Nutrient intake among US adults with disabilities.

BACKGROUND: Physical, mental and financial barriers among persons with disabilities limit their access to healthier diet. The present study investigated the relationship between disabilities and nutrient intake among US adults. METHODS: Data originated from National Health and Nutrition Examination Survey 2007-2008 and 2009-2010 waves (n = 11,811). Five disability categories include activities of daily living (ADLs), instrumental activities of daily living (IADLs), leisure and social activities (LSAs), lower extremity mobility (LEM) and general physical activities (GPAs). Nutrient intakes from food and dietary supplements were calculated from 24-h dietary recalls. Adherence to dietary reference intakes and dietary guideline recommendations was compared between people with and without disabilities and across disability categories in the statistical analysis. RESULTS: GPAs, IADLs, LSAs, LEM and ADLs occupied 24.5%, 13.3%, 9.9%, 9.2% and 9.2% of US adults, respectively (not mutually exclusive). Only 42.3%, 11.3%, 63.8%, 47.7%, 48.7%, 9.7%, 48.7%, 90.7%, 21.7% and 4.7% of adults had saturated fat, fibre, cholesterol, vitamin A, vitamin C, vitamin D, calcium, iron, sodium and potassium intakes from food within recommended levels, respectively. Dietary supplement use moderately improved vitamin C, vitamin D and calcium intakes. People with disabilities were less likely to meet recommended levels on saturated fat, fibre (except GPAs), vitamin A (except GPAs), vitamin C (except GPAs), calcium and potassium intakes than persons without disability. Nutrient intake differed across disability categories, with ADLs least likely to meet recommended intakes. CONCLUSIONS: Interventions targeting persons with disabilities through nutrition education and financial assistance are warranted to promote healthy diet and reduce disparities.

Influence of concurrent exercise or nutrition countermeasures on thigh and calf muscle size and function during 60 days of bed rest in women.

AIM: The goal of this investigation was to test specific exercise and nutrition countermeasures to lower limb skeletal muscle volume and strength losses during 60 days of simulated weightlessness (6 degrees head-down-tilt bed rest). METHODS: Twenty-four women underwent bed rest only (BR, n = 8), bed rest and a concurrent exercise training countermeasure (thigh and calf resistance training and aerobic treadmill training; BRE, n = 8), or bed rest and a nutrition countermeasure (a leucine-enriched high protein diet; BRN, n = 8). RESULTS: Thigh (quadriceps femoris) muscle volume was decreased (P < 0.05) in BR (-21 +/- 1%) and BRN (-24 +/- 2%), with BRN losing more (P < 0.05) than BR. BRE maintained (P > 0.05) thigh muscle volume. Calf (triceps surae) muscle volume was decreased (P < 0.05) to a similar extent (P > 0.05) in BR (-29 +/- 1%) and BRN (-28 +/- 1%), and this decrease was attenuated (P < 0.05) in BRE (-8 +/- 2%). BR and BRN experienced large (P < 0.05) and similar (P > 0.05) decreases in isometric and dynamic (concentric force, eccentric force, power and work) muscle strength for supine squat (-19 to -33%) and calf press (-26 to -46%). BRE maintained (P > 0.05) or increased (P < 0.05) all measures of muscle strength. CONCLUSION: The nutrition countermeasure was not effective in offsetting lower limb muscle volume or strength loss, and actually promoted thigh muscle volume loss. The concurrent aerobic and resistance exercise protocol was effective at preventing thigh muscle volume loss, and thigh and calf muscle strength loss. While the exercise protocol offset approximately 75% of the calf muscle volume loss, modification of this regimen is needed.

Resistance exercise and cyclooxygenase (COX) expression in human skeletal muscle: implications for COX-inhibiting drugs and protein synthesis.

We have shown that ibuprofen and acetaminophen block cyclooxygenase (COX) synthesis of prostaglandin PGF(2alpha) and the muscle protein synthesis increase following resistance exercise. Confusingly, these two drugs are purported to work through different mechanisms, with acetaminophen apparently unable to block COX and ibuprofen able to nonspecifically block COX-1 and COX-2. A recently discovered intron-retaining COX, now known to have three variants, has been shown to be sensitive to both drugs. We measured the expression patterns and levels of the intron 1-retaining COX-1 variants (-1b1, -1b2, and -1b3), COX-1, and COX-2 at rest and following resistance exercise to help elucidate the COX through which PGF(2alpha), ibuprofen, and acetaminophen regulate muscle protein synthesis. Skeletal muscle biopsy samples were taken from 16 individuals (8M, 8F) before, 4, and 24 h after a bout of resistance exercise and analyzed using real-time RT-PCR. Relatively few individuals expressed the intron 1-retaining COX-1b variants (COX-1b1, -1b2, and -1b3) at any time point, and when expressed, these variants were in very low abundance. COX-1 was the most abundant COX mRNA before exercise and remained unchanged (P > 0.05) following exercise. COX-2 was not expressed before exercise, but increased significantly (P < 0.05) at 4 and 24 h after exercise. The inconsistent and low levels of expression of the intron 1-retaining COX-1 variants suggest that these variants are not likely responsible for the inhibition of PGF(2alpha) production and skeletal muscle protein synthesis after resistance exercise by ibuprofen and acetaminophen. Skeletal muscle-specific inhibition of COX-1 or COX-2 by these drugs should be considered.