there was a prevalence rate of 8.5% of adults between the ages of 20 and 79 living with diabetes (Human Intelligence, 2013). According to the WHO, 86,000 people throughout Ireland were living with diabetes in the year 2000, with it expected to rise to 157,000 by the year 2030. It is estimated that 10-15% of the population has diabetes, are diagnosed with type 1 diabetes which means that they are insulin dependent (Diabetes Ireland, 2015). In Ireland, there are 854,165 adults over the age of forty that currently have type 2 diabetes or are at risk of developing it. That isn’t even the worst part of it, even more frighteningly 304,382 adults between the ages of 30-39 are also at risk of developing type 2 diabetes as they are deemed overweight and they do not achieve the recommended guidelines of 150 minutes of physical activity a week. These individuals, by doing so, leave themselves at high risk of developing chronic ill health (Diabetes Ireland, 2015). The prevalence of Diabetes is amplifying each year and is a growing problem which needs to be addressed. A major factor behind this is the increased sedentary culture which is becoming instilled in Ireland and throughout the world.
In 2012, in a document released by the American Diabetes Association (ADA), it was estimated that the costs for diabetes had risen to $245 billion in 2012, a 41% increase from $174 billion in 2007 (ADA, 2013). An international accredited study which took place in 1999 examined the costs of type 2 diabetes in Ireland and found that 10% of the Irish national budget was being spent on treating the condition; 49% was consumed on hospitalization for complications and wages, 42% on the cost of medications, 8- 9% on ambulatory care and attending non-diabetes specialists for diabetes-related concerns) (Diabetes Ireland, 2015). It is not feasible to continue to spend such a large portion of the budget on a single condition, with it looking like the costs are only going to increase, when there are cost-free ways of tackling the problem such as exercise and healthy nutrition. Some of the costs should be spent on education the population of the risks of being overweight or obese, along with the risk of maintaining low physical activity levels. Healthy nutrition and exercise workshops should be held in each workplace and every school throughout the country in order to stem the sedentary culture which we currently live in; with the stemming of this culture, we would see a change in the prevalence of type 2 diabetes.
Current Exercise Guidelines.
The current exercise guidelines which are in place from the ADA are 30 minutes of moderate to vigorous intensity aerobic exercise should be carried out 5 days per week, at least, or a total of 150 minutes per week which should be done in order to work as a management strategy for those with diabetes. “Moderate intensity” can be described as working hard enough that you could while completing the exercise but would not be able to sing. While “vigorous activity” can be described as an exercise in which you are unable to say more than a few words without the need of taking a break (ADA, 2015). The benefits of carrying out a physical activity when you have diabetes are paramount. It is shown that completing aerobic exercise enhances the body’s employment of insulin; it improves cholesterol levels while also lowering blood glucose levels and blood pressure. It is also advised to partake in resistance training along with aerobic exercise, in order to witness an improvement in their insulin sensitivity and to lower their blood glucose concentration significantly (ADA, 2015).
Pathophysiology of IIDM;
Insulin secretion, insulin resistance, and subsequent b-cell dysfunction can be defined as the factors with characterizing type 2 diabetes mellitus (Olokoba, 2012). These defects usually exist together in an individual and the causation can be mostly based around genetic and environmental factors (Kosma, 2010).
Impaired Insulin Secretion.
The release of insulin from beta-cell of the pancreatic islets is in response to alterations of the blood glucose concentration (Kosma et al, 2010). The GLUT2 transporters assist the diffusion of glucose into the beta-cells (Kosma et al, 2010). In the beta cells, adenosine triphosphate (ATP) is created through glucose metabolism. This creation of ATP leads to an increased ATP/ADP ratio, which leads to the cell become depolarised due to it inducing the closure of potassium channels. The depolarization of the cell leads to the opening of the voltage-gated calcium channels which allows the influx of extracellular calcium into the pancreatic beta cell. The exocytosis of insulin occurs due to this rise in free cytosolic calcium (Seino et al, 2002)
The release of insulin occurs in a biphasic manner from the beta cells in the pancreas in response to the sharp increase in blood glucose concentration. The first and second phase of insulin release is considerably lower, and can often be absent, in people with type 2 diabetes compared to healthy individuals. This defect in insulin release can be witnessed in normoglycemic first-degree relatives of type 2 diabetic patients (Henriksen et al, 1994).
