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Role and Management of Exercise in Diabetes Mellitus
Abstract
As more is understood about the physiology of exercise, in both normal and diabetic subjects, its role in the treatment of diabetes is becoming better defined. Whereas people with diabetes may derive many benefits from regular physical exercise, there are also several hazards that make exercise difficult to manage. In type I (insulin-dependent) diabetes, there are risks of hypoglycemia during or after exercise or of worsening metabolic control if insulin deficiency is present. Type II (non-insulin-dependent) diabetic patients treated with sulfonylureas are also at some increased risk of developing hypoglycemia during or after exercise, although this poses less of a problem than with insulin treatment. In individuals treated by diet alone, regulation of blood glucose during exercise is usually not a significant problem and exercise can be used as an adjunct to diet to achieve weight loss and improved insulin sensitivity. When obese type II diabetic patients are treated with very low calorie diets, adequate amounts of carbohydrate must be provided to ensure maintenance of normal muscle glycogen content, particularly if individuals wish to participate in high-intensity exercise that places a heavy workload on specific muscle groups. On the other hand, moderate-intensity exercise such as vigorous walking can be tolerated by individuals on very low calorie, carbohydrate-restricted diets after an appropriate period of adaptation. A number of strategies can be employed to avoid hypoglycemia in type I diabetic patients, and both type I and II diabetic patients should be examined carefully for long-term complications of their disease, which may be made worse by exercise. These considerations have led many diabetologists to consider exercise beneficial in the management of diabetes for some individuals but not recommended for everyone as a necessary part of diabetes treatment as in the past. The goals should be to teach patients to incorporate exercise into their daily lives if they wish and to develop strategies to avoid the complications of exercise. The rationale for the use of exercise as part of the treatment program in type II diabetes is much more clear than for type I diabetes; regular exercise may be prescribed as an adjunct to caloric restriction for weight reduction and as a means to improve insulin sensitivity in the obese insulin-resistant individual.
... Muscles Operation During Rest [40,67,43]: In the resting state, the muscles meet 85-90% of their energy needs via the oxidation of fatty acids. About 10% of the energy comes from oxidation of glucose and 1-2% from amino acids. ...
... Muscles Operation During Aerobic Activity [40,67,69]: Oxidation of glucose and fatty acids is the main source of energy for exercising muscles. The relative fraction of these substrates used to meet the energy needs depends on the exercise intensity, which in turn is decided based on the rate at which the individual consumes oxygen while doing this exercise. ...
... Romijn et al. [69] reported about 30% of the energy coming from the oxidation of glucose derived from locally stored glycogen when the intensity of the aerobic exercise was 65%VO 2 max. Horton [67] reported oxidation of glucose (absorbed from the blood and derived from local glycogen) providing for about 50% and almost 100% of the energy needs when the exercise intensities were 50% VO 2 max and 100%VO 2 max respectively. Most of the remaining energy needs are met by oxidation of fatty acids [70]. ...
This paper describes CarbMetSim, a discrete-event simulator that tracks the blood glucose level of a person in response to a timed sequence of diet and exercise activities. CarbMetSim implements broader aspects of carbohydrate metabolism in human beings with the objective of capturing the average impact of various diet/exercise activities on the blood glucose level. Key organs (stomach, intestine, portal vein, liver, kidney, muscles, adipose tissue, brain and heart) are implemented to the extent necessary to capture their impact on the production and consumption of glucose. Key metabolic pathways (glucose oxidation, glycolysis and gluconeogenesis) are accounted for in the operation of different organs. The impact of insulin and insulin resistance on the operation of various organs and pathways is captured in accordance with published research. CarbMetSim provides broad flexibility to configure the insulin production ability, the average flux along various metabolic pathways and the impact of insulin resistance on different aspects of carbohydrate metabolism. The simulator does not yet have a detailed implementation of protein and lipid metabolism. This paper contains a preliminary validation of the simulator’s behavior. Significant additional validation is required before the simulator can be considered ready for use by people with Diabetes.
... In the exercising state, the physical activity itself is sufficient to activate GLUT4 220 transporters [42][43][44] and hence the muscles are able to absorb sufficient glucose from the 221 bloodstream even in the absence of insulin. However, in some people with Type 1 222 Diabetes with very little insulin in circulation, glucose absorption from the bloodstream 223 is impaired even during a vigorous physical exercise [44][45][46][47]. CarbMetSim models 224 impaired glucose absorption during physical exercise using a configurable upper limit on 225 the amount of glucose absorbed by the muscles per tick during exercise. ...
... for the T2D subjects, [51] reported somewhat higher total gluconeogenesis flux during 6 819 hours after the breakfast (26.9 ± 2.2 g) than what we observed in the simulations Other results for T2D subjects in [51] were quite similar to what we observed in the glycogen is available in the liver and in the exercising muscles, the glucose production via glycogenolysis (in the liver and the exercising muscles) and gluconeogenesis (in the 841 liver and kidneys) generally matches the glucose consumption by exercising muscles 842 (and other organs) and the blood glucose level stays in the normal range [44,47] breakdown in the liver to a rate much higher than the impaired rate at which the 854 exercising muscles absorb glucose in some people with Type 1 Diabetes [44][45][46][47]. ...
... for the T2D subjects, [51] reported somewhat higher total gluconeogenesis flux during 6 819 hours after the breakfast (26.9 ± 2.2 g) than what we observed in the simulations Other results for T2D subjects in [51] were quite similar to what we observed in the glycogen is available in the liver and in the exercising muscles, the glucose production via glycogenolysis (in the liver and the exercising muscles) and gluconeogenesis (in the 841 liver and kidneys) generally matches the glucose consumption by exercising muscles 842 (and other organs) and the blood glucose level stays in the normal range [44,47] breakdown in the liver to a rate much higher than the impaired rate at which the 854 exercising muscles absorb glucose in some people with Type 1 Diabetes [44][45][46][47]. ...
This paper describes CarbMetSim, a discrete-event simulator that tracks the blood glucose level of a person in response to a timed sequence of diet and exercise activities. CarbMetSim implements broader aspects of carbohydrate metabolism in human beings with the objective of capturing the average impact of various diet/exercise activities on the blood glucose level. Key organs (stomach, intestine, portal vein, liver, kidney, muscles, adipose tissue, brain and heart) are implemented to the extent necessary to capture their impact on the production and consumption of glucose. Key metabolic pathways (glucose oxidation, glycolysis and gluconeogenesis) are accounted for in the operation of different organs. The impact of insulin and insulin resistance on the operation of various organs and pathways is captured in accordance with published research. CarbMetSim provides broad flexibility to configure the insulin production ability, the average flux along various metabolic pathways and the impact of insulin resistance on different aspects of carbohydrate metabolism. The simulator does not yet have a detailed implementation of protein and lipid metabolism.
... In The Netherlands, the prevalence rates vary between 7-14 per 1000 for women and between 5-15 per 1000 for men in the age group 30-74 years (43,44,(50)(51)(52)(53)(54)(55)(56)(57)(58)(59). Incidence estimates in the few Dutch studies performed vary between 1.5-4 per 1000 (50,51,60,61). ...
... There is evidence that physical activity increases peripheral sensitivity to insulin, especially in skeletal muscle and adipose tissue (57)(58)(59)(60). In a cross sectional study, performed in a non-diabetic population, it was shown that physical activity was related with the level of fasting insulin and C-peptide: the more active, the lower these levels (61). Another study showed that there is an association between physical activity and 2hr glucose tolerance, independent from obesity (62). ...
... To compare diabetes related and non diabetes-related mortality, we estimated a PIF on total mortality for obesity and physical inactivity for all scenarios. Based on the literature we assumed a relative risk of 1.1 for overweight and 2.0 for obesity on all-cause mortality and a relative risk of 1.4 for physical inactivity for both men and women (58)(59)(60)(61)(62)(63). The change in number of life years (Ld after each intervention was estimated for the pathway diabetes-CHD and for total mortality in the following way: ...
Diabetes mellitus comprises a clinically and genetically heterogeneous group of
disorders that have one common feature: abnormally high levels of glucose in
the blood. The most common form is non-insulin dependent diabetes mellitus
(NlDDM); about 80-90% of all diabetic patients has NlDDM. Other forms of diabetes
are insulin-dependent diabetes mellitus (lDDM) and gestational diabetes.
• In 1985, the World Health Organization (WHO) defined new criteria for diabetes
mellitus based upon the oral glucose tolerance test (OGIT). During the
OGIT test the fasting glucose level is measured, followed by the measurement of
the glucose level, 2 hours after an intake of 75 g glucose. Depending on whether
the glucose levels have been measured in the blood, plasma or serum, cut-off
values have been defined. Three diagnoses can be made: normal glUcose
tolerance, impaired glucose tolerance (IGT) or diabetes mellitus.
The OGIT is often used in epidemiological research. However, in clinical
practice, the diagnosis diabetes is usually based on the presence of the classic
symptoms of diabetes (polyuria, hunger, thirst, weight loss, tiredness) combined
with a single abnormal blood glucose level, or on two abnormal levels without
complaints measured on different occasions.
... For those with diabetes that can be managed via alterations in diet (type 2), exercise studies have documented reduced cholesterol levels and improved fitness for patients (Rimmer, Silverman, Braunschweig, Quinn, & Liu, 2002). For these same patients, physical exercise can be used for weight reduction and to achieve improved insulin sensitivity (Horton, 1988). However, for insulin-dependent (type 2) PRINTED FROM OXFORD HANDBOOKS ONLINE (www.oxfordhandbooks.com). ...
... Subscriber: Ohio State University; date: 15 July 2016 diabetics, exercise regimens require close physician monitoring, as patients may become hypoglycem during or following exercise (Horton, 1988). ...
Beginning in the 1980s, clinical psychologists have made significant contributions to the development, testing, and dissemination of psychological interventions for individuals undergoing stressful medical treatments or coping with chronic illness. This has been important, as there are elevated rates of mood and anxiety disorders among medical patients. Addressing the needs of patients with coronary heart disease (CHD), cancer, and cardio-pulmonary disease (COPD) is discussed. As is the case generally, cognitive behavior therapy (CBT), tailored to the specific medical illness/treatment circumstances of patients, plays a central role. More broadly, psychologists have been influential in contributing empirically based strategies to improve the health of all Americans. Effective behavior change methods for smoking cessation, dietary change, and increasing physical activity and improving fitness reduce morbidity and mortality and, of course, are key to reducing health-care costs. Thus, we urge psychological assessment and intervention as one element of standard, comprehensive, health care.
... On the other hand, dietary modification and management accompanied by initiation of physical workouts has long been proven to be beneficial in reducing body weight and bettering insulin sensitivity [84]. A metaanalysis on the effects of low-carbohydrate diets on CVD risk factors resulted in marked decreases in total body weight, BMI, abdominal circumference, systolic and diastolic blood pressure, triglycerides, fasting glucose, HbA1 C , plasma insulin and CRP, with a concomitant increase in HDL-cholesterol [85]. Moreover, a combination of medications and intense lifestyle modification resulted in weight reduction and decreased levels of HbA1c when compared to normally treated cases, indicating that lifestyle modification are beneficial in the management of obesity and DM [86]. ...
Obesity is a common disorder affecting millions of people worldwide. The number of overweight and obese subjects, globally, is currently 2 billion and 800 million, respectively. Projected estimates show that the number of overweight citizens will approach 60% of the world’s population by the year 2030. Oxidative stress facilitates the development of obesity by stimulating pre-adipocyte differentiation and eventual adipose accumulation. Large deposits of fat release excessive quantities of adipocytokines, resulting in chronic inflammation. The obesity-induced chronic inflammation paves the way for a large variety of systemic complications including but not limited to diabetes mellitus, hyperlipidemia, atherosclerotic lesions, cardiovascular diseases tissue and malignancy. In addition, other obesity-inducers, such as increased insulin growth factor 1, insulin resistance, and increased tissue level of leptin and low concentration of adiponectin may lead to the development of tissue malignancy. Increased physical activity coupled with a healthy food intake is crucial to the management of obesity. Anti-obesity drugs such as sibutramine, qsymia (a combination of phentermine and topiramate), and orlistat have been used to treat obesity with variable degrees of efficacy. Bariatric surgery becomes a choice in severe cases when physical activity and pharmacotherapy fail. In the obese patient with diabetes mellitus, the choice of hypoglycemic agent is important. Metformin, and sodium glucose cotransporters 2 (SGLT2) inhibitors, a new set of antidiabetic drugs can significantly reduce body weight and improve cardiorenal function. SGLT2 inhibitors, thus belong to a class of potential drugs that can be used to treat obesity. In conclusion, obesity is a “deadly” condition that can predispose individuals to many life threatening health conditions.
... The benefits are mainly related to exercise improving blood glucose levels through both a reduction of peripheral insulin resistance [151][152][153] and its capacity to induce insulin-independent glucose uptake [154]. Depending on whether the exercise is acute or chronic, the activated pathways in muscle are different (Figure 3). ...
The natural aging process is carried out by a progressive loss of homeostasis leading to a functional decline in cells and tissues. The accumulation of these changes stem from a multifactorial process on which both external (environmental and social) and internal (genetic and biological) risk factors contribute to the development of adult chronic diseases, including type 2 diabetes mellitus (T2D). Strategies that can slow cellular aging include changes in diet, lifestyle and drugs that modulate intracellular signaling. Exercise is a promising lifestyle intervention that has shown antiaging effects by extending lifespan and healthspan through decreasing the nine hallmarks of aging and age-associated inflammation. Herein, we review the effects of exercise to attenuate aging from a clinical to a cellular level, listing its effects upon various tissues and systems as well as its capacity to reverse many of the hallmarks of aging. Additionally, we suggest AMPK as a central regulator of the cellular effects of exercise due to its integrative effects in different tissues. These concepts are especially relevant in the setting of T2D, where cellular aging is accelerated and exercise can counteract these effects through the reviewed antiaging mechanisms.
