scholarly journals Muscle fiber hypertrophy in response to 6 weeks of high-volume resistance training in trained young men is largely attributed to sarcoplasmic hypertrophy

2019 ◽  
Author(s):  
Cody T. Haun ◽  
Christopher G. Vann ◽  
Shelby C. Osburn ◽  
Petey W. Mumford ◽  
Paul A. Roberson ◽  
...  

ABSTRACTCellular adaptations that occur during skeletal muscle hypertrophy in response to high-volume resistance training are not well-characterized. Therefore, we sought to explore how actin, myosin, sarcoplasmic protein, mitochondrial, and glycogen concentrations were altered in individuals that exhibited mean skeletal muscle fiber cross-sectional area (fCSA) hypertrophy following 6 weeks of high-volume resistance training. Thirty-one previously resistance-trained, college-aged males (mean ± standard deviation: 21±2 years, 5±3 training years) had vastus lateralis (VL) muscle biopsies obtained prior to training (PRE), at week 3 (W3), and at week 6 (W6). Muscle tissue from 15 subjects exhibiting PRE to W6 VL mean fCSA increases ranging from 320-1600 μm2 was further interrogated using various biochemical and histological assays as well as proteomic analysis. Seven of these individuals donated a VL biopsy after refraining from training 8 days following the last training session (W7) to determine how deloading affected biomarkers. The 15 fCSA hypertrophic responders experienced a +23% increase in mean fCSA from PRE to W6 (p<0.001) and, while muscle glycogen concentrations remained unaltered, citrate synthase activity levels decreased by 24% (p<0.001) suggesting mitochondrial volume decreased. Interestingly, both myosin and actin concentrations decreased ~30% from PRE to W6 (p<0.05). Phalloidin-actin staining similarly revealed actin concentrations per fiber decreased from PRE to W6. Proteomic analysis of the sarcoplasmic fraction from PRE to W6 indicated 40 proteins were up-regulated (p<0.05), KEGG analysis indicated that the glycolysis/gluconeogenesis pathway was upregulated (FDR sig. <0.001), and DAVID indicated that the following functionally-annotated pathways were upregulated (FDR value <0.05): a) glycolysis (8 proteins), b) acetylation (23 proteins), c) gluconeogenesis (5 proteins) and d) cytoplasm (20 proteins). At W7, sarcoplasmic protein concentrations remained higher than PRE (+66%, p<0.05), and both actin and myosin concentrations remained lower than PRE (~−50%, p<0.05). These data suggest that short-term high-volume resistance training may: a) reduce muscle fiber actin and myosin protein concentrations in spite of increasing fCSA, and b) promote sarcoplasmic expansion coincident with a coordinated up-regulation of sarcoplasmic proteins involved in glycolysis and other metabolic processes related to ATP generation. Interestingly, these effects seem to persist up to 8 days following training.

2015 ◽  
Vol 118 (8) ◽  
pp. 1040-1049 ◽  
Author(s):  
Frédéric Costes ◽  
Harry Gosker ◽  
Léonard Feasson ◽  
Marine Desgeorges ◽  
Marco Kelders ◽  
...  

Exercise training (ExTr) is largely used to improve functional capacity in patients with chronic obstructive pulmonary disease (COPD). However, ExTr only partially restores muscle function in patients with COPD, suggesting that confounding factors may limit the efficiency of ExTr. In the present study, we hypothesized that skeletal muscle adaptations triggered by ExTr could be compromised in hypoxemic patients with COPD. Vastus lateralis muscle biopsies were obtained from patients with COPD who were either normoxemic ( n = 15, resting arterial Po2 = 68.5 ± 1.5 mmHg) or hypoxemic ( n = 8, resting arterial Po2 = 57.0 ± 1.0 mmHg) before and after a 2-mo ExTr program. ExTr induced a significant increase in exercise capacity both in normoxemic and hypoxemic patients with COPD. However, ExTr increased citrate synthase and lactate dehydrogenase enzyme activities only in skeletal muscle of normoxemic patients. Similarly, muscle fiber cross-sectional area and capillary-to-fiber ratio were increased only in patients who were normoxemic. Expression of atrogenes (MuRF1, MAFbx/Atrogin-1) and autophagy-related genes (Beclin, LC3, Bnip, Gabarapl) remained unchanged in both groups. Phosphorylation of Akt (Ser473), GSK-3β (Ser9), and p70S6k (Thr389) was nonsignificantly increased in normoxemic patients in response to ExTr, but it was significantly decreased in hypoxemic patients. We further showed on C2C12 myotubes that hypoxia completely prevented insulin-like growth factor-1-induced phosphorylation of Akt, GSK-3β, and p70S6K. Together, our observations suggest a role for hypoxemia in the adaptive response of skeletal muscle of patients with COPD in an ExTr program.


