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Fig 1. Graph showing insulin sensitivity and beta cell function in people with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) (Tfalyi, 2009).
Diabetes has now hit epidemic proportions and affects over 170million people worldwide. Global estimates in 2010 also suggest that diabetes will further grow by another 50% in the following years. 90% of diabetic individuals have T2D and of this population 10% is caused by "monogenic" factors such as maturity onset diabetes, mitochondrial diabetes and a late onset of type 1 diabetes. This concludes that most diabetes in the world is accounted for by "common T2D which has multifactorial pathogenesis caused by several alterations in gene products" (Stomvoll, 2005). Throughout the course of this essay the pathophysilogy of T2D will be described in both defects leading to the disease and exercise will be discussed as a therapeutic aid.
Insulin resistance and T2D are strongly associated with excess lipid accumulation in non adipose tissue (skeletal muscle). This is most likely achieved by "interference of the accumalted lipid metabolites diacylglyceol, ceramides and long chain fatty acyl CoA with insulin signalling" (Corpeleijn, 2009). Insulin sensitivity is influenced by numerous factors including genetics, age, acute exercise, physical fitness, dietary nutrients, medications, and body fat distribution. Insulin resistance in vivo is measured using an oral glucose tolerance test, an intravenuos glucose tolerance test and a euglycaemic hyperinsulinaemic clamp. Although much work has been done on what is the main cause of insulin resistance the main area of interest seems to be with body fat distribution and in particular intra abdominal fat. The importance of intra abdominal fat and insulin sensitivity was highlighted in the following study by Fujimoto et al (1994) in which both diabetic and non diabetic japanese men were tested for free fatty acid concentration, intra abdominal fat, plasma cholesterol, low density lipoprotein density, fasting insulin and triglycerides. These were measured using computed topography. The results found that in non obese Japanese men the features of the insulin resistance syndrome seen in T2D are more strongly correlated with visceral adiposity than the other features. This makes it an important factor in preventing T2D and hence exercise is an effective means of treating T2D.
Insulin deficiency is apparent in subjects with T2D as soon as hyperglycaemia is evident. This change occurs by decreasing the functionality of the beta cells in the early insulin response to intravenous or oral glucose and also in the ability of glucose to potentiate the insulin response to non glucose secratagogues. Subjects with T2D also show a marked decrease in the potentiation by oral rather than by parenteral glucose loading which is described as "the incretin effect which is associated to glucose dependent insulinotropic peptide and glucogen like peptide secreted by enterocytes" (Kahn, 2003). The effects of insulin secretion were clearly evident in a study by Basu et al (2009). This study aimed to evaluate the effect of having T2D had on insulin secretion, action and glucose effectiveness. 25 subjects were recruited (14 of which had T2D) and underwent a mixed meal test using the triple tracer technique. The variables for examination were tested using the "Oral" minimal and C peptide models. This study found that insulin secretion, action and glucose effectiveness were all lower in diabetic subjects when compared with the non diabetic controls. The results of insulin secretion levels and glucose levels can be seen in the graphs below when a meal was ingested at time=0. The black dots indicate subjects who had T2D and the white dots indicate the controls. As is clear from the below figures insulin secretion and hence beta cell function is delayed in people with T2D and only seems to reach appropriate levels 120mins after a meal has been ingested and this level remains higher than normal still at 360mins post the meal.
Fig 2. Graphs showing glucose levels (left) and insulin secretion (right) after a meal was ingested at time=0. (Basu et al, 2009)
Exercise has a number of beneficial effects on the treatment of T2D. Exercise helps to increase energy expenditure, this may be used to prevent and change obesity, which was shown to be a factor in insulin resistance with the presense of intra abdominal fat. Also exercise "actuely increases muscle glucose transport and this effect is mediated by an increase in the glucose transport 4 isoform of the glucose transporter in skeletal muscle" (Kirwan et al, 2009). This emphasizes the therapeutic benefits of exercise in treating T2D by dealing with both insulin resistance and also insulin secretion problems. A study which highlighted these two benefits of exercise was done by Kirwan et al (2009). In this study obese people with T2D underwenth a 7 day vigorous training regeime (60min aerobic exercise at 70% of max aerobic capacity) and were tested for insulin sensitivity and insulin responsiveness before and after the intervention. The results found that exercise had increased both peripheral insulin sensitivity and responsiveness and it also surpressed hepatic glucose production.
