Dataset Information

Microvascular adaptations to resistance training are independent of load in resistance-trained young men.

ABSTRACT: Resistance training promotes microvasculature expansion; however, it remains unknown how different resistance training programs contribute to angiogenesis. Thus, we recruited experienced resistance-trained participants and determined the effect of 12 wk of either high-repetition/low-load or low-repetition/high-load resistance training performed to volitional fatigue on muscle microvasculature. Twenty men performed either a high-repetition [20-25 repetitions, 30-50% of 1-repetition maximum (1RM); n = 10] or a low-repetition (8-12 repetitions, 75-90% of 1RM; n = 10) resistance training program. Muscle biopsies were taken before and after resistance training, and immunohistochemistry was used to assess fiber type (I and II)-specific microvascular variables. High-repetition/low-load and low-repetition/high-load groups were not different in any variable before resistance training. Both protocols resulted in an increase in capillarization. Specifically, after resistance training, the capillary-to-fiber ratio, capillary contacts, and capillary-to-fiber perimeter exchange index were elevated, and sharing factor was reduced. These data demonstrate that resistance training performed to volitional failure, using either high repetition/low load or low repetition/high load, induced similar microvascular adaptations in recreationally resistance-trained young men.

SUBMITTER: Holloway TM

PROVIDER: S-EPMC6139617 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

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Microvascular adaptations to resistance training are independent of load in resistance-trained young men.

Holloway Tanya M TM Morton Robert W RW Oikawa Sara Y SY McKellar Sean S Baker Steven K SK Phillips Stuart M SM

American journal of physiology. Regulatory, integrative and comparative physiology 20180613 2

Resistance training promotes microvasculature expansion; however, it remains unknown how different resistance training programs contribute to angiogenesis. Thus, we recruited experienced resistance-trained participants and determined the effect of 12 wk of either high-repetition/low-load or low-repetition/high-load resistance training performed to volitional fatigue on muscle microvasculature. Twenty men performed either a high-repetition [20-25 repetitions, 30-50% of 1-repetition maximum (1RM); ...[more]

PMID: 29897821

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Project description:While high-load resistance training increases muscle hypertrophy, the intramuscular protein responses to this form of training remains largely unknown. In the current study, recreationally resistance-trained college-aged males (N = 15; mean ± SD: 23 ± 3 years old, 6 ± 5 years training) performed full-body, low-volume, high-load [68-90% of one repetition maximum (1RM)] resistance training over 10 weeks. Back squat strength testing, body composition testing, and a vastus lateralis biopsy were performed before (PRE) and 72 h after the 10-week training program (POST). Fiber type-specific cross-sectional area (fCSA), myofibrillar protein concentrations, sarcoplasmic protein concentrations, myosin heavy chain and actin protein abundances, and muscle tissue percent fluid were analyzed. The abundances of individual sarcoplasmic proteins in 10 of the 15 participants were also assessed using proteomics. Significant increases (p < 0.05) in type II fCSA and back squat strength occurred with training, although whole-body fat-free mass paradoxically decreased (p = 0.026). No changes in sarcoplasmic protein concentrations or muscle tissue percent fluid were observed. Myosin heavy chain protein abundance trended downward (-2.9 ± 5.8%, p = 0.069) and actin protein abundance decreased (-3.2 ± 5.3%, p = 0.034) with training. Proteomics indicated only 13 sarcoplasmic proteins were altered with training (12 up-regulated, 1 down-regulated, p < 0.05). Bioinformatics indicated no signaling pathways were affected, and proteins involved with metabolism (e.g., ATP-PCr, glycolysis, TCA cycle, or beta-oxidation) were not affected. These data comprehensively describe intramuscular protein adaptations that occur following 10 weeks of high-load resistance training. Although previous data from our laboratory suggests high-volume resistance training enhances the ATP-PCr and glycolytic pathways, we observed different changes in metabolism-related proteins in the current study with high-load training.

Project description:We sought to determine skeletal muscle genome-wide DNA methylation and transcriptome changes to one bout of lower-load (LL) versus higher-load (HL) resistance exercise. Previously trained college-aged males (n=11, age: 23±4 years old, training experience: 4 ± 3 years) performed LL or HL bouts to failure separated by one week. The HL bout (a.k.a., 80 Fail) consisted of four sets of back squats and four sets of leg extensions to failure using 80% of their estimated one-repetition maximum (i.e., est. 1-RM from 3-RM testing), whereas the LL bout (a.k.a., 30 Fail) consisted of this same paradigm using 30% of their est. 1-RM. Vastus lateralis muscle biopsies were collected before, 3 hours, and 6 hours after each exercise bout. DNA and RNA were batch-isolated from muscle and analyzed for genome-wide DNA methylation and mRNA expression using the 850k Illumina MethylationEPIC array and Clariom S mRNA microarray, respectively. Although the total number of repetitions performed were significantly greater during the 30 Fail versus 80 Fail bout (p<0.001), total training volume (sets x reps x load) was not significantly different between conditions (p=0.571). Interestingly, 30 Fail led to decreased methylation across various promoter regions, albeit the transcriptome-wide responses between bouts were largely similar. According to bioinformatics, both bouts altered post-exercise mRNA profiles related to inflammatory signaling (e.g., Toll receptor, CCKR, chemokine and cytokine signaling), apoptosis, gonadotropin-releasing hormone, and integrin signaling. Also notable, more robust DNA methylation events occurred 3 hours versus 6 hours post-exercise regardless of bout (239,951 versus 12,419 CpG sites significantly hyper- or hypomethylated at these respective time points, p<0.01). Moreover, the percentage of significantly altered mRNAs that also demonstrated significantly inversed methylation patterns across one or more CpG sites was appreciably higher at 3 hours versus 6 hours following exercise (~75% versus ~15%, respectively). In conclusion, our transcriptomic data suggest that the molecular signaling events during the early post-exercise period are largely similar between LL and HL bouts, and this may explain why similar longer-term phenotypes (e.g., myofiber hypertrophy) result from these two training modalities. Additionally, our methylome data indicate that the majority of DNA methylation changes following an acute bout of resistance exercise occur rapidly (~3 hours) following exercise in previously trained men.

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Project description:Cellular 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 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, repeated measures ANOVAs indicated that p-values approached statistical significance for both myosin and actin (p = 0.052 and p = 0.055, respectively), and forced post hoc tests indicated concentrations for both proteins decreased ~30% from PRE to W6 (p<0.05 for each target). 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.

Dataset Information

Microvascular adaptations to resistance training are independent of load in resistance-trained young men.

Publications

Microvascular adaptations to resistance training are independent of load in resistance-trained young men.

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