scholarly journals Novel time-course related linkages of skeletal muscle gene networks with blood inflammation and muscle damage markers following endurance exercise

2018 ◽  
pp. 115-117
Author(s):  
Oliver Neubauer ◽  
et. al.
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Endurance Exercise ◽  
Gene Networks ◽  
Time Course ◽  
Muscle Gene ◽  
Muscle Damage Markers

Time course-dependent changes in the transcriptome of human skeletal muscle during recovery from endurance exercise: from inflammation to adaptive remodeling

2014 ◽  
Vol 116 (3) ◽  
pp. 274-287 ◽  
Author(s):  
Oliver Neubauer ◽  
Surendran Sabapathy ◽  
Kevin J. Ashton ◽  
Ben Desbrow ◽  
Jonathan M. Peake ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Time Course ◽  
Acute Stress ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Matrix Remodeling ◽  
Molecular Signatures ◽  
Gene Sets

Reprogramming of gene expression is fundamental for skeletal muscle adaptations in response to endurance exercise. This study investigated the time course-dependent changes in the muscular transcriptome after an endurance exercise trial consisting of 1 h of intense cycling immediately followed by 1 h of intense running. Skeletal muscle samples were taken at baseline, 3 h, 48 h, and 96 h postexercise from eight healthy, endurance-trained men. RNA was extracted from muscle. Differential gene expression was evaluated using Illumina microarrays and validated with qPCR. Gene set enrichment analysis identified enriched molecular signatures chosen from the Molecular Signatures Database. Three hours postexercise, 102 gene sets were upregulated [family wise error rate (FWER), P < 0.05], including groups of genes related with leukocyte migration, immune and chaperone activation, and cyclic AMP responsive element binding protein (CREB) 1 signaling. Forty-eight hours postexercise, among 19 enriched gene sets (FWER, P < 0.05), two gene sets related to actin cytoskeleton remodeling were upregulated. Ninety-six hours postexercise, 83 gene sets were enriched (FWER, P < 0.05), 80 of which were upregulated, including gene groups related to chemokine signaling, cell stress management, and extracellular matrix remodeling. These data provide comprehensive insights into the molecular pathways involved in acute stress, recovery, and adaptive muscular responses to endurance exercise. The novel 96 h postexercise transcriptome indicates substantial transcriptional activity potentially associated with the prolonged presence of leukocytes in the muscles. This suggests that muscular recovery, from a transcriptional perspective, is incomplete 96 h after endurance exercise involving muscle damage.

Serum S100B level increases after running but not cycling exercise

2014 ◽  
Vol 39 (3) ◽  
pp. 340-344 ◽  
Author(s):  
Cintia Mussi Alvim Stocchero ◽  
Jean Pierre Oses ◽  
Giovani Santos Cunha ◽  
Jocelito Bijoldo Martins ◽  
Liz Marina Brum ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Area Under The Curve ◽  
Serum Levels ◽  
Cross Sectional Study ◽  
Intense Exercise ◽  
Cross Sectional ◽  
Serum S100b ◽  
Serum S100b Level ◽  
Muscle Damage Markers

The objective of this study was to investigate the effect of running versus cycling exercises upon serum S100B levels and typical markers of skeletal muscle damage such as creatine kinase (CK), aspartate aminotransferase (AST) and myoglobin (Mb). Although recent work demonstrates that S100B is highly expressed and exerts functional properties in skeletal muscle, there is no previous study that tries to establish a relationship between muscle damage and serum S100B levels after exercise. We conducted a cross-sectional study on 13 male triathletes. They completed 2 submaximal exercise protocols at anaerobic threshold intensity. Running was performed on a treadmill with no inclination (RUN) and cycling (CYC) using a cycle-simulator. Three blood samples were taken before (PRE), immediately after (POST) and 1 h after exercise for CK, AST, Mb and S100B assessments. We found a significant increase in serum S100B levels and muscle damage markers in RUN POST compared with RUN PRE. Comparing groups, POST S100B, CK, AST and Mb serum levels were higher in RUN than CYC. Only in RUN, the area under the curve (AUC) of serum S100B is positively correlated with AUC of CK and Mb. Therefore, immediately after an intense exercise such as running, but not cycling, serum levels of S100B protein increase in parallel with levels of CK, AST and Mb. Additionally, the positive correlation between S100B and CK and Mb points to S100B as an acute biomarker of muscle damage after running exercise.

scholarly journals Skeletal Muscle Mitochondrial Physiology in Children With Cerebral Palsy: Considerations for Healthy Aging

2021 ◽  
Vol 12 ◽  
Author(s):  
Sudarshan Dayanidhi
Keyword(s):  
Skeletal Muscle ◽  
Cerebral Palsy ◽  
Endurance Exercise ◽  
Gene Networks ◽  
Healthy Aging ◽  
Mitochondrial Protein ◽  
Mitochondrial Activity ◽  
Endurance Capacity ◽  
Inner Mitochondrial Membrane ◽  
Children With Cerebral Palsy

