Health Related Physical Fitness in Persons with Type I Diabetes - KIN 500

Health Related Physical Fitness in Persons with Type I Diabetes
KIN 500
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Instructor:	Dr. Darren Warburton
	Kyra Dickinson
	Oliver Finlay
	Yanfei Guan
	Nana Wu
Email:	darren.warburton@ubc.ca
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Health-Related Physical Fitness in Persons with Type I Diabetes

Background

What is Type I Diabetes?

Type 1 diabetes mellitus (T1D) is a chronic disease characterized by hyperglycemia and induced by immuno-mediated or idiopathic beta-cell destruction, leading to lack of insulin production (Turinese, 2017). Insulin therapy is the most common treatment for T1D, however, extensive research investigates the benefits of a more holistic approach to the prevention and maintenance of this disease. It is thought that optimal treatment should include intervention on cardiovascular risk factors, as well as integrating pharmacological treatments and lifestyle changes (Turinese, 2017).

Statistics

According to the Juvenile Diabetes Research Foundation (JDRF):

More than 300,000 Canadians live with T1D
The rate of T1D incidence among children under the age of 14 is estimated to increase by 3% annually worldwide
The life expectancy for people with T1D may be shortened by as much as 15 years
40,000 people are diagnosed with T1D each year in the U.S
Between 2001 and 2009 there was a 21% increase in the prevalence of T1D in people under age 20
$14 billion T1D-associated annual healthcare costs in the U.S

According to the Children's Diabetic Foundation:

An estimated 9 to 10% of all diabetics, including children and adults, are insulin-dependent
The Canadian Diabetes Association forecasts that diabetes will affect nearly 11% of the population by the year 2020
Approximately one million Canadians currently have diabetes without knowing it
According to the Canadian Pediatric Society, 33,000 school age children (5-18 years old) in Canada have T1D

Effects of Exercise on Metabolic Conditions

Glucose Metabolism

Physical exercise for patients with type 1 diabetes (T1D), although may seem simple to execute, harvests its own set of internal risks. The role of exercise has been studied extensively in these patients, resulting in scattered findings, with some actually revealing the worsening of glycemic control associated with exercise (Bally, 2015).

During exercise in healthy individuals, the skeletal muscle recruits local glucose and converts muscle glycogen to glucose to use as energy. This exercise-associated glucose balance is maintained by a complex hormone interplay with insulin acting as the agent that lowers glucose levels. Exercise in these healthy individuals down regulates insulin, balancing the overstimulation of GLUT4 in skeletal muscle, and increases hepatic glycogenolysis, the break down of glycogen to glucose, to maintain the insulin homeostasis and normoglycemia**. On the other hand, this pathway is compromised in patients with T1D, resulting in the need for insulin therapy to make up for the natural endogenous insulin equilibrium that the body lacks. Patients with T1D live with the fear of exercise-related hypoglycaemia*, often times deterring them from taking part in any physical activity despite desires or one’s previous lifestyle (Bally, 2017). However, one can draw some similarities between persons living with and without T1D, being that under normoglycemic conditions during aerobic exercise with the near physiological insulin doses, patients with T1D maintain normal shifts in oxidation from carbohydrates to lipids. The metabolic mechanisms under hyperglycemic*** conditions during exercise remain misunderstood and unclear (Bally, 2015).

Another condition that arises as a potential issue in patients with T1D is diabetic ketoacidosis (DKA). DKA can be defined as a state of absolute or relative insulin deficiency (Joseph, 2008). DKA occurs when the body is being deprived of the required glucose due to lack of insulin the in the body, is often associated with the body being in a hypoglycaemic state, resulting in more serious outcomes such as seizures, coma, or even death (Li, 2014), as the body is unable to utilize accumulated ketones and acids for energy. As it relates to exercise, patients suffering from T1D remain more susceptible to hypoglycaemia, because of the lack of natural physiological glucose regulation, as opposed to insulin-regulated glucose.

It is important to note that although insulin therapy is on the forefront when it comes to regulating exercise-related glucose metabolism of diabetic patients, other important determinants of glucose metabolism include the duration, intensity, and timing of exercise, glucose levels pre-exercise, and pre- and post-exercise nutrition (Bally, 2015).

