Effects of Exercise Training on Regulation of Skeletal Muscle Glucose Metabolism in Elderly Men

Biensø, Rasmus S.; Olesen, Jes; Gliemann, Lasse; Schmidt, Jakob Friis; Matzen, Mikkel Sillesen; Wojtaszewski, Jørgen F. P.; Hellsten, Ylva; Pilegaard, Henriette

doi:10.1093/gerona/glv012

Cited by 34 publications

(44 citation statements)

References 26 publications

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“…Chronic exercise training can also elevate GLUT4 abundance in muscles of older (∼60–65 years-old) humans (Bienso et al, 2015; Cox et al, 1999; Hughes et al, 1993; Prior et al, 2015). Middle-aged (16 months-old) rats (Kern et al, 1992) and older (24 months-old) mice (Willis et al, 1998) had increased muscle GLUT4 abundance after chronic exercise.…”

Section: Exercise Counteracts Age-related Changes In Insulin Sensitivitymentioning

confidence: 99%

“…Chronic strength training also elevated glucose disposal in older women and men together with greater TBC1D4 phosphorylation on Thr 642 , but not Ser 588 . Other adaptations in muscle after endurance training by older people (∼60–80 years-old) include increased hexokinase II and glycogen synthase protein abundance (Bienso et al, 2015), greater glycogen concentration (Hughes et al, 1993) and elevated capillarization (Prior et al, 2015). Chronic resistance exercise can increase muscle mass, but the magnitude of these changes is relatively modest with the exercise protocols commonly used by older people (Marcus et al, 2013).…”

Section: Exercise Counteracts Age-related Changes In Insulin Sensitivitymentioning

confidence: 99%

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Exercise Promotes Healthy Aging of Skeletal Muscle

et al. 2016

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Primary aging is the progressive and inevitable process of bodily deterioration during adulthood. In skeletal muscle, primary aging causes defective mitochondrial energetics, and reduced muscle mass. Secondary aging refers to additional deleterious structural and functional age-related changes caused by diseases and lifestyle factors. Secondary aging can exacerbate deficits in mitochondrial function and muscle mass, concomitant with the development of skeletal muscle insulin resistance. Exercise opposes deleterious effects of secondary aging by preventing the decline in mitochondrial respiration, mitigating aging-related loss of muscle mass and enhancing insulin sensitivity. This review focuses on mechanisms by which exercise promotes “healthy aging” by inducing modifications in skeletal muscle.

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Section: Exercise Counteracts Age-related Changes In Insulin Sensitivitymentioning

confidence: 99%

Section: Exercise Counteracts Age-related Changes In Insulin Sensitivitymentioning

confidence: 99%

Exercise Promotes Healthy Aging of Skeletal Muscle

et al. 2016

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“…Thus, the relationship between free-living SB and GLUT-4 which has been exhibited in young populations is likely to be present in older persons, though the latter is yet to be determined and requires further research. The evidence thus far suggests that longitudinal physical activity intervention in aged participants (60-72 years) causes an increase in vastus lateralis GLUT-4 concentration (Biensø et al 2015). It appears that this effect could also be found in acute bouts of physical activity.…”

Section: Sedentary Behaviour and Physical Activity: Impact On Glucosementioning

confidence: 99%

The emergence of sedentary behaviour physiology and its effects on the cardiometabolic profile in young and older adults

Ryan

Stebbings

Onambélé

2015

AGE

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It has recently emerged that sedentary behaviour is independent of a lack of physical activity as individuals can be sufficiently active, based on the recommended physical activity guidelines, but also spend the majority of their waking hours engaging in sedentary behaviour. Individuals who follow this pattern of physical activity and sedentary behaviour are known as 'active couch potatoes'. Sedentary behaviour has been found to have detrimental effects on cardiometabolic markers associated with cardiovascular disease. Since the positive effects of moderate-to-vigorous intensity physical activity do not necessarily negate the deleterious effects of sedentary behaviour on cardiometabolic markers, it is postulated that engaging in light physical activity is an intervention that will successfully reduce levels of sedentary behaviour and may hence improve health markers of quality of life. We propose that such lifestyle changes may be particularly relevant to older populations as these engage in sedentary behaviour for the majority of their waking hours, thereby adding to the negative aging effect on cardiometabolic markers.

