Background This paper aimed to systematically review the literature regarding the effects of resistance training (RT) performed at longer-muscle length (LML) versus shorter-muscle length (SML) on proxy measurements for longitudinal hypertrophy. Methods We included studies that satisfied the following criteria: (1) be a resistance training intervention with a comparison of LML vs SML-RT; (2) assess both fascicle length (FL) and muscle size pre- and post-intervention; (3) involve healthy adults aged ≥ 18 years; (4) be published in an English-language journal, and; (5) have a minimum training intervention duration of 4 weeks. Three databases were searched in February 2024 (Google Scholar, PubMed/Medline, Scopus) for relevant articles, alongside 'forward' and 'backward' citation searching of articles included and additions via authors' personal knowledge. The results of studies were described narratively, compared, and contrasted. Eight studies met the inclusion criteria, totaling a sample size of 120. Results Our results suggest that both muscle size and fascicle length increases may be greater following LML-RT versus SML-RT, suggesting LML-RT may lead to greater longitudinal hypertrophy than SML-RT. Notably, evidence is largely mixed; no studies to date have attempted to estimate serial sarcomere number changes from LML versus SML-RT, and all but one study used linear extrapolation methods to estimate FL, which has questionable validity. Therefore, the structural adaptations underlying hypertrophy from LML-RT remain undetermined. Conclusion In conclusion, results suggest that LML-RT may be superior to SML-RT for inducing muscle hypertrophy and, more specifically, longitudinal growth, though evidence is mixed.

We sought to examine how resistance training (RT) status in young healthy individuals, either well resistance trained (T, n = 10) or untrained (UT, n = 11), affected molecular markers with leg immobilization followed by recovery RT. All participants underwent 2 wk of left leg immobilization via a locking leg brace. Afterward, all participants underwent 8 wk (3 days/wk) of knee extensor-focused progressive RT. Vastus lateralis (VL) ultrasound-derived thickness and muscle cross-sectional area were measured at baseline (PRE), immediately after disuse (MID), and after RT (POST) with VL muscle biopsies also being collected at these time points. Both groups presented lower ultrasound-derived VL size metrics at MID versus PRE (P ≤ 0.001), and values increased in both groups from MID to POST (P < 0.05); however, VL size increased from PRE to POST in UT only (P < 0.001). Mean and type II myofiber cross-sectional area values were greater at PRE and POST versus MID (P < 0.05), with T being greater than UT throughout (P ≤ 0.012). In both groups, satellite cell number was not affected by leg immobilization but increased in response to RT (P ≤ 0.014), with T being greater than UT throughout (P = 0.004). Total RNA (ribosome content) decreased (P = 0.010) from PRE to MID while total RNA and certain endoplasmic reticulum stress proteins increased from MID to POST regardless of training status. Immobilization-induced muscle atrophy and recovery RT hypertrophy outcomes are similar between UT and T participants, and the lack of molecular signature differences between groups supports these findings. However, results are limited to younger adults undergoing noncomplicated disuse.NEW & NOTEWORTHY Formerly trained and untrained individuals demonstrate similar atrophic responses to disuse while untrained individuals exhibited a greater hypertrophic response to subsequent resistance training. The molecular responses accompanying these changes were largely similar between groups and included increases in satellite cell content with resistance training and increases in ribosome biogenesis, which was largely driven by the formerly trained group.

ABSTRACTWe examined the myofibrillar (MyoF) and non-myofibrillar (non-MyoF) proteomic profiles of the vastus lateralis (VL) muscle of younger (Y, 22±2 years old; n=5) and middle-aged participants (MA, 56±8 years old; n=6), and MA following eight weeks of knee extensor resistance training (RT, 2d/week). Shotgun/bottom-up proteomics in skeletal muscle typically yields wide protein abundance ranges that mask lowly expressed proteins. Thus, we adopted a novel approach whereby the MyoF and non-MyoF fractions were separately subjected to protein corona nanoparticle complex formation prior to digestion and Liquid Chromatography Mass Spectrometry (LC-MS) analysis. A total of 10,866 proteins (4,421 MyoF and 6,445 non-MyoF) were identified. Across all participants, the number of non-MyoF proteins detected averaged to be 5,645±266 (range: 4,888–5,987) and the number of MyoF proteins detected averaged to be 2,611±326 (range: 1,944–3,101). Differences in the non-MyoF (8.4%) and MyoF (2.5%) proteome were evident between age cohorts. Further, most of these age-related non-MyoF proteins (447/543) were more enriched in MA versus Y. Several biological processes in the non-MyoF fraction were predicted to be operative in MA versus Y including (but not limited to) increased cellular stress, mRNA splicing, translation elongation, and ubiquitin-mediated proteolysis. Non-MyoF proteins associated with splicing and proteostasis were further interrogated, and in agreement with bioinformatics, alternative protein variants, spliceosome-associated proteins (snRNPs), and proteolysis-related targets were more abundant in MA versus Y. RT in MA non-significantly increased VL muscle cross-sectional area (+6.5%, p=0.066) and significantly increased knee extensor strength (+8.7%, p=0.048). However, RT modestly altered the MyoF (∼0.3%, 11 upregulated and two downregulated proteins) and non-MyoF proteomes (∼1.0%, 56 upregulated and eight downregulated proteins, p<0.01). Further, RT did not affect predicted biological processes in either fraction. Although participant numbers were limited, these preliminary results using a novel deep proteomic approach in skeletal muscle suggest that aging and RT predominantly affects protein abundances in the non-contractile protein pool. However, the marginal proteome adaptations occurring with RT suggest either: a) this may be an aging-associated phenomenon, b) more rigorous RT may stimulate more robust effects, or c) RT, regardless of age, subtly affects skeletal muscle protein abundances in the basal state.