*hypoglycaemia = low blood glucose, less than 4.0mmoL
**normoglycaemia = normal blood glucose, 7.8mmoL
***hyperglycaemia = high blood glucose, above 11mmoL

Hormonal Response

The human body is constantly adjusting to the stresses that we unknowingly put on our bodies by way of hormone regulation. Patients with T1D in many ways are no different from healthy individuals, however critical hormonal pathways are compromised because of this disease. During exercise, T1D patients undergo a different hormonal response than that of a healthy individual because of the potential glucose increasing effect, which acts as antagonists to insulin or other counter-regulatory hormones such as cortisol, growth hormone (GH), and catecholamines (Bally, 2015).

These critical hormone responses have potential to lead to some aforementioned conditions such as hypoglycemia. Studies have shown that repetitive hypoglycaemia prior to exercise may reduce the secretion of counter-regulatory hormones, which in turn increases the risk of exercise-associated hypoglycaemia (Bally, 2015). There are also sex-differences when it comes to the hormonal regulation responses during exercise in normoglycemic conditions. These differences reveal that there is a reduced increase in catecholamines and GH in female patients with T1D (Bally, 2015).

Specific to GH during exercise, individuals with T1D are at risk of experiencing defects in secretion that contribute to an imbalance in the counter-regulation during exercise and in a hypoglycemic state (Bally, 2015). However, studies show that this is not entirely consistent within the entire T1D community, as some results revealed that under highly standardized conditions, exercise-induced secretion of GH in patients with T1D with good metabolic control is in fact comparable to the levels of a healthy individual (Bally 2015).

Dietary Considerations

Individuals living with T1D are tasked with the responsibility of not only adjusting insulin doses, but also potentially making dietary adjustments to cater to their disease. As dietary considerations relate to exercise for individuals with T1D, carbohydrates are the number one culprit. Carbohydrate ingestion is directly related to the blood-glucose state that an individual can be in, which can send the body into adverse metabolic states, whether it is hypo- or hyperglycaemic.

Carbohydrates as a general term can be categorized into different substances. For example, fructose and glucose are both carbohydrates, however, they metabolize differently, and use different enzymes to do so. Fructose is a monosaccharide absorbed through transporter GLUT5, extracted by the liver, metabolized, and can be used by other organs (Bally, 2017). Interestingly enough, fructose can and does act as an alternative energy source from glucose, without the need for insulin (Bally, 2017). This finding especially peaks the interest for individuals living with T1D, as studies have explored the efficacy of co-ingestion of glucose and fructose (Bally, 2017). It remains as future research to further study the specific types of carbohydrates, their interactions with insulin before, during and after exercise, and the mechanisms, as currently the knowledge is still quite underdeveloped.

Foods high in carbohydrates:

Sugary drinks
Sweets
Pastries
Ice cream
Bread
Pasta
Potatoes
Rice

Many studies have investigated the idea of have a carbohydrate schedule that couples with exercise and insulin administration as a way of mitigating the risks against hypoglycaemia (Bally, 2017). A 2017 study revealed some practical implications as they used a glucose-fructose co-ingestion and exercise intervention for individuals with T1D and found that by reducing the carbohydrate supplementation using co-ingestion, not only was it more convenient for the patients, but also exercise became much safer (Bally, 2017), as patients were at less risk for adverse metabolic conditions.

Additionally, another 2017 study investigated different intensity and durations exercise interventions, and how this relates to carbohydrate intake and potential effects on metabolic states. It was found that in order to mitigate the risks of hypoglycaemia during prolonged aerobic exercise, additional carbohydrate intake coupled with a reduction in insulin is required. For low to moderate intensity aerobic exercise (30-60 minutes) under basal conditions, 10-15g a carbohydrates will avoid hypoglycaemia. Lastly, during exercise in a hyperinsulinemic state (after bolus insulin), 30-60g of carbohydrates is recommended per hour of exercise; and oddly enough, this recommendation is consistent to optimize performance in healthy individuals under similar conditions (Yardley, 2017).

Insulin Therapy

Insulin therapy is the most common and effective way to manage T1D. This treatment includes exogenous insulin injected subcutaneously, in comparison to the physiological portal insulin secretion in healthy individuals (Bally, 2015). This difference in the distribution and administration of insulin plays a role in this continuous imbalance as it related to peripheral insulin levels versus portal insulin levels. However, we must not only take into account the pathway insulin takes to get into the body, but the time at which insulin is injected. For healthy individuals, insulin remains as a natural physiological feedback loop regulated by blood-glucose levels, however, patients with T1D lack this ability causing unsteady and inconsistent insulin requirements based blood-glucose levels throughout the day.

