Exercise & Type I Diabetes – A Scientific Overview

For information purposes only. Exercise at your own risk

Please note that (A surname in brackets) relates to the person who conducted a study and that “et al” just means ‘and colleagues’ i.e. that he/she had help from others to do the study.

‘To know Diabetes is to know medicine and healthcare’

(Haire-Joshu) 

Professional MMA fighter Jordan Williams has Type 1 diabetes. You can read more about him here.

Exercising with a medical condition generally requires additional supervision & precautions, but many sufferers still make it to the elite level.



The condition Diabetes Mellitus is no longer considered to be one disease, but is believed to be a group of diseases differing in etiology, biochemical features, and natural history.

Diabetes is generally characterised by a relative lack of insulin, but the acute insulin deprivation often occurring in the insulin dependent diabetes sufferers emphasises the crucial role of insulin in the regulation of metabolism (Groff, et al 1995).

Insulin has a variety of actions on metabolism, its importance being highlighted by its primary role in major functions including the controlling of glucose, decreasing hepatic glucose output, increasing glucose oxidation, glycogen deposition, lipogenesis, protein synthesis, and cell replication (Evans 2004).

The importance of insulin in the body is well documented, and Groff et al (1995) highlighted this by stating that ‘an absence of insulin not only inhibits the use of glucose by muscle and adipose tissue, but also sets into motion a sequence of events that, without effective intervention, will result in coma of the affected animal or human’. This paper will identify the metabolic and physiological effects of diabetes mellitus on the human body and the problems experienced by those affected by diabetes mellitus through participation in exercise. 

Exercise and Diabetes: An Overview

There are two types of Diabetes Mellitus, insulin-dependent (IDDM or type 1) and non-insulin dependent (NIDDM or type 2). This paper will concentrate on the difficulties associated with control of glucose levels during exercise in individuals affected with IDDM. IDDM is a less common form of the condition, which is not generally attributed to poor lifestyle.

This condition is generally caused by ‘an autoimmune process that destroys the beta cells of the pancreas causing an inability to produce insulin’ Colberg (2001) and is thought to have multi-factorial genetic influences (Onengut-Gumuscu and Concannon, 2005). One of the fundamental principles involved in controlling both conditions is the accurate regulation and maintenance of blood glucose levels. The participation in exercise then poses a problem as one of the fundamental metabolic facts involved in the exercise process is the use, and subsequent replenishment, of muscle glucose levels.

On this issue, Haire-Joshu (1992) stated that :

‘adding exercise to this issue often increases the difficulty in maintaining metabolic control since exercise, especially acute exercise bouts, can drastically alter the delicate balance of glucose’.

This was echoed by Komatsu et al (2005), who stated that ‘a persons exercise capacity is dependant on various physical factors such as neuromuscular activity, hemodynamics, respiratory mechanics, energy metabolism, and hormonal response. A decreased physiological performance of each of these can reflect in the limitation of exercise capacity’.
source/study

This highlights the sensitive process of glucose management, and the various problems arising from exercise. However, this does not mean that exercise should be avoided if you suffer from diabetes. In contrast, White (1994) found that ‘persons with NIDDM exercise has been shown to be a useful adjunct to diet for improved metabolic and weight control’. 

The role that exercise should play in the lives of diabetes sufferers may not be as clear as first thought. Exercise is of benefit in preventing, treating, and halting decline in a number of different illnesses, but its association with diabetes is less clear. It seems that diabetes is a condition suffered by people from all race, genders, and socio-economic backgrounds, with increased prevalence in certain races and society’s. 

Diabetes: Epidemiology and Demographics

Diabetes is widespread. It is ranked as one of the most common chronic diseases. In 1993, there were 11 million people who were living with the condition in the United States of America alone (Groff, et al 1995). With the levels of obesity reaching almost epidemic proportion, levels of non-insulin dependant (NIDDM or type 2) diabetes are also increasing. This was highlighted by Colberg (2001) who stated that ‘increasing incidence of type 2 diabetes is associated with a decreasing level of physical activity and an increasing prevalence in obesity’. 

According to Haire-Joshu (1992) ‘diabetes is a clinical syndrome characterised by inappropriate hyperglycaemia caused by a relative or absolute deficiency of insulin or by a resistance to the action of insulin’.
source

In 1992, it was thought that up to 200 million people suffered from a form of the condition, with 90% of the 12 million sufferers diagnosed in the USA living with NIDDM, and 18% of their 65 to 74 year old population diagnosed with NIDDM. As an example, direct medical costs in USA in 1992 accounted for 43% of total costs for diabetes as compared with only 22% for cancer, 27% for circulatory disease, and 11% for musculoskeletal diseases ( White, 1994). 

