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This study investigated the impact of menstrual cycle (MC) phases and resistance training (RT) on muscle cross-sectional area (CSA) in two MCs utilizing a within-subject design. Twenty women with regular MCs had their legs randomly allocated to either the control (CON) or RT condition, which included 16 training sessions over two MCs. CSA, estradiol (E2), and progesterone (P4) were assessed during the menstruation (M), ovulation (O), and luteal (L) phases in the first (M1, O1, L1) and second (M2, O2, L2) MCs and at the beginning of the third MC (M3). P4 values were significantly higher during the luteal phase than during menstruation (P < 0.0001) and ovulation (P < 0.0001). No significant differences in E2 concentrations were observed between the MC phases (P = 0.08). For the RT condition, the CSA showed significant increases at O2, L2, and M3 compared to baseline (M1) (all P < 0.0001). No significant changes were observed for the CON condition during the two MCs (P > 0.05). However, RT condition showed a significant change in average CSA across two MCs. Additionally, individual analyses revealed that 19 participants showed variation in CSA above or below the minimum detectable difference during the two MCs. These findings suggest that changes in muscle CSA observed during two MCs may not be exclusively attributed to RT. [ABSTRACT FROM AUTHOR]

We examined changes in skeletal muscle protein lactylation and acetylation in response to acute resistance exercise, chronic resistance training (RT), and a single endurance cycling bout. Additionally, we performed in vitro experiments to determine if different sodium lactate treatments affect myotube protein lactylation and acetylation. The acute and chronic RT study (12 college-aged participants) consisted of 10 weeks of unilateral leg extensor RT with vastus lateralis (VL) biopsies taken at baseline, 24 h following the first RT bout, and the morning of the last day of the RT bout. For the acute cycling study (9 college-aged participants), VL biopsies were obtained before, 2 h after, and 8 h after 60 min of cycling. For in vitro experiments, C2C12 myotubes were treated with varying levels of sodium lactate, including LOW (1 mM for 24 h), HIGH (10 mM for 24 h), and PULSE (10 mM for 30 min followed by 1 mM for 23.5-h). Neither acute nor chronic RT significantly affected nuclear or cytoplasmic protein lactylation. However, cytoplasmic protein acetylation was significantly reduced following one RT bout (−15%, p = 0.002) and chronic RT (−16%, p = 0.006). Cycling did not acutely alter post-exercise global protein lactylation or acetylation patterns. Lastly, varying 24 h lactate treatments did not alter nuclear or cytoplasmic protein lactylation or acetylation, cytoplasmic protein synthesis levels, or myotube diameters. These findings continue to support the idea that exercise induces more dynamic changes in skeletal muscle protein acetylation, but not lactylation. However, further human research with more sampling timepoints and a lactylomics approach are needed to determine if, at all, different exercise modalities affect skeletal muscle protein lactylation. [ABSTRACT FROM AUTHOR]

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 FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate whether baseline values and acute and chronic changes in androgen receptors (AR) markers, including total AR, cytoplasmic (cAR), and nuclear (nAR) fractions, as well as DNA-binding activity (AR-DNA), are involved in muscle hypertrophy responsiveness by comparing young nonresponder and responder individuals. After 10 wk of resistance training (RT), participants were identified as nonresponders using two typical errors (TE) obtained through two muscle cross-sectional area (mCSA) ultrasound measurements (2 × TE; 4.94%), and the highest responders within our sample were numerically matched. Muscle biopsies were performed at baseline, 24 h after the first RT session (acute responses), and 96 h after the last session (chronic responses). AR, cAR, and nAR were analyzed using Western blotting, and AR-DNA was analyzed using an ELISA-oligonucleotide assay. Twelve participants were identified as nonresponders (ΔmCSA: −1.32%) and 12 as responders (ΔmCSA: 21.35%). There were no baseline differences between groups in mCSA, AR, cAR, nAR, or AR-DNA (P > 0.05). For acute responses, there was a significant difference between nonresponders (+19.5%) and responders (−14.4%) in AR-DNA [effect size (ES) = −1.39; 95% confidence interval (CI): −2.53 to −0.16; P = 0.015]. There were no acute between-group differences in any other AR markers (P > 0.05). No significant differences between groups were observed in chronic responses across any AR markers (P > 0.05). Nonresponders and responders presented similar baseline, acute, and chronic results for the majority of the AR markers. Thus, our findings do not support the influence of AR markers on muscle hypertrophy responsiveness to RT in untrained individuals. NEW & NOTEWORTHY: We explored, for the first time, the influence of androgen receptor (AR) through the separation of cytoplasmic and nuclear cell fractions [i.e., cytoplasmic androgen receptor (cAR), nuclear androgen receptor (nAR), and androgen receptor DNA-binding activity (AR-DNA)] on muscle hypertrophy responsiveness to resistance training. The absence of muscle hypertrophy in naïve individuals does not seem to be explained by baseline values, and acute or chronic changes in AR markers. [ABSTRACT FROM AUTHOR]