Modern day patients with T1D receive insulin therapy consisting of multiple daily injections of rapid-acting insulin and long-acting basal insulin, or continuous subcutaneous insulin infusion (CSII), where almost instant reductions in insulin delivery are possible (Bally, 2015). Although each of these treatment methods proves to be effective, the primary difference between them is the flexibility maintained for rapid dose adjustments (Bally, 2015). Majority of patients decide against CSII, yet still remain regularly active, heightening the risk of adverse metabolic conditions such as hypoglycaemia, which often times takes place during and after exercise, hence why insulin doses should be reduced pre- and post-exercise. With the development and research of insulin therapy and how detrimental it is to one’s lifestyle, patients with T1D are afforded with the options to best suit their desired lifestyle without compromising metabolic health, whilst keeping the disease under control.

Seemingly simple medications that a healthy individual may take regularly or as necessary may have some serious adverse effects on an individual with T1D. For example, studies have showed that corticosteroids taken for asthma or arthritis have been associated with hyperglycaemia in individuals with T1D (Yardley, 2017). Additionally, the mental health population with T1D struggle with an array of adverse effects between insulin therapy and prescribed atypical antipsychotic drugs. As it relates to exercise the most detrimental factor would be these antipsychotic drugs reducing insulin sensitivity, causing hyperglycaemia and dehydration, putting the individual at greater risk during exercise (Yardley, 2017). Medications using phenylephrine and/or pseudoephedrine as active ingredients, including some cold and flu medications, can also lead to hyperglycaemia in patients with T1D (Yardley, 2017).

Influence of Exercise on Cardiovascular Parameters

Patients with type 1 diabetes (T1D) are at risk of high blood pressure, triacylglycerol and LDL-cholesterol, and low levels of HDL-cholesterol. These factors are related to higher risk of cardiovascular disease. Exercise can reduce the future risk of cardiovascular disease in patients with T1D, through lowering lipid levels, blood pressure, and blood sugar, and through improving body composition and quality of life. However, some previously published study also reported no changes of these outcomes in people with T1D (MacMillan et al., 2014). The heterogeneity of outcomes in these literatures may be due to many reasons including considerable variation in intervention characteristics such as program duration, prescription of exercise (combination of frequency, duration, intensity), setting (e.g. home-based, laboratory, community-based), as is now debated may be the case of cardiovascular risk factors findings in this review.

Exercise and Blood Pressure

High blood pressure (hypertension) is highly prevalent in individuals with T1D. Hypertension can lead to many complications with diabetes, including diabetic eye disease and kidney disease, or make diabetic complications. A meta-analysis of 54 randomized trials found that aerobic exercise was associated with an average reduction of 4.9/3.7 mm Hg in hypertensive patients (Whelton, Chin, Xin, & He, 2002), while consistent evidence for the benefits of exercise training on blood pressure in T1D is rare. In four prospective intervention studies, systolic and/or diastolic blood pressure were measured before and after the intervention in intervention and control or comparison groups. Salem et al. reported that a significant reduction in diastolic blood pressure of adolescents with T1D adhered to 6 months supervised intensive exercise protocol (Salem, Aboelasrar, Elbarbary, Elhilaly, & Refaat, 2010). Lehmann et al. examined adult patients with T1D and engaged in an endurance exercise program involving at least 135 min per week for 3 months, and found that systolic and diastolic blood pressure decreased significantly from 127 +/- 9 to 124 +/- 8 (P < 0.05) and from 80 +/- 5 to 77 +/- 5 mmHg (P < 0.01), respectively (Lehmann, Kaplan, Bingisser, Bloch, & Spinas, 1997). Fuchsjager-Mayrl et al. and Rigla et al. found no significant difference in change in blood pressure in adults after a 3-month intervention (Fuchsjager-Mayrl et al., 2002; Rigla et al., 2000).

