OBJECTIVE -To determine the efficacy of high-intensity progressive resistance training (PRT) on glycemic control in older adults with type 2 diabetes.RESEARCH DESIGN AND METHODS -We performed a 16-week randomized controlled trial in 62 Latino older adults (40 women and 22 men; mean Ϯ SE age 66 Ϯ 8 years) with type 2 diabetes randomly assigned to supervised PRT or a control group. Glycemic control, metabolic syndrome abnormalities, body composition, and muscle glycogen stores were determined before and after the intervention.RESULTS -Sixteen weeks of PRT (three times per week) resulted in reduced plasma glycosylated hemoglobin levels (from 8.7 Ϯ 0.3 to 7.6 Ϯ 0.2%), increased muscle glycogen stores (from 60.3 Ϯ 3.9 to 79.1 Ϯ 5.0 mmol glucose/kg muscle), and reduced the dose of prescribed diabetes medication in 72% of exercisers compared with the control group, P ϭ 0.004 -0.05. Control subjects showed no change in glycosylated hemoglobin, a reduction in muscle glycogen (from 61.4 Ϯ 7.7 to 47.2 Ϯ 6.7 mmol glucose/kg muscle), and a 42% increase in diabetes medications. PRT subjects versus control subjects also increased lean mass (ϩ1.2 Ϯ 0.2 vs. Ϫ0.1 Ϯ 0.1 kg), reduced systolic blood pressure (-9.7 Ϯ 1.6 vs. ϩ7.7 Ϯ 1.9 mmHg), and decreased trunk fat mass (Ϫ0.7 Ϯ 0.1 vs. ϩ0.8 Ϯ 0.1 kg; P ϭ 0.01-0.05).CONCLUSIONS -PRT as an adjunct to standard of care is feasible and effective in improving glycemic control and some of the abnormalities associated with the metabolic syndrome among high-risk older adults with type 2 diabetes.

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A low physical activity level is the main determinant of lower-than-normal TEE, and thus energy requirements, in women with RA.

Objective. Patients with rheumatoid arthritis (RA) lose body cell mass (BCM) by unknown mechanisms. Since the loss of BCM in normal aging individuals parallels the characteristic age-related decline in growth hormone (GH) secretion, this study was carried out to determine whether further decreased GH secretion plays a role in the pathogenesis of this loss of BCM in RA patients, termed "rheumatoid cachexia."Methods. GH secretory kinetics were determined by deconvolution analysis in 16 patients with RA and 17 healthy controls matched for age (mean ؎ SD 45.4 ؎ 13.2 years and 47.1 ؎ 14.6 years, respectively), sex, race, and body mass index. Blood samples were obtained every 20 minutes for 24 hours. Body composition was ascertained using total-body potassium (TBK) as a measure of BCM and dual x-ray absorptiometry to determine fat mass.Results. BCM was reduced in patients with RA compared with healthy controls (mean ؎ SD gm TBK 79.5 ؎ 9.5 versus 94.9 ؎ 11.9; P < 0.0005), but there was no difference in fat mass. GH kinetic parameters in patients with RA did not differ from those in controls.Conclusion. These findings suggest that GH kinetics are unaltered in RA patients compared with healthy subjects; thus, GH deficiency does not account for rheumatoid cachexia.