... Exercise is an effective non-medical intervention for the management of metabolic syndrome and DM2 [3,4]. In fact, aerobic exercise is the most studied type of exercise and most prescribed in people with common non-communicable chronic diseases, and it has shown to elicit beneficial effects in metabolic, Hb1Ac, body weight and insulin resistance control, also improving fat distribution and microcirculatory function [5,6], with a major effect achieved when combined with resistance training [7,8]. ...
Exercise is a convenient non-medical intervention, commonly recommended in metabolic syndrome and type 2 diabetes (DM2) managements. Aerobic exercise and aerobic circuit training have been shown to be able to reduce the risk of developing DM2-related complications. Growing literature proves the usefulness of Nordic walking as exercise therapy in different disease populations, therefore it has a conceivable use in DM2 management. Aims of this study were to analyze and report the effects of two different supervised exercises (gym-based exercise and Nordic walking) on anthropometric profile, blood pressure values, blood chemistry and fitness variables in obese individuals with and without DM2. In this study, 108 obese adults (aged 45-65 years), with or without DM2, were recruited and allocated into one of four subgroups: (1) Gym-based exercise program (n = 49) or (2) Nordic walking program (n = 37) for obese adults; (3) Gym-based exercise program (n = 10) or (4) Nordic walking program (n = 12) for obese adults with DM2. In all exercise subgroups, statistically significant improvements in body weight, body mass index, fat mass index, muscular flexibility and maximal oxygen uptake (VO2 max) were observed. Moreover, a higher percentage of adherence to the gym-based program compared to Nordic walking was recorded. Our findings showed that, notwithstanding the lower adherence, a supervised Nordic walk is effective as a conventional gym-based program to improve body weight control, body composition parameters, muscular flexibility and VO2 max levels in obese adults with and without type 2 diabetes.
... Diet, exercise, and drug intervention are the major treatments used to combat these defects. Some individuals with impaired fasting glucose tolerance are able to restore an almost normal blood glucose control through diet and exercise alone (Clark, 1997;Goldhaber-Fiebert et al., 2003;Horton, 1988). Physical exercise has been identified as both a catalyst for increasing glucose uptake by the muscles and impacting insulin sensitivity (Borghouts & Keizer, 2000;Goodyear & Kahn, 1998). ...
A basic model highlighting the counter-regulatory roles of insulin and glucagon is proposed to start a series of models designed to explore continuous rein control and major aspects of glucose metabolism. The three-by-three dynamical system uses black boxes to model unit processes such as the dependencies of insulin secretion rate and the glucagon secretion rate on blood glucose concentration. The dependency of basal conditions on insulin resistance and any defects in insulin or glucagon secretion are shown. Since over-production of hepatic glucose exists early in the history of diabetes, it is important that mathematical models should account for this effect by inclusion of the dynamical equation governing glucagon concentration as this illustrative model does. All solutions are consistent with gross features of the metabolic process. The model is examined for explicit and implicit assumptions affecting its validity which determines that the first extension to the model should account for glucose storage and the release of stored glucose.
... The role of exercise is not as clear in T1DM as it is in T2DM, and fear of hypoglycemia and worsening of the complications in T1DM should be taken into consideration when introducing exercise or any other regular physical activity as one of the management approaches (Horton, 1988). Increasing insulin sensitivity, lowering blood glucose level, enhancing lipid profile, reducing the risk for hypertension and positively affecting the psychological status are well-known effects of exercise on T2DM, whereas with T1DM the fluctuation between hypoand hyperglycemia can be managed by careful monitoring of blood glucose level, adjusting insulin doses and following appropriate diet (Riddell & Perkins, 2006; White & Sherman, 1999). ...
Ghrelin, a 28-amino acid peptide, is identified as the endogenous ligand of the
orphan growth hormone secretagogue-receptor type 1a. Ghrelin presents a unique
modification at Ser3 position essential for its activity. It was first discovered in the
stomach of rat in 1999. Aside from ghrelin’s role as a potent growth hormone
secretagogue and food intake modulator, ghrelin is thought to play a role in insulin
and glucagon secretion and in glucose homeostasis. A lot of contradictory data have
been reported in the literature regarding ghrelins co-localization with other hormones
in the islets of Langerhans, its role in insulin secretion and attenuation of type 2
diabetes mellitus. In this study, we investigated the effect of chronic ghrelin
treatment on glucose, body weight and insulin level in normal, STZ-induced diabetic
and ghrelin-treated male Wistar rats. We also examined the distribution pattern and
co-localization of ghrelin in the pancreatic islet of Langerhans with both pancreatic
hormones; insulin and glucagon. In addition, we examined how ghrelin treatment
influences liver function in normal and STZ-diabetic Wistar rats. Control groups
received intraperitoneal injection of normal saline while treated groups received
intraperitoneal injections of 5µg/kg ghrelin on daily basis for duration of four weeks.
Our results show that administration of ghrelin increases the serum insulin level in
both normal and diabetic rats. We also demonstrated that ghrelin co-localizes with
insulin as well as glucagon in the pancreatic islet cells and that the pattern of ghrelin
distribution is shown to alter after the onset of diabetes. Moreover, ghrelin treatment
increased insulin secretion as a result of increasing insulin-secreting β cells. In
conclusion ghrelin co-localizes with both insulin and glucagon in pancreatic islet
cells and plays a regulatory role in insulin secretion
... In the study of Baan et al. (1999), a significant inverse association between physical activity and presence of diabetes was observed.There is evidence that physical activity increases peripheral sensitivity to insulin, especially in skeletal muscle and adipose tissue (Pescatello and Dipietro, 1993;Feskens et al., 1994). Besides, physical activity may improve weight reduction by increasing the energy expenditure associated with exercise because obesity is a major risk factor for developing diabetes (Horton, 1988(Horton, & 1991. These findings, therefore, serves to strengthen the grounds for encouraging physical activity and exercise. ...
... Diet, exercise, and drug intervention are the major treatments used to combat these defects. Some individuals with impaired fasting glucose tolerance are able to restore an almost normal blood glucose control through diet and exercise alone (Clark, 1997;Goldhaber-Fiebert et al., 2003;Horton, 1988). Physical exercise has been identified as both a catalyst for increasing glucose uptake by the muscles and impacting insulin sensitivity (Borghouts & Keizer, 2000;Goodyear & Kahn, 1998). ...
A basic model highlighting the counter-regulatory roles of insulin and glucagon is proposed to start a series of models designed to explore continuous rein control and major aspects of glucose metabolism. The three-by-three dynamical system uses black boxes to model unit processes such as the dependencies of insulin secretion rate and the glucagon secretion rate on blood glucose concentration. The dependency of basal conditions on insulin resistance and any defects in insulin or glucagon secretion are shown. Since over-production of hepatic glucose exists early in the history of diabetes, it is important that mathematical models should account for this effect by inclusion of the dynamical equation governing glucagon concentration as this illustrative model does. All solutions are consistent with gross features of the metabolic process. The model is examined for explicit and implicit assumptions affecting its validity which determines that the first extension to the model should account for glucose storage and the release of stored glucose.
... Several studies have been conducted in our country to evaluate the management of diabetes in the patients practicing yoga on a regular basis (Divakar, Bhatt, & Mulla, 1978). Most of these studies were done on a small number of patients, over short periods of time and just relied on blood sugar estimations to assess the results (Shambekar & Kate, 1980). These studies also included combined Pranayama and several other yogic practices making it difficult to interpret their individual contributions (Sahay, 2007). ...
Aims: The aim of this study is to investigate the effect of yoga therapy and its influence on blood glucose parameters in patients with type 2 diabetes mellitus.
Materials and Method: This was a prospective study conducted at Diabetes Centre, KLES Dr. Prabhakar Kore Hospital and Medical Research Centre, India, from January 2016 to December 2016. A total of 1000 type 2 diabetic patients were enrolled in the study with informed consent. We assessed the patients for pre- and post-assessment blood parameters after a period of 12 months for fasting blood sugar (FBS), postprandial blood sugar (PPBS) levels, glycosylated hemoglobin (HbA1c), cholesterol, and triglycerides. A qualitative in-depth interview of the participants and therapist was conducted at baseline, end of 6 months, and end of 12 months.
Statistical Analysis: The observations were recorded and analyzed for significance using SPSS version 20.0 statistical tool.
Results: During pre-assessment, the results revealed an increase in the level of FBS (181.75 ± 71.47), PPBS (262.04 ± 97.23), HbA1c (10.30 ± 5.3), cholesterol (180.13 ± 47.1), and triglycerides (159.77 ± 110.39). However, the participants who completed the yoga therapy had significantly lower FBS (133.01 ± 46.98) (p < 0.0001), PPBS (187.67 ± 68.61) (p < 0.0001), and HbA1c (7.89 ± 1.6) (p < 0.0001) at the end of the 12th month. There was statistically significant positive correlation observed in yoga group as compared to the control group during postassessment blood parameters.
Conclusions: The results of the present study demonstrated that yoga is effective in reducing the blood glucose levels in patients with type 2 diabetes mellitus. Our study also showed positive benefits of yoga in the management of diabetes with real impact on glycemic control and lipid profile.
... The main reasons for occurrence of insulin resistance is associated with physical inactivity and or a sedentary lifestyle of the sufferer, which in turn increases PPHG. Therefore, during dietary management physical workouts prove to be beneficial in attaining desired weight with better insulin sympathy [64]. ...
Diabesity refers to the complicated conditions of diabetes and obesity occurring simultaneously within a single individual. The incidences of diabetes and obesity are growing at a rapid pace throughout the world that are mainly associated with lifestyle and dietary habits, aside from genetic vulnerability. Authors have reviewed the epidemiology and other negative aspects of diabesity followed by some of the management practices recommended. The declining of traditional lifestyles and dietary patterns is leading to a rapid increase in the prevalence of diabesity that is upcoming as a serious cause of concern world over. Diabetes, obesity, and their associated complications are without doubt a principal issue and threat in developing and under-developed nations. Diabesity has emerged as a major threat. This condition has been described as a slow poison, whose influence cannot be controlled or cured. The dietary measures offer the most viable and effective solution to diabetes onset, in addition to the obese state. The designing of a smart diet (i.e. healthy diet) and selecting gut microbiota having probiotic influence on the host can target in the weight reduction/ management, in addition to stabilizing sugar levels in the blood of an individual. Additionally, the regular physical workout can help an individual in controlling body weight and regulate other biochemical conditions which lead to various types of metabolic disorders. All of these issues are discussed in this review article which covers the causes, prevention, and control of diabesity.
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... Findings of this study, also supports this fact. Physical activity has also been emphasized as an effective cost-saving tool in the care of DM 39 . Furthermore, a cohort prospective study had also highlighted that regular aerobic exercise predicted to lower long-term morbidity and mortality among patients with DM 40 . ...
This study aimed to identify the determinants of good
glycemic control among patients with Diabetes
Mellitus (DM) in Batticaloa District, Sri Lanka. A case
control study was conducted among 339 patients with
DM in medical clinics, Teaching Hospital, Batticaloa.
Cases (n=113) were patients with DM who had fasting
blood glucose equal or less than 110 mg/dl in and
controls (n=226) were patients with DM who had
fasting blood sugar more than 110 mg/dl in at least
last 3 consecutive occasions during last 6 months.
The validated and pre-tested interviewer administered
questionnaire was used to collect data. Data collection
was carried by the trained data collector in order to avoid interviewer bias. DM duration less than 7 years
(OR 0.30, 95% CI=0.14-0.64), rural residence
(OR=2.08, 95% CI=1.04-4.15), regular exercise (OR
5.96, 95% CI=3.08-11.51), fixed time for consumption
of medication (OR 4.22, 95% CI=1.59-11.24), regular
clinic follow-up (OR 4.61, 95% CI=1.22-17.34) and
normal body weight (BMI < 23 Kg/m2) (OR 0.15, 95%
CI=0.07-0.31) were found to be the factors associated
with good glycemic control in the multivariate
logistic regression model. Patients with DM should
be advised on regular exercise, maintain the ideal
body weight, regular clinic follow-up and drug
compliance for the better glycemic control.
... Waiting 60 to 90 minutes after a meal before exercising and monitoring BG levels both during and after exercise/athletic competition are important baseline management measures (1). CHO-rich, low-glycemic index meals should be consumed 1 to 3 hours prior to exercise (59,60). Immediately before and during athletic activity, consumption of additional CHO (17 g at initiation and 17 g every 15 minutes for 60 minutes of exercise at 65% VO 2 max) has proven beneficial in maintaining BG levels both during and after exercise in patients with T1DM (61). ...
Context
Type 1 diabetes mellitus (T1DM) results from a highly specific immune-mediated destruction of pancreatic ? cells, resulting in chronic hyperglycemia. For many years, one of the mainstays of therapy for patients with T1DM has been exercise balanced with appropriate medications and medical nutrition. Compared to healthy peers, athletes with T1DM experience nearly all the same health-related benefits from exercise. Despite these benefits, effective management of the T1DM athlete is a constant challenge due to various concerns such as the increased risk of hypoglycemia. This review seeks to summarize the available literature and aid clinicians in clinical decision-making for this patient population.
Evidence Acquisition
PubMed searches were conducted for ?type 1 diabetes mellitus AND athlete? along with ?type 1 diabetes mellitus AND exercise? from database inception through November 2015. All articles identified by this search were reviewed if the article text was available in English and related to management of athletes with type 1 diabetes mellitus. Subsequent reference searches of retrieved articles yielded additional literature included in this review.
