Search

Skeletal muscle mass losses with age are associated with negative health consequences, including an increased risk of developing metabolic disease and the loss of independence. Athletes adopt numerous nutritional strategies to maximize the benefits of exercise training and enhance recovery in pursuit of improving skeletal muscle quality, mass, or function. Importantly, many of the principles applied to enhance skeletal muscle health in athletes may be applicable to support active aging and prevent sarcopenia in the healthy (non-clinical) aging population. Here, we discuss the anabolic properties of protein supplementation in addition to ingredients that may enhance the anabolic effects of protein (e.g. omega 3 s, creatine, inorganic nitrate) in older persons. We conclude that nutritional strategies used in pursuit of performance enhancement in athletes are often applicable to improve skeletal muscle health in the healthy older population when implemented as part of a healthy active lifestyle. Further research is required to elucidate the mechanisms by which these nutrients may induce favourable changes in skeletal muscle and to determine the appropriate dosing and timing of nutrient intakes to support active aging.

PURPOSE There is a lack of knowledge as to how different exercise-based cardiac rehabilitation programming affects skeletal muscle adaptations in coronary artery disease (CAD) patients. We first characterized the skeletal muscle from adults with CAD compared with a group of age- and sex-matched healthy adults. We then determined the effects of a traditional moderate-intensity continuous exercise program (TRAD) or a stair climbing-based high-intensity interval training program (STAIR) on skeletal muscle metabolism in CAD. METHODS Sixteen adults (n = 16, 61 ± 7 yr), who had undergone recent treatment for CAD, were randomized to perform (3 d·wk-1) either TRAD (n = 7, 30 min at 60%-80% of peak heart rate) or STAIR (n = 9, 3 × 6 flights) for 12 wk. Muscle biopsies were collected at baseline in both CAD and healthy controls (n = 9), and at 4 and 12 wk after exercise training in CAD patients undertaking TRAD or STAIR. RESULTS We found that CAD had a lower capillary-to-fiber ratio (C/Fi, 35% ± 25%, P = 0.06) and capillary-to-fiber perimeter exchange (CFPE) index (23% ± 29%, P = 0.034) in Type II fibers compared with healthy controls. However, 12 wk of cardiac rehabilitation with either TRAD or STAIR increased C/Fi (Type II, 23% ± 14%, P < 0.001) and CFPE (Type I, 10% ± 23%, P < 0.01; Type II, 18% ± 22%, P = 0.002). CONCLUSION Cardiac rehabilitation via TRAD or STAIR exercise training improved the compromised skeletal muscle microvascular phenotype observed in CAD patients.

We tested the hypothesis that presleep consumption of α-lactalbumin (LA), a fraction of whey with a high abundance of tryptophan, would improve indices of sleep quality and time-trial (TT) performance in cyclists relative to an isonitrogenous collagen peptide (CP) supplement lacking tryptophan. Using randomized, double-blind, crossover designs, cyclists consumed either 40 g of LA or CP 2 hr prior to sleep. In Study 1, six elite male endurance track cyclists (age 23 ± 6 years, 70.2 ± 4.4 ml·kg−1·min−1) consumed a supplement for three consecutive evenings before each 4-km TT on a velodrome track, whereas in Study 2, six well-trained cyclists (one female; age 24 ± 5 years, 66.9 ± 8.3 ml·kg−1·min−1) consumed a supplement the evening before each 4-km TT on a stationary cycle ergometer. Indices of sleep quality were assessed with wrist-based actigraphy. There were no differences between the CP and LA supplements in terms of total time in bed, total sleep time, or sleep efficiency in Study 1 (LA: 568 ± 71 min, 503 ± 67 min, 88.3% ± 3.4%; CP: 546 ± 30 min, 479 ± 35 min, 87.8% ± 3.1%; p = .41, p = .32, p = .74, respectively) or Study 2 (LA: 519 ± 90 min, 450 ± 78 min, 87.2% ± 7.6%; CP: 536 ± 62 min, 467 ± 57 min, 87.3% ± 6.4%; p = .43, p = .44, p = .97, respectively). Similarly, time to complete the 4-km TT was unaffected by supplementation in Study 1 (LA: 274.9 ± 7.6 s; CP: 275.5 ± 7.2 s; p = .62) and Study 2 (LA: 344.3 ± 22.3 s; CP: 343.3 ± 23.0 s; p = .50). Thus, relative to CP, consuming LA 2 hr prior to sleep over 1–3 days did not improve actigraphy-based indices of sleep quality or 4-km TT performance in cyclists.