INTRODUCTION: Lower-limb disuse from immobilization results in a decrease in muscle strength, volume, and function. However, muscle atrophy from disuse does not entirely account for the observed strength and functional declines. Additionally, prior engagement in resistance training (RT) has been linked to the preservation of muscular strength and neuromuscular function. Therefore, the purpose of this study was to assess the influence of a single-leg immobilization protocol, followed by structured RT rehabilitation protocol, on muscle strength, volume, and neural activation in healthy young adults with and without previous strength training experience. Methods: Participants (10 Trained (T): 8 men, 2 women; 11 Untrained (UT): 8 men, 3 women) underwent 2-weeks of left-knee immobilization at 90° knee-flexion with a hinged immobilizer knee-brace. Participants were given a pair of axillary crutches for ambulation during this time. Following immobilization, all participants underwent an 8-week structured RT rehabilitation protocol. Participants visited the laboratory for three testing sessions (baseline test on Day 0; post-immobilization at the end of week 2; and post-RT rehab at the end of week 10). Maximal knee extensor isometric strength at 45°was quantified using an isokinetic dynamometer (Biodex). Voluntary muscle activation was quantified as the root mean square (RMS) of the interference electromyography (EMG) signals derived from two indwelling fine-wire electrodes in the vastus-lateralis muscle. Additionally, a continuous wavelet transform (CWT) was performed on the EMG to determine amplitude versus frequency characteristics of the signals and how this amplitude varied with time in the 13-30 (beta) and 30-60 (piper) Hz bands. Mid-thigh muscle cross-sectional area (mCSA) and density were also quantified using peripheral quantitative computed tomography (pQCT) during all testing sessions. Results: The T group was significantly stronger (p=0.019), had greater muscle density (p=0.005) and mid-thigh mCSA (p<0.001) across all sessions when compared with the UT group. However, there were no significant time or interaction effects for strength or muscle density losses (p>0.05). While both groups demonstrated increased muscle activation across sessions (RMS: p=0.04; CWT: p=0.021), the T group demonstrated a greater increase in the neural drive from baseline to week 10 when compared with the UT group (RMS: p= 0.002; CWT: p=0.027). CONCLUSION: In younger adults with or without prior strength training experience, we find that losses in knee extensor isometric strength, muscle density, and mid-thigh mCSA are minimal following a 2-week immobilization protocol. However, certain neuromuscular adaptations during immobilization and following weight-training rehabilitation are enhanced to a greater degree in those with prior training, which is seemingly indicative of greater synchrony in descending cortical drive and motor unit recruitment. These latter findings warrant continued investigation using additional innovative methodologies (e.g., fMRI, TMS, etc.) for assessing the mechanisms underlying the effects of prehab protocols on neuromuscular adaptations. PGRF and Nix family foundation scholarship to Marina Meyer. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Abstract We examined how resistance exercise (RE), cycling exercise and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation. The 1boutRE study involved younger men (n = 8; 5 ± 2 years of RE experience) performing a lower body RE bout with vastus lateralis (VL) biopsies being obtained prior to and acutely following exercise. With the 10weekRT study, VL biopsies were obtained in 36 younger adults before and 24 h after their first/naïve RE bout. Participants also engaged in 10 weeks of resistance training and donated VL biopsies before and 24 h after their last RE bout. VL biopsies were also examined in an acute cycling study (n = 7) and a study involving 2 weeks of leg immobilization (n = 20). In the 1boutRE study, fragmentation of all MyHC isoforms (MyHCTotal) increased 3 h post‐RE (∼200%, P = 0.018) and returned to pre‐exercise levels by 6 h post‐RE. Interestingly, a greater magnitude increase in MyHC type IIa versus I isoform fragmentation occurred 3 h post‐RE (8.6 ± 6.3‐fold vs. 2.1 ± 0.7‐fold, P = 0.018). In 10weekRT participants, the first/naïve and last RE bouts increased MyHCTotal fragmentation 24 h post‐RE (+65% and +36%, P < 0.001); however, the last RE bout response was attenuated compared to the first bout (P = 0.045). Although cycling exercise did not alter MyHCTotal fragmentation, ∼8% VL atrophy with 2 weeks of leg immobilization increased MyHCTotal fragmentation (∼108%, P < 0.001). Mechanistic C2C12 myotube experiments indicated that MyHCTotal fragmentation is likely due to calpain proteases. In summary, RE and disuse atrophy increase MyHC protein fragmentation. Research into how ageing and disease‐associated muscle atrophy affect these outcomes is needed. Highlights What is the central question of this study? How different exercise stressors and disuse affect skeletal muscle myosin heavy chain fragmentation. What is the main finding and its importance? This investigation is the first to demonstrate that resistance exercise and disuse atrophy lead to skeletal muscle myosin heavy chain protein fragmentation in humans. Mechanistic in vitro experiments provide additional evidence that MyHC fragmentation occurs through calpain proteases.