There is also high prevalence of the condition in minority groups, with NIDDM being twice as common in blacks, and five times as common in Hispanics. ‘This cannot be attributed solely to the high obesity rates in Hispanics, as NIDDM levels are high even when adiposity and socio-economic status are controlled’ White (1994). 

Clinical research in the west has focused exclusively on diabetes as a physical disorder, and hence the treatments that have been researched have involved stimulating the pancreas through drugs, or by controlling the glucose levels by dietary restrictions, artificial insulin, and more recently, by physical exercise. Clinical research in India, by contrast, has recognized that diabetes is a ‘psychosomatic disorder, in which the causative factors are sedentary habits, physical, emotional and mental stress and strain’ Franz (1996). To an IDDM sufferer, the process of glucose control during exercise is one of the most important aspects of managing their condition.

Glucose Levels during Exercise During exercise, it is imperative that a working muscle is supplied with adequate amounts of oxygen, as is the ability to process and maintain muscle glucose at an acceptable level.

On this issue, Franz (1996) stated that

‘blood glucose during long-duration exercise in non-diabetic persons is maintained at a fairly stable level despite what can be a twenty fold increase in whole body oxygen, five to six fold increase in cardiac output, and an even greater increase in blood flow and oxygen consumption in the working muscles’. 

During intense exercise, the production of adenosine triphosphate (ATP) is determined by the availability of blood glucose and muscle glycogen. Though it is possible to perform light exercise with low levels of these fuels, depletion results in an inability for the muscles to sustain the contractile tension needed. If carbohydrate levels are low, utilisation of fat and protein can occur in order to generate the required energy, but this is still inadequate when compared to the energy derived from carbohydrates. In general, carbohydrate is recommended during exercise due to its rapid metabolism and absorption compared to fat and protein. 

The type of carbohydrate that is ingested can affect the potential rate of glycogen repletion. To identify this, Colberg ( 2001) measured blood sugar levels in individuals affected with IDDM post exercise. Individuals had fasted for 24 hours before being fed either glucose, white bread, or nothing and completing a period of exercise. The exercise consisted of 45 minutes of riding a cycle ergometer at 60% of maximal aerobic capacity (VO2 max, )in the morning before an injection of insulin. Without any glucose, blood sugar levels fell slightly despite having the lowest levels of circulating insulin in the morning. However, intake of 30g of glucose resulted in an excessive rise in blood sugar levels. Glucose ingestion resulted in twice the increase in blood sugars as the ingestion of white bread due to the differing glycemic indexes (GI). 

This study indicates effective management of factors affecting the rate at which glycogen stores are replenished is paramount as different carbohydrates will have differing rates of absorption according to their glycemic indexes. Alterations in Fuel Metabolism Pre and During Exercise in Persons with IDDM A major determinant of the body’s response to exercise is related to insulin availability pre-exercise. The fuel reserves of the body are affected due to often fluctuating insulin levels pre-event. Due to this fluctuation, important stores such as muscle and blood glucose are affected. 

In persons with IDDM, metabolic control is best achieved by a regular or consistent life-style that includes regular meals and snacks covered by a controlled amount of insulin. A homeostatic balance gained through frequent snacks and adequate insulin intake will inhibit the acceleration into hypoglycaemia or hyperglycaemia that would occur if the condition was poorly managed.

As an IDDM sufferer is unable to produce sufficient amount of insulin to help control the rate of glycolosis, without the introduction of insulin, exercise often resulted in a more pronounced hyperglycaemia. When treated with insulin, blood glucose levels have been shown to fall. This metabolic response varies depending on the availability of insulin at the start of exercise. Too little circulating insulin during exercise can lead to an excessive hormonal response that may elevate blood glucose levels and ketone body production.

An example of the differing effects of circulating insulin has been highlighted by Haire-Joshu (1992) who found that

‘in nonketotic persons with diabetes with mild to moderate hyperglycaemia, moderately heavy exercise 24 hours after insulin withdrawal causes blood glucose to fall. In contrast, in persons with more severe hyperglycaemia and mild ketonemia, exercise causes a significant rise in blood glucose concentration’.

This could be attributed to an overproduction of glucose from the liver or under use by the working muscles. 

Another affecting factor could be the enhancement of lipolysis during insulin deficiency which would increase the ketone and free fatty acid (FFA) levels in the blood, resulting in an inhibition of glucose uptake by the muscles.