2013 ◽  
Vol 110 (3) ◽  
pp. 538-544 ◽  
Author(s):  
Jacob M. Wilson ◽  
Ryan P. Lowery ◽  
Jordan M. Joy ◽  
Joe A. Walters ◽  
Shawn M. Baier ◽  
...  

The purpose of the present study was to determine the effects of short-term supplementation with the free acid form of β-hydroxy-β-methylbutyrate (HMB-FA) on indices of muscle damage, protein breakdown, recovery and hormone status following a high-volume resistance training session in trained athletes. A total of twenty resistance-trained males were recruited to participate in a high-volume resistance training session centred on full squats, bench presses and dead lifts. Subjects were randomly assigned to receive either 3 g/d of HMB-FA or a placebo. Immediately before the exercise session and 48 h post-exercise, serum creatine kinase (CK), urinary 3-methylhistadine (3-MH), testosterone, cortisol and perceived recovery status (PRS) scale measurements were taken. The results showed that CK increased to a greater extent in the placebo (329 %) than in the HMB-FA group (104 %) (P= 0·004, d= 1·6). There was also a significant change for PRS, which decreased to a greater extent in the placebo (9·1 (sem 0·4) to 4·6 (sem 0·5)) than in the HMB-FA group (9·1 (sem 0·3) to 6·3 (sem 0·3)) (P= 0·005, d= − 0·48). Muscle protein breakdown, measured by 3-MH analysis, numerically decreased with HMB-FA supplementation and approached significance (P= 0·08, d= 0·12). There were no acute changes in plasma total or free testosterone, cortisol or C-reactive protein. In conclusion, these results suggest that an HMB-FA supplement given to trained athletes before exercise can blunt increases in muscle damage and prevent declines in perceived readiness to train following a high-volume, muscle-damaging resistance-training session.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Christopher G. Vann ◽  
Cody T. Haun ◽  
Shelby C. Osburn ◽  
Matthew A. Romero ◽  
Paul A. Roberson ◽  
...  

Author(s):  
Michael Roberts ◽  
Matthew Romero ◽  
Christopher Mobley ◽  
Petey Mumford ◽  
Paul Roberson ◽  
...  

Background. We sought to examine how 12 weeks of resistance exercise training (RET) affected skeletal muscle myofibrillar and sarcoplasmic protein levels along with markers of mitochondrial physiology in high versus low anabolic responders. Methods. Untrained college-aged males were classified as anabolic responders in the top 25th percentile [HI; n=13, dual x-ray absorptiometry total body muscle mass change (Δ) =+3.1±0.3 kg, Δ vastus lateralis (VL) thickness =+0.59±0.05 cm, Δ muscle fiber CSA =+1426±253 μm2) and bottom 25th percentile (LO; n=12, +1.1±0.2 kg, +0.24±0.07 cm, +5±209 μm2; p<0.001 for all Δ scores compared to HI]. VL muscle prior to (PRE) and following RET (POST) was assayed for myofibrillar and sarcoplasmic protein concentrations, myosin and actin protein content, and markers of mitochondrial volume. Myofibrillar protein levels of genes related to new myofibril formation as well as whole lysate PGC1-α protein levels were also assessed. Results. Main effects of cluster (HI>LO, p=0.018, Cohen’s d=0.737) and time (PRE>POST, p=0.037, Cohen’s d=-0.589) were observed for citrate synthase activity, although no significant interaction existed. POST myofibrillar myozenin-1 protein levels were up-regulated in the LO cluster (+25%, p=0.025, Cohen’s d = 0.691). No interactions or main effects existed for other assayed markers. Our data suggest myofibrillar or sarcoplasmic protein concentrations do not differ between HI versus LO anabolic responders prior to or following a 12-week RET program. Discussion. Greater mitochondrial volume in HI responders may have facilitated greater anabolism, and myofibril myozenin-1 protein levels may represent a biomarker that differentiates anabolic responses to RET. However, mechanistic research validating these hypotheses is needed.


1997 ◽  
Vol 272 (1) ◽  
pp. R363-R369 ◽  
Author(s):  
C. Leeuwenburgh ◽  
J. Hollander ◽  
S. Leichtweis ◽  
M. Griffiths ◽  
M. Gore ◽  
...  