ABSTRACT Denervated myofibers and senescent cells are hallmarks of skeletal muscle aging. However, sparse research has examined how resistance training affects these outcomes. We investigated the effects of unilateral leg extensor resistance training on denervated myofibers, senescent cells, and associated protein markers in middle-aged participants (MA, 55±8 years old, 17 females, 9 males). We obtained vastus lateralis (VL) muscle cross-sectional area (mCSA), VL biopsies, and strength assessments before and after training. Fiber cross-sectional area (fCSA), satellite cells (Pax7+), denervated myofibers (NCAM+), senescent cells (p16+ or p21+), senescence-related proteins, and senescence-associated secretory phenotype (SASP) proteins were analyzed from biopsied muscle. Leg extensor peak torque increased after training (p<0.001), while VL mCSA trended upward (p=0.082). No significant changes were observed for fCSA, NCAM+ myofibers, or senescent (p16+ or p21+) cells, albeit satellite cells increased after training (p=0.037). While >90% satellite cells were not p16+ or p21+, most p16+ and p21+ cells were Pax7+ (>90% on average). Training altered 13/46 proteins related to muscle-nerve communication (all upregulated, p<0.05) and 10/19 proteins related to cellular senescence (9 upregulated, p<0.05). Only 1/17 SASP proteins increased with training (IGFBP-3, p=0.031). In conclusion, resistance training upregulates proteins associated with muscle-nerve communication in MA participants but does not alter NCAM+ myofibers. Moreover, while training increases senescence-related proteins in skeletal muscle, this coincided with an increase in satellite cells but not alterations in senescent cell content or SASP proteins. Hence, we interpret these collective findings as resistance training being an unlikely inducer of cellular senescence in humans.

We recently reported that resistance trained (T, n=10) and untrained (UT, n=11) young adults experience vastus lateralis (VL) muscle atrophy following two weeks of disuse, and 8 weeks of recovery resistance training (RT) promotes VL hypertrophy in both participant cohorts. However, angiogenesis targets and muscle capillary number were not examined and currently no human studies that have sought to determine if disuse followed by recovery RT affects these outcomes. Thus, we examined whether disuse and/or recovery RT affected these outcomes. All participants underwent two weeks of left leg immobilization using locking leg braces and crutches followed by eight weeks (3d/week) of knee extensor focused progressive RT. VL biopsies were obtained at baseline (PRE), immediately after disuse (MID), and after RT (POST). Western blotting was used to assay angiogenesis markers and immunohistochemistry was performed in 16/21 participants to determine type I and II muscle fiber capillary number. Significant main effects of time (p<0.05) were observed for protein levels of VEGF (MID0.100). Although disuse and recovery RT affect skeletal muscle angiogenesis-related protein targets, prior training history does not differentially affect these outcomes.