According to Kahn insulin resistance can be considered to be the biggest predictor of type 2 diabetes. Insulin carries out its biological function by interacting with an insulin receptor (IR). Following the binding of the insulin to the IR, auto-phosphorylation takes place which consists of the binding of scaffold proteins such as insulin receptor substrate (IRS) proteins. Following the phosphorylation of the IRS proteins, they interact with the p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3K) and its activation. The resulting action of PI3K leads to the accommodation of the translocating of GLUT4 containing vesicles to the surface of the cell (Muoio et al, 2008). Glucose is then transported into the cell through the GLUT4 transporter.
Insulin resistance can be characterized as the failure of the liver and adipose tissues, and skeletal muscle cells to react in the correct manner to circulating concentrations of insulin. In order to sustain normal levels of glucose concentration in the blood, the pancreas has to compensate by secreting increased levels of insulin. However, this amplified level of insulin can only be sustained for a short period of time. Following this compensatory period, the development of pre-diabetes and diabetes usually occurs, especially in individuals where beta cell dysfunction is also prominent (Vaag et al, 1992; Kosma et al, 2010).
Beta Cell Dysfunction
One of the most severe contributing factors to type 2 diabetes is beta cell dysfunction and it is triggered by insulin resistance (Ashcroft et al, 2012). Beta-cell dysfunction is more severe than insulin resistance as it impairs insulin secretion while resistance allows secretion but insulin insensitivity develops in the tissues. In order for the body to match the ever-changing metabolic demand for insulin, a normal beta cell integrity is required (Cerf, 2013). Hormones, neural inputs, and nutrient availability help sustain blood glucose levels through the careful management of insulin secretion (Schrimpe-Rutledge et al, 2012). Glucose is of huge physiological importance when it comes to the function of the beta cell and the stimulation of insulin genes, beta cell insulin secretion and proinsulin biosynthesis (Henquin et al, 2006).
Even though there has been increased understanding of the significant role that insulin resistance and beta cell dysfunction play in type 2 diabetes, it must be remembered that the metabolic disease process is inherently heterogeneous and other pathogenic considerations must be allowed for (McCulloch et al, 2014).
Diet, Obesity, and Inflammation.
Two of the most noticeable risk factors associated with an increased prevalence of impaired glucose tolerance (IGT) and type 2 diabetes are increased weight gain and decreased physical activity (Engelgau et al, 2004; Sullivan et al, 2005). Generally, individuals who are diagnosed with type 2 diabetes tend to be overweight or obese, and are carrying excess central visceral adiposity. This solidifies the idea that adipose tissue is involved in the pathophysiology of type 2 diabetes (Olokoba et al, 2012).
A major cause of resistance to insulin-mediated glucose uptake is obesity and it also leads to the beta cells becoming less sensitive to glucose (McCulloch et al, 2014). Fortunately, the solution is a simple and cheap one, active weight loss has been shown to have the ability to largely reverse these effects and return blood glucose concentration back to near normal levels (McCulloch et al, 2014). Hirosumi believes that the c-Jun amino-terminal kinase (JNK) pathway could be a central facilitator of the relationship between insulin resistance and visceral adiposity, as JNK activity is amplified in cases of high visceral adiposity, an effect that can inhibit insulin activity. In animals, the absence of JNK1 results in reduced adiposity and enhanced insulin sensitivity (Hirosumi et al., 2002).