This affecting factor was highlighted by Gordon (1993), who stated that

‘concentrations of free fatty acids increase at low insulin levels, such as what occurs during exercise or with uncontrolled diabetes, and the use of FFA in muscle increases’.

In general, the importance of FFA as a fuel, relative to carbohydrate, increases with the duration, and decreases as the exercise intensity increases. The increase in FFA lipolysis can be attributed to an increase in ketone plasma levels, and an increase in exercise.

On the relationship between increased ketone levels and increased FFA lipolysis, White (1994) stated that recent studies have suggested that ‘a defect in peripheral clearance of ketones is a major affecting factor resulting in an increase of FFA lipolysis’. An increase in exercise levels has also been attributed to this increase in FFA lipolysis.

This is due to increased ketone levels, as in severely insulin deficient persons with diabetes and hyperketonemia, strenuous exercise causes a further rise in blood ketone body levels’ White (1994). An increase in lipolysis from increased ketone levels during hypoglycaemia increases the importance of fats as a fuel, and emphasises the usability of ketones in effective metabolism. Plasma Ketone Levels During Exercise The plasma ketone levels are normally held at a low level, but may increase in situations of accelerated FFA oxidation and low carbohydrate intake or impaired use. Also, the inadequate supply of blood glucose reduces the oxaloacetate levels which inhibits the rate of oxidation through the Krebs cycle. As glucose levels diminish, the body will cease to catabolise glucose, and catabolise FFA in its place. The rate of FFA oxidation will then accelerate in order to replace the lack of energy being made available. This shift to fat catabolism, and a decrease in oxaloacetate levels, would result in an increase in ketone levels.

Even though ketone bodies make no effective contribution to the fuel supply of muscles (Evans 2004), the livers ability to distribute the ketone bodies to peripheral areas of the body results in ketone bodies providing benefit. On this issue, Groff et al (1995) stated ‘the livers ability to deliver ketone bodies to peripheral tissues such as the brain is an important mechanism for providing fuel in periods of starvation‘. 

In mild-kenotic persons with IDDM, the ability to use ketone bodies effectively during exercise is found.

According to Evans (2004)

‘recent studies suggest that a defect in peripheral clearance of ketone rather than a marked increase in ketogenesis during exercise in insulin-deprived individuals is the major factor’.

As the metabolising of muscle and blood glucose stores is an issue for sufferers of IDDM and NIDDM, the process of FFA oxidation through an increase in ketone levels will benefit the person. Even though high levels of ketone in circulating blood can disturb the body’s acid base balance (Groff et al 1995), it becomes a necessary process to provide the body with an energy source in the form of FFA.

This also highlights the responsibility of the liver during possible hypoglycaemia. Plasma Free Fatty Acid (FFA) Concentrations As stated, the levels of FFA increase when insulin levels are low. In IDDM persons, metabolising their plasma FFA levels efficiently increases in importance as the intensity of the activity increases. On a study identifying FFA levels during exercise in an IDDM sufferer, Evans (2004) identified that ‘during prolonged exercise at a low intensity (40% of VO2 max ), FFA oxidation accounts for approximately 60% of muscle oxygen consumption’. The rate of FFA uptake is not dependent of insulin as such, but there are high levels of plasma FFA in hypoglycaemic IDDM sufferers.

The relationship between FFA levels, whether basal levels of a ketotic diabetic sufferer or of one poorly managing their condition, and its utilisation by working muscles has produced a plethora of research documenting their relationship. In non-diabetic suffers, an initial decline in FFA levels during exercise is expected to be followed by a gradual rise as plasma FFA as lipolysis occurs. 

In contrast to this, Evans (2004) stated that ‘persons with diabetes with marked hyperglycaemia and ketosis already show an elevated FFA level at rest, and the rise during exercise is more marked’. As a result of this greater availability of FFA, uptake of FFA by working muscles is increased. On this issue, Haire-Joshu (1992) stated that ‘in mildly ketonic persons with diabetes, a sevenfold increase in FFA uptake by muscles was shown, as compared with a three to four fold increment in non-diabetics’. 

Hormone Regulation During Exercise Although one of the fundamental principles of the IDDM form of diabetes mellitus is often the regulation of glucose due to the lack of insulin present to regulate glucose production, persons with IDDM diabetes may have a higher level of plasma insulin present. This in turn leads to a decrease in plasma glucose which also leads to an inhibition of both gluconeogenesis and glycogenesis due to the high insulin levels present.

