Dietary protein recommendations to support healthy muscle ageing in the 21st century and beyond: considerations and future directions.

This review explores the evolution of dietary protein intake requirements and recommendations, with a focus on skeletal muscle remodelling to support healthy ageing based on presentations at the 2023 Nutrition Society summer conference. In this review, we describe the role of dietary protein for metabolic health and ageing muscle, explain the origins of protein and amino acid (AA) requirements and discuss current recommendations for dietary protein intake, which currently sits at about 0⋅8 g/kg/d. We also critique existing (e.g. nitrogen balance) and contemporary (e.g. indicator AA oxidation) methods to determine protein/AA intake requirements and suggest that existing methods may underestimate requirements, with more contemporary assessments indicating protein recommendations may need to be increased to >1⋅0 g/kg/d. One example of evolution in dietary protein guidance is the transition from protein requirements to recommendations. Hence, we discuss the refinement of protein/AA requirements for skeletal muscle maintenance with advanced age beyond simply the dose (e.g. source, type, quality, timing, pattern, nutrient co-ingestion) and explore the efficacy and sustainability of alternative protein sources beyond animal-based proteins to facilitate skeletal muscle remodelling in older age. We conclude that, whilst a growing body of research has demonstrated that animal-free protein sources can effectively stimulate and support muscle remodelling in a manner that is comparable to animal-based proteins, food systems need to sustainably provide a diversity of both plant and animal source foods, not least for their protein content but other vital nutrients. Finally, we propose some priority research directions for the field of protein nutrition and healthy ageing.

A single bout of prior resistance exercise attenuates muscle atrophy and declines in myofibrillar protein synthesis during bed-rest in older men.

Impairments in myofibrillar protein synthesis (MyoPS) during bed rest accelerate skeletal muscle loss in older adults, increasing the risk of adverse secondary health outcomes. We investigated the effect of prior resistance exercise (RE) on MyoPS and muscle morphology during a disuse event in 10 healthy older men (65-80 years). Participants completed a single bout of unilateral leg RE the evening prior to 5 days of in-patient bed-rest. Quadriceps cross-sectional area (CSA) was determined prior to and following bed-rest. Serial muscle biopsies and dual stable isotope tracers were used to determine rates of integrated MyoPS (iMyoPS) over a 7 day habitual 'free-living' phase and the bed-rest phase, and rates of acute postabsorptive and postprandial MyoPS (aMyoPS) at the end of bed rest. Quadriceps CSA at 40%, 60% and 80% of muscle length significantly decreased in exercised (EX) and non-exercised control (CTL) legs with bed-rest. The decline in quadriceps CSA at 40% and 60% of muscle length was attenuated in EX compared with CTL. During bed-rest, iMyoPS rates decreased from habitual values in CTL, but not EX, and were significantly different between legs. Postprandial aMyoPS rates increased above postabsorptive values in EX only. The change in iMyoPS over bed-rest correlated with the change in quadriceps CSA in CTL, but not EX. A single bout of RE attenuated the decline in iMyoPS rates and quadriceps atrophy with 5 days of bed-rest in older men. Further work is required to understand the functional and clinical implications of prior RE in older patient populations. KEY POINTS: Age-related skeletal muscle deterioration, linked to numerous adverse health outcomes, is driven by impairments in muscle protein synthesis that are accelerated during periods of disuse. Resistance exercise can stimulate muscle protein synthesis over several days of recovery and therefore could counteract impairments in this process that occur in the early phase of disuse. In the present study, we demonstrate that the decline in myofibrillar protein synthesis and muscle atrophy over 5 days of bed-rest in older men was attenuated by a single bout of unilateral resistance exercise performed the evening prior to bed-rest. These findings suggest that concise resistance exercise intervention holds the potential to support muscle mass retention in older individuals during short-term disuse, with implications for delaying sarcopenia progression in ageing populations.

Greater myofibrillar protein synthesis following weight-bearing activity in obese old compared with non-obese old and young individuals.