Exercise and Glycemic Control

Exercise can influence glycemic control through different pathways. Some observational studies have shown that increased exertion is associated with a lower glycosylated A1C among persons with T1D (Herbst, Kordonouri, Schwab, Schmidt, & Holl, 2007). In fact, cross-sectional studies regard regular exercise as a strong indicator of A1C in patients with T1D (Herbst et al., 2007). However, randomized controlled trails focusing on the efficacy of exercise in improving glycemic control have yielded different results. Some studies, especially those of higher physical activity and/or frequency of physical activity, report better outcome of clinically meaningful 0.4% to 1.2% absolute decrease in A1C in patients with T1D. (Campaigne, Gilliam, Spencer, Lampman, & Schork, 1984; Salem et al., 2010) In contrast, some randomized controlled trails found no difference in glycemic control between the exercise intervention group and controls. The difference may be due to the heterogeneity of participants’ inclusion criteria (age, duration of diabetes, A1C level) heterogeneity in the intervention (combination of frequency, duration, intensity). A meta-analysis of 11 randomized controlled trials evaluated 345 participants with T1D. When compared with not exercising, exercise training led to a statistically significant decrease of 0.52, showing that exercise is a beneficial option in the management of glycemic control for T1D (Quirk, Blake, Tennyson, Randell, & Glazebrook, 2014a).

Exercise and Physical Fitness

Exercise can play an important role in improving fitness. Many studies measured changes in various parameters of fitness and supported a positive effect of intervention in some area of fitness, such as improved cardiovascular fitness (Baevre, Sovik, Wisnes, & Heiervang, 1985; Campaigne et al., 1984; Faulkner, Michaliszyn, & Hepworth, 2010; Huttunen et al., 1989; Landt, Campaigne, James, & Sperling, 1985; Michaliszyn & Faulkner, 2010; Mosher, Nash, Perry, LaPerriere, & Goldberg, 1998; Newton, Wiltshire, & Elley, 2009; Rowland, Swadba, Biggs, Burke, & Reiter, 1985; Seeger et al., 2011; Sideraviciute, Gailiuniene, Visagurskiene, & Vizbaraite, 2006). Quirk et al. conducted a systematic review with meta-analysis including three randomized controlled trails and found a nonsignificant effect of exercise on maximal O2 consumption (VO2max) [standard mean difference 0.24; p=0.33](Quirk, Blake, Tennyson, Randell, & Glazebrook, 2014b).

Exercise and Lipid Profile

Patients with T1D often have less atherogenic fasting total lipid levels than controls, despite increased CVD (Janet K. Snell-Bergeon & Kristen Nadeau, 2012). Bishop et al. report that individuals with T1D have significantly lower triglycerides, total cholesterol, and LDL cholesterol and higher HDL cholesterol (Bishop et al., 2009). A meta-analysis of 5 randomized controlled trials (206 participants with T1D) found a significant reduction of 0.7 in triglycerides, a significant reduction of 0.91 in total cholesterol comparing not exercising, and nonsignificant of exercise on LDL cholesterol and HDL cholesterol (Quirk et al., 2014a). After a 12-week endurance and strength exercise program of three times a week in patients who had T1D, there was an increase in HDL cholesterol and decrease in LDL cholesterol (Mosher et al., 1998). Therefore, exercise intervention seems to improve the lipid profile with increase in HDL cholesterol, reduction in LDL cholesterol, triglycerides, total cholesterol, and may protect against cardiovascular disease. However, the dose of exercise training, rather than the intensity of exercise, may be a more important determinant of lipoprotein particle size, it is important for patients to engage in frequent and regular exercise. Exercise is apt for decreasing blood pressure, glycosylated A1C and improving physical fitness, lipid profile in patients living with type 1 diabetes. However, some studies have reported contradictory ﬁndings: exercise has no effects on cardiovascular disease risk factors. The mechanism underlying this increase is not yet fully understood. Further studies are required on the timing and method of exercise and the inﬂuence of the period on cardiovascular disease risk factors such as blood pressure, glycemic control and lipid profile.

Musculoskeletal Disorders

Introduction

It has been shown that there is an increased incidence of musculoskeletal complications in both type 1 and type 2 diabetic patients, and these complications are likely to cause further health problems and impact overall quality of life (Ardic, Soyupek, Kahraman, & Yorgancıoglu, 2003). The majority of musculoskeletal complications occurred in upper extremities, especially hands and shoulders, include limited joint mobility, Dupuytren’s disease, shoulder capsulitis (frozen shoulder), neuropathic arthropathy, flexor tenosynovitis, and carpal tunnel syndrome (Arkkila & Gautier, 2003). Although the incidence of musculoskeletal complications in lower extremities is not as high as upper extremity, they are more disabling – for instance, Charcot’s arthropathy, osteomyelitis, and diabetic foot. The understanding of the prevalence, pathogenesis, diagnosis, and treatment of musculoskeletal complications in diabetic patients is helpful for the therapy programs and further research in this area.