Results
The majority of current literature available exists as recommendations, review articles, or proposed societal guidelines, with less prospective or higher-order treatment studies available. The available literature is presented objectively with an attempt to describe clinically relevant trends and findings in the management of athletes living with T1DM.
Conclusions
Managing T1DM in the context of exercise or athletic competition is a challenging but important skill for athletes living with this disease. A proper understanding of the hormonal milieu during exercise, special nutritional needs, glycemic control, necessary insulin dosing adjustments, and prevention/management strategies for exercise-related complications can lead to successful care plans for these patients. Individualized management strategies should be created with close cooperation between the T1DM athlete and their healthcare team (including a physician and dietitian).
... Patients of Type 2 diabetes have been reported to have a twofold to fourfold increase in such risks. Blood pressure in patients decrease with exercise (Horton, 1988). High insulin levels cause hypertrophy of the tunica media -the middle muscular layer of the vascular wall. ...
Virtually everybody needs some forms and levels of exercise to stay healthy and fit. Physical activity and exercise are widely promoted as effective means to enhance health and physical functioning of individuals. Over the long term, diabetes is associated with dread conditions such as kidney failure; circulation problems; nerve damage; retinal damage and blindness; and increased rate of heart attack, stroke and hypertension. However, a major clinical research has found out that it is possible to prevent diabetes with moderate diet and exercise. This review focused on how exercise can be used to prevent and/or manage diabetes, focusing also on the risk involved in exercise for patients, if not properly programmed.
... Pivovarov et al have recently reviewed the additional benefits of physical activity to those with diabetes [4]. Previously, some young people with type 1 diabetes were restricted from organised sport [5]. It had been debated whether exercise is associated with better diabetes control [6] and a recent meta-analysis of exercise interventions to improve control had showed negligible benefit [7]. ...
Aims
To investigate young people’s attitudes to, and understanding of, physical activity on glycaemic control in Type 1 Diabetes Mellitus.
Methods
Four focus groups with 11–14 and 15–16 year olds were conducted with twelve young people with Type 1 Diabetes, from within a larger study investigating physical activity and fitness. Qualitative analysis of the focus group data was performed using Interpretative Phenomenological Analysis.
Results
Four superordinate themes were identified: Benefits of Exercise, Knowledge and Understanding, Information and Training and “You can do anything”. Young people felt that exercising helped them to manage their diabetes and had a beneficial psychological and physical impact on their bodies. They reported a lack of knowledge and understanding about diabetes among school staff and other young people. The overwhelming sense from young people was that although diabetes impacts upon their lives, with preparation, physical activity can take place as normal.
Conclusions
Whilst young people had an awareness of the physical and psychological benefits of exercise in managing their diabetes, they experienced difficulties at school. Professional support and discussions with young people, giving tailored strategies for managing Type 1 Diabetes during exercise are needed. Healthcare teams should ensure that the support and educational needs of school staff are met. Providing more opportunities to empower young people to take on the responsibility for their Type 1 Diabetes care is merited. Young people felt diabetes did not stop them from participating in activities; it is simply a part of them that needs managing throughout life.
... Exercise is a therapeutic tool, recommended by many leading diabetologists of the pre insulin era. Allen et al. was the first to demonstrate that exercise lowers the blood glucose concentration of diabetic patients and transiently improves glucose tolerance [21][22]. Physical activity is one of the principal therapies to lower blood glucose in type 2 diabetes. ...
Adherence to the treatment of diabetic patients is always a challenge. Hence the study was carried out to find out the effectiveness of the diabetic clinic, in improving the adherence of patients. Study subjects: Patients with known DM attending Diabetic clinic of Medical College Hospital, Sangli. Study design: Cross Sectional study. Study duration: 6 months. Study Tools: Pre tested proforma with written consent of the DM patient. Sampling techniques: all the patients attending diabetic clinic were interviewed once. Sample size: 282. Adherence to pharmacological treatment was 93.3 %, while adherence to non pharmacological treatment, was 78.3 % and 95 % respectively. Statistically highly significant difference was found for the adherence to advice like reducing sugar consumption, in rural and urban patients. Similarly the observed difference was found to be highly significant for the adherence to advice like carrying out daily exercise compared between male and female. Unaffordable drug price was one of the main causes of non-adherence. Adherence to treatment of diabetic patients can be improved with effective and efficient diabetic clinic.
... Regular intensive exercise in diabetes care is known to induce an immediate lowering of blood glucose levels, increased insulin sensitivity, and a decline of glycated haemoglobin (HbA1c) (8). The results from this study show that low-intensity exercise was suf -cient to produce a signi cant acute reduction of blood glucose levels in elderly type 2 diabetes patients. ...
... Varios estudios han mostrado que el ejercicio disminuye el riesgo de desarrollar diabetes, efecto más pronunciado en hombres. (12) Obesidad ...
INTRODUCCIÓN El sedentarismo es un grave problema de salud pública en nuestro país, afectando al 89% de la población chilena, siendo más frecuente en las mujeres (91%) que en los hombres (88%). El sedentarismo aumenta con la edad, de 82% en los meno-res de 25 años a 96% en los mayores de 64 años, presentando diferencias regionales, siendo levemente menor en las regio-nes del norte (I a VI Región), con tasas que varían entre 82% y 89%, en tanto las del sur fluctúan de 90% a 93%. (1) (Figura 1) Esto puede explicarse porque los niños se han vuelto menos activos físicamente y los adolescentes se vuelven físicamente inactivos después de dejar la escuela. Los adultos se enfrentan a una reducción significativa en la exigencia física en su lugar de trabajo, y durante el tiempo de ocio muy poca gente es físi-camente activa. Según el Ministerio de Salud, se define como activo a la persona que practica una actividad física fuera del horario de trabajo al menos por 30 minutos tres veces por semana, y como sedentario, a las personas con actividad física menor que este promedio. Un estilo de vida sedentario se asocia al doble riesgo de muerte prematura y a un aumento del riesgo de enfermedad cardiovascular. (2, 3) Además, el sedentarismo se asocia a otros factores de riesgo cardiovascular, como la obesidad. El entre-namiento físico tiene una amplia variedad de efectos benefi-ciosos en el curso de la aterosclerosis y reduce un 20%-25% la mortalidad total. (4, 5) Por esta razón, actualmente el ejercicio es recomendado en las guías de prevención, tanto primaria como secundaria, en las guías de manejo de la cardiopatía coronaria, de insuficiencia cardiaca y de la mayoría de las cardiopatías. En personas sanas el ejercicio se recomienda como una forma de vida saludable. En cardiópatas el ejercicio debe ser parte del tratamiento, incluido en programas de rehabilitación cardiaca. Estos programas deben ser multidisciplinarios y com-prender la educación y el manejo de los factores de riesgo car-diovascular, el entrenamiento físico, el control de los estados depresivos o ansiosos desencadenados por la enfermedad y promoción de la reinserción laboral. Figura 1.
... They have to reflect on their previous experiences and plan ahead accordingly (ADA, 2004). Exercise-related hypoglycaemia is rare among people with type 2 diabetes who are being treated with diet only or oral agents (Horton, 1988). ...
... 3 Existen suficientes pruebas en la literatura que justifican la indicación del ejercicio físico, como una herramienta terapéutica efectiva en la prevención y el tratamiento de la DM tipo 2. Diferentes estudios de intervención han demostrado que en los pacientes con tolerancia alterada a la glucosa, los programas de dieta y ejercicio disminuyen en 60 % el riesgo de desarrollar DM tipo 2. [28][29][30] En sujetos con DM tipo 2 la dieta y el ejercicio físico producen pérdida de peso, lo que favorece la reducción del uso y la dosificación de los hipoglucemiantes o los normoglucemiante orales y(o) de la insulina significativamente mayor que si se utiliza solo dieta. 31 Se ha confirmado que la intervención a través de ejercicio físico es efectiva en reducir el índice de masa corporal (IMC), los niveles de HbA1c, el riesgo coronario y el costo del tratamiento en sujetos con DM tipo 2. Además, se ha observado una correlación estadísticamente significativa entre la cantidad de la actividad física voluntaria y los efectos beneficiosos que reporta. 32 Datos de la literatura demuestran que modestos incrementos de la actividad física disminuyen la mortalidad en sujetos con DM tipo 2. 33 Boulé y otros 12 realizaron un metaanálisis y una revisión sistemática de los efectos de intervenciones estructuradas de ensayos clínicos de ejercicio físico con una duración de 8 semanas, y sus efectos sobre los niveles de HbA1c y la masa corporal en personas con DM tipo 2. Se incluyeron 12 estudios de entrenamiento aerobio y 2 que entrenaban resistencia. ...
INTRODUCTION: physical exercise is one of the more ancient methods used in treatment of diabetes mellitus and it is one of its fundamental pillars together with dietary therapy, diabetes education and the use of normoglycemic and hypoglycemic drugs. OBJECTIVES: to discuss on the more relevant features of the physical exercise role in persons presenting with diabetes mellitus. DEVELOPMENT: in cases of diabetes mellitus, the aerobic exercises are recommended, although nowadays the use of resistance exercises with small loads is not contraindicated in non-complicated diabetic patients. Its systemic practice has many benefits for the diabetes mellitus patient including the improvement of metabolic control, as well as a delay in appearance of cardiovascular diseases and the improvement of wellbeing and quality of life of those practicing it. Also, in non-diabetic persona it may to help to prevent the disease. Exercise practice is not free from risks particularly in those with complications. The hypoglycemia is the more frequent observed complication, a situation that may be prevented adjusting the therapeutical regime (diet and drugs). The physical activity is contraindicated in the diabetic persons with decompensation because of it worsen the metabolic status. The practice of high danger sports is not recommended in diabetes mellitus patients. CONCLUSIONS: the physical exercise is a fundamental pillar in treatment of diabetes mellitus even in its prevention.
... Mitochondria can be activated with well-accepted health promotion behaviors like exercise, consumption of phytochemicals, or calorie restriction (204,214). Interestingly, all of these factors are traditionally known to be beneficial to prevent and/or control T2D (215)(216)(217). A recent in vitro and in vivo experimental study reported the protective effects of resveratrol, a plant polyphenol, against PCB-mediated impairment of glucose homeostasis in adipocytes through enhanced Nrf2 signaling (218), the same pathway in which certain levels of chemicals can improve mitochondrial function, as we discussed above (204). ...
Persistent organic pollutants (POPs) are lipophilic compounds that accumulate mainly in adipose tissue. Recent human evidence links low dose POPs to an increased risk of type 2 diabetes (T2D). As humans are contaminated by POP mixtures and POPs possibly have inverted U-shaped associations with T2D, critical methodological issues arise in evaluating human findings. This review summarizes epidemiological results on chlorinated POPs and T2D, and relevant experimental evidence. It also discusses how features of POPs can affect inferences in humans. The evidence as a whole suggests that, rather than a few individual POPs, it is background exposure to POP mixtures -including organochlorine pesticides and polychlorinated biphenyls- that can increase T2D risk in humans. Inconsistent statistical significance for individual POPs may arise due to differences in POP mixtures between populations. Differences in the observed shape of the dose-response curves may reflect an inverted U-shaped association secondary to mitochondrial dysfunction or endocrine-disruption. Finally, we examine the relationship between POPs and obesity. There is evidence in animal studies that low dose POP mixtures are obesogenic. However, relationships between POPs and obesity in humans have been inconsistent. Adipose tissue plays a dual role of promoting T2D and providing a relatively safe place to store POPs. Large prospective studies with serial measurements of a broad range of POPs, adiposity, and clinically-relevant biomarkers are needed to disentangle the interrelationships among POPs, obesity and the development of T2D. Also needed are laboratory experiments that more closely mimic real-world POP doses, mixtures, and exposure duration in humans.
Introdução: A alimentação equilibrada é um fator de suma importância para a obtenção de bons resultados na musculação, pois ajuda a melhorar o desempenho físico, na diminuição da fadiga muscular e na manutenção da massa magra. Objetivo: Investigar o consumo de carboidratos e a percepção de desempenho físico em praticantes de musculação. Métodos: estudo transversal, a coleta foi realizada de março a outubro de 2023 em uma academia. Foram aplicados questionários de avaliação nutricional incluindo dados pessoais e antropométricos; recordatório de 24 horas referente ao comportamento alimentar; Questionário Internacional de Educação Física adaptado e Escala de Borg para análise do rendimento dos participantes. Resultados: Amostra de 121 desportistas (68 mulheres, 53 homens), treinando 6 dias por 1h20min a 2h30min, com consumo inadequado de carboidratos, alto teor de massa gorda e treino moderado. Conclusão: Os praticantes não possuem uma alimentação adequada de carboidratos, influenciando negativamente na composição e no rendimento muscular. Palavras-chave: Treinamento de força; musculação; carboidratos; desempenho físico.
Diabetes induces a range of macrovascular and microvascular changes, which lead to significant clinical complications. Although many studies have tried to solve the diabetic problem using drugs, it remains unclear. In this study, we investigated whether resistance exercise affects cardiovascular factors and inflammatory markers in diabetes. The study subjected Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which have genetically induced diabetes mellitus, to a resistance exercise program for 12 weeks and assessed the levels of cardiovascular factors and inflammatory markers using western blotting analysis, ELISA, and immunohistochemistry. During the training period, OLETF + exercise (EX) group exhibited lower body weight and reduced glucose levels when compared with OLETF group. Western blotting analysis, ELISA, and immunohistochemistry revealed that the levels of PAI-1, VACM-1, ICAM-1, E-selectin, TGF-β, CRP, IL-6, and TNF-α were decreased in OLETF + EX group when compared with the OLETF group. Moreover, the anti-inflammatory markers, IL-4 and IL-10, were highly expressed after exercise. Therefore, these results indicate that exercise may influence the regulation of cardiovascular factors and inflammatory markers, as well as help patients with metabolic syndromes regulate inflammation and cardiovascular function.