The mechanisms through which obesity impacts age-related muscle mass regulation are unclear. In the present study, rates of integrated myofibrillar protein synthesis (iMyoPS) were measured over 48-h prior-to and following a 45-min treadmill walk in 10 older-obese (O-OB, body fat[%]: 33 ± 3%), 10 older-non-obese (O-NO, 20 ± 3%), and 15 younger-non-obese (Y-NO, 13 ± 5%) individuals. Surface electromyography was used to determine thigh muscle "activation". Quadriceps cross-sectional area (CSA), volume, and intramuscular thigh fat fraction (ITFF) were measured by magnetic resonance imaging. Quadriceps maximal voluntary contraction (MVC) was measured by dynamometry. Quadriceps CSA and volume were greater (muscle volume, Y-NO: 1182 ± 232 cm3; O-NO: 869 ± 155 cm3; O-OB: 881 ± 212 cm3, P < 0.01) and ITFF significantly lower (m. vastus lateralis, Y-NO: 3.0 ± 1.0%; O-NO: 4.0 ± 0.9%; O-OB: 9.1 ± 2.6%, P ≤ 0.03) in Y-NO compared with O-NO and O-OB, with no difference between O-NO and O-OB in quadriceps CSA and volume. ITFF was significantly higher in O-OB compared with O-NO. Relative MVC was lower in O-OB compared with Y-NO and O-NO (Y-NO: 5.5 ± 1.6 n·m/kg-1; O-NO: 3.9 ± 1.0 n·m/kg-1; O-OB: 2.9 ± 1.1 n·m/kg-1, P < 0.0001). Thigh muscle "activation" during the treadmill walk was greater in O-OB compared with Y-NO and O-NO (Y-NO: 30.5 ± 13.5%; O-NO: 35.8 ± 19.7%; O-OB: 68.3 ± 32.3%, P < 0.01). Habitual iMyoPS did not differ between groups, whereas iMyoPS was significantly elevated over 48-h post-walk in O-OB (+ 38.6 ± 1.2%·day-1, P < 0.01) but not Y-NO or O-NO (+ 11.4 ± 1.1%·day-1 and + 17.1 ± 1.1%·day-1, respectively, both P > 0.271). Equivalent muscle mass in O-OB may be explained by the muscle anabolic response to weight-bearing activity, whereas the age-related decline in indices of muscle quality appears to be exacerbated in O-OB and warrants further exploration.

Myofibrillar Protein Synthesis and Acute Intracellular Signaling with Elastic Band Resistance Exercise in Young and Older Men.

PURPOSE: Resistance exercise training (RET) attenuates age-related muscle and strength loss ("sarcopenia"). However, compared with machine-based RET, the efficacy of cost-effective, accessible elastic band RET (EB-RET) for muscle adaptive remodeling lacks supporting mechanistic evidence. METHODS: Eight young (YM; 24 ± 4 yr) and eight older (OM; 68 ± 6 yr) untrained males consumed an oral stable isotope tracer (D 2 O) combined with serial vastus lateralis muscle biopsies to measure integrated myofibrillar protein synthesis (iMyoPS) and regulatory signaling over ~48 h before (habitual) and after an acute bout of EB-RET (6 × 12 repetitions at ~70% of one-repetition maximum). iMyoPS was determined via gas chromatography-pyrolysis-isotope ratio mass spectroscopy and regulatory signaling expression by immunoblot. RESULTS: Habitual iMyoPS did not differ between YM and OM (1.62% ± 0.21% vs 1.43% ± 0.47%·d -1 , respectively, P = 0.128). There was a significant increase in iMyoPS after EB-RET in YM (2.23% ± 0.69%·d -1 , P = 0.02), but not OM (1.75% ± 0.54%·d -1 , P = 0.30). EB-RET increased the phosphorylation of key anabolic signaling proteins similarly in YM and OM at 1 h postexercise, including p-IRS-1 Ser636/639 , p-Akt Ser473 , p-4EBP-1 Thr37/46 , p-P70S6K Thr389 , and p-RPS6 Ser240/244 , whereas p-TSC2 Thr1462 and p-mTOR Ser2448 increased only in YM (all P < 0.05). There were no differences in the expression of amino acid transporters/sensors or proteolytic markers after EB-RET. CONCLUSIONS: iMyoPS was elevated after EB-RET in YM but not OM. However, the increase in acute anabolic signaling with EB-RET was largely similar between groups. In conclusion, the capacity for EB-RET to stimulate iMyoPS may be impaired in older age. Further work may be necessary to optimize prescriptive programming in YM and OM.

Associations of Bioavailable Serum Testosterone With Cognitive Function in Older Men: Results From the National Health and Nutrition Examination Survey.

BACKGROUND: Age-associated cognitive decline may be influenced by testosterone status. However, studies evaluating the impact of bioavailable testosterone, the active, free testosterone, on cognitive function are scarce. Our study determined the relationship between calculated bioavailable testosterone and cognitive performance in older men. METHODS: We used data from the U.S. National Health and Nutrition Examination Survey (NHANES) between 2013 and 2014. This study consisted of 208 men aged ≥60 years. Bioavailable serum testosterone was calculated based on the total serum testosterone, sex hormone-binding globulin, and albumin levels, whereas cognitive performance was assessed through the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) Word List Learning Test (WLLT), Word List Recall Test (WLRT), and Intrusion Word Count Test (WLLT-IC and WLRT-IC), the Animal Fluency Test (AFT), and the Digit Symbol Substitution Test (DSST). Multiple linear regression analyses were performed upon adjustment for age, ethnicity, socioeconomic status, education level, medical history, body mass index, energy, alcohol intake, physical activity levels, and sleep duration. RESULTS: A significant positive association between bioavailable testosterone and DSST (ß: 0.049, p = .002) score was detected, with no signs of a plateau effect. No significant associations with CERAD WLLT (p = .132), WLRT (p = .643), WLLT-IC (p = .979), and WLRT-IC (p = .387), and AFT (p = .057) were observed. CONCLUSION: Calculated bioavailable testosterone presented a significant positive association with processing speed, sustained attention, and working memory in older men above 60 years of age. Further research is warranted to elucidate the impact of the inevitable age-related decline in testosterone on cognitive function in older men.