We sought to examine how resistance exercise (RE), cycling exercise, and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation in humans. In the first study (1boutRE), younger adult men (n=8; 5±2 years of RE experience) performed a lower body RE bout with vastus lateralis (VL) biopsies obtained immediately before, 3-, and 6-hours post-exercise. In the second study (10weekRT), VL biopsies were obtained in untrained younger adults (n=36, 18 men and 18 women) before and 24 hours (24h) after their first/naïve RE bout. These participants also engaged in 10 weeks (24 sessions) of resistance training and donated VL biopsies before and 24h after their last RE bout. VL biopsies were also examined from a third acute cycling study (n=7) and a fourth study involving two weeks of leg immobilization (n=20, 15 men and 5 women) to determine how MyHC fragmentation was affected. In the 1boutRE study, the fragmentation of all MyHC isoforms (MyHCTotal) increased 3 hours post-RE (~ +200%, p=0.018) and returned to pre-exercise levels by 6 hours post-RE. Immunoprecipitation of MyHCTotal revealed ubiquitination levels remained unaffected at the 3- and 6-hour post-RE time points. Interestingly, a greater increase in magnitude for MyHC type IIa versus I isoform fragmentation occurred 3-hours post-RE (8.6±6.3-fold versus 2.1±0.7-fold, p=0.018). In all 10weekRT participants, the first/naïve and last RE bouts increased MyHCTotal fragmentation 24h post-RE (+65% and +36%, respectively; p<0.001); however, the last RE bout response was attenuated compared to the first bout (p=0.045). The first/naïve bout response was significantly elevated in females only (p<0.001), albeit females also demonstrated a last bout attenuation response (p=0.002). Although an acute cycling bout did not alter MyHCTotal fragmentation, ~8% VL atrophy with two weeks of leg immobilization led to robust MyHCTotal fragmentation (+108%, p<0.001), and no sex-based differences were observed. In summary, RE and disuse atrophy increase MyHC protein fragmentation. A dampened response with 10 weeks of resistance training, and more refined responses in well-trained men, suggest this is an adaptive process. Given the null polyubiquitination IP findings, more research is needed to determine how MyHC fragments are processed. Moreover, further research is needed to determine how aging and disease-associated muscle atrophy affect these outcomes, and whether MyHC fragmentation is a viable surrogate for muscle protein turnover rates.

Background It is unclear whether chronically training close to volitional failure influences motor unit recruitment strategies during fatigue. Purpose We compared resistance training to near volitional failure vs. non-failure on individual motor unit action potential amplitude (MUAP) and surface electromyographic excitation (sEMG) during fatiguing contractions. Methods Nineteen resistance-trained adults (11 males, 8 females) underwent 5 weeks (3×/week) of either low repetitions-in-reserve (RIR; 0–1 RIR) or high RIR training (4–6 RIR). Before and after the intervention, participants performed isometric contractions of the knee extensors at 30% of maximal peak torque until exhaustion while vastus lateralis sEMG signals were recorded and later decomposed. MUAP and sEMG excitation for the vastus lateralis were quantified at the beginning, middle, and end of the fatigue assessment. Results Both training groups improved time-to-task failure (mean change = 43.3 s, 24.0%), with no significant differences between low and high RIR training groups (low RIR = 28.7%, high RIR = 19.4%). Our fatigue assessment revealed reduced isometric torque steadiness and increased MUAP amplitude and sEMG excitation during the fatiguing task, but these changes were consistent between groups. Conclusion Both low and high RIR training improved time-to-task failure, but resulted in comparable motor unit recruitment during fatiguing contractions. Our findings indicate that both low and high RIR training can be used to enhance fatiguability among previously resistance-trained adults.

Although transcriptome profiling has been used in several resistance training studies, the associated analytical approaches seldom provide in-depth information on individual genes linked to skeletal muscle hypertrophy. Therefore, a secondary analysis was performed herein on a muscle transcriptomic dataset we previously published involving trained college-aged men (n = 11) performing two resistance exercise bouts in a randomized and crossover fashion. The lower-load bout (30 Fail) consisted of 8 sets of lower body exercises to volitional fatigue using 30% one-repetition maximum (1 RM) loads, whereas the higher-load bout (80 Fail) consisted of the same exercises using 80% 1 RM loads. Vastus lateralis muscle biopsies were collected prior to (PRE), 3 h, and 6 h after each exercise bout, and 58 genes associated with skeletal muscle hypertrophy were manually interrogated from our prior microarray data. Select targets were further interrogated for associated protein expression and phosphorylation induced-signaling events. Although none of the 58 gene targets demonstrated significant bout x time interactions, ~57% (32 genes) showed a significant main effect of time from PRE to 3 h (15↑ and 17↓, p < 0.01), and ~26% (17 genes) showed a significant main effect of time from PRE to 6 h (8↑ and 9↓, p < 0.01). Notably, genes associated with the myostatin (9 genes) and mammalian target of rapamycin complex 1 (mTORC1) (9 genes) signaling pathways were most represented. Compared to mTORC1 signaling mRNAs, more MSTN signaling-related mRNAs (7 of 9) were altered post-exercise, regardless of the bout, and RHEB was the only mTORC1-associated mRNA that was upregulated following exercise. Phosphorylated (phospho-) p70S6K (Thr389) (p = 0.001; PRE to 3 h) and follistatin protein levels (p = 0.021; PRE to 6 h) increased post-exercise, regardless of the bout, whereas phospho-AKT (Thr389), phospho-mTOR (Ser2448), and myostatin protein levels remained unaltered. These data continue to suggest that performing resistance exercise to volitional fatigue, regardless of load selection, elicits similar transient mRNA and signaling responses in skeletal muscle. Moreover, these data provide further evidence that the transcriptional regulation of myostatin signaling is an involved mechanism in response to resistance exercise.

