Skeletal muscle wasting is common and insidious in patients who receive maintenance hemodialysis treatment for the management of ESRD. The objective of this study was to determine whether 12 wk of high-intensity, progressive resistance training (PRT) administered during routine hemodialysis treatment could improve skeletal muscle quantity and quality versus usual care. Forty-nine patients (62.6 ؎ 14.2 yr; 0.3 to 16.7 yr on dialysis) were recruited from the outpatient hemodialysis unit of the St. George Public Hospital (Sydney, Australia). Patients were randomized to PRT ؉ usual care (n ‫؍‬ 24) or usual care control only (n ‫؍‬ 25). The PRT group performed two sets of 10 exercises at a high intensity (15 to 17/20 on the Borg Scale) using free weights, three times per week for 12 wk during routine hemodialysis treatment. Primary outcomes included thigh muscle quantity (cross-sectional area [CSA]) and quality (intramuscular lipid content via attenuation) evaluated by computed tomography scan. Secondary outcomes included muscle strength, exercise capacity, body circumference measures, proinflammatory cytokine C-reactive protein, and quality of life. There was no statistically significant difference in muscle CSA change between groups. However, there were statistically significant improvements in muscle attenuation, muscle strength, mid-thigh and mid-arm circumference, body weight, and C-reactive protein in the PRT group relative to the nonexercising control group. These findings suggest that patients with ESRD can improve skeletal muscle quality and derive other health-related adaptations solely by engaging in a 12-wk high-intensity PRT regimen during routine hemodialysis treatment sessions. Longer training durations or more sensitive analysis techniques may be required to document alterations in muscle CSA.

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The route of estrogen replacement therapy has a major impact on the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis. Estrogen administration by the oral, but not the transdermal route, reduces IGF-I and increases GH levels in postmenopausal women. To investigate whether these perturbations have metabolic consequences, we compared the effects of 24 wk each of oral (Premarin 1.25 mg) and transdermal (Estraderm 100TTS) estrogen on energy metabolism and body composition in 18 postmenopausal women in an open-label randomized crossover study. Energy expenditure, lipid oxidation (lipid ox ), and carbohydrate oxidation (CHO ox ) were measured by indirect calorimetry in the fasted and fed state before and after 2 and 6 mon treatment. Lean body mass, fat mass, and total body bone mineral density were measured by dual X-ray absorptiometry before and after 6 mon treatment.Mean ( Ϯ SE) Luteinizing hormone levels fell to comparable levels during oral and transdermal estrogen, and bone mineral density was significantly increased by both treatments. Mean IGF-I was significantly lower during oral estrogen (77 Ϯ 7 versus 97 Ϯ 7 g/liter, P Ͻ 0.05) treatment.

Women have a higher proportion of body fat compared to men. However, women consume fewer kilojoules per kilogram lean mass and burn fat more preferentially during exercise compared with men. During gestation, women store even greater amounts of fat that cannot be solely attributed to increased energy intake. These observations suggest that the relationship between kilojoules consumed and kilojoules utilised is different in men and women. The reason for these sex differences in energy metabolism is not known; however, it may relate to sex steroids, differences in insulin resistance, or metabolic effects of other hormones such as leptin. When considering lifestyle modifications, sex differences in energy metabolism should be considered. Moreover, elucidating the regulatory role of hormones in energy homeostasis is important for understanding the pathogenesis of obesity and perhaps in the future may lead to ways to reduce body fat with less energy restriction.

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Reduction in IGF-I levels is an intrinsic effect of oral oestrogen therapy and increased GH levels may occur as a result of reduced feedback inhibition by IGF-I. Since GHBP activity is not changed by transdermal oestrogen, we conclude that the liver is a major source of circulating GHBP and that GHBP is an oestrogen sensitive protein.

OBJECTIVETo investigate changes in body composition after 12 months of high-intensity progressive resistance training (PRT) in relation to changes in insulin resistance (IR) or glucose homeostasis in older adults with type 2 diabetes.RESEARCH DESIGN AND METHODSOne-hundred three participants were randomized to receive either PRT or sham exercise 3 days per week for 12 months. Homeostasis model assessment 2 of insulin resistance (HOMA2-IR) and glycosylated hemoglobin (HbA1c) were used as indices of IR and glucose homeostasis. Skeletal muscle mass (SkMM) and total fat mass were assessed using bioelectrical impedance. Visceral adipose tissue, mid-thigh cross-sectional area, and mid-thigh muscle attenuation were quantified using computed tomography.RESULTSWithin the PRT group, changes in HOMA2-IR were associated with changes in SkMM (r = −0.38; P = 0.04) and fat mass (r = 0.42; P = 0.02). Changes in visceral adipose tissue tended to be related to changes in HOMA2-IR (r = 0.35; P = 0.07). Changes in HbA1c were related to changes in mid-thigh muscle attenuation (r = 0.52; P = 0.001). None of these relationships were present in the sham group (P > 0.05). Using ANCOVA models, participants in the PRT group who had increased SkMM had decreased HOMA2-IR (P = 0.05) and HbA1c (P = 0.09) compared with those in the PRT group who lost SkMM. Increases in SkMM in the PRT group decreased HOMA2-IR (P = 0.07) and HbA1c (P < 0.05) compared with those who had increased SkMM in the sham group.CONCLUSIONSImprovements in metabolic health in older adults with type 2 diabetes were mediated through improvements in body composition only if they were achieved through high-intensity PRT.

BackgroundDiabetes is an important risk factor for cognitive impairment. Although some studies suggest that physical exercise can minimize age-related cognitive declines or improve brain morphology or function, benefits in diabetes or impaired glucose tolerance are unclear. Therefore, our aim was to evaluate the efficacy of exercise or physical activity on cognition in adults with type 2 diabetes, insulin resistance or impaired glucose tolerance.MethodsAn electronic search for studies published from the earliest record until February 2017 was conducted using Medline, EMBASE, SPORTDiscus, CINAHL, and PsycINFO. Any experimental or observational study designs were included, as long as they were conducted in individuals of any age with type 2 diabetes, insulin resistance or impaired glucose tolerance, and they directly examined exercise/physical activity effects on cognitive outcomes or the relationship between changes in cognition and changes in either insulin resistance and glucose homeostasis. Study quality was assessed using the PEDro scale; data on participant and intervention characteristics and outcomes were extracted.ResultsSix studies enrolling 2289 participants met the eligibility criteria. Quality was modest and effect sizes variable and mostly small or negligible. Overall, four of the six studies (67%) reported significant benefits of greater exercise/physical activity participation for some aspects of cognition, but only 26% of cognitive outcomes were significant across all trials. Clinical improvements in insulin resistance/glucose homeostasis were related to improvements in cognitive function in three studies. Overall results were inconsistent, with benefits varying across exercise types and cognitive domains.ConclusionsLiterature does not provide evidence that physical activity or exercise interventions contribute to a better cognitive function in patients with type 2 diabetes or impaired glucose tolerance. Large-scale, long-term, robust randomized controlled trials are required to determine if exercise improves cognition in this high-risk cohort, and to investigate putative mechanistic links between cognition, body composition, metabolism, and inflammation in diabetes and related metabolic syndromes.