Background: Aging appears to attenuate the response of skeletal muscle protein synthesis (MPS) to anabolic stimuli such as protein ingestion (and the ensuing hyperaminoacidemia) and resistance exercise (RE). Objectives: The purpose of this study was to determine the effects of protein quality on feeding- and feeding plus RE-induced increases of acute and longer-term MPS after ingestion of whey protein (WP) and collagen protein (CP). Methods: In a double-blind parallel-group design, 22 healthy older women (mean ± SD age: 69 ± 3 y, n = 11/group) were randomly assigned to consume a 30-g supplement of either WP or CP twice daily for 6 d. Participants performed unilateral RE twice during the 6-d period to determine the acute (via [13C6]-phenylalanine infusion) and longer-term (ingestion of deuterated water) MPS responses, the primary outcome measures. Results: Acutely, WP increased MPS by a mean ± SD 0.017 ± 0.008%/h in the feeding-only leg (Rest) and 0.032 ± 0.012%/h in the feeding plus exercise leg (Exercise) (both P < 0.01), whereas CP increased MPS only in Exercise (0.012 ± 0.013%/h) (P < 0.01) and MPS was greater in WP than CP in both the Rest and Exercise legs (P = 0.02). Longer-term MPS increased by 0.063 ± 0.059%/d in Rest and 0.173 ± 0.104%/d in Exercise (P < 0.0001) with WP; however, MPS was not significantly elevated above baseline in Rest (0.011 ± 0.042%/d) or Exercise (0.020 ± 0.034%/d) with CP. Longer-term MPS was greater in WP than in CP in both Rest and Exercise (P < 0.001). Conclusions: Supplementation with WP elicited greater increases in both acute and longer-term MPS than CP supplementation, which is suggestive that WP is a more effective supplement to support skeletal muscle retention in older women than CP.This trial was registered at clinicaltrials.gov as NCT03281434.

INTRODUCTION Protein ingestion and the ensuing hyperaminoacidemia stimulates skeletal muscle protein synthesis in the postexercise period. This response facilitates muscle remodeling, which is important during intensified training. The aim of this study was to determine whether supplementation with α-lactalbumin (LA), with high leucine and tryptophan contents, would improve responses to short periods of intensified aerobic training compared with supplementation with an isonitrogenous quantity of collagen peptides (CP). METHODS Endurance-trained participants (5 male, 6 female, 24 ± 4 yr, V˙O2 = 53.2 ± 9.1 mL·kg·min, peak power output = 320 ± 48 W; means ± SD) consumed a controlled diet (1.0 g·kg·d protein) and refrained from habitual training for 11 d while taking part in this double-blind randomized, crossover trial. The two intervention phases, which consisted of brief intensified training (4 × 4-min cycling intervals at 70% of peak power output on 3 consecutive days) combined with the ingestion of LA or CP supplements after exercise (20 g) and before sleep (40 g), were separated by 4 d of washout without protein supplementation (i.e., the control phase). In response to each phase, myofibrillar (MyoPS), sarcoplasmic protein synthesis (SarcPS) rates (via H2O ingestion) and parameters of sleep quality were measured. RESULTS LA ingestion increased plasma leucine (P < 0.001) and tryptophan concentrations (P < 0.001) relative to CP. Intensified training increased MyoPS and SarcPS above the washout phase in LA- and CP-supplemented phases (P < 0.01), with increases being 13% ± 5% and 5% ± 7% greater with LA than CP for MyoPS (P < 0.01) and SarcPS, respectively (P < 0.01). CONCLUSIONS Despite an isonitrogenous diet, protein synthesis was enhanced to a greater extent when trained participants consumed LA compared with CP during intensified aerobic training, suggesting that protein quality is an important consideration for endurance-trained athletes aiming to augment adaption to exercise training.

Basketball players face multiple challenges to in-season recovery. The purpose of this article is to review the literature on recovery modalities and nutritional strategies for basketball players and practical applications that can be incorporated throughout the season at various levels of competition. Sleep, protein, carbohydrate, and fluids should be the foundational components emphasized throughout the season for home and away games to promote recovery. Travel, whether by air or bus, poses nutritional and sleep challenges, therefore teams should be strategic about packing snacks and fluid options while on the road. Practitioners should also plan for meals at hotels and during air travel for their players. Basketball players should aim for a minimum of 8 h of sleep per night and be encouraged to get extra sleep during congested schedules since back-to back games, high workloads, and travel may negatively influence night-time sleep. Regular sleep monitoring, education, and feedback may aid in optimizing sleep in basketball players. In addition, incorporating consistent training times may be beneficial to reduce bed and wake time variability. Hydrotherapy, compression garments, and massage may also provide an effective recovery modality to incorporate post-competition. Future research, however, is warranted to understand the influence these modalities have on enhancing recovery in basketball players. Overall, a strategic well-rounded approach, encompassing both nutrition and recovery modality strategies, should be carefully considered and implemented with teams to support basketball players’ recovery for training and competition throughout the season.

