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Summary: Skeletal muscle is the largest organ of the human body and plays a pivotal role in whole-body homeostasis through the maintenance of physical and metabolic health. Establishing strategies aimed at increasing the amount, and minimising loss, of muscle mass are of upmost importance. Muscle mass is primarily dictated by the meal-to-meal fluctuations in muscle protein synthesis (MPS) and muscle protein breakdown (MPB), each of which can be quantified through the use of stable isotopically labelled tracers. Importantly, both MPS and MPB can be influenced by external factors such as nutritional manipulation, specifically protein ingestion, and changes in loading via exercise. To date, research involving stable isotopic tracers has focused on determining the optimal dose, timing surrounding bouts of exercise, distribution and composition of protein to maximally stimulate MPS and inhibit MPB, both at rest and following exercise. In this review we focus on the use of these stable isotopically-labeled tracers to unravel the intricacies of skeletal muscle protein turnover in response to specific nutritional interventions.

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.

A progressive decrement in muscle mass and muscle function, sarcopoenia, accompanies ageing. The loss of skeletal muscle mass and function is the main feature of sarcopoenia. Preventing the loss of muscle mass is relevant since sarcopoenia can have a significant impact on mobility and the quality of life of older people. Dietary protein and physical activity have an essential role in slowing muscle mass loss and helping to maintain muscle function. However, the current recommendations for daily protein ingestion for older persons appear to be too low and are in need of adjustment. In this review, we discuss the skeletal muscle response to protein ingestion, and review the data examining current dietary protein recommendations in the older subjects. Furthermore, we review the concept of protein quality and the important role that nutrient-dense protein (NDP) sources play in meeting overall nutrient requirements and improving dietary quality. Overall, the current evidence endorses an increase in the daily ingestion of protein with emphasis on the ingestion of NDP choices by older adults.

PURPOSE: Previous studies have reported that low-load high-repetition (LLHR) resistance exercise can induce muscle hypertrophy to a similar extent as high-load low-repetition (HLLR). However, it is unclear which mechanical stress, such as exercise intensity, contraction number, and/or total work volume and which molecular mechanisms underpin the greater relative muscle hypertrophy after LLHR exercise.METHODS: Sprague-Dawley rats (12 weeks, N=35) were randomly allocated into control (Con, n=7), low-load low-repetition (LLLR, n=7), low-load medium-repetition (LLMR, n=7), LLHR (n=7), and HLLR (n=7) resistance exercise groups. They performed a ladder climbing exercise to evaluate the effect of exercise intensity, contraction number and work volume on the activation of satellite cells and protein synthesis signaling pathway.RESULTS: The number of active satellite cells and the phosphorylation of mTOR, p70S6K, ERK, and p38 were increased after LLHR and HLLR exercise (pp

Skeletal muscle plays a pivotal role in the maintenance of physical and metabolic health and, critically, mobility. Accordingly, strategies focused on increasing the quality and quantity of skeletal muscle are relevant, and resistance exercise is foundational to the process of functional hypertrophy. Much of our current understanding of skeletal muscle hypertrophy can be attributed to the development and utilization of stable isotopically labeled tracers. We know that resistance exercise and sufficient protein intake act synergistically and provide the most effective stimuli to enhance skeletal muscle mass; however, the molecular intricacies that underpin the tremendous response variability to resistance exercise-induced hypertrophy are complex. The purpose of this review is to discuss recent studies with the aim of shedding light on key regulatory mechanisms that dictate hypertrophic gains in skeletal muscle mass. We also aim to provide a brief up-to-date summary of the recent advances in our understanding of skeletal muscle hypertrophy in response to resistance training in humans.

Lower-load (LL), higher-repetition resistance exercise training (RET) can increase muscle mass in a similar degree as higher-load (HL), lower-repetition RET. However, little is known about how LL and HL RET modulate other aspects of the RET phenotype such as satellite cells, myonuclei, and mitochondrial proteins. We aimed to investigate changes in muscle mass, muscle strength, satellite cell activity, myonuclear addition, and mitochondrial protein content after prolonged RET with LL and HL RET.We recruited 21 young men and randomly assigned them to perform 10 wk RET (leg press, leg extension, and leg curl) three times per week with the following conditions: 80FAIL (80% one-repetition maximum [1RM] performed to volitional fatigue), 30WM (30%1RM with volume matched to 80FAIL), and 30FAIL (30%1RM to volitional fatigue). Skeletal muscle biopsies were taken from the vastus lateralis pre- and post-RET intervention.After 10 wk of RET, only 30FAIL and 80FAIL showed an increase in peak torque and type I fiber cross-sectional area (P0.05). Moreover, only 30FAIL resulted in a significant decrease in the myonuclear domain of type II muscle fibers and an increase in mitochondrial proteins related to autophagy, fission, and fusion (all P0.05).We discovered that LL RET was effective at increasing the content of several mitochondrial proteins. Similar to previous research, we found that changes in muscle mass and strength were independent of load when repetitions were performed to volitional fatigue.

