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1.
Free Radic Biol Med ; 124: 241-248, 2018 08 20.
Artigo em Inglês | MEDLINE | ID: mdl-29909291

RESUMO

Extended periods of skeletal muscle disuse result in muscle atrophy. Following limb immobilization, increased mitochondrial reactive oxygen species (ROS) production may contribute to atrophy through increases in skeletal muscle protein degradation. However, the effect of skeletal muscle disuse on mitochondrial ROS production remains unclear. This study investigated the effect of immobilization, followed by two subsequent periods of restored physical activity, on mitochondrial H2O2 emissions in adult male skeletal muscle. Middle-aged men (n = 30, 49.7 ±â€¯3.84 y) completed two weeks of unilateral lower-limb immobilization, followed by two weeks of baseline-matched activity, consisting of 10,000 steps a day, then completed two weeks of three times weekly supervised resistance training. Vastus lateralis biopsies were taken at baseline, post-immobilization, post-ambulatory recovery, and post-resistance-training. High-resolution respirometry was used simultaneously with fluorometry to determine mitochondrial respiration and hydrogen peroxide (H2O2) production in permeabilized muscle fibres. Mitochondrial H2O2 emission with complex I and II substrates, in the absence of ADP, was greater following immobilization, however, there was no effect on mitochondrial respiration. Both ambulatory recovery and resistance training, following the period of immobilization, increased in mitochondrial H2O2 emissions. These data demonstrated that 2 weeks of immobilization increases mitochondrial H2O2 emissions, but subsequent retraining periods of ambulatory recovery and resistance training also led to in robust increases in mitochondrial H2O2 emissions in skeletal muscle.


Assuntos
Exercício/fisiologia , Peróxido de Hidrogênio/metabolismo , Mitocôndrias/metabolismo , Músculo Esquelético/metabolismo , Restrição Física/fisiologia , Respiração Celular/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Treinamento de Resistência
2.
J Appl Physiol (1985) ; 125(2): 271-286, 2018 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-29698111

RESUMO

Strenuous exercise can result in skeletal muscle damage, leading to the systemic mobilization, activation, and intramuscular accumulation of blood leukocytes. Eicosanoid metabolites of arachidonic acid (ARA) are potent inflammatory mediators, but whether changes in dietary ARA intake influence exercise-induced inflammation is not known. This study investigated the effect of 4 wk of dietary supplementation with 1.5 g/day ARA ( n = 9, 24 ± 1.5 yr) or corn-soy oil placebo ( n = 10, 26 ± 1.3 yr) on systemic and intramuscular inflammatory responses to an acute bout of resistance exercise (8 sets each of leg press and extension at 80% one-repetition maximum) in previously trained men. Whole EDTA blood, serum, peripheral blood mononuclear cells (PMBCs), and skeletal muscle biopsies were collected before exercise, immediately postexercise, and at 2, 4, and 48 h of recovery. ARA supplementation resulted in higher exercise-stimulated serum creatine kinase activity [incremental area under the curve (iAUC) P = 0.046] and blood leukocyte counts (iAUC for total white cells, P < 0.001; neutrophils: P = 0.007; monocytes: P = 0.015). The exercise-induced fold change in peripheral blood mononuclear cell mRNA expression of interleukin-1ß ( IL1B), CD11b ( ITGAM), and neutrophil elastase ( ELANE), as well as muscle mRNA expression of the chemokines interleukin-8 ( CXCL8) and monocyte chemoattractant protein 1 ( CCL2) was also greater in the ARA group than placebo. Despite this, ARA supplementation did not influence the histological presence of leukocytes within muscle, perceived muscle soreness, or the extent and duration of muscle force loss. These data show that ARA supplementation transiently increased the inflammatory response to acute resistance exercise but did not impair recovery. NEW & NOTEWORTHY Daily arachidonic acid supplementation for 4 wk in trained men augmented the acute systemic and intramuscular inflammatory response to a subsequent bout of resistance exercise. Greater exercise-induced inflammatory responses in men receiving arachidonic acid supplementation were not accompanied by increased symptoms of exercise-induced muscle damage. Although increased dietary arachidonic acid intake does not appear to influence basal inflammation in humans, the acute inflammatory response to exercise stress is transiently increased following arachidonic acid supplementation.


