New evidence shows that older adults need more dietary protein than do younger adults to support good health, promote recovery from illness, and maintain functionality. Older people need to make up for age-related changes in protein metabolism, such as high splanchnic extraction and declining anabolic responses to ingested protein. They also need more protein to offset inflammatory and catabolic conditions associated with chronic and acute diseases that occur commonly with aging. With the goal of developing updated, evidence-based recommendations for optimal protein intake by older people, the European Union Geriatric Medicine Society (EUGMS), in cooperation with other scientific organizations, appointed an international study group to review dietary protein needs with aging (PROT-AGE Study Group). To help older people (>65 years) maintain and regain lean body mass and function, the PROT-AGE study group recommends average daily intake at least in the range of 1.0 to 1.2 g protein per kilogram of body weight per day. Both endurance- and resistance-type exercises are recommended at individualized levels that are safe and tolerated, and higher protein intake (ie, ≥ 1.2 g/kg body weight/d) is advised for those who are exercising and otherwise active. Most older adults who have acute or chronic diseases need even more dietary protein (ie, 1.2-1.5 g/kg body weight/d). Older people with severe kidney disease (ie, estimated GFR <30 mL/min/1.73 m(2)), but who are not on dialysis, are an exception to this rule; these individuals may need to limit protein intake. Protein quality, timing of ingestion, and intake of other nutritional supplements may be relevant, but evidence is not yet sufficient to support specific recommendations. Older people are vulnerable to losses in physical function capacity, and such losses predict loss of independence, falls, and even mortality. Thus, future studies aimed at pinpointing optimal protein intake in specific populations of older people need to include measures of physical function.

Low-volume 'sprint' interval training (SIT) stimulates rapid improvements in muscle oxidative capacity that are comparable to levels reached following traditional endurance training (ET) but no study has examined metabolic adaptations during exercise after these different training strategies. We hypothesized that SIT and ET would induce similar adaptations in markers of skeletal muscle carbohydrate (CHO) and lipid metabolism and metabolic control during exercise despite large differences in training volume and time commitment. Active but untrained subjects (23 ± 1 years) performed a constant-load cycling challenge (1 h at 65% of peak oxygen uptake (V O 2 peak ) before and after 6 weeks of either SIT or ET (n = 5 men and 5 women per group). SIT consisted of four to six repeats of a 30 s 'all out' Wingate Test (mean power output ∼500 W) with 4.5 min recovery between repeats, 3 days per week. ET consisted of 40-60 min of continuous cycling at a workload that elicited ∼65%V O 2 peak (mean power output ∼150 W) per day, 5 days per week. Weekly time commitment (∼1.5 versus ∼4.5 h) and total training volume (∼225 versus ∼2250 kJ week −1 ) were substantially lower in SIT versus ET. Despite these differences, both protocols induced similar increases (P < 0.05) in mitochondrial markers for skeletal muscle CHO (pyruvate dehydrogenase E1α protein content) and lipid oxidation (3-hydroxyacyl CoA dehydrogenase maximal activity) and protein content of peroxisome proliferator-activated receptor-γ coactivator-1α. Glycogen and phosphocreatine utilization during exercise were reduced after training, and calculated rates of whole-body CHO and lipid oxidation were decreased and increased, respectively, with no differences between groups (all main effects, P < 0.05). Given the markedly lower training volume in the SIT group, these data suggest that high-intensity interval training is a time-efficient strategy to increase skeletal muscle oxidative capacity and induce specific metabolic adaptations during exercise that are comparable to traditional ET.

This study was designed to compare the acute response of mixed muscle protein synthesis (MPS) to rapidly (i.e., whey hydrolysate and soy) and slowly (i.e., micellar casein) digested proteins both at rest and after resistance exercise. Three groups of healthy young men (n = 6 per group) performed a bout of unilateral leg resistance exercise followed by the consumption of a drink containing an equivalent content of essential amino acids (10 g) as either whey hydrolysate, micellar casein, or soy protein isolate. Mixed MPS was determined by a primed constant infusion of l-[ring-(13)C(6)]phenylalanine. Ingestion of whey protein resulted in a larger increase in blood essential amino acid, branched-chain amino acid, and leucine concentrations than either casein or soy (P < 0.05). Mixed MPS at rest (determined in the nonexercised leg) was higher with ingestion of faster proteins (whey = 0.091 +/- 0.015, soy = 0.078 +/- 0.014, casein = 0.047 +/- 0.008%/h); MPS after consumption of whey was approximately 93% greater than casein (P < 0.01) and approximately 18% greater than soy (P = 0.067). A similar result was observed after exercise (whey > soy > casein); MPS following whey consumption was approximately 122% greater than casein (P < 0.01) and 31% greater than soy (P < 0.05). MPS was also greater with soy consumption at rest (64%) and following resistance exercise (69%) compared with casein (both P < 0.01). We conclude that the feeding-induced simulation of MPS in young men is greater after whey hydrolysate or soy protein consumption than casein both at rest and after resistance exercise; moreover, despite both being fast proteins, whey hydrolysate stimulated MPS to a greater degree than soy after resistance exercise. These differences may be related to how quickly the proteins are digested (i.e., fast vs. slow) or possibly to small differences in leucine content of each protein.

Ingestion of 20 g intact protein is sufficient to maximally stimulate MPS and APS after resistance exercise. Phosphorylation of candidate signaling proteins was not enhanced with any dose of protein ingested, which suggested that the stimulation of MPS after resistance exercise may be related to amino acid availability. Finally, dietary protein consumed after exercise in excess of the rate at which it can be incorporated into tissue protein stimulates irreversible oxidation.

ObjectiveWe performed a systematic review, meta-analysis and meta-regression to determine if dietary protein supplementation augments resistance exercise training (RET)-induced gains in muscle mass and strength.Data sourcesA systematic search of Medline, Embase, CINAHL and SportDiscus.Eligibility criteriaOnly randomised controlled trials with RET ≥6 weeks in duration and dietary protein supplementation.DesignRandom-effects meta-analyses and meta-regressions with four a priori determined covariates. Two-phase break point analysis was used to determine the relationship between total protein intake and changes in fat-free mass (FFM).ResultsData from 49 studies with 1863 participants showed that dietary protein supplementation significantly (all p<0.05) increased changes (means (95% CI)) in: strength—one-repetition-maximum (2.49 kg (0.64, 4.33)), FFM (0.30 kg (0.09, 0.52)) and muscle size—muscle fibre cross-sectional area (CSA; 310 µm2 (51, 570)) and mid-femur CSA (7.2 mm2 (0.20, 14.30)) during periods of prolonged RET. The impact of protein supplementation on gains in FFM was reduced with increasing age (−0.01 kg (−0.02,–0.00), p=0.002) and was more effective in resistance-trained individuals (0.75 kg (0.09, 1.40), p=0.03). Protein supplementation beyond total protein intakes of 1.62 g/kg/day resulted in no further RET-induced gains in FFM.Summary/conclusionDietary protein supplementation significantly enhanced changes in muscle strength and size during prolonged RET in healthy adults. Increasing age reduces and training experience increases the efficacy of protein supplementation during RET. With protein supplementation, protein intakes at amounts greater than ~1.6 g/kg/day do not further contribute RET-induced gains in FFM.