(-)-Epicatechin and its colonic metabolite hippuric acid protect against dexamethasone-induced atrophy in skeletal muscle cells.

Cocoa flavanols have been shown to improve muscle function and may offer a novel approach to protect against muscle atrophy. Hippuric acid (HA) is a colonic metabolite of (-)-epicatechin (EPI), the primary bioactive compound of cocoa, and may be responsible for the associations between cocoa supplementation and muscle metabolic alterations. Accordingly, we investigated the effects of EPI and HA upon skeletal muscle morphology and metabolism within an in vitro model of muscle atrophy. Under atrophy-like conditions (24h 100µM dexamethasone (DEX)), C2C12 myotube diameter was significantly greater following co-incubation with either 25µM HA (11.19±0.39µm) or 25µM EPI (11.01±0.21µm) compared to the vehicle control (VC; 7.61±0.16µm, both P < .001). In basal and leucine-stimulated states, there was a significant reduction in myotube protein synthesis (MPS) rates following DEX treatment in VC (P = .024). Interestingly, co-incubation with EPI or HA abrogated the DEX-induced reductions in MPS rates, whereas no significant differences versus control treated myotubes (CTL) were noted. Furthermore, co-incubation with EPI or HA partially attenuated the increase in proteolysis seen in DEX-treated cells, preserving LC3 α/ß II:I and caspase-3 protein expression in atrophy-like conditions. The protein content of PGC1α, ACC, and TFAM (regulators of mitochondrial function) were significantly lower in DEX-treated versus. CTL cells (all P < .050). However, co-incubation with EPI or HA was unable to prevent these DEX-induced alterations. For the first time we demonstrate that EPI and HA exert anti-atrophic effects on C2C12 myotubes, providing novel insight into the association between flavanol supplementation and favourable effects on muscle health.

No effect of five days of bed rest or short-term resistance exercise prehabilitation on markers of skeletal muscle mitochondrial content and dynamics in older adults.

Bed rest (BR) results in significant impairments in skeletal muscle metabolism. Mitochondrial metabolism is reportedly highly sensitive to disuse, with dysregulated fission-fusion events and impaired oxidative function previously reported. The effects of clinically relevant short-term BR (≤5 days) on mitochondrial protein expression are presently unclear, as are the effects of exercise prehabilitation as a potential counteractive intervention. The present study examined the effects of a 5-day period of BR and short-term resistance exercise prehabilitation (ST-REP) on mitochondrial-protein content. Ten older men (71 ± 4 years) underwent 5 days of BR, completing four sessions of high-volume unilateral resistance exercise prehabilitation over 7 days beforehand. Muscle biopsies were obtained from the vastus lateralis in the non-exercised control and exercised legs, both pre- and post-prehabilitation and pre- and post-BR, to determine changes in citrate synthase enzyme activity and the expression of key proteins in the mitochondrial electron transport chain and molecular regulators of fission-fusion dynamics, biosynthesis, and mitophagy. We observed no significant effect of either BR or ST-REP on citrate synthase protein content, enzyme activity, or ETC complex I-V protein content. Moreover, we observed no significant changes in markers of mitochondrial fission and fusion (p-DRP1S616 , p-DRP1S637 , p-DRP1S616/S637 ratio, p-MFFS146 , Mitofillin, OPA1, or MFN2 (p > 0.05 for all). Finally, we observed no differences in markers of biosynthesis (p-AMPKT172 , p-ACCS79 , PGC1a, TFAM) or mitophagy-related signaling (ULK-1, BNIP3/NIX, LC3B I/II) (p > 0.05 for all). In contrast to previous longer-term periods of musculoskeletal disuse (i.e., 7-14 days), a clinically relevant, 5-day period of BR resulted in no significant perturbation in muscle mitochondrial protein signaling in healthy older adults, with no effect of ST-REP in the week prior to BR. Accordingly, disuse-induced muscle atrophy may precede alterations in mitochondrial content.

Monitoring Postmatch Fatigue During a Competitive Season in Elite Youth Soccer Players.

