Feeding stimulates robust increases in muscle protein synthesis (MPS); however, ageing may alter the anabolic response to protein ingestion and the subsequent aminoacidaemia. With this as background, we aimed to determine in the present study the dose -response of MPS with the ingestion of isolated whey protein, with and without prior resistance exercise, in the elderly. For the purpose of this study, thirty-seven elderly men (age 71 (SD 4) years) completed a bout of unilateral leg-based resistance exercise before ingesting 0, 10, 20 or 40 g of whey protein isolate (W0 -W40, respectively). Infusion of L-[1-13 C]leucine and L-[ring-13 C 6 ]phenylalanine with bilateral vastus lateralis muscle biopsies were used to ascertain whole-body leucine oxidation and 4 h post-protein consumption of MPS in the fed-state of non-exercised and exercised leg muscles. It was determined that whole-body leucine oxidation increased in a stepwise, dose-dependent manner. MPS increased above basal, fasting values by approximately 65 and 90 % for W20 and W40, respectively (P,0·05), but not with lower doses of whey. While resistance exercise was generally effective at stimulating MPS, W20 and W40 ingestion post-exercise increased MPS above W0 and W10 exercised values (P,0·05) and W40 was greater than W20 (P, 0·05). Based on the study, the following conclusions were drawn. At rest, the optimal whey protein dose for non-frail older adults to consume, to increase myofibrillar MPS above fasting rates, was 20 g. Resistance exercise increases MPS in the elderly at all protein doses, but to a greater extent with 40 g of whey ingestion. These data suggest that, in contrast to younger adults, in whom post-exercise rates of MPS are saturated with 20 g of protein, exercised muscles of older adults respond to higher protein doses.
In patients with type 2 diabetes, 6-month treatment with a low-glycemic index diet resulted in moderately lower HbA(1c) levels compared with a high-cereal fiber diet. Trial Registration clinicaltrials.gov identifier: NCT00438698.
Weight loss can have substantial health benefits for overweight or obese persons; however, the ratio of fat:lean tissue loss may be more important. We aimed to determine how daily exercise (resistance and/or aerobic) and a hypoenergetic diet varying in protein and calcium content from dairy foods would affect the composition of weight lost in otherwise healthy, premenopausal, overweight, and obese women. Ninety participants were randomized to 3 groups (n = 30/group): high protein, high dairy (HPHD), adequate protein, medium dairy (APMD), and adequate protein, low dairy (APLD) differing in the quantity of total dietary protein and dairy food-source protein consumed: 30 and 15%, 15 and 7.5%, or 15 and <2% of energy, respectively. Body composition was measured by DXA at 0, 8, and 16 wk and MRI (n = 39) to assess visceral adipose tissue (VAT) volume at 0 and 16 wk. All groups lost body weight (P < 0.05) and fat (P < 0.01); however, fat loss during wk 8–16 was greater in the HPHD group than in the APMD and APLD groups (P < 0.05). The HPHD group gained lean tissue with a greater increase during 8–16 wk than the APMD group, which maintained lean mass and the APLD group, which lost lean mass (P < 0.05). The HPHD group also lost more VAT as assessed by MRI (P < 0.05) and trunk fat as assessed by DXA (P < 0.005) than the APLD group. The reduction in VAT in all groups was correlated with intakes of calcium (r = 0.40; P < 0.05) and protein (r = 0.32; P < 0.05). Therefore, diet- and exercise-induced weight loss with higher protein and increased dairy product intakes promotes more favorable body composition changes in women characterized by greater total and visceral fat loss and lean mass gain.
