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Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men.

ABSTRACT: We reported, using a unilateral resistance training (RT) model, that training with high or low loads (mass per repetition) resulted in similar muscle hypertrophy and strength improvements in RT-naïve subjects. Here we aimed to determine whether the same was true in men with previous RT experience using a whole-body RT program and whether postexercise systemic hormone concentrations were related to changes in hypertrophy and strength. Forty-nine resistance-trained men (23 ± 1 yr, mean ± SE) performed 12 wk of whole-body RT. Subjects were randomly allocated into a higher-repetition (HR) group who lifted loads of ?30-50% of their maximal strength (1RM) for 20-25 repetitions/set (n = 24) or a lower-repetition (LR) group (?75-90% 1RM, 8-12 repetitions/set, n = 25), with all sets being performed to volitional failure. Skeletal muscle biopsies, strength testing, dual-energy X-ray absorptiometry scans, and acute changes in systemic hormone concentrations were examined pretraining and posttraining. In response to RT, 1RM strength increased for all exercises in both groups (P < 0.01), with only the change in bench press being significantly different between groups (HR, 9 ± 1, vs. LR, 14 ± 1 kg, P = 0.012). Fat- and bone-free (lean) body mass and type I and type II muscle fiber cross-sectional area increased following training (P < 0.01) with no significant differences between groups. No significant correlations between the acute postexercise rise in any purported anabolic hormone and the change in strength or hypertrophy were found. In congruence with our previous work, acute postexercise systemic hormonal rises are not related to or in any way indicative of RT-mediated gains in muscle mass or strength. Our data show that in resistance-trained individuals, load, when exercises are performed to volitional failure, does not dictate hypertrophy or, for the most part, strength gains.

SUBMITTER: Morton RW

PROVIDER: S-EPMC4967245 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature

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Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men.

Morton Robert W RW Oikawa Sara Y SY Wavell Christopher G CG Mazara Nicole N McGlory Chris C Quadrilatero Joe J Baechler Brittany L BL Baker Steven K SK Phillips Stuart M SM

Journal of applied physiology (Bethesda, Md. : 1985) 20160512 1

We reported, using a unilateral resistance training (RT) model, that training with high or low loads (mass per repetition) resulted in similar muscle hypertrophy and strength improvements in RT-naïve subjects. Here we aimed to determine whether the same was true in men with previous RT experience using a whole-body RT program and whether postexercise systemic hormone concentrations were related to changes in hypertrophy and strength. Forty-nine resistance-trained men (23 ± 1 yr, mean ± SE) perfo ...[more]

PMID: 27174923

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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.

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.

Project description:BackgroundIn resistance training, the role of training frequency to increase maximal strength is often debated. However, the limited data available does not allow for clear training frequency "optimization" recommendations. The purpose of this study was to investigate the effects of training frequency on maximal muscular strength and rate of perceived exertion (RPE). The total weekly training volume was equally distributed between two and four sessions per muscle group.MethodsTwenty-one experienced resistance-trained male subjects (height: 1.85 ± 0.06 m, body mass: 85.3 ± 12.3 kg, age: 27.6 ± 7.6 years) were tested prior to and after an 8-week training period in one-repetition maximum (1RM) barbell back squat and bench press. Subjects were randomly assigned to a SPLIT group (n = 10), in which there were two training sessions of squats and lower-body exercises and two training sessions of bench press and upper-body exercises, or a FULLBODY group (n = 11), in which four sessions with squats, bench press and supplementary exercises were conducted every session. In each session, the subjects rated their RPE after barbell back squat, bench press, and the full session.ResultsBoth groups significantly increased 1RM strength in barbell back squat (SPLIT group: +13.25 kg; FULLBODY group: +14.31 kg) and bench press (SPLIT group: +7.75 kg; FULLBODY group: +8.86 kg) but training frequency did not affect this increase for squat (p = 0.640) or bench press (p = 0.431). Both groups showed a significant effect for time on RPE on all three measurements. The analyses showed only an interaction effect between groups on time for the RPE after the squat exercise (p = 0.002).ConclusionWe conclude that there are no additional benefits of increasing the training frequency from two to four sessions under volume-equated conditions, but it could be favorable to spread the total training volume into several training bouts through the week to avoid potential increases in RPE, especially after the squat exercise.

