Glucose metabolism during leg exercise in man

Wahren, John; Felig, Philip; Ahlborg, Gunvor; Jorfeldt, L.

doi:10.1172/jci106772

Cited by 557 publications

(315 citation statements)

References 38 publications

Supporting

Mentioning

287

Contrasting

Unclassified

Order By: Relevance

“…The recommendation that exercise training can be used as a therapeutic means to lower blood glucose levels in NIDDM subjects stems primarily from the fact that exercise has pronounced effects upon the metabolism of glucose. Exercising muscle may indeed increase glucose uptake 7-to 20-fold [125].…”

Section: Glucose Intolerancementioning

confidence: 99%

Exercise and the metabolic syndrome

1997

View full text Add to dashboard Cite

One of the first people to introduce the metabolic syndrome -or trisyndrome mé tabolique -in the scientific literature was Camus in 1966 [1]. However, this entity did not receive much interest until Reaven in 1988 introduced syndrome X, characterised by hypertension, impairment in glucose and lipid metabolism and insulin resistance [2]. The metabolic syndrome -also called the insulin resistance syndrome -is a multifaceted syndrome characterised by five major abnormalities: obesity, hypertension, insulin resistance, glucose intolerance (impaired glucose tolerance/non-insulin-dependent diabetes mellitus (NIDDM)), and dyslipidaemia (hypertriglyceridaemia and low HDL-cholesterol). In addition, a number of other abnormalities such as microalbuminuria, hyperuricaemia, hyperfibrinogenaemia and increased levels of plasminogen activator inhibitor I and low concentrations of tissue plasminogen activator are often associated with the syndrome. The clinical importance of the metabolic syndrome is mainly due to the clustering of simultaneously occurring atherosclerotic risk factors in the same individual [2][3][4][5][6][7][8][9].The aetiology of the metabolic syndrome is poorly understood; both genetic and environmental factors are involved [2][3][4][5][6][7][8][9]. Possible common denominators for the various components of the syndrome are not known, although hyperinsulinaemia/insulin resistance are important characteristics in most of the abnormalities.The prevalence rate of the metabolic syndrome varies depending on the population studied and the definition applied. As in any syndrome, not all features are present in the same individual. The estimated prevalence rate of the metabolic syndrome in western countries is 25-35 % [2-9]. On the other hand, both Ferrannini and Rupp [8, 9] have reported that only about one-third of an adult study population was free of all major characteristics of the metabolic syndrome. Since the prevalence of hypertension, insulin resistance and glucose intolerance usually increase with increasing age, the prevalence of the metabolic syndrome will probably also rise in the aging western society.A number of pharmacological therapies can be used for the treatment of the metabolic syndrome; but the results of most of the available therapies are often unsatisfactory, although some trials with metformin and thiazolidinediones have been encouraging [6, 10, 11].Low levels of physical activity are related to most components of the metabolic syndrome [12][13][14][15][16]. Consequently this offers a unique opportunity to employ increased physical activity in the prevention and treatment of the metabolic syndrome and its components. This review will focus on the role of physical activity and exercise in the prevention and treatment of the metabolic syndrome. ObesityThe prevalence of obesity (body mass index (BMI) > 27 kg/m 2 ) is currently 25-35 % in most western societies, and is increasing [17]. If the prevalence continues to increase, as during the past decades, by the year 2230, 100 % of the adult Uni...

show abstract

Section: Glucose Intolerancementioning

confidence: 99%

Exercise and the metabolic syndrome

1997

View full text Add to dashboard Cite

show abstract

“…Insulin secretion is inhibited by increased sympathetic nervous system activity via a-adrenergic receptors, and plasma insulin concentrations decline to low levels (6,(23)(24)(25). This results in increased lipolysis in adipose tissue and increased hepatic glucose production (26,27).…”

Section: Ls Hortonmentioning

confidence: 99%

Role and Management of Exercise in Diabetes Mellitus

Horton

1988

Diabetes Care

111

View full text Add to dashboard Cite

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 highintensity exercise that places a heavy workload on specific muscle groups. On the other hand, moderateintensity 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

show abstract

“…One possible factor is the greater enzymic capacity of heart to oxidize lipids (Winder et al, 1974;Holloszy et al, 1973). Another is that the heart is a continuously contracting muscle with a high rate of glycolysis Randle, 1966) compared with perfused skeletal muscle Goodman et al, 1974;Berger et al, 1976) and presumably non-exercising muscle in vivo Wahren et al, 1971). In keeping with this notion, the glucose-fatty acid cycle has been demonstrated in brain , mammary tissue (Hawkins & Williamson, 1972;Williamson et al, 1974;Robinson & Williamson, 1977) and submaxillary glands (Thompson & Williamson, 1975), all of which have high rates of glycolysis and glucose oxidation.…”

mentioning

confidence: 93%

Effects of starvation and exercise on concentrations of citrate, hexose phosphates and glycogen in skeletal muscle and heart. Evidence for selective operation of the glucose-fatty acid cycle

Zorzano¹,

Balon²,

Brady³

et al. 1985

Biochemical Journal

View full text Add to dashboard Cite

1. Concentrations of citrate, hexose phosphates and glycogen were measured in skeletal muscle and heart under conditions in which plasma non-esterified fatty acids and ketone bodies were physiologically increased. The aim was to determine under what conditions the glucose-fatty acid cycle might be operative in skeletal muscle in vivo. 2. In keeping with the findings of others, starvation increased the concentrations of glycogen, citrate and the fructose 6-phosphate/fructose 1,6-bisphosphate ratio in heart, indicating that the cycle was operative. In contrast, it decreased glycogen and had no effect on the concentration of citrate or the fructose 6-phosphate/fructose 1,6-bisphosphate ratio in the soleus, a slow-twitch red muscle in which the glucose-fatty acid cycle has been demonstrated in vitro. 3. In fed rats, exercise of moderate intensity caused glycogen depletion in the soleus and red portion of gastrocnemius muscle, but not in heart. In starved rats the same exercise had no effect on the already diminished glycogen contents in skeletal muscle, but it decreased cardiac glycogen by 2530% . 4. After exercise, citrate and the fructose 6-phosphate/fructose 1,6-bisphosphate ratio were increased in the soleus of the starved rat. Significant changes were not observed in fed rats. 5. The data suggest that in the resting state the glucose-fatty acid cycle operates in the heart, but not in the soleus muscle, of a starved rat. In contrast, the metabolite profile in the soleus was consistent with activation of the glucose-fatty acid cycle in the starved rat during the recovery period after exercise. Whether the cycle operates during exercise itself is unclear.

show abstract

Glucose metabolism during leg exercise in man

Cited by 557 publications

References 38 publications

Exercise and the metabolic syndrome

Exercise and the metabolic syndrome

Role and Management of Exercise in Diabetes Mellitus

Effects of starvation and exercise on concentrations of citrate, hexose phosphates and glycogen in skeletal muscle and heart. Evidence for selective operation of the glucose-fatty acid cycle

Contact Info

Product

Resources

About