• MHC type
• contractile properties
• exercise prehabilitation
• hindlimb unloading
• titin

• Humans
• Rats
• Animals
• Rats, Sprague-Dawley
• Connectin
• Preoperative Exercise
• Hindlimb Suspension/adverse effects
• Hindlimb Suspension/physiology
• Muscular Atrophy/etiology
• Muscular Atrophy/prevention & control
• Muscular Atrophy/pathology
• Muscle, Skeletal
• Hindlimb

• 800-20200179 National Research Foundation of Korea
• 14-2018-0017 SNUBH Research Fund

• behaviour change
• carbohydrate periodisation
• meal timing
• nutrition support
• protein distribution
• rugby
• sports nutritionist

• molecular medicine
• metabolism

• Anabolism
• Animal protein
• Cancer
• Muscle
• Plant protein
• Protein source

• Anabolic Agents/pharmacology
• Animal Proteins, Dietary/pharmacology
• Expert Testimony
• Humans
• Muscle, Skeletal/drug effects
• Neoplasms/physiopathology
• Plant Proteins, Dietary/pharmacology

• MR/P021220/1 Medical Research Council

Although some studies have shown that a high-fat diet (HFD) adversely affects muscle extracellular matrix remodeling, the mechanisms involved in muscle trophism, inflammation, and adipogenesis have not been fully investigated. Thus, we investigated the effects of 8 weeks of paternal resistance training (RT) on gene and protein expression/activity of critical factors involved in muscle inflammation and remodeling of fathers and offspring (offspring exposed to standard chow or HFD). Animals were randomly distributed to constitute sedentary fathers (SF; n = 7; did not perform RT) or trained fathers (TF n = 7; performed RT), with offspring from mating with sedentary females. After birth, 28 male pups were divided into four groups (n = 7 per group): offspring from sedentary father submitted either to control diet (SFO-C) or high-fat diet (SFO-HF) and offspring from trained father submitted to control diet (TFO-C) or high-fat diet (TFO-HF). Our results show that an HFD downregulated collagen mRNA levels and upregulated inflammatory and atrophy pathways and adipogenic transcription factor mRNA levels in offspring gastrocnemius muscle. In contrast, paternal RT increased MMP-2 activity and decreased IL-6 levels in offspring exposed to a control diet. Paternal RT upregulated P70s6k and Ppara mRNA levels and downregulated Atrogin1 mRNA levels, while decreasing NFκ-B, IL-1β, and IL-8 protein levels in offspring exposed to an HFD. Paternal physical training influences key skeletal muscle remodeling pathways and inflammatory profiles relevant for muscle homeostasis maintenance in offspring submitted to different diets.

• adipogenic
• atrophy/hypertrophy signaling
• exercise
• gastrocnemius
• intergenerational
• proinflammatory cytokines
• protein turnover

• Heavy metal toxicity
• Selenium
• Selenocysteine
• Thioredoxin
• Thioredoxin reductase

• Atrophy
• Mechanism
• Skeletal muscle
• Treatment
• Ubiquitin proteasome system
• mTOR

• Animals
• Humans
• Muscle, Skeletal/metabolism
• Muscle, Skeletal/pathology
• Muscular Atrophy/drug therapy
• Muscular Atrophy/metabolism

• Fractional synthesis rate
• Habituated protein intake
• High protein intake
• Intrinsically labelled proteins
• Protein breakdown
• Protein synthesis
• Recommended protein intake

• Bias
• Cachexia/etiology
• Cachexia/therapy
• Combined Modality Therapy/methods
• Exercise
• Exercise Tolerance
• Fatigue/etiology
• Female
• Head and Neck Neoplasms/complications
• Humans
• Lung Neoplasms/complications
• Male
• Middle Aged
• Muscle Strength
• Neoplasms/complications
• Pancreatic Neoplasms/complications
• Patient Compliance
• Physical Endurance
• Quality of Life
• Randomized Controlled Trials as Topic
• Thinness

• Atazanavir
• Ca(2+) cycling
• Efavirenz
• HIV-1
• Ritonavir
• RyR1
• SERCA1.
• Sarcoplasmic reticulum
• Skeletal muscle weakness (dynapenia)

• aging
• inflammation
• oxidative stress
• physical activity
• sarcopenia
• satellite cells

• Aging
• Humans
• Inflammation
• Muscle, Skeletal/drug effects
• Muscle, Skeletal/metabolism
• Muscle, Skeletal/physiopathology
• Oxidative Stress
• Sarcopenia/drug therapy
• Sarcopenia/metabolism
• Sarcopenia/physiopathology
• Signal Transduction/drug effects