Limited research exists examining how resistance training to failure affects applied outcomes and single motor unit characteristics in previously trained individuals. Herein, resistance-trained adults (24 +/- 3 years old, self-reported resistance training experience was 6 +/- 4 years, 11 men and 8 women) were randomly assigned to either a low-repetitions-in-reserve (RIR; i.e., training near failure, n = 10) or high-RIR (i.e., not training near failure, n = 9) group. All participants implemented progressive overload during 5 weeks where low-RIR performed squat, bench press, and deadlift twice weekly and were instructed to end each training set with 0-1 RIR. high-RIR performed identical training except for being instructed to maintain 4-6 RIR after each set. During week 6, participants performed a reduced volume-load. The following were assessed prior to and following the intervention: (i) vastus lateralis (VL) muscle cross-sectional area (mCSA) at multiple sites; (ii) squat, bench press, and deadlift one-repetition maximums (1RMs); and (iii) maximal isometric knee extensor torque and VL motor unit firing rates during an 80% maximal voluntary contraction. Although RIR was lower in the low- versus high-RIR group during the intervention (p < 0.001), total training volume did not significantly differ between groups (p = 0.222). There were main effects of time for squat, bench press, and deadlift 1RMs (all p-values < 0.05), but no significant condition x time interactions existed for these or proximal/middle/distal VL mCSA data. There were significant interactions for the slope and y-intercept of the motor unit mean firing rate versus recruitment threshold relationship. Post hoc analyses indicated low-RIR group slope values decreased and y-intercept values increased after training suggesting low-RIR training increased lower-threshold motor unit firing rates. This study provides insight into how resistance training in proximity to failure affects strength, hypertrophy, and single motor unit characteristics, and may inform those who aim to program for resistance-trained individuals.

PURPOSE: The myostatin (MSTN) gene has been heavily researched for its role in repressing skeletal muscle hypertrophy and the anabolic mTORC1 signaling pathway. Preliminary data from our laboratory has shown a significant hypermethylation of cytosine phosphate guanine sites within the MSTN gene as well as a significant downregulation of MSTN mRNA following acute bouts of resistance exercise to failure (i.e., training at 30% one repetition maximum versus 80% one repetition maximum). This study sought to determine the changes of MSTN-related and mTORC1 signaling proteins following two bouts of resistance exercise to failure. We hypothesized there to be significant time-effects of assayed markers in response to each bout of resistance training. METHODS: Eleven previously-trained college-aged men (age: 23 ± 4 years, 11.4 ± 6.4 percent fat, 4 ± 3 years training experience) participated in this study. Each participant performed two resistance training sessions (spaced one week apart) involving either: i) 30FAIL training; 4 sets of back squats and 4 sets of leg extensors to failure at 30% of one-repetition maximum (1RM), or: ii) 80FAIL training; 4 sets of both exercises at 80% of 1RM. Vastus lateralis muscle biopsies were obtained prior to each training session (PRE), 3 hours following training (3hPOST), and 6 hours following training (6hPOST). Western blots were performed on biopsied muscle to determine the relative expression of phosphorylated (p)-mTOR (Ser2448), p-p70S6K (Thr389), p-AKT (Ser473), p-rpS6 (Ser235/236), follistatin (FST), and MSTN. RESULTS: There were no significant bout*time interactions for any of the assayed markers. There were significant differences observed for p-p70S6K (p = 0.001; PRE to 3hPOST) and FST (p = 0.021; PRE to 6hPOST). There were no significant main time effects observed for p-mTOR, p-AKT, or p-rps6. CONCLUSIONS: The two modes of resistance training elicited similar effects on p-p70S6K and FST protein expression. These results suggest, regardless of training load, mTORC1 markers and MTSN-related protein expression respond similarly in previously-trained college-aged men.

