Explore the vast range of titles available.

The purpose of this exploratory investigation was to determine if acute post‐exercise skeletal muscle myosin heavy chain fragmentation (MyHCfrag) coincides with alterations in molecular chaperones and proteolytic enzymes, select markers of mammalian target of rapamycin complex 1 (mTORC1) signalling, and/or specific gene expression signatures. Untrained males (n = 10, 23 ± 2 years) and females (n = 10, 23 ± 3 years) completed a bout of combined endurance and resistance exercise. Vastus lateralis muscle biopsies were taken before, 3 h and 24 h post‐exercise. Tissue was fractioned into myofibrillar (MF) and sarcoplasmic protein (SF) fractions for protein analysis. Differential RNA expression (DE) from those who experienced high and low MyHCfrag post‐exercise was also analysed via bulk RNA‐sequencing. MyHCfrag increased 24 h post‐exercise, albeit only four of 20 chaperone and proteolytic markers were concomitantly altered and none significantly correlated with 24 h post‐exercise MyHCfrag. Given these null findings, we explored six participants who experienced the most post‐exercise MyHCfrag versus six who experienced the least MyHCfrag with the intent of examining if post‐exercise gene signatures or signalling differed. Although mTORC1 signalling markers were similar, 799 DE transcripts were identified 24 h post‐exercise. Pathway analysis on DE differences indicated that nine of the top 10 pathways enriched in high‐MyHCfrag participants were related to inflammation. High MyHCfrag participants also presented an upregulation in extracellular matrix remodelling genes at the 24 h post‐exercise time point. Though we lack immunohistochemical data, these findings suggest that post‐exercise MyHCfrag is associated with an upregulation in an inflammatory and remodelling signature, and longer‐term studies are needed to determine if these acute outcomes align with unique adaptive responses. What is the central question of this study? Is myosin heavy chain fragmentation (MyHCfrag) following resistance exercise in humans associated with a physiological signature in skeletal muscle? What is the main finding and its importance? Higher post‐exercise MyHCfrag is associated with a gene signature indicative of inflammation and remodelling. Future research is needed to determine if these acute outcomes translate to meaningful adaptive responses with chronic training.

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.

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.

Background: Previous research indicates that gastrointestinal discomfort from milk consumption may be attributable to A1 β-casein, rather than lactose intolerance alone. A2 milk (free of A1 β-casein) consumption may result in fewer symptoms compared to conventional milk containing both A1/A2 β-casein. Objective: In this five-week, double-blind, double-crossover study, we assessed the physiological responses to doses escalating in volume of lactose-free conventional milk (Lactaid), A2 milk, and lactose-free A2 milk in fluid milk-avoiding participants. Methods: Each milk type was consumed over three separate weeks with three increasing doses across five days per week, >one week washout. Gastrointestinal symptoms, blood glucose, and breath gases were monitored for twenty-four, two-, and three-hours post-consumption, respectively. Sensory evaluation was completed for each sample. Results: Fifty-three participants consented and were randomized, with forty-eight participants completing the study. Overall, symptoms were minimal. On Days 1 and 3, lower ratings of bloating and flatulence were observed in A2 compared to lactose-free A2. Breath hydrogen responses reflected lactose content, but were higher in lactose-free A2 than Lactaid on Day 5. Thirty-three participants were deemed lactose-intolerant and had higher fasting and average breath hydrogen for all samples. The only symptom corresponding to the increase in breath hydrogen among these participants was flatulence after A2 consumption. Surprisingly, flatulence was apparently higher for lactose-tolerant individuals when consuming Lactaid compared to A2. Conclusions: These findings suggest that adults who avoid conventional fluid milk consumption may experience minimal GI discomfort from lactose-free and/or A1-free milks.

Background: Wearable technology has increased in popularity due to its live feedback and ability to adjust within training sessions. In addition to heart rate (HR) monitoring, measuring power and internal load may provide useful insight and a more comprehensive view of training differences. Objectives: Assess the efficacy of wearable technology in endurance runners to determine changes in performance variables with varying wind resistance. Methods: A quasi-experimental study was designed and recruited twelve endurance-trained runners currently running ≥120 min/week for the past 3 months. Participants completed two sessions: V̇O2peak testing, and a 20-min run at 70% V̇O2peak. The run was evenly divided into no wind resistance (W0) and 16.1 km/h wind resistance (W16). Power was assessed via a power meter and internal/external load measured via surface EMG sensor-embedded compression shorts. A HR sensor was used and V̇O2 and RER were monitored using a metabolic cart. Paired t-tests were used to compare differences and Pearson correlations were conducted for each segment. Significance was set a priori at p0.05. Results: There were significant differences in power (W16 W0; p=0.002), as well as a strong positive correlation between power and internal load for W0 (r=0.692; p=0.013) and W16 (r=0.657; p=0.02). Conclusions: The lack of significance changes in HR, V̇O2, and RER demonstrates a sustained similar physiological response. The significant increase observed in power suggests the power meter can be useful in differentiating wind resistance, and the positive correlations suggest a combination of these devices may be beneficial in distinguishing performance changes during fluctuating conditions.

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 (MyHC ) increased 3 hours post-RE (~ +200%, p=0.018) and returned to pre-exercise levels by 6 hours post-RE. Immunoprecipitation of MyHC 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 MyHC 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 MyHC fragmentation, ~8% VL atrophy with two weeks of leg immobilization led to robust MyHC 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.

We sought to examine how resistance training (RT) status in young healthy individuals, either well-trained (T, n=10 (8 males)) or untrained (UT, n=11 (8 males)), affected muscle size and molecular markers with leg immobilization followed by recovery RT. All participants underwent two weeks of left leg immobilization via the use of crutches and a locking leg brace. After this two-week period, all participants underwent eight weeks (3 d/week) 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 collected at these time points. T and UT presented lower ultrasound derived VL size (cross-sectional area and thickness) values 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 (fCSA) values demonstrated a main effect of time where PRE and POST were greater than MID (p<0.05) and main effect of training status where T was greater than UT (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 across all time points (p=0.004). Additionally, ribosome content (total RNA) decreased (p=0.010) from PRE to MID while the endoplasmic reticulum stress proteins (BiP, Xbp1s, and CHOP) increased from MID to POST regardless of training status. Finally, the phosphorylation states of mechanistic target of rapamycin complex-1 signaling proteins were not significantly altered for either group throughout the intervention. In conclusion, 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, these data are limited to younger adults undergoing non-complicated disuse. Thus, further investigation to determine the impact of training status on prolonged leg immobilization models mirroring current medical protocols (e.g., following orthopedic injury and surgery) is warranted.

The purpose of this study was to evaluate the effectiveness of three different physical training approaches to improving cadets’ fitness variables. Retrospective data for male and female land management law enforcement officers attending a 15-week training program at three separate time points were provided for analysis. The time points reflected the three different training approaches, including calisthenic training (CT) = 83, functional fitness training (FT) = 90, and strength training (ST) = 110. Inferential data analysis was used to find which mode of exercise had the greatest impact on body composition, cardiovascular endurance, muscular strength, agility, and flexibility. All groups displayed decreases in body fat percentage, with weight loss being more significant within the CT and FT groups, while the ST group increased in body weight. The CT group had the greatest flexibility increases compared to the FT and ST groups. ST training elicited significantly smaller changes in cardiovascular endurance than the FT and CT groups. ST training showed greater improvements in lean mass, while CT and FT showed greater increases in flexibility and endurance. These results suggest that training protocols can increase performance and optimize the abilities to perform job tasks in tactical athletes.