Physical therapists commonly treat people with diabetes for a wide variety of diabetes-associated impairments, including those from diabetes-related vascular disease. Diabetes is associated with both microvascular and macrovascular diseases affecting several organs, including muscle, skin, heart, brain, and kidneys. A common etiology links the different types of diabetes-associated vascular disease. Common risk factors for vascular disease in people with diabetes, specifically type 2 diabetes, include hyperglycemia, insulin resistance, dyslipidemia, hypertension, tobacco use, and obesity. Mechanisms for vascular disease in diabetes include the pathologic effects of advanced glycation end product accumulation, impaired vasodilatory response attributable to nitric oxide inhibition, smooth muscle cell dysfunction, overproduction of endothelial growth factors, chronic inflammation, hemodynamic dysregulation, impaired fibrinolytic ability, and enhanced platelet aggregation. It is becoming increasingly important for physical therapists to be aware of diabetes-related vascular complications as more patients present with insulin resistance and diabetes. The opportunities for effective physical therapy interventions (such as exercise) are significant.

Objective-Our objective was to examine the effects of exercise training (EXS) on quality of life (QoL) in highly active antiretroviral therapy (HAART)-treated HIV-positive (HIV+) subjects with body fat redistribution (BFR) in Rwanda.Methods-The effects of a randomised controlled trial of EXS on QoL were measured using World Health Organisation Quality of Life (WHOQOL)-BREF in HIV+ subjects with BFR randomised to EXS (n = 50; BFR + EXS) or no exercise training (n = 50; BFR + noEXS). Conclusions-Exercise training improved several components of QoL in HAART-treated HIV+ African subjects with BFR. Exercise training is an inexpensive and efficacious strategy for Results-At

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Barth syndrome (BTHS) is a mitochondrial myopathy characterized by reports of exercise intolerance. We sought to determine if 1) BTHS leads to abnormalities of skeletal muscle O(2) extraction/utilization and 2) exercise intolerance in BTHS is related to impaired O(2) extraction/utilization, impaired cardiac function, or both. Participants with BTHS (age: 17 ± 5 yr, n = 15) and control participants (age: 13 ± 4 yr, n = 9) underwent graded exercise testing on a cycle ergometer with continuous ECG and metabolic measurements. Echocardiography was performed at rest and at peak exercise. Near-infrared spectroscopy of the vastus lateralis muscle was continuously recorded for measurements of skeletal muscle O(2) extraction. Adjusting for age, peak O(2) consumption (16.5 ± 4.0 vs. 39.5 ± 12.3 ml·kg(-1)·min(-1), P < 0.001) and peak work rate (58 ± 19 vs. 166 ± 60 W, P < 0.001) were significantly lower in BTHS than control participants. The percent increase from rest to peak exercise in ejection fraction (BTHS: 3 ± 10 vs. control: 19 ± 4%, P < 0.01) was blunted in BTHS compared with control participants. The muscle tissue O(2) saturation change from rest to peak exercise was paradoxically opposite (BTHS: 8 ± 16 vs. control: -5 ± 9, P < 0.01), and the deoxyhemoglobin change was blunted (BTHS: 0 ± 12 vs. control: 10 ± 8, P < 0.09) in BTHS compared with control participants, indicating impaired skeletal muscle extraction in BTHS. In conclusion, severe exercise intolerance in BTHS is due to both cardiac and skeletal muscle impairments that are consistent with cardiac and skeletal mitochondrial myopathy. These findings provide further insight to the pathophysiology of BTHS.

BackgroundAn increasingly large share of diet comes from ultra-processed foods (UPFs), which are assemblages of food substances designed to create durable, convenient and palatable ready-to-eat products. There is increasing evidence that high UPF consumption is indicative of poor diet and is associated with obesity and metabolic disorders. This study sought to examine the relationship between percent of energy intake from ultra-processed foods (PEI-UPF) during pregnancy and maternal gestational weight gain, maternal lipids and glycemia, and neonatal body composition. We also compared the PEI-UPF indicator against the US government’s Healthy Eating Index-2010 (HEI-2010).MethodsData were used from a longitudinal study performed in 2013–2014 at the Women’s Health Center and Obstetrics & Gynecology Clinic in St. Louis, MO, USA. Subjects were pregnant women in the normal and obese weight ranges, as well as their newborns (n = 45). PEI-UPF and the Healthy Eating Index-2010 (HEI-2010) were calculated for each subject from a one-month food frequency questionnaire (FFQ). Multiple regression (ANCOVA-like) analysis was used to analyze the relationship between PEI-UPF or HEI-2010 and various clinical outcomes. The ability of these dietary indices to predict clinical outcomes was also compared with the predictive abilities of total energy intake and total fat intake.ResultsAn average of 54.4 ± 13.2% of energy intake was derived from UPFs. A 1%-point increase in PEI-UPF was associated with a 1.33 kg increase in gestational weight gain (p = 0.016). Similarly, a 1%-point increase in PEI-UPF was associated with a 0.22 mm increase in thigh skinfold (p = 0.045), 0.14 mm in subscapular skinfold (p = 0.026), and 0.62 percentage points of total body adiposity (p = 0.037) in the neonate.DiscussionPEI-UPF (percent of energy intake from ultra-processed foods) was associated with and may be a useful predictor of increased gestational weight gain and neonatal body fat. PEI-UPF was a better predictor of all tested outcomes than either total energy or fat intake, and a better predictor of the three infant body fat measures than HEI-2010. UPF consumption should be limited during pregnancy and diet quality should be maximized in order to improve maternal and neonatal health.