CONTEXT: Countermovement jump (CMJ) and perceived wellness measures are useful for monitoring fatigue. Fatigue indicators should simultaneously show sensitivity to previous load and demonstrate influence on subsequent physical output; however, these factors have not been examined. OBJECTIVE: To explore the efficacy of CMJ and wellness measures to both detect postmatch fatigue and predict subsequent physical match output in elite youth soccer players. DESIGN: Cross-sectional study. PATIENTS OR OTHER PARTICIPANTS: Sixteen soccer players (18 ± 1 years) from 36 English Football League Youth Alliance League fixtures. MAIN OUTCOME MEASURE(S): Physical match outputs (total distance, high-speed running, very high-speed running, and accelerations and decelerations [AD]) were recorded using a 10-Hz global positioning system and 200-Hz accelerometer device during competitive match play. The CMJ height and perceived wellness were assessed weekly and daily, respectively, as indirect indicators of fatigue. Four subunits of wellness (perceived soreness, energy, general stress, and sleep) were measured using customized psychometric questionnaires. RESULTS: Simple linear regression showed that match AD predicted energy (R2 = 0.08, P = .001), stress (R2 = 0.09, P < .001), and total wellness (R2 = 0.06, P = .002) at 2 days postmatch. The CMJ (R2 = 0.05, P = .002), stress (R2 = 0.08, P < .001), sleep (R2 = 0.03, P = .034), and total wellness (R2 = 0.05, P = .006) measures at 5 days prematch predicted AD during the subsequent match. CONCLUSIONS: The CMJ and wellness measures may be useful for detecting postmatch fatigue. Wellness scores, but not CMJ, at 5 days prematch influenced subsequent match output and therefore may be used to plan and periodize training for the upcoming microcycle.

Acute resistance exercise training does not augment mitochondrial remodelling in master athletes or untrained older adults.

Background: Ageing is associated with alterations to skeletal muscle oxidative metabolism that may be influenced by physical activity status, although the mechanisms underlying these changes have not been unraveled. Similarly, the effect of resistance exercise training (RET) on skeletal muscle mitochondrial regulation is unclear. Methods: Seven endurance-trained masters athletes ([MA], 74 ± 3 years) and seven untrained older adults ([OC]. 69 ± 6 years) completed a single session of knee extension RET (6 x 12 repetitions, 75% 1-RM, 120-s intra-set recovery). Vastus lateralis muscle biopsies were collected pre-RET, 1 h post-RET, and 48h post-RET. Skeletal muscle biopsies were analyzed for citrate synthase (CS) enzyme activity, mitochondrial content, and markers of mitochondrial quality control via immunoblotting. Results: Pre-RET CS activity and protein content were ∼45% (p < .001) and ∼74% greater in MA compared with OC (p = .006). There was a significant reduction (∼18%) in CS activity 48 h post-RET (p < .05) in OC, but not MA. Pre-RET abundance of individual and combined mitochondrial electron transport chain (ETC) complexes I-V were significantly greater in MA compared with OC, as were markers of mitochondrial fission and fusion dynamics (p-DRP-1Ser616, p-MFFSer146, OPA-1 & FIS-1, p < .05 for all). Moreover, MA displayed greater expression of p-AMPKThr172, PGC1α, TFAM, and SIRT-3 (p < .05 for all). Notably, RET did not alter the expression of any marker of mitochondrial content, biogenesis, or quality control in both OC and MA. Conclusion: The present data suggest that long-term aerobic exercise training supports superior skeletal muscle mitochondrial density and protein content into later life, which may be regulated by greater mitochondrial quality control mechanisms and supported via superior fission-fusion dynamics. However, a single session of RET is unable to induce mitochondrial remodelling in the acute (1h post-RET) and delayed (48 h post-RET) recovery period in OC and MA.

Short-term step reduction reduces citrate synthase activity without altering skeletal muscle markers of oxidative metabolism or insulin-mediated signaling in young males.

Mitochondria are critical to skeletal muscle contractile function and metabolic health. Short-term periods of step reduction (SR) are associated with alterations in muscle protein turnover and mass. However, the effects of SR on mitochondrial metabolism/muscle oxidative metabolism and insulin-mediated signaling are unclear. We tested the hypothesis that the total and/or phosphorylated protein content of key skeletal muscle markers of mitochondrial/oxidative metabolism, and insulin-mediated signaling would be altered over 7 days of SR in young healthy males. Eleven, healthy, recreationally active males (means ± SE, age: 22 ± 1 yr, BMI: 23.4 ± 0.7 kg·m2) underwent a 7-day period of SR. Immediately before and following SR, fasted-state muscle biopsy samples were acquired and analyzed for the assessment of total and phosphorylated protein content of key markers of mitochondrial/oxidative metabolism and insulin-mediated signaling. Daily step count was significantly reduced during the SR intervention (13,054 ± 833 to 1,192 ± 99 steps·day-1, P < 0.001). Following SR, there was a significant decline in maximal citrate synthase activity (fold change: 0.94 ± 0.08, P < 0.05) and a significant increase in the protein content of p-glycogen synthase (P-GSS641; fold change: 1.47 ± 0.14, P < 0.05). No significant differences were observed in the total or phosphorylated protein content of other key markers of insulin-mediated signaling, oxidative metabolism, mitochondrial function, or mitochondrial dynamics (all P > 0.05). These results suggest that short-term SR reduces the maximal activity of citrate synthase, a marker of mitochondrial content, without altering the total or phosphorylated protein content of key markers of skeletal muscle mitochondrial metabolism and insulin signaling in young healthy males.NEW & NOTEWORTHY Short-term (7 day) step reduction reduces the activity of citrate synthase without altering the total or phosphorylated protein content of key markers of skeletal muscle mitochondrial metabolism and insulin signaling in young healthy males.