Obese patients tend to have a high concentration of free fatty acids which pose a severe risk for patients with type 2 diabetes (McCulloch et al, 2014). This high level of free fatty acids which they are harboring can inhibit insulin secretion and insulin-stimulated glucose uptake in those with type 2 diabetes. This can lead to a metabolic overload of the liver and muscles which causes mitochondrial dysfunction along with the impairment of fatty acid oxidation. This metabolic overload paired with physical inactivity leads to lipid-derived intermediates gathering in the mitochondria which add further to the mitochondrial stress and insulin resistance. The development of hepatic insulin resistance and hepatic steatosis is encouraged by the re-routing of free fatty acids into the endoplasmic reticulum and cytoplasm due to the impaired fatty acid oxidation (Muoio et al, 2008). This increased level of fatty acids leads to the disruption of the insulin signaling cascade which eliminates the insulin activation associated with the PI3K activity (Dresner et al, 1999).
Adiponectin has been shown to decrease bloody fatty free acid levels and is related to improved lipid profiles, it has been shown to enhance glycaemic control and decrease inflammation in patients with diabetes (Mantzaros et al, 2005). A deficit in adiponectin has been shown to be related to the development of insulin resistance and therefore type 2 diabetes (Kadowaki et al, 2006).
Leptin has been linked to obese individuals and increased insulin resistance. As adipocyte mass and stored fat increases, so does the magnitude of leptin secretion (McCulloch et al, 2014). In a study completed on mice, an increase in glucose tolerance can be seen when there is an absence of leptin when the mice were being fed their regular diet. However, once a high-fat diet was introduced to the mice, it was seen that they gained weight and increased insulin resistance occurred. Through this valuable insight, it can be suggested that leptin could play a role in the development of obesity-related type 2 diabetes (McCulloch et al, 2014).
Adipocytes also release a protein called retinol-binding protein 4 (RBP4). In obese patients who have type 2 diabetes or are glucose intolerant, there is a correlation between RBP4 and insulin resistance. RBP4 has been shown to decrease in patients who have increased their physical activity levels due to the decrease in insulin resistance.
Effect of Exercise on Type 2 Diabetes.
As I have already mentioned, over 80% of the diabetic population is considered overweight or obese. Inevitably, a link has been made been type 2 diabetes and obesity, as we can see there is a strong correlation between the two.
Effect of exercise on glycemia and insulinemia
Exercise has been shown to a have a positive effect on both glycemia and insulinemia, thus having a positive effect on individuals who are affected by type 2 diabetes. As we know already, in resting conditions, glucose uptake tends to be most reliable on insulin. The transportation of glucose into the cell cytoplasm is facilitated by the translocation of GLUT-4 to the cell membrane (Suh et al, 2007). With the onset of exercise, if the duration is long enough and the intensity high enough, there is a significant improvement in the uptake and utilization of glucose. The more intense the exercise is, the greater the effect it has on glycemia as an increased amount of carbohydrates will be metabolized in order to match the energy requirements associated with the increased intensity (Suh et al, 2007). As we know abnormal amounts of glucose concentration in the blood lead to insulin secretion defects which are a cause of type 2 diabetes. A decrease in blood glucose concentrations helps prevent this insulin secretion impairment and can be used as an effective method of treating and preventing type 2 diabetes.
Effect of Exercise on Carbohydrate and Fat Oxidation in Type 2 Diabetes.
Carbohydrate oxidation has been shown to improve in individuals with type 2 diabetes with the help of increased exercise, even with the uptake of glucose being impaired through insulin-dependent pathways. This is shown to be true as the majority of glucose taken in during exercise is through insulin independent pathways (Sigal et al, 2006).
It is thought that the best part of carbohydrate oxidation that takes place during exercise in individuals with type 2 diabetes is independent of the actual exercise intensity. Carbohydrate is used as a substrate during exercise and is readily available as an energy source as glycogen in the muscle and glycogen in the blood. It is considered to be dependent on the intensity of the exercise as to how much you use (Colberg et al, 2010).
In a study conducted by Lima, a cycle ergometer test was carried out and fat oxidation levels were measured. The study showed that fat oxidation was increased in individuals with type 2 diabetes while high-intensity exercises prolonged this exercise further. Fat oxidation was also increased post-exercise in those with type 2 diabetes compared to those who aren’t diagnosed with it.