INTRODUCTION: Older adults can experience periods of inactivity related to disease or illness, which can hasten the development of physical disability, in part, through reductions in skeletal muscle strength and power. To date no study has characterized adaptations in skeletal muscle physical function in response to reduced daily physical activity. METHODS: Participants (15 men, 69±2 years, 15 women, 68±4 years) restricted their daily steps (

Previous longitudinal studies suggest that left ventricular (LV) structure is unaltered with resistance exercise training (RT) in young men. However, evidence from aerobic exercise training suggests that early changes in functional LV wall mechanics may occur prior to and independently of changes in LV size, although short-term changes in LV mechanics and structural remodelling in response to RT protocols have not been reported. Therefore, the purpose of this study was to examine the effects of RT on LV mechanics in healthy men performing 2 different time-under-tension protocols. Forty recreationally trained men (age: 23 ± 3 years) were randomized into 12 weeks of whole-body higher-repetition RT (20–25 repetitions/set to failure at ∼30%–50% 1 repetition maximum (1RM); n = 13), lower-repetition RT (8–12 repetitions/set to failure at ∼75%–90% 1RM; n = 13), or an active control period (n = 14). Speckle tracking echocardiography was performed at baseline and following the intervention period. Neither RT program altered standard measures of LV volumes (end-diastolic volume, end-systolic volume, or ejection fraction; P > 0.05) or indices of LV mechanics (total LV twist, untwisting rate, twist-to-shortening ratio, untwisting-to-twist ratio, or longitudinal strain; P > 0.05). This is the first longitudinal study to assess both LV size and mechanics after RT in healthy men, suggesting a maintenance of LV size and twist mechanics despite peripheral muscle adaptations to the training programs. These results provide no evidence for adverse LV structural or functional remodelling in response to RT in young men and support the positive role of RT in the maintenance of optimal cardiovascular function, even with strenuous RT.

Background: Cardiac rehabilitation exercise reduces the risk of secondary cardiovascular disease. Interval training is a time-efficient alternative to traditional cardiac rehabilitation exercise and stair climbing is an accessible means. We aimed to assess the effectiveness of a high-intensity interval stair climbing intervention on improving cardiorespiratory fitness (V˙O2peak) compared to standard cardiac rehabilitation care.Methods: Twenty participants with coronary artery disease (61 ± 7 years, 18 males, two females) were randomly assigned to either traditional moderate-intensity exercise (TRAD) or high-intensity interval stair climbing (STAIR). V˙O2peak was assessed at baseline, following 4 weeks of six supervised exercise sessions and after 8 weeks of ~24 unsupervised exercise sessions. TRAD involved a minimum of 30 min at 60–80%HRpeak, and STAIR consisted of three bouts of six flights of 12 stairs at a self-selected vigorous intensity (~90 s/bout) separated by recovery periods of walking (~90 s). This study was registered as a clinical trial at clinicaltrials.gov (NCT03235674).Results: Two participants could not complete the trial due to the time commitment of the testing visits, leaving n = 9 in each group who completed the interventions without any adverse events. V˙O2peak increased after supervised and unsupervised training in comparison to baseline for both TRAD [baseline: 22.9 ± 2.5, 4 weeks (supervised): 25.3 ± 4.4, and 12 weeks (unsupervised): 26.5 ± 4.8 mL/kg/min] and STAIR [baseline: 21.4 ± 4.5, 4 weeks (supervised): 23.4 ± 5.6, and 12 weeks (unsupervised): 25 ± 6.2 mL/kg/min; p (time) = 0.03]. During the first 4 weeks of training (supervised) the STAIR vs. TRAD group had a higher %HRpeak (101 ± 1 vs. 89 ± 1%; p ≤ 0.001), across a shorter total exercise time (7.1 ± 0.1 vs. 36.7 ± 1.1 min; p = 0.009). During the subsequent 8 weeks of unsupervised training, %HRpeak was not different (87 ± 8 vs. 96 ± 8%; p = 0.055, mean ± SD) between groups, however, the STAIR group continued to exercise for less time per session (10.0 ± 3.2 vs. 24.2 ± 17.0 min; p = 0.036).Conclusions: Both brief, vigorous stair climbing, and traditional moderate-intensity exercise are effective in increasing V˙O2peak, in cardiac rehabilitation exercise programmes.