Obesity drives an excessive triglycerides accumulation in adipose tissue, which incites immune cell infiltration, causing fibrosis and inflammation, causing local hypoxia in adipocytes, and ultimately insulin resistance. The extracellular matrix (ECM) complex network of proteins and proteoglycans that offer a scaffold for cells controlling differentiation, migration, repair, survival, and development, and ECM remodeling is required for healthy adipose tissue expansion. To understand the molecular mechanism of this process is a challenge in order to prevent or treat metabolic diseases. This chapter describes the different ECM components and their function related to adipose tissue and their contribution to restore or maintain insulin sensitivity and the whole body metabolism.
Nowadays, respiratory infections are one of the main causes of death worldwide. It was always thought that the respiratory tract was devoid of its microbiota, but it was a few years ago when this changed. It has not only been described but also the pulmonary microbial community is altered in the context of various respiratory disorders. Despite the lack of knowledge about its role in health and disease, there is evidence indicating that the use of probiotics may have beneficial effects during respiratory disorders since they can modulate the immune system both directly and indirectly.
I MÉTABOLISME ÉNERGÉTIQUE ET ADAPTATION À L'EFFORT CHEZ L'ENFANT NORMAL (p515)
A Caractéristiques spécifiques
B Adaptation à l'effort
II ADAPTATIONS MÉTABOLIQUES LORS DE L'EXERCICE PHYSIQUE CHEZ L'ENFANT DIABÉTIQUE (p521)
A Exercice isolé
B Entraînement physique
C Aptitude physique
III RECOMMANDATIONS PRATIQUES (p529)
A Explication des rôles du glucose et de l'insuline
B Que faire lors d'un exercice physique?
C Quels sports
Background: Understanding diabetes mobile apps functionality is fundamental to diabetes self-management because of the reliance of many patients with diabetes on these apps.
Objectives: The aim of this study is to perform a review of diabetes mobile apps to discover users’ sentiments and qualitatively examine the review comments to understand the perceptions of positive, neutral, and negative sentimental users of the apps.
Method: A total of 2678 user review comments obtained from the google play store were analysed from 47 diabetes mobile apps to understand user sentiments following clinical Self-management Indicators (SMIs) shown in previous research. Pearson correlation analysis was conducted to determine the association between the SMIs present in the apps’ and user review indicators such as rating score, user sentiment and the number of downloads. The users’ review comments were thematically screened using grounded theory to establish the themes to describe their perception of the apps.
Results: After evaluating SMIs such as weight tracking/BMI, sugar level monitoring, diet/Calories management, medication reminder, etc., 74.47% of the apps were found to have Sugar Level Monitoring(SLM) capabilities with 10.64% designed to track weight/BMI. There are 53.19% of the apps that can manage diet/calories and have data storage and security SMIs, however, less than 30% of them provide medication adherence, exercise management, doctor's appointment scheduling, and diabetes information repository. The number of the SMIs included in apps did not influence users’, but the value derived from the functionality of the apps.
Conclusions: Users are satisfied with the apps that are easy to use, setup, provide good analytics for blood sugar monitoring and have uncrowded graphical outputs and user interface. Proper data management and contemporary information about diabetes are among the identified challenges of the apps that were found to crash relentlessly on downloading, uploading, installing, and setup.
The science of yoga is an ancient one. It is a rich heritage of our culture. Several older books make a mention of the usefulness of yoga in the treatment of certain diseases and preservation of health in normal individuals. The effect of yogic practices on the management of diabetes has not been investigated well. We carried out well designed studies in normal individuals and those with diabetes to assess the role of yogic practices on glycaemic control, insulin kinetics, body composition exercise tolerance and various co morbidities like hypertension and dyslipidemia. These studies were both short term and long term. Yoga therapists prescribe specific regimens of postures, breathing, exercise and relaxation techniques to suit individual needs. Medical research shows that yoga therapy is among effective complementary therapies for several common ailments. Hence it has been concluded that Yoga cannot "cure" diabetes, but there are several ways yoga can be beneficial in controlling diabetes. There was a decrease in free fatty acids. There was an increase in lean body mass and decrease in body fat percentage. The number of insulin receptors was also increased. There was an improvement in insulin sensitivity and decline in insulin resistance. All these suggest that yogic practices have a role even in the prevention of diabetes. Keyword: Yoga, Diabetes. INTRODUCTION There are different approaches to yoga including spiritual, therapeutic, and developmental However, the underlying premise of mind-body exercise modalities like yoga is that the physiological state of the body can affect emotions, thoughts, and attitudes, which in turn have a reciprocal effect on the body. Diabetes mellitus has reached epidemic proportions worldwide as we enter the new millennium. The World Health Organization (WHO) has commented there is 'an apparent epidemic of diabetes, which is strongly related to lifestyle and economic change'. Over the next decade the projected number will exceed 200 million. Most will have type-2 diabetes, and all are at risk for the development of complications The science of yoga is an ancient one. It is a rich heritage of our culture. Several older books make a mention of the usefulness of yoga in the treatment of certain diseases and preservation of health in normal individuals. It has now become the subject of modern scientific evaluation. Apart from its spiritual philosophy, yoga has been utilized as a therapeutic tool to achieve positive health and cure disease. This concept is promoted in Hatha yoga and Ghatastha yoga by the yoga preceptors. Interest has been evinced in this direction by many workers and studies on the effect of yoga on hypertension, diabetes, asthma, obesity and other common ailments have been carried out. Diabetes by the following mechanisms: exercise effect, changes in biochemical and hormonal profile, elimination of stress and instilling a sense of discipline. To assess these postulations normal individuals and diabetics were investigated with a carefully chalked out protocol for the effect of yogic practices on exercise tolerance, obesity, hypertension, and insulin kinetics and lipid metabolism. Diabetes represents a spectrum of metabolic disorders, which has become a major health challenge worldwide. The unprecedented economic development and rapid
Whereas exercise training is key in the management of patients with cardiovascular disease (CVD) risk (obesity, diabetes, dyslipidaemia, hypertension), clinicians experience difficulties in how to optimally prescribe exercise in patients with different CVD risk factors. Therefore, a consensus statement for state-of-the-art exercise prescription in patients with combinations of CVD risk factors as integrated into a digital training and decision support system (the EXercise Prescription in Everyday practice & Rehabilitative Training (EXPERT) tool) needed to be established. EXPERT working group members systematically reviewed the literature for meta-analyses, systematic reviews and/or clinical studies addressing exercise prescriptions in specific CVD risk factors and formulated exercise recommendations (exercise training intensity, frequency, volume and type, session and programme duration) and exercise safety precautions, for obesity, arterial hypertension, type 1 and 2 diabetes, and dyslipidaemia. The impact of physical fitness, CVD risk altering medications and adverse events during exercise testing was further taken into account to fine-tune this exercise prescription. An algorithm, supported by the interactive EXPERT tool, was developed by Hasselt University based on these data. Specific exercise recommendations were formulated with the aim to decrease adipose tissue mass, improve glycaemic control and blood lipid profile, and lower blood pressure. The impact of medications to improve CVD risk, adverse events during exercise testing and physical fitness was also taken into account. Simulations were made of how the EXPERT tool provides exercise prescriptions according to the variables provided. In this paper, state-of-the-art exercise prescription to patients with combinations of CVD risk factors is formulated, and it is shown how the EXPERT tool may assist clinicians. This contributes to an appropriately tailored exercise regimen for every CVD risk patient.
The etiology of type I and type II diabetes differs and so do the nutritional challenges during and after exercise. For type I diabetics, exercise may cause hypoglycemia. To avoid hypoglycemia, a carbohydrate-rich meal should be eaten 1 to 3 hours prior to exercise and the insulin dose reduced. During exercise, at least 40 g glucose per hour should be ingested; more if the insulin dose is not reduced. After exercise, it is important to rebuild the glycogen stores to reduce the risk for hypoglycemia. Carbohydrates should always be available during training and in the recovery period. Despite these difficulties, exercise is recommended for type I diabetics and competition at high level is possible. Exercise prevents development of type II diabetes and improves metabolic regulation. For type II diabetics, exercise is normally performed to improve insulin sensitivity and to reduce body weight. Carbohydrates should only be supplied to prevent hypoglycemia.
Type 1 diabetes is a chronic disease that can lead to many serious complications if not properly managed. The patient and physician must work together to optimize glucose control involving both insulin administration and caloric intake. Exercise has numerous benefits and the type 1 diabetic should take advantage of these benefits. Athletes with type 1 diabetes are capable of undertaking a wide array of exercise activities and there are no longer firm contraindications to certain sports for diabetic patients. This article will aid the sports physician in understanding the effects of exercise on diabetes, educating patients to exercise safely, advising when exercise is contraindicated, and providing guidelines for optimal management of the diabetic athlete.
The effect of exercise training on glucose tolerance and insulin sensitivity was studied in rats receiving a modern-westernized high fat diet, in which 42% of total energy was provided in fat.
Rats were either permitted to exercise actively (group E) or forced to be in the sedentary condition (group S) for the first two weeks. In the next 2 weeks, rats in both groups were subjected to either active exercise (group EE and SE) or the sedentary condition (group ES and SS). An intraperitoneal glucose tolerance test and insulin sensitivity test were performed at the end of the first and the second 2 weeks.
No significant difference was found among the groups in blood glucose levels after glucose challenge. However, the insulin levels in the groups E, SE and EE were significantly lower than those in the groups S, SS and ES, respectively. Sensitivity to exogenous insulin was higher in the group EE and SE than in the group ES and SS, respectively. The epididymal fat pads of the groups S, ES and SS were heavier than those of the group E, EE and SE, respectively.
These findings altogether showed that exercise training restrained the increase in the body fat of rats receiving a high fat diet and improved their sensitivity to endogenous and exogenous insulin. However, discontinuation of exercise rapidly lowered the insulin sensitivity. These findings suggest that continuous exercise is especially important for the prevention and treatment of diabetes mellitus, even under a westernized high fat diet.
The pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) remains uncertain. Although over the past few years many of the abnormalities present in the disease have been identified, the mechanism or mechanisms by which these develop have not been established (Table 4.1). The two major abnormalities that are present in essentially all patients with overt NIDDM are insulin resistance and defective insulin secretion.1 Which of these is primary remains an area of considerable controversy. Since both are essentially present in all patients with NIDDM, the assumption may be that both are required for the clinical expression of this disease. In populations in which there is a high occurrence of NIDDM, such as the Pima Indians or South Pacific islanders, insulin resistance can be detected prior to the development of overt glucose intolerance or prior to detectable abnormalities in insulin secretion.2 This suggests that in these groups, insulin resistance might be the primary abnormality, and in susceptible individuals this could ultimately result in abnormalities in insulin secretion and the full development of NIDDM.
There has been growing public concern regarding the ethical conduct of healthcare professionals. This is often reflected as complaints about poor ethical conduct and an increasing use of litigation against healthcare practitioners. In order to formulate ethical curriculum germane to every region, the first step may be to determine the current basic knowledge and attitudes of the healthcare practitioners in the region. There have been few standard yardsticks designed to measure what is known and known and practised, so that educational efforts may be better targeted. Physicians and nurses work closely together for patient-care, With this background the present study is an attempt to elucidate the knowledge, attitude but the professional relations between the two categories may have differences with respect to their attitudes towards patient-care . and practice of the physicians and nurses in relation to healthcare ethics and law.
Prescription of exercise therapy for diabetics is a difficult task. Experience shows that the skilled clinicians are able to express their practical knowledge linguistically in the form of conditional statements (if ...then). Linguistic values are a source of linguistic uncertainty, which can be described using fuzzy set theory. The set of rules represents the linguistic model of the problem to be solved.
The fuzzy expert system could assist the doctors in the exercise therapy prescription. Developed consulting fuzzy expert system represents a useful support for the indication of exercise therapy, choice of suitable physical activity and its regulation.
The knowledge base is formed by expert’s statements that determine the relations between significant (input and output) factors. The knowledge base should be regularly refined and perfected.
Noninsulin-dependent diabetes mellitus (NIDDM)* is a heterogenous disease that is genetically determined and, in most people, is dependent on aging and/or obesity for its expression. It is characterized frequently by a resistance to the metabolic effects of insulin (1,2) and always by a relatively impaired insulin secretory response to a high ambient glucose concentration both in the overnight fasting state and after oral or iv administration of glucose (3,4). Whether an impairment in insulin secretion or insulin resistance or both precedes the development of NIDDM is controversial. The contribution of each appears to be highly variable (5).
Diabetes mellitus is characterized by hyperglycemia resulting from either an absolute or relative insulin deficiency, and affects over 16 million people in the United States. Diabetes is classified into several types (1), but the most frequently encountered categories are types 1 and 2 diabetes. Type 1 diabetes results from pancreatic-cell destruction, which causes in an absolute insulin deficiency. On the other hand, type 2 diabetes is characterized initially by insulin resistance followed by a progressive decline in insulin secretion (2).