Prevalence

Cagliero, Apruzzese, Perlmutter, & Nathan (2002) reported the incidence of muscuskeletal complications (adhesive capsulitis, carpal tunnel syndrome, Dupuytren’s disease, and flexor tenosynovitis) of 100 type 1 and 100 type 2 diabetic patients and 100 control patients. The results showed that diabetic patients had a significantly higher prevalence of adhesive capsulitis (12% vs. 0%, P < 0.01), Dupuytren’s disease (16% vs. 3%, P < 0.01), flexor tenosynovitis (16% vs. 3%, P < 0.01), carpal tunnel syndrome (12% vs. 2%, P < 0.04) than control patients. Overall, the prevalence of musculoskeletal complications was significantly higher in diabetic patients than controls (36% vs. 9%, P < 0.01). In addition, the study showed that the types of diabetics and sex difference are factors that influence the prevalence. A higher prevalence was found in patients with T1D compared to type 2 diabetes, and it is also higher in female diabetic patients than males (Cagliero, Apruzzese, Perlmutter, & Nathan, 2002). Another study systematically analyzed the prevalence of muscuskeletal complications in patients with and without diabetes, and found similar results: the incidence of adhesive capsulitis, limited joint mobility, Dupuytren’s contracture, carpal tunnel syndrome, flexor tenosynovitis and diffuse idiopathic skeletal hyperostosis is much higher in diabetic patients than people without diabetes (Smith, Burnet, & McNeil, 2003). While as the improvement in diabetes treatment and higher standard of glycemic control, a survey in UK diabetic population showed that the prevalence of limited joint mobility had decreased form 43% to 23% between the 1980s and 2002 (Lindsay et al., 2005). However, the incidence of limited joint mobility showed an increasing trend with longer duration of diabetics (Lindsay et al., 2005). Based on findings of previous research, it can be concluded that diabetic patients have an increased chance to be influenced by muscuskeletal complications compared to people without diabetes. Diabetic patients and physicians should be aware of related conditions and get them treated at the early stages.

Clinical Features and Diagnosis

Limited joint mobility (LJM), also known as diabetic stiff hand syndrome or diabetic cheiroarthopathy, is characterized by tight, thick skin on the dorsum of the hand, increased resistance of joint passive extension, and limited mobility of the metacarpophalangeal joints (Chammas et al., 1995). Clinically, LJM can be diagnosed through the disability of folding two palms completely together with the wrists reaching the greatest flexion, or failure of any joint to make contact (Arkkila & Gautier, 2003). The severity of LJM can be reflected by the joint movement and goniometrically measured. Normally, LJM is not painful and disabling enough to seek treatment (Chammas et al., 1995).

Dupuytren’s disease (DD), or Dupuytren’s contracture, is characterized by digital or palmar thickening, tethering or contracture of the hands (Smith et al., 2003). For diabetic patients, DD mostly affects the bilateral middle and ring fingers, resulting in certain degree of deformity when flexing the fingers.

Shoulder capsulitis (SC), is a syndrome of pain, stiffness and inability in shoulder for a few months. It is clinically diagnosed by restricted range of movement of shoulder joint in at three planes.

Neuropathic arthropathy is a destructive arthropathy with progressive degeneration of a weight bearing joint, marked by bone destruction, bone resorption, and even deformity finally, which can lead to sensory loss of an area, and most happens in the tarsometatarsal and tarsal joints. The clinical diagnosis of neuropathic arthropathy is based on evident unilateral swelling, raised skin temperature, joint instability and effusion (Bálint, Korda, Hangody, & Bálint, 2003).

Carpal tunnel syndrome (CTS) is caused by the compression of the median nerve as it travels through the wrist at the carpal tunnel (Burton, Chesterton, & Davenport, 2014). The symptoms include paraesthesia like pain and numbness in the thumb, index, middle, and lateral side of the ring fingers (Smith et al., 2003).