Although several reports have hypothesized that exercise may increase skeletal muscle protein lactylation, empirical evidence in humans is lacking. Thus, we adopted a multi-faceted approach to examine if acute and subchronic resistance training (RT) altered skeletal muscle protein lactylation levels. In mice, we also sought to examine if surgical ablation-induced plantaris hypertrophy coincided with increases in muscle protein lactylation. To examine acute responses, participants’ blood lactate concentrations were assessed before, during, and after eight sets of an exhaustive lower body RT bout (n = 10 trained college-aged men). Vastus lateralis biopsies were also taken before, 3-h post, and 6-h post-exercise to assess muscle protein lactylation. To identify training responses, another cohort of trained college-aged men (n = 14) partook in 6 weeks of lower-body RT (3x/week) and biopsies were obtained before and following the intervention. Five-month-old C57BL/6 mice were subjected to 10 days of plantaris overload (OV, n = 8) or served as age-matched sham surgery controls (Sham, n = 8). Although acute resistance training significantly increased blood lactate responses ∼7.2-fold ( p < 0.001), cytoplasmic and nuclear protein lactylation levels were not significantly altered at the post-exercise time points, and no putative lactylation-dependent mRNA was altered following exercise. Six weeks of RT did not alter cytoplasmic protein lactylation ( p = 0.800) despite significantly increasing VL muscle size (+3.5%, p = 0.037), and again, no putative lactylation-dependent mRNA was significantly affected by training. Plantaris muscles were larger in OV versus Sham mice (+43.7%, p < 0.001). However, cytoplasmic protein lactylation was similar between groups ( p = 0.369), and nuclear protein lactylation was significantly lower in OV versus Sham mice ( p < 0.001). The current null findings, along with other recent null findings in the literature, challenge the thesis that lactate has an appreciable role in promoting skeletal muscle hypertrophy.

We examined how set-volume equated resistance training using either the back squat (SQ) or hip thrust (HT) affected hypertrophy and various strength outcomes. Untrained college-aged participants were randomized into HT (n = 18) or SQ (n = 16) groups. Surface electromyograms (sEMG) from the right gluteus maximus and medius muscles were obtained during the first training session. Participants completed 9 weeks of supervised training (15–17 sessions), before and after which gluteus and leg muscle cross-sectional area (mCSA) was assessed via magnetic resonance imaging. Strength was also assessed prior to and after the training intervention via three-repetition maximum (3RM) testing and an isometric wall push test. Gluteus mCSA increases were similar across both groups. Specifically, estimates [(−) favors HT (+) favors SQ] modestly favored the HT versus SQ for lower [effect ±SE, −1.6 ± 2.1 cm2; CI95% (−6.1, 2.0)], mid [−0.5 ± 1.7 cm2; CI95% (−4.0, 2.6)], and upper [−0.5 ± 2.6 cm2; CI95% (−5.8, 4.1)] gluteal mCSAs but with appreciable variance. Gluteus medius + minimus [−1.8 ± 1.5 cm2; CI95% (−4.6, 1.4)] and hamstrings [0.1 ± 0.6 cm2; CI95% (−0.9, 1.4)] mCSA demonstrated little to no growth with small differences between groups. mCSA changes were greater in SQ for the quadriceps [3.6 ± 1.5 cm2; CI95% (0.7, 6.4)] and adductors [2.5 ± 0.7 cm2; CI95% (1.2, 3.9)]. Squat 3RM increases favored SQ [14 ± 2 kg; CI95% (9, 18),] and hip thrust 3RM favored HT [−26 ± 5 kg; CI95% (−34, −16)]. 3RM deadlift [0 ± 2 kg; CI95% (−4, 3)] and wall push strength [−7 ± 12N; CI95% (−32, 17)] similarly improved. All measured gluteal sites showed greater mean sEMG amplitudes during the first bout hip thrust versus squat set, but this did not consistently predict gluteal hypertrophy outcomes. Squat and hip thrust training elicited similar gluteal hypertrophy, greater thigh hypertrophy in SQ, strength increases that favored exercise allocation, and similar deadlift and wall push strength increases.