Body shape, daily physical-activity, cardiovascular risk factors and disease complications of diabetic patients were analyzed by the survey of mailed questionnaires. Of the 6,800 men who were randomly selected, 1,731 responded. The subjects were divided into two groups according to age (middle-aged group ; 40-60 yrs, old-aged group ; over 60 yrs). The physical-activity performed by the diabetic patients was similar to that of non-diabetic patients in the middle-aged group. However, in the old-aged group the diabetic patients performed significantly less physical-activity than that of the non-diabetic cohort. The prevalence of coronary heart disease of diabetic patients in the old-aged group was significantly higher than their age-matched non-diabetic cohort. Also, in the old-aged group, the age at onset of hypercholesteremia of diabetic patients occurred significantly earlier than that of non-diabetic cohort. The onset of the cardiovascular complications (hypertension and hypercholesteremia) of diabetes mellitus in patients with an earlier onset (40-49 yrs) of diabetes mellitus was related to their obesity, in diabetic patients with a later-onset (over 60 yrs) of diabetes mellitus there was no relationship with obesity and physical-activity throughout life are important in preventing onset and progression of coronary heart disease of the diabetic patient.
The current advocacy of intensive insulin therapy regimens involving multiple daily subcutaneous injections places a heavy burden of compliance on patients, and has prompted interest in developing alternative, less invasive routes of delivery. Various efforts have been made to develop alternative methods for administering insulin, among which is the RapidMistTM Diabetes Management System. This is based on a proprietary formulation technology that allows a liquid, aerosolized pharmaceutical formulation to be delivered accurately into the mouth of the patient as a spray. This introduces a high-velocity, fine-particle aerosol (OralinTM) into the patient's mouth, thus inducing a markedly increased deposition of the preparation over the mucosal membrane, the deposition being much larger than occurs with conventional technology. This rapidly moving, fine particle aerosol is able to traverse the thin membrane so that the insulin molecules are absorbed rapidly into the bloodstream (aided by absorption enhancers) and reach the peripheral circulation within 10 min of application. Studies conducted in patients with type 1 and type 2 diabetes showed clearly that OralinTM has a more rapid absorption and metabolic control than subcutaneously injected insulin. This novel, pain-free, oral insulin formulation has notable attributes of rapid absorption, a simple (user-friendly) administration technique, precise dose control.(comparable to injection within one unit), and bolus delivery of drug. A simplified.approach to pain-free prandial insulin delivery offered by this technique will significantly reduce the incidence of key complications.by allowing increased patient.compliance with consistent drug administration to regulate patients' blood glucose levels. This chapter describes the recent results.of clinical studies (in type 1 and type 2 diabetes patients) by comparing the efficacy of OralinTM with subcutaneously injected insulin.
As reported in the first part of this paper, regular physical exertion can improve the metabolic, clinical and mental state of patients with diabetes. However, since exertion may be associated with a number of adverse effects and risks, the diabetologist and the sports practictioner should carefully evaluate the basal state of the patients together, according to their own specific expertise. In this respect, a diagnostic algorithm is proposed, based on the glycemic profile over several days, the level of glycosylated haemoglobin and an indepth investigation in order to detect cardiac, retinal, renal and nervous disturbances and the diabetic foot. The analysis of the results will indicate the most appropriate sports and the most suitable training program (length and frequency of the training sessions and exertion intensity) for each individual. Practising a number of sports should be prohibited to diabetic patients, due to the high death risk (which can involve other partecipants) if hypoglycemia occurs. Some sports are generically inadvisable because of the high risk of injury or because their practice is associated with a marked elevation of arterial pressure. Finally, preclusion to specific sports may be dictated by the presence of one or more diabetes-induced organ diseases. As the effects of training on glucose metabolism are unpredictable in the single individual, each patient must be taught to be able to self-manage his/her disease and complications, and the diabetologist must assess and certify such a capability, by law. The medical cooperation should continue during the follow-up of the exercising patient, with a specific metabolic surveillance provided by the diabetologist, and serial evaluations of patient fitness and tolerance to training by the sports practitioner. Such interdisciplinary cooperation could overcome a still deficient regulations on this issue and ensure that exercising patients with diabetes are under appropriate medical surveillance.
For many years, athletes with “diabetes” have struggled to find enough information and appropriate levels of care and input to allow elite performance to be maintained. The diagnosis of diabetes has been standardized by the World Health Organization (WHO) and is based on typical symptoms as well as blood glucose levels in defined parameters. There are several types of diabetes but almost all fall into two broad categories; type 1 (T1DM) and type 2 (T2DM) diabetes. Glucose homeostasis is finely balanced in health with tissues in the body, particularly the brain, requiring a steady supply of glucose to function. Increased glucose requirements in exercise are met by muscle glycogenolysis and glucose uptake. Individuals with T2DM are usually overweight and may have risk factors for cardiovascular disease, therefore before commencing an exercise regimen it is prudent to ensure a medical examination is performed.
A prospective, randomized, double-blind, placebo-controlled study S erum IGF-I is reduced in adoles-cents with type 1 diabetes, and in-jections of IGF-I improve glycemic control (1). The fact that sulfonylureas can increase IGF-I directly and indepen-dent of insulin has not been included in standard literature (2). The first observa-tion of a stimulatory effect on serum IGF-I was made in hypophysectomized rats (3). In in vitro experiments, glibenclamide stimulated growth of human chondro-cytes via IGF-I and independent of insulin (4). Glibenclamide and glimepiride had dose-dependent stimulatory effects on IGF-I transcription and production in hu-man liver cells (HuH7) (5). We recruited 40 pubertal patients with type 1 diabetes of a duration of 1 year (negative for C-peptide) at Ulm (n 20) and Bern (n 20). They were ran-domly allocated at the start of treatment and each participant underwent a 6-week course of either glimepiride (one daily dose of 8.2 mol 4 mg; n 20) or placebo (n 20) in addition to the mul-tiple injection intensive insulin therapy (Table 1). One patient receiving glimepi-ride was withdrawn because of viral en-cephalitis. The primary end point in our study had been defined as the increment of IGF-I between start of treatment and 6 – 8 weeks thereafter. Assuming a SD of 200 ng/ml, we estimated that in a two-sided statistical test with an level of 0.05 and a power of 80%, sample sizes of 17 patients per group would be sufficient to attain a significant result, if a true rise in IGF-I from 300 ng/ml (5th percentile) to 500 ng/ml (50th percentile) occurred. The study protocol was approved by the local ethics committees at both centers. At the time of allocation, both groups were not relevantly different regarding age, sex, weight, height, blood pressure, insulin dose, fasting serum glucose, hypo-glycemic events, IGF-I, IGF binding pro-tein-3 (IGFBP-3), HbA 1c , or serum lipids. No remarkable changes (Mann-Whitney U test) in IGF-I or IGFBP-3 could be ob-served during glimepiride treatment (Ta-ble 1). When compared with the placebo group, no differences could be found. Glimepiride did not influence weight, blood pressure, insulin dosage, fasting serum glucose, rate of hypoglycemias, HbA 1c , or serum lipids. In adolescents with type 1 diabetes, the peripheral mode of application of in-sulin is likely to lead to IGF-I insuffi-ciency, consecutively to growth hormone hypersecretion and an insulin-resistant state. In case oral sulfonylureas could effectively increase IGF-I, they could pre-sent a suitable therapeutic option because they are inexpensive, easy to administer, and do not endanger patients by hypogly-cemias. An increase of IGF-I to the upper normal range would be desirable and would not likely be associated with severe side effects (6). For safety reasons, glimepiride, which exhibited a higher stimulatory ef-fect on IGF-I than glibenclamide (5), was given at a usual dose. We anticipated that a treatment duration of 6 weeks should be sufficient to induce a change in IGF-I. The reason why IGF-I did not increase signif-icantly probably lies in the low serum concentrations of glimepiride (median 0.16 mol/l) achieved with our protocol. Glimepiride levels were up to four times higher in the cell culture experiments (5). The authors consider it appropriate to suggest further studies using higher con-centrations of sulfonylureas.
The different aspects that contribute to quality of life in patients with diabetes mellitus, such as mood, are of great importance for the treatment of this disease. These aspects not only influence the well-being of patients but also influence treatment adherence, therefore affecting the course of the disease. A panel of experts from Argentina, Chile, and Uruguay performed a review of the main aspects affecting quality of life in patients with diabetes: physical activity, mood disorders, and sexual activity. The consensus of the panel was that physical activity is important in the treatment of patients with diabetes because it reduces morbidity, mortality, and disease complications, and it should be performed on a regular basis, bearing in mind the patient's characteristics. Increased physical activity is associated with better glycemic control, and in individuals with glucose intolerance, it delays progression toward diabetes. In patients with diabetes, there is a high prevalence of depression, which can influence treatment adherence. Therefore, early detection of depression is essential to improve the course of diabetes. Regarding sexual activity, erectile dysfunction may be a significant sign in the case of suspected diabetes and the early diagnosis of vasculopathy in patients with diabetes. In conclusion, greater emphasis should be placed on improving patient knowledge, early detection, and multidisciplinary approaches to deal with the aspects of diabetes that affect patients' quality of life.
The purpose of this study was to analyze the effects of 6 months of aqua aerobic exercise in obese patients with
Type II Diabetes Mellitus. A total of 24 adults (mean age 56.12±6.27 years; 12 men mean age 55.83±3.37 years and women mean age 56.41±8.41 years) with diet controlled or oral hypoglycemic medications controlled type 2
diabetes, were recruited. Exercise sessions were supervised by a certified exercise trainer three times per
week for a period of six months. Testing was done three times: initial testing, testing after 3 months (transitive
testing) and final testing after 6 months. Statistically significant differences were determined between the first
and the second trial in HbA1c (HbA1c decreased 4.28%, p<0.05), the first and third trial in HbA1c (HbA1c
decreased 7.03%, p<0.05), while between the second and third trial the decrease in HbA1c was the lowest (2.87%, p<0.05). Statistically significant differences between trials were also determined for the values of total
cholesterol and HDL and LDL cholesterol and body weight. Statistically significant and linear decrease was
found for the values of blood glucose between before training values of glucose and the values of glucose after
training. In conclusion, this study showed that aqua aerobic training has a positive effect on glycemic control,
body weight and lipid profile among patients with type II diabetes mellitus.
Nine trained cyclists were studied to determine the effects of caffeine (CAF), and glucose polymer (GP) feedings on work production (kpm) during two hr of isokinetic cycling exercise (80 rpm). Ingestion of 250 mg of CAF 60 min prior to the ride was followed by ingestion of an additional 250 mg fed at 15 min intervals over the first 90 min of the exercise. This treatment significantly increased work production by 7.4% and Vo2 by 7.3% as compared to control (C) while the subjects' perception of exertion remained unchanged. Ingestion of approximately 90 g of GP during the first 90 min (12.8 g/15 min) of the exercise had no effect on total work production or Vo2. It was, however, effective in reducing the rate of fatigue over the last 30 min of cycling. Although GP maintained blood glucose and insulin levels (P less than or equal to 0.05) above those of the C and CAF trials, total CHO utilization did not differ between treatments. During the last 70 min of the CAF trial, however, fat oxidation was elevated 31% and appeared to provide the substrate needed for the increased work production during this period of exercise. These data, therefore, demonstrate an enhanced rate of lipid catabolism and work production following the ingestion of caffeine.
Human diabetics on intermediate and long-acting insulin occasionaly become hypoglycemic during exercise. We have shown previously that during exercise, hypoglycemia did not occur in depancreatized insulin-infused dogs because the increments in glucose production and utilization were proportional and of the same magnitude as in normal dogs. Therefore, to elucidate the mechanism of the glucose-lowering effect of strenuous exercise, we measured glucose production and utilization, metabolic clearance of glucose, and serum immunoreactive insulin in postabsorptive depancreatized dogs 8 h after a subcutaneous injection of protamine zinc and crystalline insulin. During rest, plasma glucose was stable, but ranged between hypoglycemia and hyperglycemia. Hyperglycemia was associated with overproduction of glucose, indicating insulin deficiency despite normal or elevated serum immunoreactive insulin. Glucose clearance, as in normal dogs, increased threefold but glucose production increased only marginally (50%) and, consequently, glucose decreased in plasma. The decrease of plasma glucose was directly proportional to the preexercise concentration and production of glucose. The magnitude of inhibition glucose production was not correlated with the serum immunoreactive insulin indicating either that some released insluin was not active or that a moderate immunoreactive insulin increment induced a near-maximal inhibition. It is concluded that in depancreatized dogs injected with protamine zinc insulin, exercise accelerates mobilization of insulin from its injection site presumably because of increased blood and lymph flow. Glucose utilization did not exceed that in normal dogs, but hepatic glucose production failed to increase sufficiently to meet the needs of muscle in exercise.
Seven men were studied during 30 min of treadmill exercise (approximately 70% VO2 max) to determine the effects of increased availability of plasma free fatty acids (FFA) and elevated plasma insulin on the utilization of muscle glycogen. This elevation of plasma FFA (1.01 mmol/1) with heparin (2,000 units) decreased the rate of muscle glycogen depletion by 40% as compared to the control experiment (FFA = 0.21 mmol/1). The ingestion of 75 g of glucose 45 min before exercise produced a 3.3-fold increase in plasma insulin and a 38% rise in plasma glucose at 0 min of exercise. Subsequent exercise increased muscle glycogen utilization and total carbohydrate (CHO) oxidation 17 and 13%, respectively, when compared to the control trial. This elevation of plasma insulin produced hypoglycemia (less than 3.5 mmol/1) in most subjects throughout the exercise. These data illustrate the regulatory influence of both plasma insulin and FFA on the rate of CHO usage during prolonged severe muscular activity.
Body composition, maximal oxygen uptake, plasma lipids, glucose and lipid tolerance, and plasma insulin were examined in middle-aged, physically well-trained men in comparison with randomly selected men of the same age. The well-trained men were characterized by a small adipose tissue consisting of small fat cells, and probably by an increased muscle mass. They had an elevated maximal oxygen uptake. Fasting plasma lipids were low. Assimilation of 100 g glucose perorally was very rapid and occurred while insulin concentrations in plasma were much lower than in controls. Fasting plasma insulin values were also low. Intravenous lipid tolerance test showed a rapid removal rate of triglycerides. Analyses of glucose metabolism in vitro in muscle biopsies from these men showed an increased activity in several metabolic pathways. Succinic oxidase activity, as a marker of aerobic capacity as well as glycogen contents, was also increased. These results indicate that physical training is a potent factor for regulation of plasma insulin levels. It was suggested that qualitative and quatitative changes in muscle capacity to metabolize glucose are in some way involved in this regulation.