Protein Source and Quality for Skeletal Muscle Anabolism in Young and Older Adults: A Systematic Review and Meta-Analysis.

BACKGROUND: There is much debate regarding the source/quality of dietary proteins in supporting indices of skeletal muscle anabolism. OBJECTIVE: We performed a systematic review and meta-analysis to determine the effect of protein source/quality on acute muscle protein synthesis (MPS) and changes in lean body mass (LBM) and strength, when combined with resistance exercise (RE). METHODS: A systematic search of the literature was conducted to identify studies that compared the effects of ≥2 dose-matched, predominantly isolated protein sources of varying "quality." Three separate models were employed as follows: 1) protein feeding alone on MPS, 2) protein feeding combined with a bout of RE on MPS, and 3) protein feeding combined with longer-term resistance exercise training (RET) on LBM and strength. Further subgroup analyses were performed to compare the effects of protein source/quality between young and older adults. A total of 27 studies in young (18-35 y) and older (≥60 y) adults were included. RESULTS: Analysis revealed an effect favoring higher-quality protein for postprandial MPS at rest [mean difference (MD): 0.014%/h; 95% CI: 0.006, 0.021; P < 0.001] and following RE (MD: 0.022%/h; 95% CI: 0.014, 0.030; P < 0.00001) in young (model 1: 0.016%/h; 95% CI: -0.004, 0.036; P = 0.12; model 2: 0.030%/h; 95% CI: 0.015, 0.045; P < 0.0001) and older (model 1: 0.012%/h; 95% CI: 0.006, 0.018; P < 0.001; model 2: 0.014%/h; 95% CI: 0.007, 0.021; P < 0.001) adults. However, although higher protein quality was associated with superior strength gains with RET [standardized mean difference (SMD): 0.24 kg; 95% CI: 0.02, 0.45; P = 0.03)], no effect was observed on changes to LBM (SMD: 0.05 kg; 95% CI: -0.16, 0.25; P = 0.65). CONCLUSIONS: The current review suggests that protein quality may provide a small but significant impact on indices of muscle protein anabolism in young and older adults. However, further research is warranted to elucidate the importance of protein source/quality on musculoskeletal aging, particularly in situations of low protein intake.

The role of protein hydrolysates for exercise-induced skeletal muscle recovery and adaptation: a current perspective.

The protein supplement industry is expanding rapidly and estimated to have a multi-billion market worth. Recent research has centred on understanding how the manufacturing processes of protein supplements may impact muscle recovery and remodeling. The hydrolysed forms of protein undergo a further heating extraction process during production which may contribute to amino acids (AA) appearing in circulation at a slightly quicker rate, or greater amplitude, than the intact form. Whilst the relative significance of the rate of aminoacidemia to muscle protein synthesis is debated, it has been suggested that protein hydrolysates, potentially through the more rapid delivery and higher proportion of di-, tri- and smaller oligo-peptides into circulation, are superior to intact non-hydrolysed proteins and free AAs in promoting skeletal muscle protein remodeling and recovery. However, despite these claims, there is currently insufficient evidence to support superior muscle anabolic properties compared with intact non-hydrolysed proteins and/or free AA controls. Further research is warranted with appropriate protein controls, particularly in populations consuming insufficient amounts of protein, to support and/or refute an important muscle anabolic role of protein hydrolysates. The primary purpose of this review is to provide the reader with a current perspective on the potential anabolic effects of protein hydrolysates in individuals wishing to optimise recovery from, and maximise adaptation to, exercise training.

The effect of short-term exercise prehabilitation on skeletal muscle protein synthesis and atrophy during bed rest in older men.