Magnetic resonance imaging (MRI) is the current gold standard for measuring changes in muscle size (cross‐sectional area [CSA] and volume) but can be cost‐prohibitive and resource‐intensive. We evaluated the validity of B‐mode ultrasonography (US) as a low‐cost alternative to MRI for measuring muscle hypertrophy and atrophy in response to resistance training and immobilization, respectively. Fourteen young men performed 10wk of unilateral resistance training (RT) to induce muscle hypertrophy. In the final two weeks of the 10wk, the subjects’ contralateral leg was immobilized (IMB). The cross‐sectional area of the vastus lateralis (VLCSA) was measured at the mid‐thigh before and after each intervention using MRI (VLCSAMRI) and US (VLCSAUS). The relationship and agreement between methods were assessed. Reliability of US measurements ranged from good to excellent in all comparisons (ICC >0.67). VLCSA significantly increased after 10 weeks of RT (VLCSAUS: 7.9 ± 3.8%; VLCSAMRI: 7.8 ± 4.5%) and decreased after 2 weeks of IMB (VLCSAUS: −8.2%±5.8%; VLCSAMRI: −8.7 ± 6.1%). Significant correlations were identified between MRI and US at each time point measured (all r > 0.85) and, importantly, between MRI‐ and US‐derived changes in VLCSA. Bland‐Altman analysis revealed minimal bias in US measurements relative to the MRI (−0.5 ± 3.0%) and all measurements were within the upper and lower limits of agreement. Our data suggest that B‐mode ultrasonography can be a suitable alternative to MRI for measuring changes in muscle size in response to increased and decreased muscle loading in young men., We demonstrate that ultrasound‐derived measurements of vastus lateralis hypertrophy and atrophy induced by resistance training and immobilization are significantly correlated with MRI‐derived measurements. The reliability of our ultrasound technique was also in the range of good‐excellent. Together, these data suggest that B‐mode ultrasonography is a suitable alternative for the assessment of muscle hypertrophy and atrophy under conditions of dynamic loading in young men.

The mechanistic target of rapamycin complex-1 (mTORC-1) is a key nutrient and contraction-sensitive protein that regulates a pathway leading to skeletal muscle growth. Utilizing a multiplex assay, we aimed to examine the phosphorylation status of key mTORC-1-related signalling molecules in response to protein feeding and resistance exercise. Eight healthy men (age, 22.5 ± 3.1 years; mass, 80 ± 9 kg; 1-repetition maximum leg extension, 87 ± 5 kg) performed 4 sets of unilateral leg extensions until volitional failure. Immediately following the final set, all participants consumed a protein-enriched beverage. A single skeletal muscle biopsy was obtained from the vastus lateralis before (Pre) with further bilateral biopsies at 1 h (1 h exercised legs (FEDEX) and 1 h nonexercised legs (FED)) and 3 h (3 h FEDEX and 3 h FED) after drink ingestion. Phosphorylated AktSer473was significantly elevated from Pre at 1 h FEDEX. Phosphorylated p70S6K1Thr412was significantly increased above Pre at 1 h FEDEX and 1 h FED and was still significantly elevated at 3 h FEDEX but not 3 h FED. Phosphorylated rpS6Ser235/236was also significantly increased above Pre at 1 h FEDEX and 1 h FED with 1 h FEDEX greater than 1 h FED. Our data highlight the utility of a multiplex assay to assess anabolic signalling molecules in response to protein feeding and resistance exercise in humans. Importantly, these changes are comparable with those as previously reported using standard immunoblotting and protein activity assays.

Carotid artery longitudinal wall motion (CALM) exhibits reduced magnitude in older adults and in individuals with chronic diseases, although longitudinal data are lacking to indicate how changes in CALM might develop over time. Therefore, the aim of this study was to investigate the effect of exercise training in healthy men on CALM using a retrospective design. Carotid ultrasound data were analysed from two previous studies in which men performed 12 wk of moderate-intensity continuous exercise training (n = 9), sprint-interval training (n = 7), higher-repetition resistance exercise training (n = 15) or lower-repetition resistance exercise training (n = 15). The CALM pattern was unaltered after 12 wk of exercise training, regardless of exercise mode, with no differences in systolic or diastolic CALM magnitudes (p > 0.05), similar to carotid intima-media thickness (p > 0.05). Our findings suggest that CALM is resistant to transient changes in lifestyle factors, similar to wall thickness in otherwise healthy populations.