The muscle glycogen content of the quadriceps femoris muscle was determined in 9 healthy subjects with the aid of the needle biopsy technique. The glycogen content could be varied in the individual subjects by instituting different diets after exhaustion of the glycogen store by hard exercise. Thus, the glycogen content after a fat ± protein (P) and a carbohydrate-rich (C) diet varied maximally from 0.6 g/100g muscle to 4.7 g. In all subjects, the glycogen content after the C diet was higher than the normal range for muscle glycogen, determined after the mixed (M) diet. After each diet period, the subjects worked on a bicycle ergometer at a work load corresponding to 75 per cent of their maximal O2 uptake, to complete exhaustion. The average work time was 59, 126 and 189 min after diets P, M and C, and a good correlation was noted between work time and the initial muscle glycogen content. The total carbohydrate utilization during the work periods (54–798 g) was well correlated to the decrease in glycogen content. It is therefore concluded that the glycogen content of the working muscle is a determinant for the capacity to perform long-term heavy exercise. Moreover, it has been shown that the glycogen content and, consequently, the long-term work capacity can be appreciably varied by instituting different diets after glycogen depletion.
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Glycogen synthesis rate in skeletal muscle studied in six juvenile diabetic and six non-diabetic males ingesting a carbohydrate rich diet during 12 h of resting recovery after exhaustive bicycle exercise. The diabetic subjects took their regular insulin. Blood samples and muscle biopsies were obtained at rest prior to exercise, immediately after cessation of exercise and after 2,4,6.9 and 12 h of recovery. A marked decrease in muscle glycogn content was observed in response to exercise in both groups of subjects. Mean glycogen utilization rate was the same in the two groups. Glycogen synthesis rate during the first 4 h or recovery was 6.4 +/- 0.6 mmol glucosyl units/kg w.w./h in the diabetic subjects and 7.2 +/- 0.7 mmol glycosyl units/kg w.w./h in the non-diabetic subjects. During the next 8 h glycogen synthesis rate was approximately 1/3 of that being 2.0 +/- 0.3 and 2.4 +/- 0.5 mmol glucosyl units/kg w.w./h in the two groups respectively. Glycogen synthetase I-activity increased markedly in response to exercise in both groups of subjects. However, no differences were observed between the groups. No significant differences in muscle glucose 6-phosphate concentrations were observed between the two groups. Plasma glucose levels were significantly higher in the diabetic than in the non-diabetic subjects. It is concluded that glycogen synthesis during recovery following prolonged severe exercise can proceed at the same rate in diabetic subjects taking their regular insulin as in non-diabetic subjects.
Stimulated by increasing evidence of an inverse relationship between plasma high-density lipoprotein cholesterol level and frequency of coronary heart disease, we determined concentrations of fasting plasma cholesterol, triglyceride, and lipoproteins in 41 very active men (running greater than 15 miles/wk for the previous year) 35-59 years of age (mean age, 47) and in a comparison group of men of similar age, randomly selected from three northern California communities. The runners had significantly (p less than 0.05) decreased mean plasma triglyceride (70 versus 146 mg/100 ml), total plasma cholesterol (200 versus 210 mg/100 ml), and low-density lipoprotein (LDL) cholesterol (125 versus 139 mg/100 ml) concentrations, and a higher mean level of high-density lipoprotein (HDL) cholesterol (64 versus 43 mg/100 ml) than the comparison group (n equals 147 for HDL and LDL; n equals 743 for total cholesterol and triglycerides). These very active men exhibited a plasma lipoprotein profile resembling that of younger women rather tan of sedentary, middle-aged men. This characteristic, and apparently advantageous, pattern could be only partially accounted for by differences in adiposity between runners and control subjects.
The influence of vigorous activity in man on plasma lipids and lipoproteins is reviewed, with particular emphasis on high density lipoproteins. Both cross sectional and longitudinal (or training) studies have been reported, many of them of less than ideal design. Nonetheless, a consistent pattern emerges in which increased exercise levels lead to lower plasma concentrations of triglycerides and very low density lipoproteins, and of low density lipoproteins. High density lipoprotein levels increase. Sometimes, but not uniformly, plasma total cholesterol level falls as the result of these changes. The increase in plasma high density lipoprotein appears to be the result largely of an increase in the less dense HDL2 subfraction. Plasma apolipoprotein A-I levels (but not apo-A-II levels) seem to increase concomitantly. The precise biochemical mechanism responsible for these changes has not been elucidated; but the recent finding of increased lipoprotein lipase activity in adipose tissue and muscle of endurance runners suggests that increased lipolytic rate of triglyceride-rich lipoproteins may be an initial step in a sequence of events leading to higher plasma levels of HDL-2.
Summary Metabolic and hormonal effects of muscular exercise were studied in juvenile-type diabetics in relation to the prevailing degree of metabolic control and compared with those in healthy control subjects. Two groups of diabetic patients, one in moderate metabolic control and one in ketosis due to insulin withdrawal, were subjected to a 3 hour bicycle ergometer test of comparable, mild work intensity. In both groups of diabetics the exercise-induced rise in blood lactate was similar, but was significantly higher than in control subjects. Blood alanine levels showed a transient, significant rise in both diabetic groups, but not in controls. Blood concentrations of branch-chained amino acids remained unchanged. In the moderately controlled diabetics, exercise induced a marked fall of blood glucose and increases in blood levels of free fatty acids (FFA), ketone bodies and glucagon, which were comparable to the exercise effects in normal controls. In ketotic diabetics, however, exercise led to an additional rise in blood glucose concentration and to increases in ketone body, glucagon and cortisol levels. Significant correlations were found between the exercise effect on blood glucose and initial blood levels of glucose, FFA, ketone bodies and branch chained amino acids: pre-exercise values of above 325 mg/dl glucose, 1173 mol/l FFA, 2.13 mmol/l ketone bodies and 0.74 mmol/l branch chained amino acids led to increased blood glucose levels on exercise, whereas below these limits glucose fell during the exercise test. These findings seem to be, at least in part, explained by the hypothesis of a permissive effect of insulin during stimulation of muscle glucose uptake by exercise. The increased circulating levels of glucagon and cortisol during exercise in ketotic diabetics might represent additional hyperglycaemic and, probably more important, lipolytic and ketogenic stimuli. The results suggest that in moderately controlled, non-ketotic diabetics blood glucose falls during exercise; in ketotic, relatively insulin deficient patients, muscular activity has adverse metabolic and hormonal effects: a further increase in blood glucose, plasma glucagon and cortisol and a rapid aggravation of ketosis.
Submaximal bicycle ergometry was used in the evaluation of cardiac function in 22 patients with juvenile diabetes and 21 age-matched control subjects. Six patients had moderate to severe retinopathy and 2 had peripheral neuropathy. Half of the patients, but only 3 of the controls, were smokers. No differences were found in BP, serum cholesterol, triglycerides and serum creatinine levels between diabetics and controls. None had proteinuria. Patients with juvenile diabetes had higher heart rates (HR) at rest as well as during and after exercise than the healthy controls. Diabetics also had a reduced HR response to postural changes compared with the controls. Five diabetics and one control had a pathological exercise ECG (0.05 less than P less than 0.1) that may indicate early non-symptomatic coronary heart disease. The observed changes in HR may be due to autonomic neuropathy.
Six juvenile diabetics [age, 31 ± 2 yr (mean and SEM); duration of diabetes, 15 ± 4 yr] with signs of autonomic neuropathy (decreased beat-to-beat variation in heart rate during deep breathing) and seven control patients of similar age (27 ± 1 yr) and duration of diabetes (14 ± 2 yr) performed graded exercise oh an ergometer cycle. Resting heart rate was higher and the increase in heart rate at the lowest work load (50 W) was diminished in patients with autonomic neuropathy compared with control patients (P < 0.001), indicating a vagal defect.
The relationships in autonomic neuropathy between heart rate and systolic blood pressure, respectively, and relative work load (expressed as oxygen uptake — in percent—of individual maximal oxygen uptake) were identical with previous findings in normal subjects during beta-adrenergic receptor blockade, indicating impaired sympathetic activity. Maximal heart rate was 157 ± 9 min−1 in autonomic neuropathy and 181 ± 4 in controls, P < 0.05; maximal systolic blood pressure was 179 ± 11 mm Hg and 197 ± 5, respectively.
The greatest tolerable work load was significantly less in patients with autonomic neuropathy (125 ± 13 vs. 161 ± 9 w, P < 0.05). Similarly, maximal oxygen uptake was reduced (1.68 ± 0.21 vs. 2.78 ± 0.18 L/min, 25 ± 3 vs. 38 ± 2 ml/min/kg, P < 0.005).
In conclusion, diabetics with decreased beat-to-beat variation in heart rate displayed signs of cardiovascular dysfunction of parasympathetic as well as sympathetic origin during graded exercise.
Normal subjects were infused 1) with epinephrine (50 ng/(kg.min)) for 180 min followed by epinephrine plus glucagon (3 ng/(kg.min)) for 60 min after which the epinephrine infusion rate was increased (125 ng/(kg.min)) or 2) with epinephrine plus somatostatin (500 microgram/h) for 180 min. Epinephrine increased glucose production and plasma glucagon transiently but caused persistent suppression of glucose clearance and sustained hyperglycemia (despite increased plasma insulin and gluconeogenic substrates); glucose production increased again on addition of glucagon and on increasing the epinephrine infusion rate. During epinephrine plus somatostatin, glucose production still increased transiently, but further suppression of glucose clearance caused more marked hyperglycemia. In conclusion, 1) in man hyperepinephrinemia within the physiological range caused sustained suppression of glucose clearance but only a transient increase in glucose production; 2) this transient hepatic response a) was not due to glycogen or substrate depletion, b) occurred without changes in plasma glucagon or insulin, c) was specific for epinephrine but permitted subsequent responses to changes in plasma epinephrine; 3) epinephrine can serve as a physiological regulator of glucose homeostasis in man both by increasing glucose production and by decreasing glucose clearance.
We studied the effect of physical training on in vivo tissue sensitivity to insulin and insulin binding to monocytes in six previously untrained healthy adults. Physical training (one hour of cycle-ergometer exercise four times per week for six weeks) failed to alter body weight but resulted in a 20 per cent increase (P less than 0.02) in maximal aerobic power (VO2 max) and a 30 per cent increase (P less than 0.01) in insulin-mediated glucose uptake (determined by the insulin clamp technique). The increase in insulin sensitivity correlated directly with the rise in VO2 max (P less than 0.05). Binding of [125I]insulin to monocytes also rose by 35 per cent after physical training (P less than 0.02), primarily because of an increase in the concentration of insulin receptors. Our data indicate that physical training increases tissue sensitivity to insulin in proportion to the improvement in physical fitness. Physical training may have a role in the management of insulin-resistant states, such as obesity and maturity-onset diabetes, that is independent of its effects on body weight.
To investigate whether leg exercise accelerates the absorption of exogenous insulin from its subcutaneous depot in insulin-treated diabetics, and whether the glycemic response to exercise in these patients is related to alterations in the insulin absorption process, the authors studied 9 insulin-dependent diabetics and 4 normal subjects during rest and exercise. The diabetics received the regular dose of intermediate-acting insulin, reduced by 20 U, and their morning breakfast. One hour after the meal, 20 U regular insulin (Actrapid, labeled with 125I or unlabeled) was injected into the arm or the leg. Exercise (90 ± 10 W) was initiated 35 min later for 3 consecutive 10-min periods. In controls, no insulin was injected. Plasma glucagon and C-peptide levels were not changed during exercise, but blood ketone bodies and lactate levels increased significantly. Whether the insulin was injected into the moving or resting limb, external counting over the injection site demonstrated no exercise-induced alteration of the disappearance of 125I-radiation during the exercise period, but revealed a small postexercise enhancement of 125I disappearance only after leg injection. Determination of plasma insulin levels in 4 diabetics with newly insulin-treated diabetes revealed that circulating insulin had increased by 70% 30 min after the subcutaneous administration of regular insulin and had then plateaued for 45 min. Leg exercise had no additional effect on plasma insulin levels during the physical activity. In normals, exercise lowered circulating plasma insulin to a level approximately one-fifth that in diabetics. Regardless of the insulin injection site, there was an identical glycemic response to exercise, i.e., a pronounced fall of glycemia by 15% immediately and by 50% 30 min after the onset of exercise. In normals glucose homeostasis was not disturbed by exercise. This study demonstrates that moderate leg exercise does not necessarily accelerate the absorption of exogenous insulin; however, it can induce an acute and profound fall in glycemia, which presumably is due to the presence of a fixed hyperinsulinemic state in these patients rather than an alteration of the mobilization of insulin from its subcutaneous depot. Although this study investigated only a specific situation, the results indicate the possibility that exercise-induced hypoglycemia in insulin-treated diabetics is not necessarily prevented by changing the insulin injection site to nonmoving parts of the body.
