Focal adhesion kinase phosphorylation was greater at 8 weeks after ECC RT and was muscle region-specific. FAK activity correlated to contraction-dependent architectural remodelling, suggesting a potential role of FAK in orienting muscle structural changes in response to distinct mechanical stimuli.
The insertion/deletion polymorphism in the gene for the regulator of vascular tone, angiotensin-converting enzyme (ACE), is the prototype of a genetic influence on physical fitness and this involves an influence on capillary supply lines and dependent aerobic metabolism in skeletal muscle. The respective interaction of ACE-I/D genotype and training status on local metabolic and angiogenic reactions in exercised muscle is not known. Toward this end we characterized the metabolomic and angiogenic response in knee extensor muscle, m. vastus lateralis, in 18 untrained and 34 endurance-trained (physically active,VO2max > 50 mL min −1 kg −1 ) white British men to an exhaustive bout of one-legged cycling exercise. We hypothesized that training status and ACE-I/D genotype affect supply-related muscle characteristics of exercise performance in correspondence to ACE expression and angiotensin 2 levels. ACE-I/D genotype and training status developed an interaction effect on the cross-sectional area (CSA) of m. vastus lateralis and mean CSA of slow type fibers, which correlated with peak power output (r ≥ 0.44). Genotype × training interactions in muscle also resolved for exercise-induced alterations of 22 metabolites, 8 lipids, glycogen concentration (p = 0.016), ACE transcript levels (p = 0.037), and by trend for the pro-angiogenic factor tenascin-C post exercise (p = 0.064). Capillary density (p = 0.001), capillary-to-fiber ratio (p = 0.010), systolic blood pressure (p = 0.014), and exercise-induced alterations in the pro-angiogenic protein VEGF (p = 0.043) depended on the ACE-I/D genotype alone. Our observations indicate that variability in aerobic performance in the studied subjects was in part reflected by an ACE-I/D-genotype-modulated metabolic phenotype of a major locomotor muscle. Repeated endurance exercise appeared to override this genetic influence in skeletal muscle by altering the ACE-related metabolic response and molecular aspects of the angiogenic response to endurance exercise.
Background: Muscle atrophy and fatty infiltration are limiting factors for successful rotator cuff (RC) repair. Quantitative data regarding these hallmarks of degenerative muscle changes after RC repair in humans are scarce. By utilizing a new application of the 6-point Dixon magnetic resonance imaging technology, 3-dimensional volume and fat fraction analysis of the whole RC muscle have become possible. Purpose: Quantitative analysis of atrophy and fatty infiltration of the supraspinatus muscle after healed and failed RC tendon-to-bone repair. Study Design: Cohort study; Level of evidence, 3. Methods: Muscle volume and fat fraction were measured preoperatively and at 3 and 12 months postoperatively in 19 failed and 21 healed arthroscopic supraspinatus tendon repairs, with full muscle volume segmentation and magnetic resonance Dixon sequences. Results: In both groups, the muscle volume initially decreased 3 months after RC repair by –3% in intact ( P = .140) and –10% in failed repair ( P = .004) but recovered between 3 and 12 months to 103% ( P = .274) in intact and 92% ( P = .040) in failed repairs when compared with the preoperative volume (difference of change between groups, preoperative to 12 month: P = .013). The supraspinatus muscle’s fat fraction did not significantly change after successful repair (6.5% preoperative, 6.6% after 3 months, and 6.7% after 12 months; all nonsignificant). There was, however, a significant increase from 7.8% to 10.8% at 3 months ( P = .014) and 11.4% at 12 months ( P = .020) after failed repair (difference between groups at 3- and 12-month follow-up: P = .018 and P = .001, respectively). Conclusion: After successful arthroscopic repair, RC tendon tear–induced fatty infiltration can be almost stopped, and muscle atrophy can even be slightly reversed. In case of a failed repair, however, these changes are further pronounced during the first 3 postoperative months but seem to stabilize thereafter.
Introduction Gene polymorphisms are associated with athletic phenotypes relying on maximal or continued power production and affect the specialization of skeletal muscle composition with endurance or strength training of untrained subjects. We tested whether prominent polymorphisms in genes for angiotensin converting enzyme (ACE), tenascin-C (TNC), and actinin-3 (ACTN3) are associated with the differentiation of cellular hallmarks of muscle metabolism and contraction in high level athletes. Methods Muscle biopsies were collected from m. vastus lateralis of three distinct phenotypes; endurance athletes ( n = 29), power athletes ( n = 17), and untrained non-athletes ( n = 63). Metabolism-, and contraction-related cellular parameters (such as capillary-to-fiber ratio, capillary length density, volume densities of mitochondria and intramyocellular lipid, fiber mean cross sectional area (MCSA) and volume densities of myofibrils) and the volume densities of sarcoplasma were analyzed by quantitative electron microscopy of the biopsies. Gene polymorphisms of ACE (I/D (insertion/deletion), rs1799752), TNC (A/T, rs2104772), and ACTN3 (C/T, rs1815739) were determined using high-resolution melting polymerase chain reaction (HRM-PCR). Genotype distribution was assessed using Chi 2 tests. Genotype and phenotype effects were analyzed by univariate or multivariate analysis of variance and post hoc test of Fisher. P -values below 0.05 were considered statistically significant. Results The athletes demonstrated the specialization of metabolism- and contraction-related cellular parameters. Differences in cellular parameters could be identified for genotypes rs1799752 and rs2104772, and localized post hoc when taking the interaction with the phenotype into account. Between endurance and power athletes these concerned effects on capillary length density for rs1799752 and rs2104772, fiber type distribution and volume densities of myofibrils (rs1799752), and MSCA (rs2104772). Endurance athletes carrying the I-allele of rs1799752 demonstrated 50%-higher volume densities of mitochondria and sarcoplasma, when power athletes that carried only the D-allele showed the highest fiber MCSAs and a lower percentage of slow type muscle fibers. Discussion ACE and tenascin-C gene polymorphisms are associated with differences in cellular aspects of muscle metabolism and contraction in specifically-trained high level athletes. Quantitative differences in muscle fiber type distribution and composition, and capillarization in knee extensor muscle explain, in part, identified associations of the insertion/deletion genotypes of ACE (rs1799752) with endurance- and power-type Sports.
The findings of this study help to understand how and to which extent a neurological lesion of the supplying suprascapular nerve could influence the pattern of anatomic-physiological muscular changes after rotator cuff tendon tears.
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