Declines in strength and muscle function with age—sarcopenia—contribute to a variety of negative outcomes including an increased risk of: falls, fractures, hospitalization, and reduced mobility in older persons. Population-based estimates of the loss of muscle after age 60 show a loss of ~1% per year while strength loss is more rapid at ~3% per year. These rates are not, however, linear as periodic bouts of reduced physical activity and muscle disuse transiently accelerate loss of muscle and declines in muscle strength and power. Episodic complete muscle disuse can be due to sickness-related bed rest or local muscle disuse as a result of limb immobilization/surgery. Alternatively, relative muscle disuse occurs during inactivity due to illness and the associated convalescence resulting in marked reductions in daily steps, often referred to as step reduction (SR). While it is a “milder” form of disuse, it can have a similar adverse impact on skeletal muscle health. The physiological consequences of even short-term inactivity, modeled by SR, show losses in muscle mass and strength, as well as impaired insulin sensitivity and an increase in systemic inflammation. Though seemingly benign in comparison to bed rest, periodic inactivity likely occurs, we posit, more frequently with advancing age due to illness, declining mental health and declining mobility. Given that recovery from inactivity in older adults is slow or possibly incomplete we hypothesize that accumulated periods of inactivity contribute to sarcopenia. Periodic activity, even in small quantities, and protein supplementation may serve as effective strategies to offset the loss of muscle mass with aging, specifically during periods of inactivity. The aim of this review is to examine the recent literature encompassing SR, as a model of inactivity, and to explore the capacity of nutrition and exercise interventions to mitigate adverse physiological changes as a result of SR.

Loading of skeletal muscle leads to remodeling of myofibrillar and extracellular matrix proteins to withstand metabolic stress and unloading results in the opposite. In humans, the heterogenous response to altered loading greatly complicates molecular modeling of the underpinning processes. We utilized a within-person paired Hypertrophy and Atrophy (‘HypAt’) strategy that reduced response heterogeneity by ~40%. We applied a new genome-wide transcriptome analysis methodology to model mRNA, the 3’ or 5’ untranslated regions (UTR, sites of translation regulation) and proteome-constrained networks. We discovered > 4 times more regulated genes compared with similarly sized studies while 1,000 genes were only modified at their UTRs. A core of 141 genes were consistently modulated in proportion to muscle growth, across three independent studies (n=100). This new model revealed, at a pathway level, direct interactions between the proteome features of exercise-trained muscle, and the molecular processes underpinning muscle aging and insulin sensitivity.

Purpose:Self–myofascial release (SMR) is a common exercise and therapeutic modality shown to induce acute improvements in joint range of motion (ROM) and recovery; however, no long-term studies have been conducted. Static stretching (SS) is the most common method used to increase joint ROM and decrease muscle stiffness. It was hypothesized that SMR paired with SS (SMR+SS) compared with SS alone over a 4-wk intervention would yield greater improvement in knee-extension ROM and hamstring stiffness.Methods:19 men (22 ± 3 y) with bilateral reduced hamstring ROM had each of their legs randomly assigned to either an SMR+SS or an SS-only group. The intervention consisted of 4 repetitions of SS each for 45 s or the identical amount of SS preceded by 4 repetitions of SMR each for 60 s and was performed on the respective leg twice daily for 4 wk. Passive ROM, hamstring stiffness, rate of torque development (RTD), and maximum voluntary contraction (MVC) were assessed pre- and postintervention.Results:Passive ROM (P < .001), RTD, and MVC (P < .05) all increased after the intervention. Hamstring stiffness toward end-ROM was reduced postintervention (P = .02). There were no differences between the intervention groups for any variable.Conclusion:The addition of SMR to SS did not enhance the efficacy of SS alone. SS increases joint ROM through a combination of decreased muscle stiffness and increased stretch tolerance.

Summary Loading of skeletal muscle changes the tissue phenotype reflecting altered metabolic and functional demands. In humans, heterogeneous adaptation to loading complicates the identification of the underpinning molecular regulators. A within-person differential loading and analysis strategy reduces heterogeneity for changes in muscle mass by ∼40% and uses a genome-wide transcriptome method that models each mRNA from coding exons and 3′ and 5′ untranslated regions (UTRs). Our strategy detects ∼3–4 times more regulated genes than similarly sized studies, including substantial UTR-selective regulation undetected by other methods. We discover a core of 141 genes correlated to muscle growth, which we validate from newly analyzed independent samples (n = 100). Further validating these identified genes via RNAi in primary muscle cells, we demonstrate that members of the core genes were regulators of protein synthesis. Using proteome-constrained networks and pathway analysis reveals notable relationships with the molecular characteristics of human muscle aging and insulin sensitivity, as well as potential drug therapies., Graphical Abstract, Highlights • Muscle loading and unloading regulate the untranslated regions of mRNA • Regulated genes form functional networks central to muscle plasticity • 141 genes correlate with muscle growth in 3 independent validation cohorts • Several growth-correlated network genes directly regulate myocyte protein synthesis, Stokes et al. identify and validate a core set of genes that are regulated in proportion to the magnitude of muscle protein turnover with loading. Several of these genes correlate with muscle growth only at their 3′ or 5′ untranslated region, and a subset directly influences protein synthesis in vitro.