The global outbreak of COVID-19 has led to governments and local authorities implementing nationwide lockdowns in an attempt to encourage social distancing and minimize the spread of the virus. Only essential businesses have been able to remain open, with non-essential businesses and activities either closing or restricting services. With no group training sessions allowed, canceled matches, an inability to work and the closure of eating establishments, Rugby Union players have experienced disruption to their daily lives. Two surveys were distributed among Rugby Union athletes to explore (1) the influence of COVID-19 lockdown restrictions on Rugby Union players' nutrition and training habits and (2) how nutrition habits in New Zealand Rugby Union players change after lockdown restrictions were lifted. In total, 258 respondents completed Survey 1 (84.1% male, 26.4% professional/semi-professional). Of the respondents, 58% indicated they lived with family during lockdown. Total food intake was reported to be higher in 36% of respondents. Fruit and vegetable intake was lower (17%) and packaged/convenience food intake higher (26%) in a minority of respondents. In total, 106 respondents completed Survey 2 (84.9% male, 34.0% professional/semi-professional). Of the respondents, 72% prepared and 67% purchased their own food. Less than half of respondents consumed high-protein food more than twice daily either during or following lockdown. Compared to during lockdown, motivation to train and exercise was greater in 58% of respondents following lockdown. Dieticians and nutritionists within clubs provided most of the nutrition knowledge to athletes however other unreliable sources were identified, such as social media and family members. The ongoing pandemic has presented significant challenges for athletes concerning training and nutrition habits and the current study provides some insight into these. Coaches and performance staff should ensure athletes receive appropriate nutritional and training support whilst being aware of the unique demands the individuals' may face.

• COVID-19
• Rugby Union
• athlete
• nutrition habits
• social distancing measures
• training

• Chronic fatigue syndrome
• Environmental factors
• Infection
• Inflammation
• Ionizing radiation
• Myalgic encephalomyelitis
• Neuro-immune
• Nutritional deficiencies

Ageing is accompanied by a severe muscle function decline presumably caused by structural and functional adaptations at the central and peripheral level. Although researchers have reported an extensive analysis of the alterations involving muscle intrinsic properties, only a limited number of studies have recognised the importance of the central nervous system, and its reorganisation, on neuromuscular decline. Neural changes, such as degeneration of the human cortex and function of spinal circuitry, as well as the remodelling of the neuromuscular junction and motor units, appear to play a fundamental role in muscle quality decay and culminate with considerable impairments in voluntary activation and motor performance. Modern diagnostic techniques have provided indisputable evidence of a structural and morphological rearrangement of the central nervous system during ageing. Nevertheless, there is no clear insight on how such structural reorganisation contributes to the age-related functional decline and whether it is a result of a neural malfunction or serves as a compensatory mechanism to preserve motor control and performance in the elderly population. Combining leading-edge techniques such as high-density surface electromyography (EMG) and improved diagnostic procedures such as functional magnetic resonance imaging (fMRI) or high-resolution electroencephalography (EEG) could be essential to address the unresolved controversies and achieve an extensive understanding of the relationship between neural adaptations and muscle decline.

• aging
• cerebral cortex
• dynapenia
• elderly
• motor unit
• muscle strength
• neural
• neuroplasticity
• sarcopenia

Skeletal muscle atrophy is encountered in many clinical conditions, but a pharmacological treatment has not yet been established. Cistanche tubulosa (Schenk) Wight is an herbal medicine used in traditional Japanese and Chinese medicine. In the current study, we investigated the effect of C. tubulosa extract (CTE) on atrophied muscle in vivo. We also investigated hindlimb cast immobilization in mice and devised a novel type of hindlimb-immobilizing cast, consisting of sponge-like tape and a thin plastic tube. Using this method, 3 out of 4 groups of mice (n = 11 for each group) were cast-immobilized in the hindlimbs and administered CTE or vehicle for 13 days. A sham procedure was performed in the mice of the fourth group to which the vehicle was administered. Next, the triceps surae muscles (TS) were excised. To analyze the effect of the novel cast system and CTE administration on muscle atrophy, we evaluated TS wet weight and myofiber cross-sectional area (CSA). We also determined MyHC IId/IIx expression levels by western blotting, since their increase is a hallmark of disuse muscle atrophy, suggesting slow-to-fast myofiber type shift. Moreover, we performed two tests of hindlimb performance. The novel cast immobilization method significantly reduced TS wet weight and myofiber CSA. This was accompanied by deterioration of hindlimb function and an increase in MyHC IId/IIx expression. CTE administration did not alter TS wet weight or myofiber CSA; however, it showed a trend of amelioration of the loss of hindlimb function and of suppression of the increased MyHC IId/IIx expression in cast-immobilized mice. Our novel hindlimb cast immobilization method effectively induced muscle atrophy. CTE did not affect muscle mass, but suppressed the shift from slow to fast myofiber type in cast-immobilized mice, ameliorating hindlimb function deterioration.