To examine the effects of leg exercise on insulin absorption from various injection sites, 125I-labelled rapid actin insulin (9 units) was injected subcutaneously into the leg, arm or abdomen of patients with insulin-dependent diabetes before one hour of intermittent leg (bicycle) exercise and on a resting, control day. Insulin disappearance from the leg increased by 135 per cent during the first 10 minutes of leg exercise (P less than 0.05) and remained 50 per cent above resting levels after 60 minutes (P less than 0.02). Leg exercise had no effect on insulin disappearance from the arm, but insulin disappearance from the abdomen was reduced during the post-exercise recovery period (P less than 0.02). As compared to leg injection, arm or abdominal injection reduced the hypoglycemic effect of exercise by 57 per cent (P less than 0.02) and 89 per cent (P less than 0.005), respectively. Leg exercise accelerates insulin absorption from the leg. Arm or abdominal injection avoids this acceleration during leg exercise and reduces exercise-induced hypoglycemia.
Insulin secretion and glucose tolerance were examined in 6 highly conditioned athletes in comparison with a control group of 115 normal healthy persons. During glucose infusion the athletes showed low insulin secretion although there was no difference in the levels of blood glucose compared to the control group. It is concluded that under physiologic conditions the extent of insulin secretion is not dependent only upon the blood glucose levels. The results show that a lack of insulin response can occur as a consequence of adaption to physical training. A reduced insulin response, therefore, does not necessarily indicate a diabetic or prediabetic state.
The urinary excretion of albumin was measured in insulin-dependent diabetics under ordinary conditions of life and in response to exercise. Possible mechanisms of exercise induced albuminuria in diabetics were also investigated. Under ordinary conditions of life the insulin-treated diabetics, as a group, had a higher mean urinary albumin excretion than normal controls; however, half of the diabetics had albumin excretion rates within the control range. A given exercise load (600 kpm/min for 20 min) produced an exaggerated albumin excretion in diabetics, particularly evident in the post-exercise period. The elevated urinary albumin excretion was due to an increased transglomerular passage of albumin, not to reduced tubular reabsorption. The increase was not associated with differences in blood pressure or urine flow between controls and diabetics. This exercise test has proved to be a suitable provocation test to unmask abnormalities in the glomerular handling of albumin that might not be recognisable at rest.
The importance of the sympatho-adrenal system for the pancreatic hormonal response to exercise and, furthermore, the role of glucagon and catecholamines for the hepatic glycogen depletion during exercise were studied. Rats were either surgically adrenomedullectomized and chemically sympathectomized with 6-hydroxydopamine or shamtreated. Two weeks later the rats had either rabbit-antiglucagon serum or normal rabbit serum injected. Subsequently the rats either rested or swam with a tail weight for 75 min. Immediately afterwards cardiac blood was drawn and liver and muscle tissue collected. In control rats in spite of an increase in blood glucose concentrati4ns during exercise plasma insulin concentrations were unchanged, while glucagon concentrations increased. In sympathectomized rats, compared to control rats, glucagon concentrations increased less, and insulin concentrations were higher, although glucose concentrations were lower during exercise. Sympathectomy completely abolished the exercise-induced decrease in liver and muscle glycogen concentrations, whereas neither glycogen depletion nor plasma catecholamine concentrations were influenced by the administration of glucagon antibodies. These findings indicate that the sympatho-adrenal system enhances glucagon secretion as well as muscular and hepatic glycogen depletion but inhibits insulin secretion in exercising rats. The increase in glucagon concentrations, however, does not enhance hepatic glycogen depletion at the work load used.
Glucose (100 g) was ingested 15 min after bicycle exercise until exhaustion at a work load corresponding to 70% of maximal uptake (series 1), 14--15 h after an identical exercise period, no food being taken in the interval (series 2), and by nonexercised control subjects. Splanchnic glucose output in the exercised groups rose to values 50--300% greater than in controls, amounting to (over 135 min) 59 +/- 5 g in series 1 and 58 +/- 6 in series 2 compared to 28 +/- 6 in controls. The glycogen concentration of quadriceps muscle in series 1 was 65 +/- 2 mmol glycosyl U/kg wet wt before exercise, 16 +/- 13 at the end of work, and 32 +/- 4 at 135 min after glucose ingestion. In series 2, muscle glycogen concentration was 20 +/- 3 immediately after exercise and rose to 44 +/- 5 over the ensuing 14--15 h in spite of continued fasting. It rose to 56 +/- 3 at 135 min after glucose loading. Repletion of leg muscle glycogen after glucose feeding could account for 50--66% of total splanchnic glucose release. It is concluded that during postexercise recovery, a greater proportion of an oral glucose load escapes hepatic retention, allowing repletion of muscle glycogen to take precedence over hepatic glycogen repletion.
Summary Previous studies in man and pancreatectomized dogs have indicated that alterations of the pharmacokinetics of subcutaneously injected insulin during physical activity may contribute to exercise-induced hypoglycaemia in insulin-treated diabetic patients. We have directly measured the appearance of subcutaneously injected insulin in the circulation and assessed its distribution to different tissues using a recently developed semisynthetic homogeneous [3H]insulin as a tracer. Following subcutaneous injection in rats of [3H]insulin in amounts insufficient to exert significant biological activity in intact animals, circulating levels of exogenous insulin were measured as plasma radioactivity co-migrating with insulin during gel filtration chromatography. Strenuous treadmill running accelerated the mobilization of subcutaneously injected [3H] insulin and resulted in a significant elevation of circulating levels of exogenous insulin early during exercise, followed by decreased levels in the post-exercise period. In addition, exercise induced a redistribution of 3H radioactivity in tissues, mainly increasing that found in skeletal muscle. This direct demonstration of altered pharmacokinetics of subcutaneously injected insulin during exercise provides, at least in part, a mechanism for the exercise-induced hypoglycemia seen following insulin injections in animals and during insulin treatment in man.
The influence of 12 h of fasting after prolonged severe exercise on the muscle glycogen concentration was studed in 5 normal subjects. The subjects exercised in the post absorptive state at 70% of max. Vo2 till exhaustion, then rested for 12 h. No food was allowed during recovery. Blood samples and muscle biopsies were obtained before exercise, immediately after the cessation of exercise, and after 2, 4, 6, 9 and 12 h of recovery. Muscle glycogen content decreased from 70.4 +/- 3.0 to 21.6 +/- 3.9 mmol glucosyl units/kg w.w. in response to exercise. After 4 h of recovery muscle glycogen had increased to 28.8 +/- 3.6 mmol glucosyl units/kg (P less than 0.025). During the next 8 h of recovery no further increase in glycogen concentration was observed. Mean plasma glucose concentration was observed. Mean plasma glucose concentration decreased from 5.25 +/- 0.16 to 4.37 +/- 0.18 mmol/l during exercise (P less than 0.001). No change in the plasma glucose level was observed during recovery. Immunoreactive insulin (IRI) concentration decreased from 15.9 +/- 1.0 to 10.2 +/- 0.5 micromicron/ml (P less than 0.001) during exercise, and remained at this level during recovery. It is concluded that some muscle glycogen repletion may occur after prolonged, severe exercise even under fasting conditions. It is suggested that this may proceed through an increased hepatic gluconeogenesis.
It is not known whether training enhances insulin sensitivity in patients with diabetes and whether this results in a greater improvement in glucose tolerance than is reported in control subjects. In an attempt to answer these questions, we assessed the effects of physical training on glucose tolerance and serum insulin in several patients with maturity-onset diabetes. This report describes the effects of 3-6 months of physical training on a bicycle ergometer in six midle-aged men in whom diabetes was associated with fasting hyperglycemia and deficient insulin secretion. The effect of the training regimen on plasma triglycerides and cholesterol is also described. In the present study, four subjects experienced a decrease in cholesterol that averaged 26 mg/dl and was not associated with a change in body weight or water. The fifth subject in whom cholesterol was determined had an increase of 20 mg/dl after training, even though his plasma triglycerides had diminished. The increment in plasma cholesterol in this individual, in part, may have been related to seasonal variation, as his initial determinations were done during the summer and his later determinations in March, when plasma levels may be in excess of 20 mg/dl higher. The results suggest that the role of physical training in the therapy of diabetes requires further consideration. Additional studies are needed to define the intensity and frequency of exercise needed to produce and maintain biochemical improvement in the diabetic. Also, it remains to be determined if certain patients will benefit more than others. Individuals with deficient insulin secretion were reported here. As training seems to enhance insulin sensitivity, it may well be that maturity-onset diabetics with hyperinsulinism and insulin resistance would show even greater improvement.
In order to study the effect of exercise on the mobilization of exogenous insulin we have injected semisynthetic [ 3H]insulin in rats and diabetic patients and followed its circulating levels at rest and during exercise. (In previous experiments on rats we have shown that treadmill exercise does potentiate the hypoglycemic effect of subcutaneously injected unlabeled insulin, analogous to observations in normal and diabetic man.
Both obesity and physical working capacity are related to glucose tolerance, and a high frequency of pathological oral glucose intolerance is also found among men who are unfit and obese. Middle-aged men who are normoglycemic but have a pathological oral glucose tolerance test (OGTT) have an increased risk for developing diabetes. Moreover, cardiovascular diseases are also more common among these men. In obese men the insulin level during OGTT was reduced by physical training. The question then arises whether middle-aged men with pathological OGTT and similar body weights as age-matched controls also can benefit from physical training. The authors present a summary of several studies still in progress that deal with this question.
1. The interaction of insulin and isometric exercise on glucose uptake by skeletal muscle was studied in the isolated perfused rat hindquarter. 2. Insulin, 10 m-i.u./ml, added to the perfusate, increased glucose uptake more than 10-fold, from 0.3-0.5 to 5.2-5.4 mumol/min per 30g of muscle in hindquarters of fed and 48h-starved rats respectively. In contrast, it did not stimulate glucose uptake in hindquarters from rats in diabetic ketoacidosis. 3. In the absence of added insulin, isometric exercise, induced by sciatic-nerve stimulation, increased glucose uptake to 4 and 3.4 mumol/min per 30g of muscle in fed and starved rats respectively. It had a similar effect in rats with moderately severe diabetes, but it did not increase glucose uptake in rats with diabetic ketoacidosis or in hindquarters of fed rats that had been "washed out" with an insulin-free perfusate. Insulin, at concentrations which did not stimulate glucose uptake in resting muscle, restored the stimulatory effect of exercise in these situations. 4. The stimulation of glucose uptake by exercise was independent of blood flow and the degree of tissue hypoxia; also it could not be reproduced by perfusing resting muscle with a medium previously used in an exercise experiment. 5. At rest glucose was not detectable in muscle cell water of fed and starved rats even when perfused with insulin. In the presence of insulin, a small accumulation of glucose, 0.25 mM, was noted in the muscle of ketoacidotic diabetic rats, suggesting inhibition of glucose phosphorylation, as well as of transport. 6. During exercise, the calculated intracellular concentration of glucose in the contracting muscle increased to 1.1-1.6mM in the fed, starved and moderately diabetic groups. Insulin significantly increased the already high rates of glucose uptake by the hindquarters of these animals but it did not alter the elevated intracellular concentration of glucose. 7. In severely diabetic rats, exercise did not cause glucose to accumulate in the cell in the absence of insulin. In the presence of insulin, it increased glucose uptake to 6.1 mumol/min per 30g of muscle and intracellular glucose to 0.72 mM. 8. The data indicate that the stimulatory effect of exercise on glucose uptake requires the presence of insulin. They suggest that in the absence of insulin, glucose uptake is not enhanced by exercise owing to inhibition of glucose transport into the cell.
To characterize glucoregulation during exercise in insulin treated non-obese diabetics, the response to controlled exercise after an overnight fast was compared to that of normal controls. The diabetics were divided into two groups: ten received insulin by continuous iv infusion while nine received one-third their usual intermediate acting insulin by sc injection in the thigh 1 h prior to exercise. Exercise was on a bicycle ergometer for 45 min at 50% maximum O 2 consumption. In the sc insulin group glucose was 227 ± 16 mg/dl at rest and exercise induced a progressive fall to 156 ± 18 mg/dl at the end of the exercise period. In both insulin-infused diabetic subjects and normal controls exercise did not affect plasma glucose. Glucose turnover was measured by a method employing 3- 3H-glucose by primed infusion. Glucose production in the normal controls increased approximately two-fold with exercise and glucose disappearance paralleled production. Similarly, in the normoglycemic insulin-infused diabetics, glucose production and disappearance increased synchronously. By contrast, in the sc insulin diabetics, there was decreased glucose production despite increased disappearance, accounting for the fall in plasma glucose. Plasma immunoreactive insulin (IRI) increased during exercise when insulin was administered by subcutaneous injection. These studies demonstrate: a) moderate exercise in diabetics receiving sc insulin is associated with a rapid fall in plasma glucose; b) plasma glucose in diabetics receiving insulin by constant iv infusion is unaffected by exercise; c) the fall in plasma glucose during exercise in sc treated diabetics is the result of decreased glucose production, perhaps related to insulin mobilization from the sc depot injection site.
Eight men were studied during graded (47, 77, and 100% of maximal oxygen uptake) and prolonged (76%) exhaustive treadmill running. During graded exercise the glucagon concentration increased 35% from 81 plus or minus 7 pg/ml (mean and SE) at rest to 109 plus or minus 17 after the heaviest load. During prolonged exercise glucagon increased progressively to three times (226 plus or minus 40) the resting value. Norepinephrine increased from 0.40 plus or minus 0.06 ng/ml to 2.22 plus or minus 0.39, epinephrine from 0.07 plus or minus 0.01 to 0.42 plus or minus 0.13 during graded, and to 1.51 plus or minus 0.08 and 0.33 plus or minus 0.04, respectively, during prolonged exercise. Insulin concentrations were depressed during work except for the heaviest load. Fatty acids rose throughout prolonged exercise, whereas blood glucose significantly diminished 30 min afterward. Glucagon concentrations correlated significantly with norepinephrine and epinephrine concentrations during prolonged and with epinephrine during graded exercise. Although increments in catecholamines were similar, the glucagon secretion was larger during prolonged than during graded exercise. While increments in catecholamines might explain increased glucagon secretion during graded exercise, they cannot account completely for the rise of glucagon during prolonged exercise.