Resistance training promotes microvasculature expansion; however, it remains unknown how different resistance training programs contribute to angiogenesis. Thus, we recruited experienced resistance-trained participants and determined the effect of 12 wk of either high-repetition/low-load or low-repetition/high-load resistance training performed to volitional fatigue on muscle microvasculature. Twenty men performed either a high-repetition [20–25 repetitions, 30–50% of 1-repetition maximum (1RM); n = 10] or a low-repetition (8–12 repetitions, 75–90% of 1RM; n = 10) resistance training program. Muscle biopsies were taken before and after resistance training, and immunohistochemistry was used to assess fiber type (I and II)-specific microvascular variables. High-repetition/low-load and low-repetition/high-load groups were not different in any variable before resistance training. Both protocols resulted in an increase in capillarization. Specifically, after resistance training, the capillary-to-fiber ratio, capillary contacts, and capillary-to-fiber perimeter exchange index were elevated, and sharing factor was reduced. These data demonstrate that resistance training performed to volitional failure, using either high repetition/low load or low repetition/high load, induced similar microvascular adaptations in recreationally resistance-trained young men.

Background In older persons, muscle loss is accelerated during physical inactivity and hypoenergetic states, both of which are features of hospitalization. Protein supplementation may represent a strategy to offset the loss of muscle during inactivity, and enhance recovery on resumption of activity. Objective We aimed to determine if protein supplementation, with proteins of substantially different quality, would alleviate the loss of lean mass by augmenting muscle protein synthesis (MPS) while inactive during a hypoenergetic state. Design Participants (16 men, mean ± SD age: 69 ± 3 y; 15 women, mean ± SD age: 68 ± 4 y) consumed a diet containing 1.6 g protein · kg-1 · d-1, with 55% ± 9% of protein from foods and 45% ± 9% from supplements, namely, whey protein (WP) or collagen peptides (CP): 30 g each, consumed 2 times/d. Participants were in energy balance (EB) for 1 wk, then began a period of energy restriction (ER; -500 kcal/d) for 1 wk, followed by ER with step reduction (ER + SR

Mechanistic target of rapamycin (mTOR) resides as two complexes within skeletal muscle. mTOR complex 1 [mTORC1–regulatory associated protein of mTOR (Raptor) positive] regulates skeletal muscle growth, whereas mTORC2 [rapamycin-insensitive companion of mTOR (Rictor) positive] regulates insulin sensitivity. To examine the regulation of these complexes in human skeletal muscle, we utilized immunohistochemical analysis to study the localization of mTOR complexes before and following protein-carbohydrate feeding (FED) and resistance exercise plus protein-carbohydrate feeding (EXFED) in a unilateral exercise model. In basal samples, mTOR and the lysosomal marker lysosomal associated membrane protein 2 (LAMP2) were highly colocalized and remained so throughout. In the FED and EXFED states, mTOR/LAMP2 complexes were redistributed to the cell periphery [wheat germ agglutinin (WGA)-positive staining] (time effect; P = 0.025), with 39% (FED) and 26% (EXFED) increases in mTOR/WGA association observed 1 h post-feeding/exercise. mTOR/WGA colocalization continued to increase in EXFED at 3 h (48% above baseline) whereas colocalization decreased in FED (21% above baseline). A significant effect of condition (P = 0.05) was noted suggesting mTOR/WGA colocalization was greater during EXFED. This pattern was replicated in Raptor/WGA association, where a significant difference between EXFED and FED was noted at 3 h post-exercise/feeding (P = 0.014). Rictor/WGA colocalization remained unaltered throughout the trial. Alterations in mTORC1 cellular location coincided with elevated S6K1 kinase activity, which rose to a greater extent in EXFED compared with FED at 1 h post-exercise/feeding (P < 0.001), and only remained elevated in EXFED at the 3 h time point (P = 0.037). Collectively these data suggest that mTORC1 redistribution within the cell is a fundamental response to resistance exercise and feeding, whereas mTORC2 is predominantly situated at the sarcolemma and does not alter localization.