• aging
• cancer
• epigenetics
• inflammation
• physical exercise

• COX-2
• Pain
• diet
• exercises
• nutritional supplementation
• omega-3

• Adolescent
• Adult
• Humans
• Leg
• Male
• Muscle Fibers, Fast-Twitch/drug effects
• Muscle Fibers, Fast-Twitch/pathology
• Muscle Fibers, Slow-Twitch/drug effects
• Muscle Fibers, Slow-Twitch/pathology
• Muscle Strength/drug effects
• Muscle Strength/physiology
• Muscular Atrophy/diagnostic imaging
• Muscular Atrophy/etiology
• Muscular Atrophy/prevention & control
• Nandrolone Decanoate/administration & dosage
• Quadriceps Muscle/diagnostic imaging
• Quadriceps Muscle/drug effects
• Quadriceps Muscle/pathology
• Restraint, Physical/adverse effects
• Tomography, X-Ray Computed
• Young Adult

• atrophy
• inactivity
• muscle function
• physical activity

• activity of daily living
• acute and critical illness
• muscle mass
• quality of life
• rehabilitation and nutritional treatment

• Activities of Daily Living
• Acute Disease/rehabilitation
• Acute Disease/therapy
• Critical Illness/rehabilitation
• Critical Illness/therapy
• Humans
• Nutrition Therapy
• Physical Therapy Modalities
• Quality of Life

• Chronic fatigue syndrome
• Cytokines
• Delayed hypersensitivity
• Immunoglobulins
• Lymphocyte transformation
• Nutrients

• cancer survivors
• cancer treatments
• physical activity treatments
• physical exercise
• psycho-physical symptoms

• Excessive exercise
• Mitochondria
• Muscle atrophy
• Physical exercise

• Exercise
• Humans
• Mitochondria, Muscle/physiology
• Muscle Contraction
• Muscle, Skeletal/physiopathology
• Muscular Atrophy/prevention & control

• cachexia
• cancer
• exercise
• multimodal treatment
• muscle wasting
• nutritional intervention

• Exercise
• aging
• cardiac cachexia
• heart failure
• physical function
• protein supplementation
• weakness

• Botulinum toxin-A
• CD34
• Mesenchymal stem cells
• Muscle atrophy

• aging
• bone health
• nutrition
• osteosarcopenic obesity
• physical activity

The response to resistance training and protein supplementation in the latissimus dorsi muscle (LDM) has never been investigated. We investigated the effects of resistance training (RT) and protein supplementation on muscle mass, strength, and fiber characteristics of the LDM. Eighteen healthy young subjects were randomly assigned to a progressive eight-week RT program with a normal protein diet (NP) or high protein diet (HP) (NP 0.85 vs. HP 1.8 g of protein·kg⁻¹·day⁻¹). One repetition maximum tests, magnetic resonance imaging for cross-sectional muscle area (CSA), body composition, and single muscle fibers mechanical and phenotype characteristics were measured. RT induced a significant gain in strength (+17%, p < 0.0001), whole muscle CSA (p = 0.024), and single muscle fibers CSA (p < 0.05) of LDM in all subjects. Fiber isometric force increased in proportion to CSA (+22%, p < 0.005) and thus no change in specific tension occurred. A significant transition from 2X to 2A myosin expression was induced by training. The protein supplementation showed no significant effects on all measured outcomes except for a smaller reduction of 2X myosin expression. Our results suggest that in LDM protein supplementation does not further enhance RT-induced muscle fiber hypertrophy nor influence mechanic muscle fiber characteristics but partially counteracts the fast-to-slow fiber shift.