Skeletal muscle contractile proteins require a constant supply of energy to produce force needed for movement. Energy (ATP) is primarily produced by mitochondrial organelles, located within and around muscle fibers, by oxidative phosphorylation that couples electron flux through the electron transport chain to create a proton gradient across the inner mitochondrial membrane that is in turn used by the ATP synthase. Mitochondrial networks increase in size by biogenesis to increase mitochondrial abundance and activity in response to endurance exercise, while their function and content reduce with constant inactivity, such as during muscle atrophy. During healthy aging, there is an overall decline in mitochondrial activity and abundance, increase in mitochondrial DNA mutations, potential increase in oxidative stress, and reduction in overall muscular capacity. Many of these alterations can be attenuated by consistent endurance exercise. Children with cerebral palsy (CP) have significantly increased energetics of movement, reduced endurance capacity, and increased perceived effort. Recent work in leg muscles in ambulatory children with CP show a marked reduction in mitochondrial function. Arm muscles show that mitochondrial protein content and mitochondria DNA copy number are lower, suggesting a reduction in mitochondrial abundance, along with a reduction in markers for mitochondrial biogenesis. Gene expression networks are reduced for glycolytic and mitochondrial pathways and share similarities with gene networks with aging and chronic inactivity. Given the importance of mitochondria for energy production and changes with aging, future work needs to assess changes in mitochondria across the lifespan in people with CP and the effect of exercise on promoting metabolic health.

scholarly journals Does exercising at a certain time-of-day affect athletes skeletal muscle damage markers? A systematic review and meta-analysis

2019 ◽  
Vol 5 (1) ◽  
pp. 1670529 ◽  
Author(s):  
Efrem Kentiba ◽  
Argachew Adane ◽  
Mezgebe Mena ◽  
Zerihun Zekarias ◽  
Zenebech Abera ◽  
...  
Keyword(s):  
Systematic Review ◽  
Skeletal Muscle ◽  
Muscle Damage ◽  
Meta Analysis ◽  
Time Of Day ◽  
Skeletal Muscle Damage ◽  
Muscle Damage Markers

scholarly journals Vitamin D Promotes Skeletal Muscle Regeneration and Mitochondrial Health

2021 ◽  
Vol 12 ◽  
Author(s):  
Christine M. Latham ◽  
Camille R. Brightwell ◽  
Alexander R. Keeble ◽  
Brooke D. Munson ◽  
Nicholas T. Thomas ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Muscle Damage ◽  
Muscle Regeneration ◽  
Muscle Injury ◽  
Time Course ◽  
Active Form ◽  
Skeletal Muscle Regeneration ◽  
Optimal Timing

Vitamin D is an essential nutrient for the maintenance of skeletal muscle and bone health. The vitamin D receptor (VDR) is present in muscle, as is CYP27B1, the enzyme that hydroxylates 25(OH)D to its active form, 1,25(OH)D. Furthermore, mounting evidence suggests that vitamin D may play an important role during muscle damage and regeneration. Muscle damage is characterized by compromised muscle fiber architecture, disruption of contractile protein integrity, and mitochondrial dysfunction. Muscle regeneration is a complex process that involves restoration of mitochondrial function and activation of satellite cells (SC), the resident skeletal muscle stem cells. VDR expression is strongly upregulated following injury, particularly in central nuclei and SCs in animal models of muscle injury. Mechanistic studies provide some insight into the possible role of vitamin D activity in injured muscle. In vitro and in vivo rodent studies show that vitamin D mitigates reactive oxygen species (ROS) production, augments antioxidant capacity, and prevents oxidative stress, a common antagonist in muscle damage. Additionally, VDR knockdown results in decreased mitochondrial oxidative capacity and ATP production, suggesting that vitamin D is crucial for mitochondrial oxidative phosphorylation capacity; an important driver of muscle regeneration. Vitamin D regulation of mitochondrial health may also have implications for SC activity and self-renewal capacity, which could further affect muscle regeneration. However, the optimal timing, form and dose of vitamin D, as well as the mechanism by which vitamin D contributes to maintenance and restoration of muscle strength following injury, have not been determined. More research is needed to determine mechanistic action of 1,25(OH)D on mitochondria and SCs, as well as how this action manifests following muscle injury in vivo. Moreover, standardization in vitamin D sufficiency cut-points, time-course study of the efficacy of vitamin D administration, and comparison of multiple analogs of vitamin D are necessary to elucidate the potential of vitamin D as a significant contributor to muscle regeneration following injury. Here we will review the contribution of vitamin D to skeletal muscle regeneration following injury.