Discrepancies regarding the effect of resistance exercise training (RET) on arterial stiffness have led to uncertainty regarding the effect of RET on cardiovascular health. Confounding our understanding in this area are the roles of the following: load (heavier vs lighter), participant cardiovascular health, and arterial stiffness assessment method. We aimed to investigate the effects of a heavier versus a lighter load resistance training protocol on both central and local arterial stiffness in previously trained young men. Participants were randomly assigned to a 12-wk supervised whole-body RET program consisting of three sets of 8-12 repetitions (heavier-load, lower-repetition [LR]; n = 16) or three sets of 20-25 repetitions (lighter-load, higher-repetition [HR]; n = 16) to volitional failure, or a control group who maintained their regular activity habits (n = 14). Central arterial stiffness (carotid-femoral pulse wave velocity), local arterial stiffness (common carotid arterial distensibility), and left ventricular mass were measured before and after 12 wk of RET. There was a reduction in carotid-femoral pulse wave velocity in both LR (6.24 ± 0.56 vs 5.77 ± 0.76 m·s; P < 0.05) and HR (6.42 ± 0.70 vs 5.72 ± 0.60 m·s; P < 0.05) with no changes in carotid distensibility (P = 0.52) or left ventricular mass allometrically scaled to fat-free mass (P = 0.60). There were no changes in any variable in the control group. Using current criterion-standard assessment methods, central arterial stiffness was reduced after resistance training, regardless of the load lifted during RET, with no effect on local carotid artery distensibility or left ventricular mass. Our results support a role of RET in the promotion of positive adaptations in vascular function.

We provide novel evidence of the effect of lifting markedly different (lighter vs. heavier) loads (mass per repetition) during whole-body resistance training on the development of muscle strength and hypertrophy in previously trained persons. Using a large sample size (n = 49), and contradicting dogma, we report that the relative load lifted per repetition does not determine skeletal muscle hypertrophy or, for the most part, strength development. In line with our previous work, acute postexercise systemic hormonal changes were unrelated to strength and hypertrophic gains., We reported, using a unilateral resistance training (RT) model, that training with high or low loads (mass per repetition) resulted in similar muscle hypertrophy and strength improvements in RT-naïve subjects. Here we aimed to determine whether the same was true in men with previous RT experience using a whole-body RT program and whether postexercise systemic hormone concentrations were related to changes in hypertrophy and strength. Forty-nine resistance-trained men (23 ± 1 yr, mean ± SE) performed 12 wk of whole-body RT. Subjects were randomly allocated into a higher-repetition (HR) group who lifted loads of ∼30-50% of their maximal strength (1RM) for 20–25 repetitions/set (n = 24) or a lower-repetition (LR) group (∼75–90% 1RM, 8–12 repetitions/set, n = 25), with all sets being performed to volitional failure. Skeletal muscle biopsies, strength testing, dual-energy X-ray absorptiometry scans, and acute changes in systemic hormone concentrations were examined pretraining and posttraining. In response to RT, 1RM strength increased for all exercises in both groups (P < 0.01), with only the change in bench press being significantly different between groups (HR, 9 ± 1, vs. LR, 14 ± 1 kg, P = 0.012). Fat- and bone-free (lean) body mass and type I and type II muscle fiber cross-sectional area increased following training (P < 0.01) with no significant differences between groups. No significant correlations between the acute postexercise rise in any purported anabolic hormone and the change in strength or hypertrophy were found. In congruence with our previous work, acute postexercise systemic hormonal rises are not related to or in any way indicative of RT-mediated gains in muscle mass or strength. Our data show that in resistance-trained individuals, load, when exercises are performed to volitional failure, does not dictate hypertrophy or, for the most part, strength gains.

It is well accepted that daily protein intake is an important dietary consideration to limit and treat age-related declines in muscle mass, strength, and function. Furthermore, we propose that there is a growing appreciation for the need to consider protein intake on a per-meal basis rather than simply focusing on the total daily protein intake. The existence of a saturable dose-response relationship between muscle protein synthesis (MPS) and the quantity of protein consumed in a single meal/bolus provides the rationale for promoting an even/balanced pattern of daily protein intake. We hypothesize that a balanced/even protein intake pattern with the ingestion a quantity of protein shown to optimally stimulate MPS at each meal may be an effective strategy to alleviate sarcopenic muscle loss. In this review we examine the available evidence supporting the influence of dietary protein intake pattern on muscle protein turnover, muscle mass, and muscle function. We present several practical considerations that, it is proposed, should be taken into account when translating a per-meal protein recommendation into dietary advice for older adults.