• myosin isoform
• nutrition
• single muscle fiber mechanics
• strength training
• supplementation
• whey protein

• Adult
• Body Composition
• Diet
• Dietary Proteins/administration & dosage
• Humans
• Male
• Muscle Fibers, Skeletal/drug effects
• Muscle Fibers, Skeletal/physiology
• Resistance Training
• Superficial Back Muscles/drug effects
• Superficial Back Muscles/physiology
• Young Adult

Counteracting muscle atrophy induced by mechanical unloading/inactivity is of great clinical need and challenge. A therapeutic agent that could counteract muscle atrophy following mechanical unloading in safety is desired. This study showed that natural product Icaritin (ICT) could increase the phosphorylation level of Phosphatidylinositol 3 kinase (PI3K) at p110 catalytic subunit and promote PI3K/Akt signaling markers in C2C12 cells. This study further showed that the high dose ICT treatment could significantly attenuate the decreases in the phosphorylation level of PI3K at p110 catalytic subunit and its downstream markers related to protein synthesis, and inhibit the increases in protein degradation markers at mRNA and protein levels in rat soleus muscle following 28-day hindlimb unloading. In addition, the decreases in soleus muscle mass, muscle fiber cross-sectional area, twitch force, specific force, contraction time and half relaxation time could be significantly attenuated by the high dose ICT treatment. The low dose ICT treatment could moderately attenuate the above changes induced by unloading. Wortmannin, a specific inhibitor of PI3K at p110 catalytic subunit, could abolish the above effects of ICT in vitro and in vivo, indicating that PI3K/Akt signaling could be required by ICT to counteract skeletal muscle atrophy following mechanical unloading.

• Akt
• exercise
• histone deacetylase (HDAC)
• insulin receptor substrate 1 (IRS1)
• metabolism
• myotubes

• AMP-Activated Protein Kinases/metabolism
• Animals
• Atrophy/drug therapy
• Atrophy/genetics
• Cell Line
• Dose-Response Relationship, Drug
• Extracellular Space/metabolism
• Glucose/metabolism
• Histone Deacetylase Inhibitors/pharmacology
• Humans
• Insulin Receptor Substrate Proteins/metabolism
• Mechanistic Target of Rapamycin Complex 1
• Mice
• Multiprotein Complexes/metabolism
• Muscle Fibers, Skeletal/drug effects
• Muscle Fibers, Skeletal/metabolism
• Oxygen Consumption
• Peptides, Cyclic/pharmacology
• Phosphatidylinositol 3-Kinases/metabolism
• Proto-Oncogene Proteins c-akt/metabolism
• Signal Transduction/drug effects
• TOR Serine-Threonine Kinases/metabolism

Step-reduction (SR) in older adults results in muscle atrophy and an attenuated rise in postprandial muscle protein synthesis (MPS): anabolic resistance. Knowing that resistance exercise (RT) can enhance MPS, we examined whether RT could enhance MPS following 2 weeks of SR. In addition, as we postulated that SR may impair feeding-induced vasodilation limiting nutrient delivery to muscle, we also examined whether citrulline (CIT), as an arginine and nitric oxide precursor, could attenuate muscle anabolic resistance accompanying SR. We used a unilateral leg model to compare older subjects’ who had undergone SR to a loaded condition of SR plus RT (SR + RT). Thirty older men (70 ± 1 years) underwent 14 days of SR (<1500 steps/day) with supplementation of either 5 g/day CIT or glycine placebo. Throughout SR, subjects performed unilateral low-load RT thrice weekly. We assessed muscle protein synthesis in the postabsorptive and postprandial state (20 g whey isolate plus 15 g glycine or as micellar-whey with 5 g CIT or 15 g glycine, n = 10/group). As MPS was similar after ingestion of either whey isolate, micellar-whey, or micellar-whey + CIT data related to different dietary groups were collapsed to compare SR and SR + RT legs. Subjects’ daily steps were reduced by 80 ± 2% during SR (P < 0.001) compared with baseline. Leg fat-free mass decreased with SR (−124 ± 61 g) and increased in the SR + RT (+126 ± 68 g; P = 0.003). Myofibrillar FSR was lower (P < 0.0001) in the SR as compared with the SR + RT leg in the postabsorptive (0.026 ± 0.001%/h vs. 0.045 ± 0.001%/h) and postprandial states (0.055 ± 0.002%/h vs. 0.115 ± 0.003%/h). We conclude that low-load RT, but not supplementation with CIT, can attenuate the deleterious effects of SR in aging muscle.

• Anabolic resistance
• resistance training
• sarcopenia
• step‐reduction

• HSP70
• PGC1-α
• bed rest
• immobilization
• mitophagy
• oxidative stress
• superoxide dismutase
• unloading

• Adult
• Cachexia/etiology
• Cachexia/therapy
• Exercise
• Humans
• Neoplasms/complications
• Thinness

Exercise and rehabilitation approaches in palliative care programs for cancer patients affect patients’ symptoms, physical functioning, muscle strength, emotional wellbeing, psychological symptoms, functional capacities, quality of life, mortality and morbidity positively. Based on scientific data, palliative cancer patients should be recommended to participate in exercise programs. There is no standard approach to recipe an exercise regimen for a palliative cancer survivor. Studies for demonstrating the positive effects of exercising in palliative care patients are increasing in number day by day. At this point, increasing awareness about exercising in the entire team monitoring the patient and our efforts in this matter seems to be very important.