BACKGROUND: Poor recovery from periods of disuse accelerates age-related muscle loss, predisposing individuals to the development of secondary adverse health outcomes. Exercise prior to disuse (prehabilitation) may prevent muscle deterioration during subsequent unloading. The present study aimed to investigate the effect of short-term resistance exercise training (RET) prehabilitation on muscle morphology and regulatory mechanisms during 5 days of bed rest in older men. METHODS: Ten healthy older men aged 65-80 years underwent four bouts of high-volume unilateral leg RET over 7 days prior to 5 days of inpatient bed rest. Physical activity and step-count were monitored over the course of RET prehabilitation and bed rest, whilst dietary intake was recorded throughout. Prior to and following bed rest, quadriceps cross-sectional area (CSA), and hormone/lipid profiles were determined. Serial muscle biopsies and dual-stable isotope tracers were used to determine integrated myofibrillar protein synthesis (iMyoPS) over RET prehabilitation and bed rest phases, and acute postabsorptive and postprandial myofibrillar protein synthesis (aMyoPS) rates at the end of bed rest. RESULTS: During bed rest, daily step-count and light and moderate physical activity time decreased, whilst sedentary time increased when compared with habitual levels (P < 0.001 for all). Dietary protein and fibre intake during bed rest were lower than habitual values (P < 0.01 for both). iMyoPS rates were significantly greater in the exercised leg (EX) compared with the non-exercised control leg (CTL) over prehabilitation (1.76 ± 0.37%/day vs. 1.36 ± 0.18%/day, respectively; P = 0.007). iMyoPS rates decreased similarly in EX and CTL during bed rest (CTL, 1.07 ± 0.22%/day; EX, 1.30 ± 0.38%/day; P = 0.037 and 0.002, respectively). Postprandial aMyoPS rates increased above postabsorptive values in EX only (P = 0.018), with no difference in delta postprandial aMyoPS stimulation between legs. Quadriceps CSA at 40%, 60%, and 80% of muscle length decreased significantly in EX and CTL over bed rest (0.69%, 3.5%, and 2.8%, respectively; P < 0.01 for all), with no differences between legs. No differences in fibre-type CSA were observed between legs or with bed rest. Plasma insulin and serum lipids did not change with bed rest. CONCLUSIONS: Short-term resistance exercise prehabilitation augmented iMyoPS rates in older men but did not offset the relative decline in iMyoPS and muscle mass during bed rest.

Enhanced Cycling Time-Trial Performance During Multiday Exercise With Higher-Pressure Compression Garment Wear.

PURPOSE: Compression garments are widely used as a tool to accelerate recovery from intense exercise and have also gained traction as a performance aid, particularly during periods of limited recovery. This study tested the hypothesis that increased pressure levels applied via high-pressure compression garments would enhance "multiday" exercise performance. METHODS: A single-blind crossover design, incorporating 3 experimental conditions-loose-fitting gym attire (CON), low-compression (LC), and high-compression (HC) garments-was adopted. A total of 10 trained male cyclists reported to the laboratory on 6 occasions, collated into 3 blocks of 2 consecutive visits. Each "block" consisted of 3 parts, an initial high-intensity protocol, a 24-hour period of controlled rest while wearing the applied condition/garment (CON, LC, and HC), and a subsequent 8-km cycling time trial, while wearing the respective garment. Subjective discomfort questionnaires and blood pressure were assessed prior to each exercise bout. Power output, oxygen consumption, and heart rate were continuously measured throughout exercise, with plasma lactate, creatine kinase, and myoglobin concentrations assessed at baseline and the end of exercise, as well as 30 and 60 minutes postexercise. RESULTS: Time-trial performance was significantly improved during HC compared with both CON and LC (HC = 277 [83], CON = 266 [89], and LC = 265 [77] W; P < .05). In addition, plasma lactate was significantly lower at 30 and 60 minutes postexercise on day 1 in HC compared with CON. No significant differences were observed for oxygen consumption, heart rate, creatine kinase, or subjective markers of discomfort. CONCLUSION: The pressure levels exerted via lower-limb compression garments influence their effectiveness for cycling performance, particularly in the face of limited recovery.

Exploring the Impact of Obesity on Skeletal Muscle Function in Older Age.

Sarcopenia is of important clinical relevance for loss of independence in older adults. The prevalence of obesity in combination with sarcopenia ("sarcopenic-obesity") is increasing at a rapid rate. However, whilst the development of sarcopenia is understood to be multi-factorial and harmful to health, the role of obesity from a protective and damaging perspective on skeletal muscle in aging, is poorly understood. Specifically, the presence of obesity in older age may be accompanied by a greater volume of skeletal muscle mass in weight-bearing muscles compared with lean older individuals, despite impaired physical function and resistance to anabolic stimuli. Collectively, these findings support a potential paradox in which obesity may protect skeletal muscle mass in older age. One explanation for these paradoxical findings may be that the anabolic response to weight-bearing activity could be greater in obese vs. lean older individuals due to a larger mechanical stimulus, compensating for the heightened muscle anabolic resistance. However, it is likely that there is a complex interplay between muscle, adipose, and external influences in the aging process that are ultimately harmful to health in the long-term. This narrative briefly explores some of the potential mechanisms regulating changes in skeletal muscle mass and function in aging combined with obesity and the interplay with sarcopenia, with a particular focus on muscle morphology and the regulation of muscle proteostasis. In addition, whilst highly complex, we attempt to provide an updated summary for the role of obesity from a protective and damaging perspective on muscle mass and function in older age. We conclude with a brief discussion on treatment of sarcopenia and obesity and a summary of future directions for this research field.