Skeletal muscle plays an indispensable role in metabolic health and physical function. A decrease in muscle mass and function with advancing age exacerbates the likelihood of mobility impairments, disease development, and early mortality. Therefore, the development of non-pharmacological interventions to counteract sarcopenia warrant significant attention. Currently, resistance training provides the most effective, low cost means by which to prevent sarcopenia progression and improve multiple aspects of overall health. Importantly, the impact of resistance training on skeletal muscle mass may be augmented by specific dietary components (i.e., protein), feeding strategies (i.e., timing, per-meal doses of specific macronutrients) and nutritional supplements (e.g., creatine, vitamin-D, omega-3 polyunsaturated fatty acids etc.). The purpose of this review is to provide an up-to-date, evidence-based account of nutritional strategies to enhance resistance training-induced adaptations in an attempt to combat age-related muscle mass loss. In addition, we provide insight on how to incorporate the aforementioned nutritional strategies that may support the growth or maintenance of skeletal muscle and subsequently extend the healthspan of older individuals.

Exercise training causes epigenetic changes in skeletal muscle, although it is unclear how resistance exercise (RE) affects histone modifications. The present study was carried out to investigate the effects of acute RE and RE training on gene expression profiles and histone modifications in human skeletal muscle. Healthy male adults were assigned to acute RE (n = 9, age = 20.5±4.3yr, BMI = 28.0±6.8kg/m2) or RE training (n = 21, age = 23.7±2.5yr, BMI = 24.2±2.7kg/m2) groups. Biopsy samples were obtained from the vastus lateralis muscle before and three hours after a single bout of acute RE, or 3-days after 10 weeks of RE training. RNA sequencing analysis revealed that 153 genes with GO terms including muscle development, stress response, metabolism, cell death, and transcription factor were significantly up-regulated (+291% vs. pre-acute RE) upon acute RE. Expressions of these genes were also greater (+9.6% vs. pre-RE training, p

Background Limited data are available examining dietary interventions for optimizing protein and leucine intake to stimulate muscle protein synthesis (MPS) in older humans. Objectives We aimed to investigate the aminoacidemia and appetite responses of older adults after consuming breakfast, a meal frequently consumed with high-carbohydrate and below-par amounts of protein and leucine for stimulating MPS. Methods Five men and 3 women (means ± SD; age: 74 ± 7 y, BMI: 25.7 ± 4.9 kg/m2, fat- and bone-free mass: 63 ± 7 kg) took part in this experiment in which they consumed breakfasts with low-protein (LP = 13 ± 2 g), high-protein (HP = 32 ± 5 g), and LP followed by a protein- and leucine-enriched bar formulation 2 h later (LP + Bar = 29 ± 2 g). The LP, HP, and LP + Bar breakfast conditions contained 519 ± 86 kcal, 535 ± 83 kcal, and 739 ± 86 kcal, respectively. Blood samples were drawn for 6 h and analyzed for amino acid, insulin, and glucose concentrations. Visual analog scales were assessed for hunger, fullness, and desire to eat. Results The net AUC for essential amino acid (EAA) exposure was similar between the LP + Bar and HP conditions but greater in the HP condition compared with the LP condition. Peak leucinemia was higher in the LP + Bar condition compared with the HP, and both were greater than the LP condition. Net leucine exposure was similar between HP and LP + Bar, and both were greater than LP. Hunger was similarly reduced in LP + Bar and HP, and LP + Bar resulted in a greater hunger reduction than LP. Both LP + Bar and HP resulted in greater net fullness scores than LP. Conclusions Consuming our bar formulation increased blood leucine availability and net exposure to EAAs to a similar degree as consuming a high-protein meal. High-protein at breakfast results in a greater net exposure to EAAs and leucine, which could support MPS in older persons. This study was registered at clinicaltrials.gov as NCT03712761., There are practical limitations for older persons to sufficiently increase daily protein intake. Dietary recommendations aimed to prevent or minimize sarcopenia may benefit from inclusion of supplementing with unique formulations containing milk proteins with free leucine.