Effect of long-term exercise on skeletal muscle lipid composition

Morgan, TE; Short, F. A.; Cobb, L. A.

doi:10.1152/ajplegacy.1969.216.1.82

Cited by 78 publications

(47 citation statements)

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“…IMTG content does not appear to be correlated with obesity in humans (11,29) but does correlate with obesity in rats (43). IMTG content is increased in trained compared with untrained human muscle (20,24). Data on the contribution of VLDL-TG to fat oxidation during exercise in the literature are not consistent (13,20,26).…”

Section: Discussionmentioning

confidence: 98%

Effect of exercise training at different intensities on fat metabolism of obese men

Aggel-Leijssen

Saris

Wagenmakers

et al. 2002

Journal of Applied Physiology

111

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. Effect of exercise training at different intensities on fat metabolism of obese men. J Appl Physiol 92: 1300-1309, 2002; 10.1152/japplphysiol.00030.2001.-The present study investigated the effect of exercise training at different intensities on fat oxidation in obese men. Twenty-four healthy male obese subjects were randomly divided in either a low-[40% maximal oxygen consumption (V O2 max)] or high-intensity exercise training program (70% V O2 max) for 12 wk, or a nonexercising control group. Before and after the intervention, measurements of fat metabolism at rest and during exercise were performed by using indirect calorimetry, [U-13 C]palmitate, and [1,2-13 C]acetate. Furthermore, body composition and maximal aerobic capacity were measured. Total fat oxidation did not change at rest in any group. During exercise, after low-intensity exercise training, fat oxidation was increased by 40% (P Ͻ 0.05) because of an increased non-plasma fatty acid oxidation (P Ͻ 0.05). Highintensity exercise training did not affect total fat oxidation during exercise. Changes in fat oxidation were not significantly different among groups. It was concluded that lowintensity exercise training in obese subjects seemed to increase fat oxidation during exercise but not at rest. No effect of high-intensity exercise training on fat oxidation could be shown. low intensity; stable isotopes; acetate correction factor; [ 13 C]palmitate OBESITY IS ASSOCIATED with an impaired ability to use fat as a fuel. This may contribute to the development and maintenance of large fat stores. Upper body obesity is associated with an impaired postabsorptive free fatty acid (FFA) utilization in skeletal muscle in women (6). Isoprenaline-induced fat oxidation and skeletal muscle FFA uptake are impaired in obese men, and no improvement was found after weight loss (1-3). Lean, formerly obese women have lower fasting fat oxidation rates compared with lean, never-obese women (32). Moreover, in Pima Indians, a population with a high prevalence of obesity, weight gain is association with a low 24-h fat-to-carbohydrate oxidation ratio (49). Several explanations have been proposed for this reduced fat utilization in obesity, such as a low activity of enzymes of ␤-oxidation (50), low skeletal muscle lipoprotein lipase activity (7), and impaired mobilization of fat stores (1). Interventions that will increase the capacity of the skeletal muscle to utilize fat may, therefore, make an important contribution to weight management in obese individuals and individuals at risk for obesity.Endurance exercise training is known to increase fat oxidation during submaximal exercise at a fixed workload in lean subjects (14,17,23,30,38). Cross-sectional studies also report higher fat oxidation during exercise after an overnight fast (18,20,21,40,45) or with glucose (19, 47) in trained compared with sedentary men. Some studies also found an enhanced resting fat oxidation after endurance training (5, 31, 34). Thus endurance exercise training appears to have the capacity to increase ...

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Section: Discussionmentioning

confidence: 98%

Effect of exercise training at different intensities on fat metabolism of obese men

Aggel-Leijssen

Saris

Wagenmakers

et al. 2002

Journal of Applied Physiology

111

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“…Exercise training has been reported to increase muscle triglyceride content (25,26), and chronic exercise increases insulin sensitivity (27,28) as well as the capacity for fatty acid oxidation (29). Studies of exercise physiology indicate that skeletal muscle triglyceride can contribute substantially to the mixture of substrates oxidized by exercising skeletal muscle (30 -32).…”

Section: -Associations Of Adipose Tissue Located Beneath the Fascia Lmentioning

confidence: 99%

Skeletal Muscle Triglyceride

2001

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Recent evidence derived from four independent methods indicates that an excess triglyceride storage within skeletal muscle is linked to insulin resistance. Potential mechanisms for this association include apparent defects in fatty acid metabolism that are centered at the mitochondria in obesity and in type 2 diabetes. Specifically, defects in the pathways for fatty acid oxidation during postabsorptive conditions are prominent, leading to diminished use of fatty acids and increased esterification and storage of lipid within skeletal muscle. These impairments in fatty acid metabolism during fasting conditions may be related to a metabolic inflexibility in insulin resistance that is not limited to defects in glucose metabolism during insulin-stimulated conditions. Thus, there is substantial evidence implicating perturbations in fatty acid metabolism during accumulation of skeletal muscle triglyceride and in the pathogenesis of insulin resistance. Weight loss by caloric restriction improves insulin sensitivity, but the effects on fatty acid metabolism are less conspicuous. Nevertheless, weight loss decreases the content of triglyceride within skeletal muscle, perhaps contributing to the improvement in insulin action with weight loss. Alterations in skeletal muscle substrate metabolism provide insight into the link between skeletal muscle triglyceride accumulation and insulin resistance, and they may lead to more appropriate therapies to improve glucose and fatty acid metabolism in obesity and in type 2 diabetes. Diabetes Care 24:933-941, 2001N early all individuals with type 2 diabetes are markedly insulin resistant, and the majority of them are obese. This review examines mechanisms that might contribute to the association between insulin resistance and obesity, emphasizing 1), established and newer concepts of regional adipose tissue distribution, and 2), triglyceride content within skeletal muscle. Physiological and cellular mechanisms that lead to an excess accumulation of lipids within skeletal muscle will also be examined. The hypothesis that is addressed in this review is that tissue accumulation of triglyceride makes a major contribution to skeletal muscle insulin resistance and occurs due to reduced reliance on free fatty acid oxidation during postabsorptive conditions. Abdominal Adipose Tissue Distribution and Insulin ResistanceObesity, even if not complicated by diabetes, is associated with insulin-resistant glucose metabolism in skeletal muscle. Considerable insight into the link between obesity and insulin resistance has been gained from studies of adipose tissue distribution. Omental and mesenteric adipose tissue, so-called visceral adiposity, is recognized as a depot strongly associated with insulin resistance of skeletal muscle (1), as well as with dyslipidemia (2) and increased risks for hypertension and glucose intolerance (1,3,4). For example, Banerji et al. (5) observed that variance in visceral adiposity accounted for much of the inter-individual variation in insulin resistance among a cohort o...

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“…[33,34] Interestingly, TG storage within the muscle cell can be increased by regular endurance training. [3,35,36] …”

Section: Factors Limiting Fatty Acid Uptake By Muscle Cellsmentioning

confidence: 99%

“…[59,61] Trained muscles store more intracellular fat and also express a higher LPL activity, which will favour the maximising of FA flux to the mitochondria. [8,9,58,[63][64][65] This may enhance the capacity to utilise intramuscular TG as fuel [3,35,36,60,61,63] while using less blood-borne FA. The advantage of a shift from extracellular to intracellular stores of FA [66,67] is that potential barriers in overall FA utilisation, such as the endothelium and the sarcolemma, are irrelevant when intracellular TG is utilised.…”

Section: Endurance Trainingmentioning

confidence: 99%