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- Nilsson, Andreas, 1973-, et al.
(författare)
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Detrimental Links Between Inflammation and Muscle Mass are Moderated by Physical Activity in Older Adults
- 2019
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Ingår i: Medicine & Science in Sports & Exercise. - : Lippincott Williams & Wilkins. - 0195-9131 .- 1530-0315. ; 51:6, s. 215-215
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- While age-related elevations in systemic inflammation may contribute to the accelerated loss of skeletal muscle mass, previous findings have been based on a limited number of biomarkers. Moreover, whether links between inflammation and muscle mass are independent of protein intake and habitual physical activity (PA) remain unknown.PURPOSE: The aim of the study was to explore links between skeletal muscle mass and inflammatory biomarkers in older women with different metabolic risk status, while accounting for adherence to guidelines on protein intake and PA.METHODS: Skeletal muscle mass index (SMI) was assessed in 112 women (67±1.5 years) by bioelectrical impedance together with the equation of Janssen et al. (2002) to obtain muscle mass expressed in relation to body weight. Fasting blood samples were obtained following standardized protocols. Acute-phase proteins C-reactive protein (CRP) and fibrinogen were determined, together with the following inflammatory biomarkers: Adiponectin, Oncostatin-M (OSM), Leukemia inhibitory factor-receptor (LIF-R), Interleukin-6 (IL-6), IL-8, IL-12, and IL-18. Protein intake and PA were determined during 6 days by food record and accelerometry, respectively. Classification of metabolic risk status was based on the metabolic syndrome. Multivariate regression models were used to explore links between SMI and inflammatory biomarkers while adjusting for adherence to PA and protein intake guidelines and metabolic risk status.RESULTS: Variations in SMI were inversely linked to levels of CRP (β-coefficient: -0.47; p< 0.05) and OSM (-0.20 p< 0.05), where the OSM link was attenuated after further adjustment for PA. In contrast, positive links between SMI and adiponectin (0.19 p< 0.05) and LIF-R (0.24 p< 0.05) were observed, which both remained significant in fully adjusted models. Links to other biomarkers were non-significant.CONCLUSIONS: Several inflammatory markers are linked to skeletal muscle mass in older adults, where detrimental or beneficial actions are indicated depending on the biomarker. While adherence to PA guidelines moderates some of these links, others seem unaffected by either PA and protein intake or metabolic risk status. Further research is needed to elucidate mechanisms underlying these observations.
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- Rundqvist, Håkan C., et al.
(författare)
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Systemic Effect On Myotube Size After Sprint Exercise Combined With Nutrients
- 2018
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Ingår i: Medicine & Science in Sports & Exercise. - : Lippincott Williams & Wilkins. - 0195-9131 .- 1530-0315. ; 50:5S, s. 807-807
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- PURPOSE: To study systemic effects of sprint exercise combined with nutrient ingestion on muscle cell hypertrophy. It was hypothesized that the size of human muscle cells increases when they are exposed to post-exercise serum in nutrient but not in placebo condition. Previously studies have shown that oral ingestion of essential amino acids (EAA) and carbohydrate results in higher activation of Akt/mTOR signalling and higher rate of muscle protein synthesis following sprintexercise in humans. Both local and systemic factors may contribute to these effects. Moreover, If the nutrient-induced effects on signalling and muscle protein synthesis result into muscle hypertrophy is not known. In this study we “isolate” the systemic effects by exposing cultured muscle cells for post sprint exercise serum from either nutrient ingestions or placebo.METHODS: This study is based on a previous study, were healthy subjects performed three 30-s sprints with 20 minutes rest in between. Subjects ingested a flavoured drink containing EAA and maltodextrin (nutrient) or only flavoured water (placebo) during the sprint exercise session up to 15 min after the last sprint in a randomized order with one month interval. Blood samples were collected before during and up to 200 minutes after the last sprint and were analyzed for EEA, insulin lactate and glucose. Human myoblasts were isolated from vastus lateralis and differentiated into multinucleated myotubes, which were cultured in serum collected from 5 subjects fromthe sprint exercise study described above. Blood samples, obtained at 80 min after the last sprint, were chosen since the peak values for the accumulation of insulin and EAA occur approximately atthat time point.RESULTS: Both serum insulin (6-fold; P<0.05) and plasma leucine levels (2.6-fold; P<0.01) were higher after nutrient compared to placebo 80 min post-exercise. Plasma lactate and glucose levels did not differ between the conditions. Myotube size was 16% larger after exposure to post sprint exercise serum obtained during nutrient as compared to placebo (P<0.05).CONCLUSIONS: Systemic factors may stimulate muscle hypertrophy after sprint exercise when combined with nutrient ingestion. If such a systemic effect may be counteracted by intracellular metabolic perturbations after sprint exercise is not known.
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- Tarum, Janelle, 1991-, et al.
(författare)
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Electrical pulse stimulation : an in vitro exercise model for the induction of human skeletal muscle cell hypertrophy. A proof-of-concept study
- 2017
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Ingår i: Experimental Physiology. - : John Wiley & Sons. - 0958-0670 .- 1469-445X. ; 102:11, s. 1405-1413
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Tidskriftsartikel (refereegranskat)abstract
- New Findings:What is the central question of this study?Is electrical pulse stimulation (EPS) an in vitro exercise model able to elicit the hypertrophy of human muscle cells?What is the main finding and its importance?The addition of a restitution period of 8h after EPS induces the enlargement of human muscle cells, a major physiological end-point to resistance exercise. This is supported by downregulationof myostatin, a negative regulator of muscle mass, and increased phosphorylated mTOR and 4E-BP1, key factors in the growth cascade. This proof-of-concept study provides a model of physiologically mediated muscle growth, which will be the basis for future studies aiming to depict molecular events governing the hypertrophy of human muscle cells.Electrical pulse stimulation (EPS) of muscle cells has previouslybeenused as an in vitro exercise model. The present study aimedto establish an EPS protocol promoting the hypertrophy ofhuman muscle cells, which represents a major physiological end-point to resistance exercise in humans. We hypothesized that adding a resting period after EPS would be crucial for the occurrence of the morphological change. Myoblasts obtained from human muscle biopsies (n=5) were differentiated into multinucleated myotubes and exposed to 8h of EPS consisting of 2ms pulses at 12V, with a frequency of 1Hz. Myotube size was assessed using immunohistochemistry immediately, 4 and 8h after completed EPS. Gene expression and phosphorylation status of selected markers of hypertrophy were assessed using RT-PCR and Western blotting, respectively. Release of the myokine interleukin-6 in culture medium was measured using enzyme-linked immunosorbent assay. We demonstrated a significant increase (31 +/- 14%; P=0.03) in the size of myotubes when EPS was followed by an 8h resting period, but not immediately or 4h after completion of EPS. The response was supported by downregulation (P=0.04) of the gene expression of myostatin, a negative regulator of muscle mass, and an increase in phosphorylated mTOR (P=0.03) and 4E-BP1 (P=0.01), which are important factors in the cellular growth signalling cascade. The present work demonstrates that EPS is an in vitro exercise model promoting the hypertrophy of human muscle cells, recapitulating a major physiological end-point to resistance exercise in human skeletal muscle.
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