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“…, BMI of 25 ± 1 kg/m 2 and a median age of 30 years (range [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40]. There was a 100-200-fold increase in TNF-α, IL-6 and IL-10 during KET [13].…”

Section: Resultsmentioning

confidence: 95%

“…KET was associated with compromised glycogen synthesis evident by increased phosphorylation of the inhibiting site 3a [32]. In addition to regulation by phosphorylation, GS activity is dependent on substrate availability, and the ablated glucose uptake in skeletal muscle is likely to contribute further to impairment of glycogen synthesis [33,34].…”

Section: Discussionmentioning

confidence: 99%

Metabolic effects of insulin in a human model of ketoacidosis combining exposure to lipopolysaccharide and insulin deficiency: a randomised, controlled, crossover study in individuals with type 1 diabetes

et al. 2017

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Aims/hypothesis Diabetic ketoacidosis (DKA) is often caused by concomitant systemic inflammation and lack of insulin. Here we used an experimental human model to test whether and how metabolic responses to insulin are impaired in the early phases of DKA with a specific focus on skeletal muscle metabolism. Methods Nine individuals with type 1 diabetes from a previously published cohort were investigated twice at Aarhus University Hospital using a 120 min infusion of insulin (3.0/1.5 mU kg) after an overnight fast under: (1) euglycaemic conditions (CTR) or (2) hyperglycaemic ketotic conditions (KET) induced by an i.v. bolus of lipopolysaccharide and 85% reduction in insulin dosage. The primary outcome was insulin resistance in skeletal muscle. Participants were randomly assigned to one of the two arms at the time of screening using www.randomizer.org. The study was not blinded. Results All nine volunteers completed the 2 days and are included in the analysis. Circulating concentrations of glucose and 3-hydroxybutyrate increased during KET (mean ± SEM 17.7 ± 0.6 mmol/l and 1.6 ± 0.2 mmol/l, respectively), then decreased after insulin treatment (6.6 ± 0.7 mmol/l and 0.1 ± 0.07 mmol/l, respectively). Prior to insulin infusion (KET vs CTR) isotopically determined endogenous glucose production rates were 17 ± 1.7 μmol kg (p = 0.77) and urea excretion rates were 16.9 ± 2.4 g/day vs 7.3 ± 1.7 g/day (p = 0.01). Insulin failed to stimulate forearm glucose uptake and glucose oxidation in KET compared with CTR (p < 0.05). Glycogen synthase phosphorylation was impaired in skeletal muscle. Conclusions/interpretation In KET, hyperglycaemia is primarily driven by increased endogenous glucose production. Insulin stimulation during early phases of DKA is associated with reduced glucose disposal in skeletal muscle, impaired glycogen synthase function and lower glucose oxidation. This underscores the presence of muscle insulin resistance in the pathogenesis of DKA.

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Effects of Exercise Training on Regulation of Skeletal Muscle Glucose Metabolism in Elderly Men

Abstract: The present results suggest that exercise training improves glucose regulation in elderly subjects by enhancing the capacity and acute regulation of glucose uptake and by enhancing intracellular glucose removal to glycogen synthesis rather than glucose oxidation.

Cited by 34 publications

References 26 publications

Exercise Promotes Healthy Aging of Skeletal Muscle

Exercise Promotes Healthy Aging of Skeletal Muscle

The emergence of sedentary behaviour physiology and its effects on the cardiometabolic profile in young and older adults

Metabolic effects of insulin in a human model of ketoacidosis combining exposure to lipopolysaccharide and insulin deficiency: a randomised, controlled, crossover study in individuals with type 1 diabetes

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