Treatment

For curing musculoskeletal disorders in diabetic patients, there are no specific programs or medications, however, physical activity interventions have proved to be an optimal treatment. Physical activities that include strength, aerobic and anaerobic training is perceived beneficial to glycemic control and physical functioning improvement in diabetic patients (Backonja et al., 1999), which may help reducing or curing the musculoskeletal disorders. Additionally, the non-pharmacological, low cost nature, and other benefits to the cardiovascular and aerobic health, are important factors in recognizing physical activity as the best choice in treating musculoskeletal disorders. For specific disorders, for example, LJM or DD, in addition to optimizing glycemic control through exercise, individualized therapy or surgery is an alternative treatment. Overall, in preventing diabetic hand/shoulder complications, the flexor tendon stretching and strengthening exercises may be effective. In treating lower-extremity complications, good hygiene and stretching of the plantar fascia, lower extremities, and strengthening exercises would also be useful (Lindsay et al., 2005). According to Bálint (2003), an important part of treatment is the confirmation of diagnosis to the patients, and ensure the patients acquiring direction and treatment from the physicians before further deterioration. However, preventing diabetic complications by well glycemic control, is the most important and effective in reducing the affection of musculoskeletal disorders in diabetic patients.

High Performance

Physiology

In high performance athletes, the engagement in higher-intensity and more prolonged bouts of exercise, be it in training or game-play, demands that the body will utilise greater amounts of carbohydrates than at lower exercise intensities, where lipids may also provide a useful fuel source. Subsequently, if the activity is sustained, muscle glycogen and blood glucose stores may become depleted. This glycogen store depletion is increased during bouts of higher-intensity, repeated interval training, as the preferred fuel source switches to muscle glycogen stores and consequently, the risk of hypoglycaemia increases.

In contrast, shorter, more intense activities performed in isolated bouts, such as sprinting or power lifting, are predominantly anaerobic activities, which result in muscles rapidly utilising high energy phosphate compounds, and, only consume intramuscular stores of glycogen if the bouts extend beyond ten seconds in duration.

The endocrinological response to high-intensity, and stressful competitive exercise must also be considered. Release of epinephrine and cortisol caused by significant sympathetic nervous system responses in stress situations, will raise blood glucose levels. Subsequently, a transient hyperglycaemic response can be brought about, which requires an administration of insulin to correct. If such a response remains uncorrected, elevated blood glucose levels may remain for up to three hours post exercise, irrespective of pre-exertional levels.

Athletes must guard against hypoglycaemia resulting from ongoing muscle glycogen replacement in muscles post-exercise, which is largely insulin independent, until glycogen levels increase, particularly during the “window of opportunity” from 30 minutes up to two hours after physical activity.

Athletes with type 1 diabetes who train regularly, generally exhibit a heightened sensitivity to insulin, which allows more efficient uptake of blood glucose into muscle cells both acutely and chronically with exercise. Acute changes are likely related to heightened muscle glycogen repletion following physical exertion, although some results have reported an unchanged insulin sensitivity the morning after a competitive marathon in normoglycemic athletes with type 1 diabetes, despite significant glycogen depletion. This may be explained by enhanced lipid oxidation following exhaustive exercise, which is a normal occurrence, combined with some degree of muscular damage to create a transient state of insulin resistance.

Chronic exercise-related changes in insulin sensitivity are caused by adaptive changes in muscle tissue, which result in enhanced insulin-mediated glucose transport by insulin-sensitive glucose transporter (GLUT4) proteins and lower hepatic glucose output.

The nature of the training stimulus also affects the types of change that occur, with aerobic training resulting in an increase in the proportion of lipids used during low- or moderate-intensity activity. By metabolising lipids more effectively, muscle glycogen stores and blood glucose can be spared, which allows for better glycemic control during exertion.

Training related changes in fuel utilisation reduce the magnitude of compensatory adjustments to carbohydrate or insulin intake administered to maintain glycemic control, in comparison to pre-training norms. Subsequently, training adaptations reduce overall insulin requirements, irrespective of the insulin regimen adopted. However, as the heightened state of insulin action declines after only one to two days of inactivity, exercise regimens must remain consistent and be considered following periods of detraining.

Resistance training also enhances insulin sensitivity and blood glucose utilisation. Therefore, athletes with type 1 diabetes, who gain muscle mass from resistance work will also reduce their overall insulin requirements and must subsequently lower their insulin doses both acutely and chronically.