The counterregulatory hormones, along with insulin, monitor glucose production, but even if the counterregulatory response is high ‘the hepatic glucose production cannot match the rate of peripheral glucose use, and blood glucose falls’ Haire-Joshu (1992). The counterregulatory hormones involved, mainly glucagon, play a large part in keeping a homeostatic glucose balance during exercise. Adrenaline, which reflects the ‘fight or flight’ sympathetic system activation, has been shown to be ‘of major importance in stimulating glycogenolysis in both liver and muscle and in stimulating lipolysis in adipose tissue.

An increase in response to high intensity exercise or declining blood glucose also stimulates hepatic glycogenolysis and lipolysis’. The use of other hormones, such as growth hormone, are less important to glucose control as they are less vital during short term exercise, but they become effective as the duration of the exercise increases. On this, Haire-Joshu (1992) stated that ‘growth hormone is less important in response to short-term exercise, but they increase lipolysis, decrease insulin-stimulated glucose uptake in peripheral tissues, and increase hepatic gluconeogenesis over longer periods of exercise’.

As shown, poor working of counterregulatory hormones, along with insulin production, are major effecting factors. The impact that poor counterregulatory hormone control can have has been highlighted by White (1994) who explored persons who exercise when in moderately poor control of their diabetes. After the resulting increase in glucoregulatory hormone secretion, he stated that ‘ insulin deficiency plus a high concentration of counterregulatory hormones enhances gluconeogenesis at levels 2 to 3 times those seen in nondiabetic persons, resulting in an exaggerated increase in hepatic glucose production and circulating plasma glucose concentrations’. 

Post-Exercise Glucose Levels

After exercise, at most intensity’s, muscle glycogen stores are mostly depleted. Replenishment of these stores can often take several hours, and begins with an increased insulin sensitivity of the exercised muscles. According to Rasta’s et al (2004), ‘whole body insulin sensitivity has been found to be increased for at least 48 hours following 1 hour of bicycling at a moderate intensity’. This resulting increase in insulin sensitivity will probably result in hypoglycaemia in athletes with IDDM.

The 48 hour duration post-exercise where a diabetic athlete is at risk of becoming hypoglycaemic without adequate intervention is one that was the basis of a study carried out by Evans (2004). He investigated the effects of different insulin adjustments in nine persons with IDDM. When hypoglycaemia occurred, it was noted 5 hours after exercise 5 out of 8 times. A similar study carried out by McDonald (1987) selected 300 young people with IDDM. Post-exercise hypoglycaemia occurred in 48 of the subjects during the two year study period. The incidence of hypoglycaemia varied from 3 to 31 hours after exercise, but was most common 6 to 15 hours after exercise. Hypoglycaemia 1 or 2 hours after exercise was relatively uncommon. He concluded by stating that ‘the incidence of hypoglycaemia varied from 3 to 31 hours after exercise, but was most common between 6 and 15 hours after exercise’ (McDonald 1987). The above study highlights the importance of taking on carbohydrates straight after exercise to replenish the spent stores. If none are ingested, they may become hypoglycaemic within 6, or even 31 hours of exercise. 

Conclusion

With one of the fundamental factors of diabetes being the management of glucose levels, diabetic athletes have to have a good knowledge of contributing factors in order to effectively control the condition. It has been shown that exercise is not to be avoided if you are a diabetes sufferer. In fact in NIDDM, it is of paramount importance in controlling the condition and the general poor lifestyle which may have contributed to its onset. The issue of exercise to an IDDM sufferer is less clear. It is the less common form of the condition and seems to be linked to ones genetics.

The condition is controlled by regular injections of insulin and adequate carbohydrate consumption. To a person exercising with the IDDM condition, the type of carbohydrate consumed is important as the GI of the food needs to be taken into consideration.

The time of ingestion of the carbohydrate is also a factor as research has been cited showing that the onset of hypoglycaemia can occur after 6 hours and up to 31 hours later. In IDDM, the inhibition of replenishing glucose stores leads to possible hypoglycaemia, or ketosis due to increased ketone levels in the blood, and this in turn leads to increased fat metabolism by the working muscles.

These adverse factors only occur from poor management of the condition, and exercise is not directly attributed to hypoglycaemia or hyperglycaemia. In summary, the body deals with the loss of insulin by placing a number of systematic processes in place in order to provide the muscles with the necessary fuel. These processes are all related to the metabolism of FFA to counter the lack of glucose present. Careful dietary control both in terms of what is consumed and when, is particularly important for diabetics when engaging in exercise.

About Drew

MMA, Fitness & Marketing enthusiast from North Wales, UK. A Stoic Hippy with no hair. Not to boast but - 1st Class Degree in Sports Science from Loughborough, MSc in Nutrition from the University of Liverpool. 20 years experience of weight & fitness training.
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