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Fluctuations in the skeletal muscle power-velocity relationship and interferon-? after a muscle-damaging event in humans.

ABSTRACT: BACKGROUND:Skeletal muscle power is velocity-dependent under constant load conditions. Interferon (IFN)-? is an inflammatory cytokine that regulates skeletal muscle recovery following insult in experimental animals. It is unknown if the power-velocity relationship and IFN-? are modulated after a muscle-damaging event in humans. Therefore, the purpose of this study was to identify the power-velocity relationship and circulating IFN-? concentration responses to a muscle-damaging event in humans. METHODS:Nine healthy males participated in this study. Each subject had one leg randomly assigned as the control leg. The other leg served as the treatment leg and performed an intense-stretch-shortening cycling (SSC) exercise protocol to induce muscle damage. To measure muscle damage and the power-velocity relationship, unilateral peak isometric force and power output (forces and velocities) measurements were performed prior to, immediately after, and during the days following the SSC protocol. The circulating IFN-? concentrations were measured in serum samples obtained prior to, immediately after, and during the days following the SSC protocol. Statistical significance of single-leg isometric force and power output data were assessed using a two-way (time and leg treatment) analysis of variance (ANOVA) with repeated measures, followed by a Tukey's honestly significant difference (HSD) to test multiple pairwise comparisons. The statistical significance of the IFN-? data were assessed using a one-way (time) ANOVA with repeated measures, followed by a Tukey's HSD to test multiple pairwise comparisons. RESULTS:In the treatment leg, significant (P < 0.05) peak isometric force deficits occurred immediately and persisted several days after the SSC protocol, thereby identifying muscle damage-induced weakness. During muscle weakness in the treatment leg, peak power was significantly (P < 0.05) depressed and the velocities at peak power were significantly (P < 0.05) slower. Interestingly, circulating IFN-? concentrations decreased at 2 and 3 days after compared to those immediately following the SSC protocol. CONCLUSION:We conclude that the velocity to achieve a compromised peak power is reduced, and speculatively, the circulating IFN-? excursion could be influential on the recovery of skeletal muscle after a muscle-damaging event in humans.

SUBMITTER: Barker T

PROVIDER: S-EPMC3707101 | biostudies-literature | 2012 Oct

REPOSITORIES: biostudies-literature

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Fluctuations in the skeletal muscle power-velocity relationship and interferon-γ after a muscle-damaging event in humans.

Barker Tyler T Henriksen Vanessa T VT Martins Thomas B TB Kjeldsberg Carl R CR Hill Harry R HR

Extreme physiology & medicine 20121001 1

<h4>Background</h4>Skeletal muscle power is velocity-dependent under constant load conditions. Interferon (IFN)-γ is an inflammatory cytokine that regulates skeletal muscle recovery following insult in experimental animals. It is unknown if the power-velocity relationship and IFN-γ are modulated after a muscle-damaging event in humans. Therefore, the purpose of this study was to identify the power-velocity relationship and circulating IFN-γ concentration responses to a muscle-damaging event in h ...[more]

PMID: 23849351

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Project description:BackgroundSarcopenia is a disease diagnosed in the elderly. In patients with sarcopenia, the muscle mass decreases every year. The occurrence of sarcopenia is greatly affected by extrinsic factors such as eating habits, exercise, and lifestyle. The present study aimed to determine the relationship between muscle mass traits and genes affected by epigenetic factors with three different adjustment methods using Korean Genome and Epidemiology Study (KOGES) data.ResultsWe conducted a demographic study and DNA methylation profiling by three studies according to the muscle mass index (MMI) adjustment methods: appendicular skeletal muscle mass divided by body weight (MMI1); appendicular skeletal muscle mass divided by square of height (MMI2); appendicular skeletal muscle mass divided by BMI (MMI3). We analyzed differentially methylated regions (DMRs) for each group. We then restricted our subjects to be top 30% (T30) and bottom 30% (B30) based on each MMI adjustment method. Additionally, we performed enrichment analysis using PathfindR to evaluate the relationship between identified DMRs and sarcopenia. A total of 895 subjects were included in the demographic study. The values of BMI, waist, and hip showed a significant difference in all three groups. Among 446 participants, 44 subjects whose DNA methylation profiles were investigated were included for DNA methylation analysis. The results of enrichment analysis showed differences between groups. In the women group through MMI1 method, only the glutamatergic synapse pathway showed a significant result. In the men group through MMI2 method, the adherens junction pathway was the most significant. Women group through MMI2 method showed similar results, having an enriched Rap1 signaling pathway. In men group through MMI3 method, the Fc epsilon RI signaling pathway was the most enriched. Particularly, the notch signaling pathway was significantly enriched in women group through MMI3 method.ConclusionThis study presents results about which factor should be concerned first in muscle mass index (MMI) adjustment. The present study suggested that GAB2 and JPH3 in MMI1 method, HLA-DQB1 and TBCD in MMI2 method, GAB2, NDUFB4 and ISPD in MMI3 method are potential genes that can have an impact on muscle mass. It could enable future epigenetic studies of genes based on annotation results. The present study is a nationwide study in Korea with the largest size up to date that compares adjustment indices for MMI in epigenetic research.

Dataset Information

Fluctuations in the skeletal muscle power-velocity relationship and interferon-? after a muscle-damaging event in humans.

Publications

Fluctuations in the skeletal muscle power-velocity relationship and interferon-γ after a muscle-damaging event in humans.

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