The effect of endurance training on glutathione (GSH) status and antioxidant enzyme system was investigated in skeletal muscle, heart, and liver of female Sprague-Dawley rats pair fed an isocaloric diet. Ten weeks of treadmill training (25 m/min, 10% grade for 2 h/day, 5 days/wk) increased citrate synthase activity in the deep vastus lateralis (DVL) and soleus muscles by 79 and 39%, respectively (P < 0.01), but not in the heart or liver. In DVL, GSH content was increased 33% (P < 0.05) with training, accompanied by a 64% (P < 0.05) increase in glutamate content but no change in cysteine. Trained rats showed a 62 and 27% higher GSH peroxidase (GPX) and superoxide dismutase (SOD) activity, respectively (P < 0.05), in DVL compared with control rats. In contrast, GSH content and glutathione reductase (GR) activity in soleus declined with training (P < 0.05), whereas activities of GPX and SOD remained unchanged. Training did not alter GSH status in the liver or plasma but significantly decreased the GSH-to glutathione disulfide ratio in the heart. In addition, GR activity in the liver and GSH sulfur-transferase activity in the heart and DVL were significantly lower in the trained vs control rats DVL muscle had threefold higher gamma-glutamyl transpeptidase activity compared with other tissues; however no significant alteration was observed in the activity of gamma-glutamyltranspeptidase or gamma-glutamylcysteine synthetase in the liver, heart, or skeletal muscle. These data indicate that endurance training can cause tissue- and muscle fiber-specific adaptation of antioxidant systems and that GSH homeostasis in extrahepatic tissues may be determined by utilization and uptake of GSH via the gamma-glutamyl cycle.


2017 ◽  
Author(s):  
Jackson J. Fyfe ◽  
David J. Bishop ◽  
Jonathan D. Bartlett ◽  
Erik D. Hanson ◽  
Mitchell J. Anderson ◽  
...  

1.AbstractCombining endurance training with resistance training (RT) may attenuate skeletal muscle hypertrophic adaptation versus RT alone; however, the underlying mechanisms are unclear. We investigated changes in markers of ribosome biogenesis, a process linked with skeletal muscle hypertrophy, following concurrent training versus RT alone. Twenty-three males underwent eight weeks of RT, either performed alone (RT group, n = 8), or combined with either high-intensity interval training (HIT+RT group, n = 8), or moderate-intensity continuous training (MICT+RT group, n = 7). Muscle samples (vastus lateralis) were obtained before training, and immediately before, 1 h and 3 h after the final training session. Training-induced changes in basal expression of the 45S ribosomal RNA (rRNA) precursor (45S pre-rRNA), and 5.8S and 28S mature rRNAs, were greater with concurrent training versus RT. However, during the final training session, RT further increased both mTORC1 (p70S6K1 and rps6 phosphorylation) and 45S pre-rRNA transcription-related signalling (TIF-1A and UBF phosphorylation) versus concurrent training. These data suggest that when performed in a training-accustomed state, RT induces further increases mTORC1 and ribosome biogenesis related signalling in human skeletal muscle versus concurrent training; however, changes in ribosome biogenesis markers were more favourable following a period of short-term concurrent training versus RT performed alone.


Author(s):  
Michael Roberts ◽  
Matthew Romero ◽  
Christopher Mobley ◽  
Petey Mumford ◽  
Paul Roberson ◽  
...  

Background. We sought to examine how 12 weeks of resistance exercise training (RET) affected skeletal muscle myofibrillar and sarcoplasmic protein levels along with markers of mitochondrial physiology in high versus low anabolic responders. Methods. Untrained college-aged males were classified as anabolic responders in the top 25th percentile [HI; n=13, dual x-ray absorptiometry total body muscle mass change (Δ) =+3.1±0.3 kg, Δ vastus lateralis (VL) thickness =+0.59±0.05 cm, Δ muscle fiber CSA =+1426±253 μm2) and bottom 25th percentile (LO; n=12, +1.1±0.2 kg, +0.24±0.07 cm, +5±209 μm2; p<0.001 for all Δ scores compared to HI]. VL muscle prior to (PRE) and following RET (POST) was assayed for myofibrillar and sarcoplasmic protein concentrations, myosin and actin protein content, and markers of mitochondrial volume. Myofibrillar protein levels of genes related to new myofibril formation as well as whole lysate PGC1-α protein levels were also assessed. Results. Main effects of cluster (HI>LO, p=0.018, Cohen’s d=0.737) and time (PRE>POST, p=0.037, Cohen’s d=-0.589) were observed for citrate synthase activity, although no significant interaction existed. POST myofibrillar myozenin-1 protein levels were up-regulated in the LO cluster (+25%, p=0.025, Cohen’s d = 0.691). No interactions or main effects existed for other assayed markers. Our data suggest myofibrillar or sarcoplasmic protein concentrations do not differ between HI versus LO anabolic responders prior to or following a 12-week RET program. Discussion. Greater mitochondrial volume in HI responders may have facilitated greater anabolism, and myofibril myozenin-1 protein levels may represent a biomarker that differentiates anabolic responses to RET. However, mechanistic research validating these hypotheses is needed.


PLoS ONE ◽  
2019 ◽  
Vol 14 (6) ◽  
pp. e0215267 ◽  
Author(s):  
Cody T. Haun ◽  
Christopher G. Vann ◽  
Shelby C. Osburn ◽  
Petey W. Mumford ◽  
Paul A. Roberson ◽  
...  

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