Nutritional Strategies to Offset Disuse-Induced Skeletal Muscle Atrophy and Anabolic Resistance in Older Adults: From Whole-Foods to Isolated Ingredients.

Preserving skeletal muscle mass and functional capacity is essential for healthy ageing. Transient periods of disuse and/or inactivity in combination with sub-optimal dietary intake have been shown to accelerate the age-related loss of muscle mass and strength, predisposing to disability and metabolic disease. Mechanisms underlying disuse and/or inactivity-related muscle deterioration in the older adults, whilst multifaceted, ultimately manifest in an imbalance between rates of muscle protein synthesis and breakdown, resulting in net muscle loss. To date, the most potent intervention to mitigate disuse-induced muscle deterioration is mechanical loading in the form of resistance exercise. However, the feasibility of older individuals performing resistance exercise during disuse and inactivity has been questioned, particularly as illness and injury may affect adherence and safety, as well as accessibility to appropriate equipment and physical therapists. Therefore, optimising nutritional intake during disuse events, through the introduction of protein-rich whole-foods, isolated proteins and nutrient compounds with purported pro-anabolic and anti-catabolic properties could offset impairments in muscle protein turnover and, ultimately, the degree of muscle atrophy and recovery upon re-ambulation. The current review therefore aims to provide an overview of nutritional countermeasures to disuse atrophy and anabolic resistance in older individuals.

Quadriceps muscle electromyography activity during physical activities and resistance exercise modes in younger and older adults.

BACKGROUND: Understanding the root cause of the age-related impairment in muscle adaptive remodelling with resistance exercise training (RET) and developing pragmatic and accessible resistance exercise for older adults, are essential research directives. METHODS: We sought to determine whether indices of quadriceps muscle EMG activity in response to different modes of RET and activities of daily living (ADL), differed between 15 healthy younger (25 ± 3 years) and 15 older (70 ± 5 years) adults. On four separate days, participants completed a maximal voluntary contraction (MVC) of the knee extensors, followed by a 15 m walking task, stair climbing task (i.e. ADL) and lower-limb RET through body-weight squats (BW-RET) and seated knee extensions on a machine (MN-RET) or via elastic bands (EB-RET). Surface quadriceps electromyography (EMG) was measured throughout all tasks to provide indirect estimates of changes in muscle activity. RESULTS: MVC was significantly greater in young vs. older adults (Young: 256 ± 72 vs. Old: 137 ± 48 N·m, P < 0.001). EMG activity during all exercise tasks was significantly higher in older vs. younger adults when expressed relative to maximal EMG achieved during MVC (P < 0.01, for all). In addition, relative quadriceps muscle EMG activity was significantly greater in EB-RET (Young: 20.3 ± 8.7 vs. Old: 37.0 ± 10.7%) and MN-RET (Young: 22.9 ± 10.3, vs. Old: 37.8 ± 10.8%) compared with BW-RET (Young: 8.6 ± 2.9 vs. Old: 27.0 ± 9.3%), in young and older adults (P < 0.001). However, there was no significant difference in quadriceps EMG between EB-RET and MN-RET (P > 0.05). CONCLUSIONS: In conclusion, relative quadriceps muscle EMG activity was higher across a range of activities/exercise modes in older vs. younger adults. The similar quadriceps muscle EMG activity between EB-RET and MN-RET provides a platform for detailed investigation of the neuromuscular and muscle metabolic responses to such pragmatic forms of RET to strengthen the evidence-base for this mode of RET as a potential countermeasure to sarcopenia.

Influence of muscle oxygenation and nitrate-rich beetroot juice supplementation on O2 uptake kinetics and exercise tolerance.