Another benefit of exercise is its ability to stimulate vascular function. This is important in T2D as "mortality from T2D is largely attributable to atheroscelrotic macrovascular complications" (Maiorana et al, 2001). The benefit of two different types of exercise on this function will now be looked at. This includes studies by Maorana et al (2001) and Madden et al (2009). In these studies it was shown that both short term aerobic (3months) and medium term (16 weeks) combined aerobic and resistance training increased flow mediated dilation (1.7%-5%)(Maiorana et al, 2001) seen in the figure 3 below, and also reduced arterial stiffness (decrease of 20.7% in radial pulse wace velocity and 13.9% in femoral pulse wave velocity)(Madden et al, 2009). These are vital elements of the risk factors in cardiovascular disease which is associated with T2D and in such exercise can be used as a therapeutic aid.
Fig.3 Graph showing increase in flow mediated dilation (top) after exercise intervention (Maiorana et al, 2001).
Although exercise is widely accepted as a therapeutic form of treating people with T2D the mode and intensity of which exercise is best suited is often debated. The following table (table 1) looks at some different studies done on different types of exercise and each one's respective effects on treating T2D.
Dunstan et al, 2002
High intensity resistance training
Men, women (N=36) between 60-80 years
Intervention group: subjects completed HI resistance training and a moderate weight loss program
Control Group: subjects completed a moderate weight loss program
IRM bench and leg extension
Blood samples, plasma glucose, serum total cholesterol, triglycerides, serum insulin and insulin sensitivity (homestasis model)
HI resistance training was effective in improving glycaemic control in older populations with T2D, improved muscular strength was another benefit of this approach.
Castenenda et al, 2002
Moderate resistance training
Latino men/women N=62, average age=66
Intervention Group: subjects performed resistance sessions 3 times a week
Control Group subjects maintained normal daily activity levels
Glycemic and metabolic control, body composition, physical acitivity, muscle strength
Resistance training improved glycemic control, increased fat free mass, reduced abdominal adiposity, systolic blood pressure and increased muscle strength.
Sigal et al, 2007
Aerobic alone, resistance alone and both combined
Adults aged 39-70years, N=231
Combined Aerobic group and resistance group and
Trained 3 times a week for 22 weeks.
Haemoglobin levels, body composition, plasma lipid levels and blood pressure
The combined aerobic and resistance group improved glycemic control more so than either group alone.
Table.1 Studies showing effects of different modes and intensities of exercise on treatment of T2D.
As can be seen from this table all types of exercise benefit patients suffering with T2D with the greatest effects shown on programs that incorporate both an aerobic element and resistance element. This not only increases insulin sensitivity and secretion levels but also help fight obesity and increase muscular strength. There are a lot of considerations however when setting an exercise program for people with T2D and sometimes people may be limited to one type of training. Before setting off on an exercise program a person with T2D should: monitor blood glucose levels before, during and after a training session and consult a physician as different levels of T2D exist rangng from severe to moderate. Also when training athletes should reduce the amount of insulin they inject while training, this could be done by injectin insulin into sites that are not being used in the activity such as the stomach as insulin is absorbed more rapidly from sites involved in physical activity (UK Diabetes, 2008). However an interesting phenomenon described as the "athlete's paradox" has been developed by Dube et al (2007) in a study which they found that "endurance trained athletes who possess a high oxidative capacity and enhanced insulin sensitivity also have higher intamyocellular lipid content" (Dube, 2007). This is interesting as a high level of this substance is associated with developing T2D, however work is ongoing in the area and further studies are needed before being concerned with this phenomenon. Overall it can be seen that T2D has a complex pathophysiology and that exercise does work as a therapeutic aid in the fight against this growing disease.