The aim of this study was to compare the effects of progressive overload in resistance training on muscle strength and cross-sectional area (CSA) by specifically comparing the impact of increasing load (LOADprog) versus an increase in repetitions (REPSprog). We used a within-subject experimental design in which 39 previously untrained young persons (20 men and 19 women) had their legs randomized to LOADprog and REPSprog. Outcomes were assessed before and after 10 weeks of training. Muscle strength was assessed using the one repetition maximum (1RM) test on the leg extension exercise, and the CSA of the vastus lateralis was assessed by ultrasonography. Both protocols increased 1RM values from pre (LOADprog: 52.90±16.32 kg; REPSprog: 51.67±15.84 kg) to post (LOADprog: 69.05±18.55 kg, REPSprog: 66.82±17.95 kg), with no difference between them (P +>+0.05). Similarly, both protocols also increased in CSA values from pre (LOADprog: 21.34±4.71 cm²; REPSprog: 21.08±4.62 cm²) to post (LOADprog: 23.53±5.41 cm², REPSprog: 23.39±5.19 cm²), with no difference between them (P +>+0.05). In conclusion, our findings indicate that the progression of overload through load or repetitions can be used to promote gains in strength and muscle hypertrophy in young men and women in the early stages of training. [ABSTRACT FROM AUTHOR]

Context: Low-load resistance training (LL) and neuromuscular electrostimulation (NES), both combined with blood flow restriction (BFR), emerge as effective strategies to maintain or increase muscle mass. It is well established that LL-BFR promotes similar increases in muscle cross-sectional area (CSA) and lower rating of perceived exertion (RPE) and pain compared with traditional resistance training protocols. On the other hand, only 2 studies with conflicting results have investigated the effects of NES-BFR on CSA, RPE, and pain. In addition, no study directly compared LL-BFR and NES-BFR. Objective: The aim of the study was to compare the effects of LL-BFR and NES-BFR on vastus lateralis CSA, RPE, and pain. Individual response for muscle hypertrophy was also compared between protocols. Design: Intrasubject longitudinal study. Setting: University research laboratory. Intervention: Fifteen healthy young males (age = 23 [5] y; weight = 77.6 [11.3] kg; height = 1.76 [0.08] m). Main outcome measures: Vastus lateralis CSA was measured through ultrasound at baseline (pre) and after 20 training sessions (post). The RPE and pain responses were obtained through modified 10-point scales, handled during all training sessions. Results: Both protocols demonstrated significant increases in muscle CSA (P < .0001). However, the LL-BFR demonstrated significantly greater CSA changes compared with NES-BFR (LL-BFR = 11.2%, NES-BFR = 4.6%; P < .0001). Comparing individual increases in CSA, 12 subjects (85.7% of the sample) presented greater muscle hypertrophy for LL-BFR than for the NES-BFR protocol. In addition, LL-BFR produced significantly lower RPE and pain responses (P < .0001). Conclusions: The LL-BFR produced significantly greater increases in CSA with significant less RPE and pain than NES-BFR. In addition, LL-BFR resulted in greater individual muscle hypertrophy responses for most subjects compared with NES-BFR. [ABSTRACT FROM AUTHOR]