Transcriptome and translational signaling following endurance exercise in trained skeletal muscle: impact of dietary protein

2011 ◽  
Vol 43 (17) ◽  
pp. 1004-1020 ◽  
Author(s):  
David S. Rowlands ◽  
Jasmine S. Thomson ◽  
Brian W. Timmons ◽  
Frédéric Raymond ◽  
Andreas Fuerholz ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Matrix ◽  
Endurance Exercise ◽  
Translation Initiation ◽  
Time Course ◽  
Muscle Development ◽  
Acid Metabolism ◽  
Axonal Guidance ◽  
Nucleic Acid Metabolism ◽  
Protein Feeding

Postexercise protein feeding regulates the skeletal muscle adaptive response to endurance exercise, but the transcriptome guiding these adaptations in well-trained human skeletal muscle is uncharacterized. In a crossover design, eight cyclists ingested beverages containing protein, carbohydrate and fat (PTN: 0.4, 1.2, 0.2 g/kg, respectively) or isocaloric carbohydrate and fat (CON: 1.6, 0.2 g/kg) at 0 and 1 h following 100 min of cycling. Biopsies of the vastus lateralis were collected at 3 and 48 h following to determine the early and late transcriptome and regulatory signaling responses via microarray and immunoblot. The top gene ontology enriched by PTN were: muscle contraction, extracellular matrix - signaling and structure, and nucleoside, nucleotide, and nucleic acid metabolism (3 and 48 h); developmental processes, immunity, and defense (3 h); glycolysis, lipid and fatty acid metabolism (48 h). The transcriptome was also enriched within axonal guidance, actin cytoskeletal, Ca2+, cAMP, MAPK, and PPAR canonical pathways linking protein nutrition to exercise-stimulated signaling regulating extracellular matrix, slow-myofibril, and metabolic gene expression. At 3 h, PTN attenuated AMPKα1Thr172 phosphorylation but increased mTORC1Ser2448, rps6Ser240/244, and 4E-BP1-γ phosphorylation, suggesting increased translation initiation, while at 48 h AMPKα1Thr172 phosphorylation and PPARG and PPARGC1A expression increased, supporting the late metabolic transcriptome, relative to CON. To conclude, protein feeding following endurance exercise affects signaling associated with cell energy status and translation initiation and the transcriptome involved in skeletal muscle development, slow-myofibril remodeling, immunity and defense, and energy metabolism. Further research should determine the time course and posttranscriptional regulation of this transcriptome and the phenotype responding to chronic postexercise protein feeding.

scholarly journals Transient transcriptional events in human skeletal muscle at the outset of concentric resistance exercise training

2014 ◽  
Vol 116 (1) ◽  
pp. 113-125 ◽  
Author(s):  
A. J. Murton ◽  
R. Billeter ◽  
F. B. Stephens ◽  
S. G. Des Etages ◽  
F. Graber ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Muscle Damage ◽  
Time Course ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Transcriptional Response ◽  
Physiological Adaptation ◽  
Multiple Time ◽  
Αb Crystallin

We sought to ascertain the time course of transcriptional events that occur in human skeletal muscle at the outset of resistance exercise (RE) training in RE naive individuals and determine whether the magnitude of response was associated with exercise-induced muscle damage. Sixteen RE naive men were recruited; eight underwent two sessions of 5 × 30 maximum isokinetic knee extensions (180°/s) separated by 48 h. Muscle biopsies of the vastus lateralis, obtained from different sites, were taken at baseline and 24 h after each exercise bout. Eight individuals acted as nonexercise controls with biopsies obtained at the same time intervals. Transcriptional changes were assessed by microarray and protein levels of heat shock protein (HSP) 27 and αB-crystallin in muscle cross sections by immunohistochemistry as a proxy measure of muscle damage. In control subjects, no probe sets were significantly altered (false discovery rate < 0.05), and HSP27 and αB-crystallin protein remained unchanged throughout the study. In exercised subjects, significant intersubject variability following the initial RE bout was observed in the muscle transcriptome, with greatest changes occurring in subjects with elevated HSP27 and αB-crystallin protein. Following the second bout, the transcriptome response was more consistent, revealing a cohort of probe sets associated with immune activation, the suppression of oxidative metabolism, and ubiquitination, as differentially regulated. The results reveal that the initial transcriptional response to RE is variable in RE naive volunteers, potentially associated with muscle damage and unlikely to reflect longer term adaptations to RE training. These results highlight the importance of considering multiple time points when determining the transcriptional response to RE and associated physiological adaptation.

Time course of ultrastructural changes in skeletal muscle after two types of exercise

1982 ◽  
Vol 52 (4) ◽  
pp. 910-913 ◽  
Author(s):  
M. A. Nimmo ◽  
D. H. Snow
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Ultrastructural Study ◽  
Time Course ◽  
Ultrastructural Changes ◽  
Mitochondrial Structure ◽  
Mitochondrial Alterations ◽  
Thoroughbred Horses ◽  
Muscle Biopsies

To ascertain the effects of sprint and endurance exercise on the time course of skeletal muscle mitochondrial changes, an ultrastructural study was conducted on four Thoroughbred horses. Skeletal muscle biopsies were taken at various intervals during and after the exercise. Transient mitochondrial alterations of varying degrees were observed following both types of exercise and were considered to be related to the development of fatigue. The degree of distortion of mitochondrial structure is considered not to represent the in vivo condition but the state of responsiveness to the fixation medium.

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