Assuntos
Ácido Araquidônico/administração & dosagem , Exercício/fisiologia , Inflamação/tratamento farmacológico , Treinamento de Resistência/efeitos adversos , Adolescente , Adulto , Antígeno CD11b/metabolismo , Quimiocina CCL2/metabolismo , Creatina Quinase/metabolismo , Suplementos Nutricionais , Humanos , Inflamação/metabolismo , Interleucina-1beta/metabolismo , Interleucina-8/metabolismo , Elastase de Leucócito/metabolismo , Leucócitos Mononucleares/efeitos dos fármacos , Leucócitos Mononucleares/metabolismo , Masculino , Força Muscular/efeitos dos fármacos , Músculo Esquelético/efeitos dos fármacos , Músculo Esquelético/metabolismo , Mialgia/tratamento farmacológico , Mialgia/metabolismo , RNA Mensageiro/metabolismo , Adulto Jovem
3.
J Appl Physiol (1985) ; 124(4): 1080-1091, 2018 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-29389245

RESUMO

Arachidonic acid (ARA), a polyunsaturated ω-6 fatty acid, acts as precursor to a number of prostaglandins with potential roles in muscle anabolism. It was hypothesized that ARA supplementation might enhance the early anabolic response to resistance exercise (RE) by increasing muscle protein synthesis (MPS) via mammalian target of rapamycin (mTOR) pathway activation and/or the late anabolic response by modulating ribosome biogenesis and satellite cell expansion. Nineteen men with ≥1 yr of resistance-training experience were randomized to consume either 1.5 g daily ARA or a corn-soy-oil placebo in a double-blind manner for 4 wk. Participants then undertook fasted RE (8 sets each of leg press and extension at 80% 1-repetition maximum), with vastus lateralis biopsies obtained before exercise, immediately postexercise, and at 2, 4, and 48 h of recovery. MPS (measured via stable isotope infusion) was not different between groups ( P = 0.212) over the 4-h recovery period. mTOR pathway members p70 S6 kinase and S6 ribosomal protein were phosphorylated postexercise ( P < 0.05), with no difference between groups. 45S preribosomal RNA increased 48 h after exercise only in ARA ( P = 0.012). Neural cell adhesion molecule-positive satellite cells per fiber increased 48 h after exercise ( P = 0.013), with no difference between groups ( P = 0.331). Prior ARA supplementation did not alter the acute anabolic response to RE in previously resistance-trained men; however, at 48 h of recovery, ribosome biogenesis was stimulated only in the ARA group. The findings do not support a mechanistic link between ARA and short-term anabolism, but ARA supplementation in conjunction with resistance training may stimulate increases in translational capacity. NEW & NOTEWORTHY Four weeks of daily arachidonic acid supplementation in trained men did not alter their acute muscle protein synthetic or anabolic signaling response to resistance exercise. However, 48 h after exercise, men supplemented with arachidonic acid showed greater ribosome biogenesis and a trend toward greater change in satellite cell content. Chronic arachidonic acid supplementation does not appear to regulate the acute anabolic response to resistance exercise but may augment muscle adaptation in the following days of recovery.


Assuntos
Ácido Araquidônico/administração & dosagem , Proteínas Musculares/biossíntese , Músculo Esquelético/efeitos dos fármacos , Treinamento de Resistência , Adulto , Suplementos Nutricionais , Humanos , Sistema de Sinalização das MAP Quinases , Masculino , Ribossomos/metabolismo , Células Satélites de Músculo Esquelético , Adulto Jovem
4.
Artigo em Inglês | MEDLINE | ID: mdl-29413364