From the above, we can see the positive effects that exercise can have on those with type 2 diabetes. The increase in carbohydrate and fat oxidation have positive effects on factors which characterize type 2 diabetes such as obesity and abnormal glycogen levels. The carbohydrate oxidation helps to lower the glycogen levels through the oxidation and also through the use of it as an energy source. As we know high blood glucose levels lead to insulin impairments which can begin the onset of type 2 diabetes, so exercise is an effective way of preventing and treating those that are pre-diabetic or diabetic. They are capable of doing this as they both contribute to increased insulin sensitivity and reduce body fat, which would reduce adipocytes which would help prevent the onset of type 2 diabetes and would help treat it.
Effect of Exercise on Blood Pressure.
Individuals with type 2 diabetes are at high risk of also developing hypertension. It has been shown though that hypertension can be treated with single bouts of exercise whether it be aerobic or resistance, while also increasing the likelihood of hypotension. Exercise stimulates the release of Nitric Oxide which helps lower blood pressure following exercise.
The benefits of hypotension following exercise are numerous and highly beneficial but can be dependent on the intensity of the exercise performed. An individual with type 2 diabetes appears to react better to high-intensity exercise, which works them above the lactate threshold. Completing exercise at this intensity has shown to reduce systolic blood pressure much more significantly than lower intensity exercise (Lima et al, 2008).
The above shows that just a single bout of exercise elicits numerous benefits which can help improve the treatment and prevention of type 2 diabetes. It lowers blood pressure, improves glucose control, increases carbohydrate and fat oxidation. The metabolic stresses which exercise onsets increase the carbohydrate oxidation during the bout of exercise, which leads to an elevated O2 consumption post exercise. This then has a knock on effect which leads to an increased fat oxidation at rest, along with an improvement in insulin sensitivity, glucose tolerance and a decrease in blood glucose levels. These effects can last from 2 to 72 hours depending on the length and intensity of the exercise. Should regular intensive exercise be adhered to there is no doubt that physical activity would act as an effective treatment for type 2 diabetes, and it certainly would prevent the onset of diabetes initially.
The prevalence of type 2 diabetes increases in the older population. In the older generation, we know that their muscle mass declines the older they become, along with the degeneration being helped along by type 2 diabetes. Resistance training is what is required for those in the older population in order to achieve a more effective management and treatment of diabetes. The optimal training programme for treating and managing type 2 diabetes should include a mixture of resistance training, cardiorespiratory training, and endurance training. While it is necessary to train the various systems in order to reap multiple benefits from each, another important factor of varying training is that it increases the adherence rate of individuals so it helps with the treatment and management of type 2 diabetes (Eriksson, 1999).
It is clear that the diabetes epidemic is a serious one with the prevalence of the condition growing each year, along with it costing the state millions upon millions to treat. It is a chronic disease which can seriously affect a person’s quality of life as it can often be debilitating.
While currently it is generally being treated through the prescription of drugs such as metformin, this shouldn’t be the go-to management of diabetes. It doesn’t particularly improve quality of life while it does help regulate insulin and glucose, this can be done through a cost-free means. The use of exercise as the treatment would reduce costs, improve quality of life, and also give the individuals much more autonomy over their own life.
A single lifestyle intervention is the best way to treat and prevent the onset of diabetes. Introducing a healthier diet and increased physical activity in their life can help counteract the onset of impaired insulin sensitivity, beta cell dysfunction, and insulin resistance. It helps to do this by reducing the likelihood of being obese or overweight.
Lifestyle intervention workshops are the way forward for the treatment of type 2 diabetes such as teachings about how to improve your diet and how to gradually improve your physical activity levels. While immediately it may not have a massive effect, in the long term it would reduce costs and decrease the prevalence of type 2 diabetes throughout the world as a new fitness culture would be instilled in the youth upwards.