We recently reported that vastus lateralis (VL) cross-sectional area (CSA) increases after 7 weeks of resistance training (RT, 2 days/week), with declines occurring following 7 weeks of subsequent treadmill high-intensity interval training (HIIT) (3 days/week). Herein, we examined the effects of this training paradigm on skeletal muscle proteolytic markers. VL biopsies were obtained from 11 untrained college-aged males at baseline (PRE), after 7 weeks of RT (MID), and after 7 weeks of HIIT (POST). Tissues were analysed for proteolysis markers, and in vitro experiments were performed to provide additional insights. Atrogene mRNAs (TRIM63, FBXO32, FOXO3A) were upregulated at POST versus both PRE and MID (P < 0.05). 20S proteasome core protein abundance increased at POST versus PRE (P = 0.031) and MID (P = 0.049). 20S proteasome activity, and protein levels for calpain-2 and Beclin-1 increased at MID and POST versus PRE (P < 0.05). Ubiquitinated proteins showed model significance (P = 0.019) with non-significant increases at MID and POST (P > 0.05). in vitro experiments recapitulated the training phenotype when stimulated with a hypertrophic stimulus (insulin-like growth factor 1; IGF1) followed by a subsequent AMP-activated protein kinase activator (5-aminoimidazole-4-carboxamide ribonucleotide; AICAR), as demonstrated by larger myotube diameter in IGF1-treated cells versus IGF1 followed by AICAR treatments (I+A; P = 0.017). Muscle protein synthesis (MPS) levels were also greater in IGF1-treated versus I+A myotubes (P < 0.001). In summary, the loss in RT-induced VL CSA with HIIT coincided with increases in several proteolytic markers, and sustained proteolysis may have driven this response. Moreover, while not measured in humans, we interpret our in vitro data to suggest that (unlike RT) HIIT does not stimulate MPS. New FindingsWhat is the central question of this study?Determining if HIIT-induced reductions in muscle hypertrophy following a period of resistance training coincided with increases in proteolytic markers.What is the main finding and its importance?Several proteolytic markers were elevated during the HIIT training period implying that increases in muscle proteolysis may have played a role in HIIT-induced reductions in muscle hypertrophy.

The purpose of this study was to improve our understanding of the relative contributions of biomechanical, anthropometric, and psychological factors in explaining maximal bench press (BP) strength in a heterogeneous, resistance-trained sample. Eighteen college-aged participants reported to the laboratory for three visits. The first visit consisted of psychometric testing. The second visit assessed participants' anthropometrics, additional psychometric outcomes, and bench press one repetition maximum (1RM). Participants performed isometric dynamometry testing for horizontal shoulder adduction and elbow extension at a predicted sticking point joint position. Multiple linear regression was used to examine the relationships between the biomechanical, anthropometric, and psychological variables and BP 1RM. Our primary multiple linear regression accounted for 43% of the variance in BP strength (F(3,14) = 5.34, p = 0.01; R2 = 0.53; adjusted R2 = 0.43). The sum of peak isometric net joint moments from the shoulder and elbow had the greatest standardized effect (0.59), followed by lean body mass (0.27) and self-efficacy (0.17). The variance in BP 1RM can be similarly captured (R2 = 0.48) by a single principal component containing anthropometric, biomechanics, and psychological variables. Pearson correlations with BP strength were generally greater among anthropometric and biomechanical variables as compared to psychological variables. These data suggest that BP strength among a heterogeneous, resistance-trained population is explained by multiple factors and is more strongly associated with physical than psychological variables.

Background Progressive overload is a principle of resistance training exercise program design that typically relies on increasing load to increase neuromuscular demand to facilitate further adaptations. However, little attention has been given to another way of increasing demand—increasing the number of repetitions. Objective This study aimed to compare the effects of two resistance training programs: (1) increasing load while keeping repetition range constant vs (2) increasing repetitions while keeping load constant. We aimed to compare the effects of these programs on lower body muscle hypertrophy, muscle strength, and muscle endurance in resistance-trained individuals over an 8-week study period. Methods Forty-three participants with at least 1 year of consistent lower body resistance training experience were randomly assigned to one of two experimental, parallel groups: A group that aimed to increase load while keeping repetitions constant (LOAD: n = 22; 13 men, nine women) or a group that aimed to increase repetitions while keeping load constant (REPS: n = 21; 14 men, seven women). Subjects performed four sets of four lower body exercises (back squat, leg extension, straight-leg calf raise, and seated calf raise) twice per week. We assessed one repetition maximum (1RM) in the Smith machine squat, muscular endurance in the leg extension, countermovement jump height, and muscle thickness along the quadriceps and calf muscles. Between-group effects were estimated using analyses of covariance, adjusted for pre-intervention scores and sex. Results Rectus femoris growth modestly favored REPS (adjusted effect estimate (CI 90% ), sum of sites: 2.8 mm [−0.5, 5.8]). Alternatively, dynamic strength increases slightly favored LOAD (2.0 kg [−2.4, 7.8]), with differences of questionable practical significance. No other notable between-group differences were found across outcomes (muscle thicknesses, <1 mm; endurance, <1%; countermovement jump, 0.1 cm; body fat, <1%; leg segmental lean mass, 0.1 kg), with narrow CIs for most outcomes. Conclusion Both progressions of repetitions and load appear to be viable strategies for enhancing muscular adaptations over an 8-week training cycle, which provides trainers and trainees with another promising approach to programming resistance training.