The factors that underpin heterogeneity in muscle hypertrophy following resistance exercise training (RET) remain largely unknown. We examined circulating hormones, intramuscular hormones, and intramuscular hormone-related variables in resistance-trained men before and after 12 weeks of RET. Backward elimination and principal component regression evaluated the statistical significance of proposed circulating anabolic hormones (e.g., testosterone, free testosterone, dehydroepiandrosterone, dihydrotestosterone, insulin-like growth factor-1, free insulin-like growth factor-1, luteinizing hormone, and growth hormone) and RET-induced changes in muscle mass (n = 49). Immunoblots and immunoassays were used to evaluate intramuscular free testosterone levels, dihydrotestosterone levels, 5α-reductase expression, and androgen receptor content in the highest- (HIR; n = 10) and lowest- (LOR; n = 10) responders to the 12 weeks of RET. No hormone measured before exercise, after exercise, pre-intervention, or post-intervention was consistently significant or consistently selected in the final model for the change in: type 1 cross sectional area (CSA), type 2 CSA, or fat- and bone-free mass (LBM). Principal component analysis did not result in large dimension reduction and principal component regression was no more effective than unadjusted regression analyses. No hormone measured in the blood or muscle was different between HIR and LOR. The steroidogenic enzyme 5α-reductase increased following RET in the HIR (P < 0.01) but not the LOR (P = 0.32). Androgen receptor content was unchanged with RET but was higher at all times in HIR. Unlike intramuscular free testosterone, dihydrotestosterone, or 5α-reductase, there was a linear relationship between androgen receptor content and change in LBM (P < 0.01), type 1 CSA (P < 0.05), and type 2 CSA (P < 0.01) both pre- and post-intervention. These results indicate that intramuscular androgen receptor content, but neither circulating nor intramuscular hormones (or the enzymes regulating their intramuscular production), influence skeletal muscle hypertrophy following RET in previously trained young men.

Older and younger men completed 12 weeks of resistance training and ingested either 500 mL of chocolate milk or placebo daily. Training increased strength in both age groups (p < 0.05), with no supplementation effect. Type I muscle fibre area increased with training (p = 0.008) with no effect of age or supplementation. Type II fibre area increased (p = 0.014) in young men only with no supplementation effect. Chocolate milk did not enhance skeletal muscle hypertrophy following training.

Increases in limb blood flow in response to nutrition are reduced in older age. Muscle microvascular blood flow (MBF) in response to nutrition is also reduced with advancing age and this may contribute to age-related 'anabolic resistance'. Resistance exercise training (RET) can rejuvenate limb blood flow responses to nutrition in older individuals. We report here that 20 weeks of RET also restores muscle MBF in older individuals. Restoration of MBF does not, however, enhance muscle anabolic responses to nutrition.The anabolic effects of dietary protein on skeletal muscle depend on adequate skeletal muscle perfusion, which is impaired in older people. This study explores fed state muscle microvascular blood flow, protein metabolism and exercise training status in older men. We measured leg blood flow (LBF), muscle microvascular blood volume (MBV) and muscle protein turnover under post-absorptive and fed state (i.v. Glamin to double amino acids, dextrose to sustain glucose ∼7-7.5 mmol l(-1) ) conditions in two groups: 10 untrained men (72.3 ± 1.4 years; body mass index (BMI) 26.5 ± 1.15 kg m(2) ) and 10 men who had undertaken 20 weeks of fully supervised, whole-body resistance exercise training (RET) (72.8 ± 1.4 years; BMI 26.3 ± 1.2 kg m(2) ). We measured LBF by Doppler ultrasound and muscle MBV by contrast-enhanced ultrasound. Muscle protein synthesis (MPS) was measured using [1, 2-(13) C2 ] leucine with breakdown (MPB) and net protein balance (NPB) by ring-[D5 ] phenylalanine tracers. Plasma insulin was measured via ELISA and indices of anabolic signalling (e.g. Akt/mTORC1) by immunoblotting from muscle biopsies. Whereas older untrained men did not exhibit fed-state increases in LBF or MBV, the RET group exhibited increases in both LBF and MBV. Despite our hypothesis that enhanced fed-state circulatory responses would improve anabolic responses to nutrition, fed-state increases in MPS (∼50-75%; P 0.001) were identical in both groups. Finally, whereas only the RET group exhibited fed-state suppression of MPB (∼-38%; P 0.05), positive NPB achieved was similar in both groups. We conclude that RET enhances fed-state LBF and MBV and restores nutrient-dependent attenuation of MPB without robustly enhancing MPS or NPB.