Strategies that decrease postprandial glucose excursions, including digestive enzyme inhibition, and low glycemic index diets result in lower diabetes incidence and coronary heart disease (CHD) risk, possibly through lower postprandial oxidative damage to lipids and proteins. We therefore assessed the effect of decreasing postprandial glucose excursions on measures of oxidative damage. Fifteen healthy subjects ate 2 bread control meals and 3 test meals: almonds and bread; parboiled rice; and instant mashed potatoes, balanced in carbohydrate, fat, and protein, using butter and cheese. We obtained blood samples at baseline and for 4 h postprandially. Glycemic indices for the rice (38 +/- 6) and almond meals (55 +/- 7) were less than for the potato meal (94 +/- 11) (P < 0.003), as were the postprandial areas under the insulin concentration time curve (P < 0.001). No postmeal treatment differences were seen in total antioxidant capacity. However, the serum protein thiol concentration increased following the almond meal (15 +/- 14 mmol/L), indicating less oxidative protein damage, and decreased after the control bread, rice, and potato meals (-10 +/- 8 mmol/L), when data from these 3 meals were pooled (P = 0.021). The change in protein thiols was also negatively related to the postprandial incremental peak glucose (r = -0.29, n = 60 observations, P = 0.026) and peak insulin responses (r = -0.26, n = 60 observations, P = 0.046). Therefore, lowering postprandial glucose excursions may decrease the risk of oxidative damage to proteins. Almonds are likely to lower this risk by decreasing the glycemic excursion and by providing antioxidants. These actions may relate to mechanisms by which nuts are associated with a decreased risk of CHD.
Heavy, whole-body resistance exercise with the consumption of milk versus carbohydrate in the early postexercise period resulted in greater muscle mass accretion, strength gains, fat mass loss, and a possible reduction in bone turnover in women after 12 wk. Our results, similar to those in men, highlight that milk is an effective drink to support favorable body composition changes in women with resistance training.
Nut consumption has been associated with reduced coronary heart disease (CHD) risk. In addition to cholesterol-lowering properties, almonds have been shown to lower oxidized LDL concentrations. However, little is known regarding their effects on other markers of oxidative stress. The dose-response effects of whole almonds, taken as snacks, were compared with low-saturated fat (<5% energy) whole-wheat muffins (control) in the therapeutic diets of hyperlipidemic subjects. In a randomized crossover study, 27 hyperlipidemic men and women consumed 3 isoenergetic (mean 423 kcal/d or 1770 kJ/d) supplements each for 1 mo. Supplements consisted of full-dose almonds (73 +/- 3 g/d), half-dose almonds plus half-dose muffins (half-dose almonds), and full-dose muffins (control). Subjects were assessed at wk 0, 2 and 4. Mean body weights differed < or = 300 g between treatments, although the weight loss on the half-dose almond treatment was greater than on the control (P < 0.01). At 4 wk, the full-dose almonds reduced serum concentrations of malondialdehyde (MDA) (P = 0.040) and creatinine-adjusted urinary isoprostane output (P = 0.026) compared with the control. Serum concentrations of alpha- or gamma-tocopherol, adjusted or unadjusted for total cholesterol, were not affected by the treatments. Almond antioxidant activity was demonstrated by their effect on 2 biomarkers of lipid peroxidation, serum MDA and urinary isoprostanes, and supports the previous finding that almonds reduced oxidation of LDL-C. Antioxidant activity provides an additional possible mechanism, in addition to lowering cholesterol, that may account for the reduction in CHD risk with nut consumption.
Genome-wide association studies (GWAS), relying on hundreds of thousands of individuals, have revealed >200 genomic loci linked to metabolic disease (MD). Loss of insulin sensitivity (IS) is a key component of MD and we hypothesized that discovery of a robust IS transcriptome would help reveal the underlying genomic structure of MD. Using 1,012 human skeletal muscle samples, detailed physiology and a tissue-optimized approach for the quantification of coding (>18,000) and non-coding (>15,000) RNA (ncRNA), we identified 332 fasting IS-related genes (CORE-IS). Over 200 had a proven role in the biochemistry of insulin and/or metabolism or were located at GWAS MD loci. Over 50% of the CORE-IS genes responded to clinical treatment; 16 quantitatively tracking changes in IS across four independent studies (P = 0.0000053: negatively: AGL, G0S2, KPNA2, PGM2, RND3 and TSPAN9 and positively: ALDH6A1, DHTKD1, ECHDC3, MCCC1, OARD1, PCYT2, PRRX1, SGCG, SLC43A1 and SMIM8). A network of ncRNA positively related to IS and interacted with RNA coding for viral response proteins (P < 1 × 10−48), while reduced amino acid catabolic gene expression occurred without a change in expression of oxidative-phosphorylation genes. We illustrate that combining in-depth physiological phenotyping with robust RNA profiling methods, identifies molecular networks which are highly consistent with the genetics and biochemistry of human metabolic disease.
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