Aging Athletes

Athletes’ management of exercise-related hypoglycaemia can evolve over time, as the body’s ability to cope with repeat bouts of exercise diminishes. Hypoglycaemia-associated autonomic failure (HAAF) can lead to a decreased release of glucose-raising hormones like glucagon and epinephrine in response to exercise. HAAF is more likely to occur following a prior bout of exercise in the previous 24-48 hours or a prior hypoglycaemic event, with subsequent responses being exacerbated by the length and magnitude of the event.

A single episode of hypoglycaemia or a single bout of exercise, in an individual with type 1 diabetes can blunt the body’s normal counter-regulatory defences (neuroendocrine and autonomic nervous system responses) against subsequent hypoglycaemia or exercise. This is more common in individuals demonstrating signs of type 1 diabetes for 5 years or longer.

Ageing athletes can take longer to recover from bouts of exercise due to decreased rates of muscle repair, carbohydrate repletion and energy replacement. Therefore, relative exercise intensities increase when individuals work at the same absolute intensity due to a decline in maximal aerobic capacity with ageing. Ageing athletes also exhibit a gradual loss of muscle mass, which can affect total storage capacity for muscle glycogen.

Supplementation

An area of performance preparation and recovery requiring close scrutiny by athletes with type I diabetes is that of ergogenic supplementation.

Ergogenic protein and amino acid supplements release substantial amounts of nitrogen when metabolised and as such will add extra stress on the kidneys due to the increased excretive demands. This can be significant for those athletes that may demonstrate pre-existing damage from long-term diabetes.

Creatine monohydrate supplementation has also been shown to harm kidneys demonstrating markers of existing damage, particularly during the initial creatine loading period. However, research in this area is limited to animal models and has yet to be tested on human subjects.

Caffeine is often used to enhance performance through its stimulatory affect on the central nervous system to reduce perception of fatigue and work effort. However, supplementation can increase fluid loss and contribute to states of dehydration when taken prior to exertion, especially in hot environments, and, therefore, care must be taken to ensure adequate fluids are consumed. Studies have also shown that caffeine affects insulin sensitivity, with higher habitual caffeine consumption being associated with higher insulin sensitivity, whilst acutely caffeine intake has been demonstrated to lower insulin sensitivity and increase glucose concentrations.

Carbohydrate loading prior to competition can result in hyperglycaemia before, during, and/or after exercise if adequate insulin is not administered. Studies have demonstrated enhanced glycogen storage and better glycaemic control when a loading diet comprised of 50% of the calories from carbohydrate intake is utilised in comparison to a 60% carbohydrate diet. Furthermore, liver glycogen repletion is linked to tighter blood glucose control. Carbohydrate loading before and after exercise also reduces formation of glucose transport proteins (GLUT4) and insulin sensitivity.

In contrast, if carbohydrate is consumed before exercise and excessive compensatory insulin is given, hypoglycaemia can occur. Athletes should always carry a source of rapidly absorbable carbohydrate (e.g., glucose tablets, glucose polymers, sugary drink or hard candy) that can be easily consumed before, during and after exertion in the event of onset of a hypoglycaemic state.

Rapid restoration of muscle glycogen can be achieved by consuming carbohydrate within 30 minutes after glycogen-depleting exercise and this strategy may actually prevent late-onset hypoglycaemia that can occur up to 24 hours after exercise.

Insulin sensitivity is elevated immediately post-exercise, and during this window, blood glucose uptake into muscle to reform glycogen can be achieved with minimal circulating insulin. As reduced rates of net muscle glycogen repletion occur in individuals with poorly controlled type 1 diabetes, it is imperative to maintain good glycemic control during this post-exercise recovery period, in order to ensure that subsequent exercise performance is not impaired. Therefore, some additional insulin may be needed to cover carbohydrate intake post-exercise.

Testing

Blood glucose response to exercise varies from person to person and from sport to sport. Therefore, frequent blood glucose monitoring is the key to success, especially as exercise can often mask the symptoms of both hypo- and hyperglycaemia. For example, a study conducted in adolescents with type 1 diabetes, adolescent boys with type 1 diabetes tended to underestimate their blood sugar when it was high and overestimate it when it was low (Riddell & Bar-Or, 2002). Therefore, it is possible for athletes to be hypoglycaemic or hyperglycaemic during exercise even though their perception is that their blood sugar is levels are within the normal range.

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