• Palliative care
• Cancer
• Exercise
• Rehabilitation
• Muscle

• atrophy
• botulinum toxin
• contractile function
• embryonic stem cells
• skeletal muscle

• Aged
• Exercise
• Exercise Therapy
• Frail Elderly
• Humans
• Muscle Strength/physiology
• Muscle, Skeletal/physiopathology
• Nutritional Status
• Physical Endurance
• Randomized Controlled Trials as Topic
• Resistance Training
• Sarcopenia/therapy

Prolonged inactivity induces muscle loss due to an activation of proteolysis and decreased protein synthesis; the latter is also involved in the recovery of muscle mass. The aim of the present work was to explore the evolution of muscle mass and protein metabolism during immobilization and recovery and assess the effect of a nutritional strategy for counteracting muscle loss and facilitating recovery. Adult rats (6–8 months) were subjected to unilateral hindlimb casting for 8 days (I0–I8) and then permitted to recover for 10 to 40 days (R10–R40). They were fed a Control or Experimental diet supplemented with antioxidants/polyphenols (AOX) (I0 to I8), AOX and leucine (AOX + LEU) (I8 to R15) and LEU alone (R15 to R40). Muscle mass, absolute protein synthesis rate and proteasome activities were measured in gastrocnemius muscle in casted and non-casted legs in post prandial (PP) and post absorptive (PA) states at each time point. Immobilized gastrocnemius protein content was similarly reduced (-37%) in both diets compared to the non-casted leg. Muscle mass recovery was accelerated by the AOX and LEU supplementation (+6% AOX+LEU vs. Control, P<0.05 at R40) due to a higher protein synthesis both in PA and PP states (+23% and 31% respectively, Experimental vs. Control diets, P<0.05, R40) without difference in trypsin- and chymotrypsin-like activities between diets. Thus, this nutritional supplementation accelerated the recovery of muscle mass via a stimulation of protein synthesis throughout the entire day (in the PP and PA states) and could be a promising strategy to be tested during recovery from bed rest in humans.

• Absorption, Physiological
• Animals
• Antioxidants/pharmacology
• Biomarkers/metabolism
• Body Weight/drug effects
• Dietary Supplements
• Eating/drug effects
• Immobilization/adverse effects
• Leucine/blood
• Leucine/pharmacology
• Male
• Muscle Proteins/biosynthesis
• Muscle Proteins/metabolism
• Muscle, Skeletal/anatomy & histology
• Muscle, Skeletal/drug effects
• Muscle, Skeletal/metabolism
• Muscle, Skeletal/physiology
• Organ Size/drug effects
• Oxidation-Reduction/drug effects
• Postprandial Period/drug effects
• Rats
• Recovery of Function/drug effects

• Cachexia
• Cancer
• Muscle mass
• Muscle strength
• Physical exercise

• hiv
• chronic disease and hiv
• nutrition
• physical activity
• interventions
• cardiometabolic disease
• malnutrition
• antiretroviral therapy (art)
• multivitamin supplementation
• vitamin d

• Acquired Immunodeficiency Syndrome/complications
• Acquired Immunodeficiency Syndrome/immunology
• Acquired Immunodeficiency Syndrome/physiopathology
• Acquired Immunodeficiency Syndrome/therapy
• Bone Density
• Chronic Disease
• Dietary Supplements
• Disease Progression
• Dyslipidemias/complications
• Dyslipidemias/immunology
• Dyslipidemias/prevention & control
• Exercise
• Female
• HIV Seropositivity/complications
• HIV Seropositivity/immunology
• HIV Seropositivity/physiopathology
• HIV Seropositivity/therapy
• Humans
• Insulin Resistance/immunology
• Male
• Malnutrition/complications
• Malnutrition/immunology
• Malnutrition/prevention & control
• Nutritional Status
• Obesity/complications
• Obesity/immunology
• Obesity/prevention & control
• Quality of Life
• Vitamins/therapeutic use

• 1 R01 HL095127 NHLBI NIH HHS
• 1 R01 HD060325 NICHD NIH HHS
• 1R01 NR012885 NINR NIH HHS
• R01 HL095127 NHLBI NIH HHS
• R01 HD060325 NICHD NIH HHS
• R01 NR012885 NINR NIH HHS