Project description:The factors that underpin heterogeneity in muscle hypertrophy following resistance exercise training (RET) remain largely unknown. We examined circulating hormones, intramuscular hormones, and intramuscular hormone-related variables in resistance-trained men before and after 12 weeks of RET. Backward elimination and principal component regression evaluated the statistical significance of proposed circulating anabolic hormones (e.g., testosterone, free testosterone, dehydroepiandrosterone, dihydrotestosterone, insulin-like growth factor-1, free insulin-like growth factor-1, luteinizing hormone, and growth hormone) and RET-induced changes in muscle mass (n = 49). Immunoblots and immunoassays were used to evaluate intramuscular free testosterone levels, dihydrotestosterone levels, 5?-reductase expression, and androgen receptor content in the highest- (HIR; n = 10) and lowest- (LOR; n = 10) responders to the 12 weeks of RET. No hormone measured before exercise, after exercise, pre-intervention, or post-intervention was consistently significant or consistently selected in the final model for the change in: type 1 cross sectional area (CSA), type 2 CSA, or fat- and bone-free mass (LBM). Principal component analysis did not result in large dimension reduction and principal component regression was no more effective than unadjusted regression analyses. No hormone measured in the blood or muscle was different between HIR and LOR. The steroidogenic enzyme 5?-reductase increased following RET in the HIR (P < 0.01) but not the LOR (P = 0.32). Androgen receptor content was unchanged with RET but was higher at all times in HIR. Unlike intramuscular free testosterone, dihydrotestosterone, or 5?-reductase, there was a linear relationship between androgen receptor content and change in LBM (P < 0.01), type 1 CSA (P < 0.05), and type 2 CSA (P < 0.01) both pre- and post-intervention. These results indicate that intramuscular androgen receptor content, but neither circulating nor intramuscular hormones (or the enzymes regulating their intramuscular production), influence skeletal muscle hypertrophy following RET in previously trained young men.

Project description:The load in resistance training is considered to be a critical variable for neuromuscular adaptations. Therefore, it is important to assess the effects of applying different loads on the development of maximal strength and muscular hypertrophy. The aim of this study was to systematically review the literature and compare the effects of resistance training that was performed with low loads versus moderate and high loads in untrained and trained healthy adult males on the development of maximal strength and muscle hypertrophy during randomized experimental designs. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines (2021) were followed with the eligibility criteria defined according to participants, interventions, comparators, outcomes, and study design (PICOS): (P) healthy males between 18 and 40 years old, (I) interventions performed with low loads, (C) interventions performed with moderate or high loads, (O) development of maximal strength and muscle hypertrophy, and (S) randomized experimental studies with between- or within-subject parallel designs. The literature search strategy was performed in three electronic databases (Embase, PubMed, and Web of Science) on 22 August 2021. Results: Twenty-three studies with a total of 563 participants (80.6% untrained and 19.4% trained) were selected. The studies included both relative and absolute loads. All studies were classified as being moderate-to-high methodological quality, although only two studies had a score higher than six points. The main findings indicated that the load magnitude that was used during resistance training influenced the dynamic strength and isometric strength gains. In general, comparisons between the groups (i.e., low, moderate, and high loads) showed higher gains in 1RM and maximal voluntary isometric contraction when moderate and high loads were used. In contrast, regarding muscle hypertrophy, most studies showed that when resistance training was performed to muscle failure, the load used had less influence on muscle hypertrophy. The current literature shows that gains in maximal strength are more pronounced with high and moderate loads compared to low loads in healthy adult male populations. However, for muscle hypertrophy, studies indicate that a wide spectrum of loads (i.e., 30 to 90% 1RM) may be used for healthy adult male populations.

Dataset Information

Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men.

Publications

Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men.

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