The purpose of this study was to evaluate differences in changes in muscle strength and muscle thickness (MT) of the plantar flexor muscles between traditional resistance training (RT) involving passive rest and RT combined with inter-set stretch in the calf raise exercise. Employing a within-subject design, 21 young, healthy men performed plantar flexion exercises twice per week in both a traditional RT (TRAD) format and combined with a 20-second inter-set stretch (STRETCH). One leg was randomly assigned to the TRAD condition and the contralateral leg performed the STRETCH condition throughout the 8-week study period. Dependent variables included MT of the lateral gastrocnemius (LG), medial gastrocnemius (MG) and the soleus (SOL), and isometric strength of the plantar flexors. Results indicated a potential beneficial hypertrophic effect of STRETCH compared to TRAD for the SOL [0.7 mm, CI90% = (0, 1.6)], while the LG had more ambiguous effects [0.4 mm (-0.4, 1.3)] and MG effects were equivocal [0 mm (-0.6, 0.7)]. In general, LG demonstrated greater standardized growth [z = 1.1 (1, 1.3)] as compared to MG [z = 0.3 (0.2, 0.5)] and SOL [z = 0.3 (0.2, 0.5)]. Measures of isometric strength showed a modest advantage to STRETCH. In conclusion, loaded inter-set stretch may enhance MT of the soleus but effects on the gastrocnemii appear uncertain or unlikely in untrained men; plantar flexor strength appears to be modestly enhanced by the interventional strategy.

Human muscle fibers are generally classified by myosin heavy chain (MHC) isoforms characterized by slow to fast contractile speeds. Type I, or slow-twitch fibers, are seen in high abundance in elite endurance athletes, such as long-distance runners and cyclists. Alternatively, fast-twitch IIa and IIx fibers are abundant in elite power athletes, such as weightlifters and sprinters. While cross-sectional comparisons have shown marked differences between athletes, longitudinal data have not clearly converged on patterns in fiber type shifts over time, particularly between slow and fast fibers. However, not all fiber type identification techniques are created equal and, thus, may limit interpretation. Hybrid fibers, which express more than one MHC type (I/IIa, IIa/IIx, I/IIa/IIx), may make up a significant proportion of fibers. The measurement of the distribution of fibers would necessitate the ability to identify hybrid fibers, which is best done through single fiber analysis. Current evidence using the most appropriate techniques suggests a clear ability of fibers to shift between hybrid and pure fibers as well as between slow and fast fiber types. The context and extent to which this occurs, along with the limitations of current evidence, are discussed herein.

Objectives: To conduct a systematic review and multilevel meta-analysis of the current literature as to the effects of interval training (IT) vs moderate intensity continuous training (MICT) on measures of body composition, both on a whole-body and regional level. Design: Systematic review and meta-analysis. Data sources: English-language searches of PubMed/MEDLINE, Scopus, and CINAHL conducted in accordance with PRISMA guidelines. Eligibility criteria for selecting studies: a) randomized controlled trials that directly compared IT vs MICT body composition using a validated measure in healthy children and adults; b) training was carried out a minimum of once per week for at least four weeks; c) published in a peer-reviewed English language journal or on a pre-print server. Results: The main model for fat mass effects revealed a trivial standardized point estimate with high precision for the interval estimate, with negligible heterogeneity. The main model for lean mass effects revealed a trivial standardized point estimate with high precision for the interval estimate, with negligible heterogeneity. The GRADE summary of findings suggested high certainty for both main model effects. In comparison to non-intervention control groups, the IT conditions resulted in small reductions in fat mass and trivial increases in lean mass. The MICT conditions also produced small reductions in fat mass, and trivial increases in lean mass. Analysis of regional fat loss revealed trivial between group comparative treatment effects for upper body, lower body and trunk regions with minimal differences between regions. Conclusion: Our findings provide compelling evidence that the intensity of effort during endurance exercise has minimal influence on longitudinal changes in fat mass and lean mass.