RESUMO

Arachidonic acid (ARA), an omega-6 polyunsaturated fatty acid (PUFA), is the metabolic precursor to the eicosanoid family of lipid mediators. Eicosanoids have potent pro-inflammatory actions, but also act as important autocrine/paracrine signaling molecules in skeletal muscle growth and development. Whether dietary ARA is incorporated into skeletal muscle phospholipids and the resulting impact on intramuscular inflammatory and adaptive processes in-vivo is not known. In the current study, resistance trained men (≥1 year) received dietary supplementation with 1.5g/day ARA (n=9, 24 ± 1.5 years) or placebo (n=10, 26 ± 1.3 years) for 4-weeks while continuing their normal training regimen. Plasma and vastus lateralis muscle biopsies were collected in an overnight fasted state at baseline and week 4. ARA supplementation increased plasma content of ARA and gamma-linolenic acid, while decreasing relative abundance of linoleic acid, eicosapentaenoic acid, and dihomo-gamma-linolenic acid. In skeletal muscle, ARA and dihomo-gamma-linolenic acid content increased, whereas alpha-linolenic-acid was reduced. Compared to placebo, ARA supplementation reduced circulating platelet and monocyte number, and decreased the mRNA expression of the immune cell surface markers; neutrophil elastase/CD66b and interleukin 1-beta, in peripheral blood mononuclear cells. In muscle, ARA supplementation increased mRNA expression of the myogenic regulatory factors; MyoD and myogenin, but had no effect on a range of immune cell markers or inflammatory cytokines. These data show that dietary ARA supplementation can rapidly and safely modulate plasma and muscle fatty acid profile and promote myogenic gene expression in resistance trained men, without a risk of increasing basal systemic or intramuscular inflammation.


Assuntos
Ácido Araquidônico/farmacologia , Inflamação/dietoterapia , Lipídeos/análise , Músculo Esquelético/efeitos dos fármacos , Adolescente , Adulto , Ácido Araquidônico/administração & dosagem , Análise Química do Sangue , Composição Corporal/efeitos dos fármacos , Suplementos Nutricionais , Ácidos Graxos/análise , Ácidos Graxos/sangue , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Leucócitos Mononucleares/efeitos dos fármacos , Metabolismo dos Lipídeos/efeitos dos fármacos , Lipídeos/sangue , Masculino , Músculo Esquelético/metabolismo
5.
Mol Nutr Food Res ; 62(7): e1701028, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29377592

RESUMO

Limb immobilization results in a rapid loss of muscle size and strength. The resultant alterations in signaling pathways governing myogenesis, catabolism, and mitochondrial biogenesis are likely to include posttranscriptional regulation mediated by altered microRNAs (miRNAs). Given that protein ingestion exerts an anabolic action and may act as a countermeasure to mitigate muscle loss with immobilization, it is important to examine miRNA in this context. The objective of the study is therefore to characterize the vastus lateralis miRNA response to 14 days of disuse in males (45-60 years) randomized to receive supplementation with 20 g d-1 of dairy protein (n = 12) or isocaloric carbohydrate placebo (n = 13). Biopsies are collected before and after a 2-week immobilization period. Of the 24 miRNAs previously identified in myogenic regulation, seven (miR-133a, -206, -15a, -451a, -126, -208b, and let-7e) are increased with immobilization irrespective of group; five (miR-16, -494, let-7a, -7c, and 7d) increased only in the carbohydrate group; and eight (miR-1, -486, -23a, -23b, -26a, -148b, let-7b, and -7g) are divergently expressed between groups (suppressed with protein). The ability of protein supplementation to differentially regulate miRNAs involved in key muscle regulatory pathways following short-term limb immobilization reflects potential protective function in mitigating muscle loss during limb immobilization.


Assuntos
Suplementos Nutricionais , Regulação da Expressão Gênica , MicroRNAs/metabolismo , Proteínas do Leite/uso terapêutico , Músculo Esquelético/metabolismo , Atrofia Muscular/prevenção & controle , Restrição Física/efeitos adversos , Bebidas , Biópsia por Agulha , Desjejum , Estudos de Coortes , Perfilação da Expressão Gênica , Humanos , Joelho , Extremidade Inferior , Masculino , Pessoa de Meia-Idade , Músculo Esquelético/patologia , Atrofia Muscular/etiologia , Atrofia Muscular/metabolismo , Atrofia Muscular/patologia , Músculo Quadríceps
6.
J Appl Physiol (1985) ; 124(3): 717-728, 2018 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-29122965