We tested the hypothesis that acute supplementation with nitrate (NO3-)-rich beetroot juice (BR) would improve quadriceps muscle oxygenation, pulmonary oxygen uptake (V˙O2) kinetics and exercise tolerance (Tlim) in normoxia and that these improvements would be augmented in hypoxia and attenuated in hyperoxia. In a randomised, double-blind, cross-over study, ten healthy males completed two-step cycle tests to Tlim following acute consumption of 210 mL BR (18.6 mmol NO3-) or NO3--depleted beetroot juice placebo (PL; 0.12 mmol NO3-). These tests were completed in normobaric normoxia [fraction of inspired oxygen (FIO2): 21%], hypoxia (FIO2: 15%) and hyperoxia (FIO2: 40%). Pulmonary V˙O2 and quadriceps tissue oxygenation index (TOI), derived from multi-channel near-infrared spectroscopy, were measured during all trials. Plasma [nitrite] was higher in all BR compared to all PL trials (P < 0.05). Quadriceps TOI was higher in normoxia compared to hypoxia (P < 0.05) and higher in hyperoxia compared to hypoxia and normoxia (P < 0.05). Tlim was improved after BR compared to PL ingestion in the hypoxic trials (250 ± 44 vs. 231 ± 41 s; P = 0.006; d = 1.13), with the magnitude of improvement being negatively correlated with quadriceps TOI at Tlim (r = -0.78; P < 0.05). Tlim was not improved following BR ingestion in normoxia (BR: 364 ± 98 vs. PL: 344 ± 78 s; P = 0.087, d = 0.61) or hyperoxia (BR: 492 ± 212 vs. PL: 472 ± 196 s; P = 0.273, d = 0.37). BR ingestion increased peak V˙O2 in hypoxia (P < 0.05), but not normoxia or hyperoxia (P > 0.05). These findings indicate that BR supplementation is more likely to improve Tlim and peak V˙O2 in situations when skeletal muscle is more hypoxic.

Contralateral fatigue during severe-intensity single-leg exercise: influence of acute acetaminophen ingestion.

Exhaustive single-leg exercise has been suggested to reduce time to task failure (Tlim) during subsequent exercise in the contralateral leg by exacerbating central fatigue development. We investigated the influence of acetaminophen (ACT), an analgesic that may blunt central fatigue development, on Tlim during single-leg exercise completed with and without prior fatiguing exercise of the contralateral leg. Fourteen recreationally active men performed single-leg severe-intensity knee-extensor exercise to Tlim on the left (Leg1) and right (Leg2) legs without prior contralateral fatigue and on Leg2 immediately following Leg1 (Leg2-CONTRA). The tests were completed following ingestion of 1-g ACT or maltodextrin [placebo (PL)] capsules. Intramuscular phosphorus-containing metabolites and substrates and muscle activation were assessed using 31P-MRS and electromyography, respectively. Tlim was not different between Leg1ACT and Leg1PL conditions (402 ± 101 vs. 390 ± 106 s, P = 0.11). There was also no difference in Tlim between Leg2ACT-CONTRA and Leg2PL-CONTRA (324 ± 85 vs. 311 ± 92 s, P = 0.10), but Tlim was shorter in Leg2ACT-CONTRA and Leg2PL-CONTRA than in Leg2CON (385 ± 104 s, both P < 0.05). There were no differences in intramuscular phosphorus-containing metabolites and substrates or muscle activation between Leg1ACT and Leg1PL and between Leg2ACT-CONTRA and Leg2PL-CONTRA (all P > 0.05). These findings suggest that levels of metabolic perturbation and muscle activation at Tlim are not different during single-leg severe-intensity knee-extensor exercise completed with or without prior fatiguing exercise of the contralateral leg. Despite contralateral fatigue, ACT ingestion did not alter neuromuscular responses, muscle metabolites, or exercise performance.

Montmorency cherry supplementation improves 15-km cycling time-trial performance.

AIM: Montmorency cherries are rich in polyphenols that possess antioxidant, anti-inflammatory and vasoactive properties. We investigated whether 7-day Montmorency cherry powder supplementation improved cycling time-trial (TT) performance. METHODS: 8 trained male cyclists ([Formula: see text]: 62.3 ± 10.1 ml kg-1 min-1) completed 10-min steady-state (SS) cycling at ~ 65% [Formula: see text] followed by a 15-km TT on two occasions. Participants consumed 6 pills per day (Montmorency cherry powder, MC; anthocyanin 257 mg day-1 or dextrose powder, PL) for a 7-day period, 3 pills in the morning and evening. Capillary blood [lactate] was measured at baseline, post SS and post TT. Pulmonary gas exchange and tissue oxygenation index (TOI) of m. vastus lateralis via near-infrared spectroscopy, were measured throughout. RESULTS: TT completion time was 4.6 ± 2.9% faster following MC (1506 ± 86 s) supplementation compared to PL (1580 ± 102 s; P = 0.004). Blood [lactate] was significantly higher in MC after SS (PL: 4.4 ± 2.1 vs. MC: 6.7 ± 3.3 mM, P = 0.017) alongside an elevated baseline TOI (PL: 68.7 ± 2.1 vs. MC: 70.4 ± 2.3%, P = 0.018). DISCUSSION: Montmorency cherry supplementation improved 15-km cycling TT performance. This improvement in exercise performance was accompanied by enhanced muscle oxygenation suggesting that the vasoactive properties of the Montmorency cherry polyphenols may underpin the ergogenic effects.