SKELETAL muscle constitutes 40 per cent of body weight in normal human beings and accounts for 35 to 40 per cent of total oxygen consumption in the resting state. During exercise, consumption of oxygen and metabolic fuels increases markedly to provide the adenosine triphosphate (ATP) necessary for the contractile process. The purpose of this communication is to review the patterns of fuel utilization and production during exercise. Emphasis will be placed on glucose homeostasis and the hormonal factors that contribute to its regulation. The studies reviewed from our laboratories are of the interorgan exchange of substrates in subjects examined in . . .
Urinary albumin excretion during exercise was measured with a radioimmunological method in a group of 13 young male diabetic patients and in a comparable control group. The duration of diabetes was 2-18 years; they had no proteinuria (Albustix¿) and no other signs of renal disease. There was no difference in the basal albumin excretion. In the diabetics the average albumin excretion was doubled during exercise at 600 kpm/min for 20 min, from 9.1 mug/min to 18.7 mug/min (P less than 0.005). No significant change was seen in the controls. These results strongly suggest that abnormal glomerular filter properties are present in patients with relatively short duration of diabetes - that is, in patients who are known to have thickened glomerular basement membrane. The exercise provocation test may be useful in other fields of renal pathophysiology.
Unlabelled:
In order to elucidate the role of insulin and glucagon during strenuous exercise (100 m/min, slope 10-12 degrees), we have determined the rates of production (Ra), utilization (Rd), and metabolic clearance (M) of glucose in normal dogs before pancreatectomy and 2 wk after total pancreatectomy (a) when they were being maintained on constant intraportal basal insulin infusion, (245 muU/kg-min) and (b) when insulin supply had been withheld before and during exercise. Such an intense exercise induced in normal dogs a prompt decrease in mean immunoreactive serum insulin (IRI) from 20 +/- 3 to 11 +/- 2 muU/ml. In depancreatized insulin-infused dogs serum IRI during rest and exercise was between 14 +/- 1 and 12 +/- 2 muU/ml. In the third group, after cessation of insulin infusion, IRI decreased by 76% (from 17 +/- 5 to 4 +/- 1) and did not decrease futher during exercise. During exercise, serum immunoreactive glucagon (IRG) increased threefold in normal dogs. In depancreatized dogs serum IRG was the same as in normal resting dogs (indicating a nonpancreatic source of the hormone) but it did not increase during exercise. In normal dogs exercise induced proportional increases in Ra, Rd, and M (threefold) and normoglycemia was maintained. Changes in glucose turnover in depancreatized insulin-infused dogs were similar to those seen in normal dogs suggesting that a decrease in insulin secretion and a rise in IRG are not essential to prevent hypoglycemia in diabetic dogs. With the cessation of insulin infusion in resting depancreatized dogs, Ra increased, M decreased, and hyperglycemia ensued. During exercise, Ra continued to rise, but M did not increase significantly.
Conclusions:
(a) Regulation of glucose production by liver during exercise is multifactorial. A decrease in IRI and an increase in IRG are not the only factors which can promote delivery of glucose to the peripheral tissues. The insulin glucagon molar ratio was found not to be an essential metabolic functional unit in regulating glucose metabolism during exercise. (b) It is hypothesized that increases in blood flow and capillary surface area can lead to an increase in the amount of insulin delivered to the muscle even when serum levels of IRI are reduced during exercies. It is suggested that small, but adequate amounts of insulin (as found in normal and depancreatized insulin-infused dogs) are essential in regulating glucose uptake in the working muscle. (c) Since totally depancreatized dogs had normal serum levels of IRG (originating presumably from the gastrointestinal tract), the question of essentiality of basal glucagon activity in glucose homeostasis during exercise could not be resolved by these experiments. It appears, however, that regulation of secretion of nonpancreatic glucagon differs from that of pancreatic glucagon.
We studied the effects of ingesting either a snack food (S) (260 kcal) or placebo (P) 30 min before intermittent cycle exercise at 70% maximal O2 consumption on endurance performance and muscle glycogen depletion in eight healthy human males. Immediately before exercise there were significantly greater increases in plasma glucose (PG) (S +28 +/- 9.7; P +0.1 +/- 0.8 mg/dl) and insulin (S +219 +/- 61.5; P -7 +/- 5.5 pmol/l) (P less than 0.05) following S feeding compared with P. These differences were no longer present by the end of the first exercise period. There were no differences in endurance times (S 52 +/- 6.4; P 48 +/- 5.6 min) or in the extent of muscle glycogen depletion following exercise (S 56 +/- 14.7; P 50 +/- 15.5 micrograms/mg protein) between the two groups. PG was maintained at base-line (prefeeding) concentrations following S, whereas there was a tendency for PG to steadily decrease after P. Total grams of carbohydrate oxidized during exercise did not differ between the two groups (S 120; P 118 g). These results demonstrate that the ingestion of a mixed-macronutrient snack 30 min before exercise does not impair endurance performance nor increase the extent of muscle glycogen depletion during high-intensity cycle exercise in untrained adult male subjects.
The effects of prior high-intensity cycle exercise (85% VO2 max) to muscular exhaustion on basal and insulinstimulated glucose metabolism were studied in obese, insulin-resistant, and normal subjects. Six obese (30.4% fat) and six lean (14.5% fat) adult males underwent two separate, two-level hyperinsulinemic-euglycemic clamp studies (100-min infusions at 40 and 400 mU/m2/min), with and without exercise 12 h earlier. Carbohydrate oxidation was estimated by indirect calorimetry using a ventilated hood system, and endogenous glucose production by D-(3-3H)-glucose infusion. Glycogen content and glycogen synthase activity (GS %l) were measured in vastus lateralis muscle biopsies before and at the end of each insulin clamp procedure.
After exercise, the obese and lean subjects had comparably low muscle glycogen concentrations (0.10 versus 0.08 mg/g protein, respectively), and equal activation of muscle GS activity (54.4 versus 45.3 GS %l, respectively). In the obese subjects, insulin-stimulated glucose disposal was increased significantly, but not totally corrected to normal. In both groups there was a comparable increase in nonoxidative glucose disposal (NOGD), whereas glucose oxidation was decreased and lipid oxidation was increased. Thus, the major effect of prior exercise was to increase insulin-stimulated glucose disposal in the obese subjects and to alter the pathways of glucose metabolism to favor NOGD and decrease glucose oxidation.
No correlation was found between the exercise-induced increase in GS %l and NOGD, except in the normal subjects during maximal insulin stimulation. Thus, glycogen synthase activity does not appear to be ratelimiting fpr NOGD at physiologic insulin concentrations. Our findings suggest that a single bout of glycogendepleting exercise can increase glucose disposal for at least 12–14 h in obese subjects with insulin resistance.
Impaired glucose tolerance is a well documented consequence of absolute bedrest in man. Previous studies have shown a decrease in forearm glucose uptake during intravenous glucose infusion after fourteen days of bedrest. Bedrest is associated not only with physical inactivity but with a change in gravitational vector. This study was designed to examine the individual contributions of these factors to the glucose intolerance of bedrest. Thus, glucose tolerance tests were carried out in exercising subjects at bedrest and in rhesus monkeys immobilized in the vertical plane. Exercise in man improved glucose tolerance during bedrest, and vertically immobilized monkeys demonstrated significant glucose intolerance. It is concluded that the glucose intolerance of bedrest is a function of the decrease in physical activity.
Five severely obese subjects with decreased glucose tolerance but without marked hyperinsulinemia were trained physically, producing a slight circulatory adaptation and an increase in muscle aerobic enzyme activity. The patients ate ad libitum, and no decrease of body fat was found after training. Glucose tolerance did not change. Fasting plasma insulin, as well as the sum of insulin values, decreased after an intravenous glucose tolerance test, but not after a peroral glucose tolerance test. Excretion of 17-ketogenic steroids was unaltered. It was concluded that physical training can cause a decrease in plasma insulin in glucose-intolerant patients without marked hyperinsulinemia, concomitant with minor effects on oxygen transport system, and no effects on body fat, glucose tolerance, enteric insulinogenic factors, and 17-ketogenic steroid excretion.
The glucose and urea production and the uptake of gluconeogenic precursors by the liver were measured with the liver vein catheterization technique in two series of healthy subjects after 4 days on a well-defined normo-caloric diet. After a normal mixed diet the net splanchnic glucose production was 0.87 mmol/min. The glucose derived from maximum gluconeogenesis was 0.31 mmol/min. By using a liver biopsy technique in a similar series, the glycogenolysis was found to be 0.54 mmol glucose/min. After a carbohydrate-poor diet the splanchnic glucose production had decreased to 0.30 mmol/min. In this situation the liver was deprived of most of its glycogen, as shown earlier by direct determination of glycogen in liver biopsy specimens. The uptake of gluconeogenic substrates corresponded to the net glucose production. The decreased glucose production during carbohydrate-poor diet did not result in any significant change of the blood glucose level. This indicates a considerable decrease of the peripheral uptake of glucose.
Liver glycogen content was determined in specimens obtained by repeated percutaneous biopsies during starvation and under various dietary conditions in 19 human subjects. During rest and following an overnight fast, there was a decrease in liver glycogen content by a mean of 0.30 mmol glucosyl units per kg wet liver tissue per min during a further 4 hours' starvation. Prolonged starvation or carbohydrate-poor normocaloric diet decreased the liver glycogen from a mean of 232 to 24–55 mmol glucosyl units per kg within 24 hours. During an additional period of up to 9 days on the carbohydrate-poor diet the liver glycogen remained at a low level. Refeeding with a carbohydrate-rich diet gave a rapid increase of the liver glycogen to supernormal values, 424–624 mmol glucosyl units per kg wet liver tissue.
The relationship between muscle glycogen level and glycogen synthetase activity was studied in normal man. Under basal conditions 27% of the total activity was in the I form. Lowering glycogen by exercise increased I activity to 75%. As glycogen increased back to basal level during carbohydrate feeding, I activity decreased to 25%. Increase of glycogen above normal level did not further affect I activity. Total activity remained unchanged. An inverse relationship between glycogen level and per cent I activity was established in human muscle.
Summary Blood glucose and plasma insulin during glucose loads were measured in nine obese patients before and twice the days after a submaximal work of long duration. All subjects showed lower plasma insulin values the day after exercise. The insulin/glucose ratio was decreased indicating an increased insulin sensitivity. The effect could be demonstrated with the peroral as well as with the intravenous glucose test. The effect was remaining for four to six days after exercise in seven of the nine patients studied. The insulin concentration the day after exercise was well within the range of values of non-obese, non-exercising controls. No parallel lowering of plasma triglycerides was observed. It was concluded that an acute, submaximal, prolonged work produces a considerable decrease of plasma insulin levels during several days in hyperinsulinemic obese patients.
Arterial concentrations and net substrate exchange across the leg and splanchnic vascular bed were determined for glucose, lactate, pyruvate, and glycerol in healthy postabsorptive subjects at rest and during 40 min of exercise on a bicycle ergometer at work intensities of 400, 800, and 1200 kg-m/min. Rising arterial glucose levels and small decreases in plasma insulin concentrations were found during heavy exercise. Significant arterial-femoral venous differences for glucose were demonstrated both at rest and during exercise, their magnitude increasing with work intensity as well as duration of the exercise performed. Estimated glucose uptake by the leg increased 7-fold after 40 min of light exercise and 10- to 20-fold at moderate to heavy exercise. Blood glucose uptake could at this time account for 28-37% of total substrate oxidation by leg muscle and 75-89% of the estimated carbohydrate oxidation. Splanchnic glucose production increased progressively during exercise reaching levels 3 to 5-fold above resting values at the heavy work loads. Close agreement was observed between estimates of total glucose turnover during exercise based on leg glucose uptake and splanchnic glucose production. Hepatic gluconeogenesis-estimated from splanchnic removal of lactate, pyruvate, glycerol, and glycogenic amino acids-could supply a maximum of 25% of the resting hepatic glucose production but could account for only 6-11% of splanchnic glucose production after 40 min of moderate to heavy exercise. IT IS CONCLUDED THAT: (a) blood glucose becomes an increasingly important substrate for muscle oxidation during prolonged exercise of this type: (b) peripheral glucose utilization increases in exercise despite a reduction in circulating insulin levels: (c) increased hepatic output of glucose, primarily by means of augmented glycogenolysis, contributes to blood glucose homeostasis in exercise and provides an important source of substrate for exercising muscle.
Ten obese patients were subjected to physical training, which resulted in an increased maximal oxygen consumption and an increased isometric muscle strength. Body weight increased, due primarily to an increase in body fat, but also, in some cases, to an increase in body cell mass, determined by isotope dilution techniques. Fat cell diameter was unchanged. Peroral glucose tolerance test with plasma radioimmuochemically determined insulin in these patients showed no changes in blood glucose values after training but a marked decrease in insulin values. This was interpreted to be due to an increased insulin sensitivity of tissues. Since the body fat mass was not decreased it was not considered likely that the increased insulin sensitivity was due to adipose tissue factors. This augmentation of insulin sensitivity was furthermore not related to the increase in body cell mass and therefore probably not to an increase in muscle mass. It was concluded that muscle probably is an important determinant for insulin sensitivity in obesity.
The disappearance time for glucose, infused after exercise of various intensities, decreased with increasing work load as related to the subject's maximal oxygen uptake. Plasma immunoreactive insulin levels followed glucose levels closely. It appears that the mechanisms which are responsible for the increased rate of glucose transport into the cells are activated in proportion to the intensity of the exercise rather than to the total energy utilization.