RESUMO

Muscle disuse results in the loss of muscular strength and size, due to an imbalance between protein synthesis (MPS) and breakdown (MPB). Protein ingestion stimulates MPS, although it is not established if protein is able to attenuate muscle loss with immobilization (IM) or influence the recovery consisting of ambulatory movement followed by resistance training (RT). Thirty men (49.9 ± 0.6 yr) underwent 14 days of unilateral leg IM, 14 days of ambulatory recovery (AR), and a further six RT sessions over 14 days. Participants were randomized to consume an additional 20 g of dairy protein or placebo with a meal during the intervention. Isometric knee extension strength was reduced following IM (-24.7 ± 2.7%), partially recovered with AR (-8.6 ± 2.6%), and fully recovered after RT (-0.6 ± 3.4%), with no effect of supplementation. Thigh muscle cross-sectional area decreased with IM (-4.1 ± 0.5%), partially recovered with AR (-2.1 ± 0.5%), and increased above baseline with RT (+2.2 ± 0.5%), with no treatment effect. Myofibrillar MPS, measured using deuterated water, was unaltered by IM, with no effect of protein. During AR, MPS was increased only with protein supplementation. Protein supplementation did not attenuate the loss of muscle size and function with disuse or potentiate recovery but enhanced myofibrillar MPS during AR. NEW & NOTEWORTHY Twenty grams of daily protein supplementation does not attenuate the loss of muscle size and function induced by 2 wk of muscle disuse or potentiate recovery in middle-age men. Average mitochondrial but not myofibrillar muscle protein synthesis was attenuated during immobilization with no effect of supplementation. Protein supplementation increased myofibrillar protein synthesis during a 2-wk period of ambulatory recovery following disuse but without group differences in phenotype recovery.


Assuntos
Imobilização/efeitos adversos , Proteínas do Leite/uso terapêutico , Músculo Esquelético/efeitos dos fármacos , Atrofia Muscular/prevenção & controle , Citrato (si)-Sintase/metabolismo , Suplementos Nutricionais , Exercício , Humanos , Masculino , Pessoa de Meia-Idade , Proteínas do Leite/farmacologia , Proteínas Musculares/biossíntese , Proteínas Musculares/metabolismo , Força Muscular/efeitos dos fármacos , Músculo Esquelético/diagnóstico por imagem , Músculo Esquelético/metabolismo , Atrofia Muscular/etiologia , Proteínas Ligases SKP Culina F-Box/metabolismo
7.
Nutr Metab (Lond) ; 14: 9, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28127382

RESUMO

BACKGROUND: The milk fat globule membrane (MFGM) is primarily composed of polar phospho- and sphingolipids, which have established biological effects on neuroplasticity. The present study aimed to investigate the effect of dietary MFGM supplementation on the neuromuscular system during post-natal development. METHODS: Growing rats received dietary supplementation with bovine-derived MFGM mixtures consisting of complex milk lipids (CML), beta serum concentrate (BSC) or a complex milk lipid concentrate (CMLc) (which lacks MFGM proteins) from post-natal day 10 to day 70. RESULTS: Supplementation with MFGM mixtures enriched in polar lipids (BSC and CMLc, but not CML) increased the plasma phosphatidylcholine (PC) concentration, with no effect on plasma phosphatidylinositol (PI), phosphatidylethanolamine (PE), phosphatidylserine (PS) or sphingomyelin (SM). In contrast, muscle PC was reduced in rats receiving supplementation with both BSC and CMLc, whereas muscle PI, PE, PS and SM remained unchanged. Rats receiving BSC and CMLc (but not CML) displayed a slow-to-fast muscle fibre type profile shift (MyHCI → MyHCIIa) that was associated with elevated expression of genes involved in myogenic differentiation (myogenic regulatory factors) and relatively fast fibre type specialisation (Myh2 and Nfatc4). Expression of neuromuscular development genes, including nerve cell markers, components of the synaptogenic agrin-LRP4 pathway and acetylcholine receptor subunits, was also increased in muscle of rats supplemented with BSC and CMLc (but not CML). CONCLUSIONS: These findings demonstrate that dietary supplementation with bovine-derived MFGM mixtures enriched in polar lipids can promote neuromuscular development during post-natal growth in rats, leading to shifts in adult muscle phenotype.

8.
Front Physiol ; 7: 546, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27917127

RESUMO

A maternal high-fat (HF) diet during pregnancy can lead to metabolic compromise, such as insulin resistance in adult offspring. Skeletal muscle mitochondrial dysfunction is one mechanism contributing to metabolic impairments in insulin resistant states. Therefore, the present study aimed to investigate whether mitochondrial dysfunction is evident in metabolically compromised offspring born to HF-fed dams. Sprague-Dawley dams were randomly assigned to receive a purified control diet (CD; 10% kcal from fat) or a high fat diet (HFD; 45% kcal from fat) for 10 days prior to mating, throughout pregnancy and during lactation. From weaning, all male offspring received a standard chow diet and soleus muscle was collected at day 150. Expression of the mitochondrial transcription factors nuclear respiratory factor-1 (NRF1) and mitochondrial transcription factor A (mtTFA) were downregulated in HF offspring. Furthermore, genes encoding the mitochondrial electron transport system (ETS) respiratory complex subunits were suppressed in HF offspring. Moreover, protein expression of the complex I subunit, NDUFB8, was downregulated in HF offspring (36%), which was paralleled by decreased maximal catalytic linked activity of complex I and III (40%). Together, these results indicate that exposure to a maternal HF diet during development may elicit lifelong mitochondrial alterations in offspring skeletal muscle.

9.
Inflamm Bowel Dis ; 22(2): 268-78, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26588088

RESUMO

BACKGROUND: Inflammation is a factor potentially underpinning skeletal muscle mass. Intestinal-derived inflammation in inflammatory bowel disease (IBD) results in loss of muscle mass; however, the underlying mechanism is unclear. The interleukin 10 gene-deficient (Il10-/-) mouse is a genetically modified animal model of IBD that can be used to study the effect of intestinal-derived inflammation on muscles. METHODS: Il10-/- and C57BL/6 wild-type (WT) mice were inoculated with intestinal bacteria to induce colon inflammation at the fifth week of age. Skeletal muscles were collected between 7 and 14 weeks of age for analysis of muscle weight, myofiber cross-sectional area (CSA), and molecular markers of inflammation and anabolism pathways, with a focus on ribosome biogenesis. RESULTS: Il10-/- animals that developed colon inflammation had a marked increase in muscle immunoglobulin G (IgG) compared with WT. Inflamed Il10-/- animals had impaired muscle mass gain and smaller myofiber CSA. Intramuscular IgG deposition negatively correlated with muscle mass. After the onset of muscle inflammation, Il10-/- mice had decreased levels of total and ribosomal RNAs (45S, 28S, 18S, and 5.8S rRNAs). Inflammation inversely correlated with muscle levels of total RNA and 28S rRNA which in turn positively correlated with muscle mass. The abundance of growth-related proteins (p70S6K and upstream binding factor, UBF) was decreased in Il10-/- mice. CONCLUSIONS: Muscle inflammation and associated decline of ribosome biogenesis lead to muscle growth impairment in Il10-/- mice. This may have implications for maintenance of muscle mass in conditions associated with chronic intestinal-derived inflammation.


Assuntos
Colo/patologia , Modelos Animais de Doenças , Inflamação/patologia , Doenças Inflamatórias Intestinais/etiologia , Interleucina-10/fisiologia , Músculo Esquelético/patologia , Ribossomos/patologia , Animais , Western Blotting , Colo/metabolismo , Colo/microbiologia , Enterococcus/patogenicidade , Técnicas Imunoenzimáticas , Inflamação/metabolismo , Inflamação/microbiologia , Doenças Inflamatórias Intestinais/patologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Músculo Esquelético/metabolismo , Músculo Esquelético/microbiologia , Doenças Musculares/etiologia , Doenças Musculares/patologia , Biogênese de Organelas , Reação em Cadeia da Polimerase em Tempo Real , Ribossomos/metabolismo
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