High-intensity interval training (HIIT) may elicit different skeletal muscle responses compared to work-matched moderate-intensity continuous training (MICT). The effect of work-matched HIIT versus MICT on myofibrillar protein synthesis remains to be determined. In the present study, we assessed the effect of short-term HIIT versus MICT on myofibrillar protein synthesis rates using a single-leg within-participant design. Ten healthy young men (age: 20 ± 1 years) performed six to eight training sessions with each leg over 2 weeks while ingesting deuterated water to assess myofibrillar protein synthesis. One leg was randomly assigned to perform HIIT and the other MICT. Skeletal muscle biopsies were collected at rest from one leg before and after a 2-week habituation period and from both legs after the training period to assess myofibrillar protein synthesis rates. HIIT and MICT increased single-leg maximal power output (main effect, p < .01), with no differences between legs (interaction: p = .61). Myofibrillar protein synthesis rates did not differ between the habituation period, MICT, or HIIT (1.39 ± 0.16%, 1.24 ± 0.30%, and 1.42 ± 0.31% per day, respectively; p = .29). In conclusion, we observed no detectable differences in daily myofibrillar protein synthesis rates between HIIT or work-matched MICT when assessed over a 2-week exercise training period in recreationally active young adult men.

Aerobic and resistance exercise (RE) induce distinct molecular responses. One hypothesis is that these responses are antagonistic and unfavorable for the anabolic response to RE when concurrent exercise is performed. This thesis may also depend on the participants' training status and concurrent exercise order. We measured free-living myofibrillar protein synthesis (MyoPS) rates and associated molecular responses to resistance-only and concurrent exercise (with different exercise orders), before and after training. Moderately active men completed one of three exercise interventions (matched for age, baseline strength, body composition, and aerobic capacity): resistance-only exercise (RE, n = 8), RE plus high-intensity interval exercise (RE+HIIE, n = 8), or HIIE+RE (n = 9). Participants trained 3 days/week for 10 weeks; concurrent sessions were separated by 3 h. On the first day of Weeks 1 and 10, muscle was sampled immediately before and after, and 3 h after each exercise mode and analyzed for molecular markers of MyoPS and muscle glycogen. Additional muscle, sampled pre- and post-training, was used to determine MyoPS using orally administered deuterium oxide (D2 O). In both weeks, MyoPS rates were comparable between groups. Post-exercise changes in proteins reflective of protein synthesis were also similar between groups, though MuRF1 and MAFbx mRNA exhibited some exercise order-dependent responses. In Week 10, exercise-induced changes in MyoPS and some genes (PGC-1ɑ and MuRF1) were dampened from Week 1. Concurrent exercise (in either order) did not compromise the anabolic response to resistance-only exercise, before or after training. MyoPS rates and some molecular responses to exercise are diminished after training.

A majority of human genes produce non-protein-coding RNA (ncRNA), and some have roles in development and disease. Neither ncRNA nor human skeletal muscle is ideally studied using short-read sequencing, so we used a customized RNA pipeline and network modelling to study cell-type specific ncRNA responses during muscle growth at scale. We completed five human resistance-training studies (n = 144 subjects), identifying 61% who successfully accrued muscle-mass. We produced 288 transcriptome-wide profiles and found 110 ncRNAs linked to muscle growth in vivo, while a transcriptome-driven network model demonstrated interactions via a number of discrete functional pathways and single-cell types. This analysis included established hypertrophy-related ncRNAs, including CYTOR-which was leukocyte-associated (false discovery rate [FDR] = 4.9 × 10-7). Novel hypertrophy-linked ncRNAs included PPP1CB-DT (myofibril assembly genes, FDR = 8.15 × 10-8), and EEF1A1P24 and TMSB4XP8 (vascular remodelling and angiogenesis genes, FDR = 2.77 × 10-5). We also discovered that hypertrophy lncRNA MYREM shows a specific myonuclear expression pattern in vivo. Our multi-layered analyses established that single-cell-associated ncRNA are identifiable from bulk muscle transcriptomic data and that hypertrophy-linked ncRNA genes mediate their association with muscle growth via multiple cell types and a set of interacting pathways.

Skeletal muscle mass losses with age are associated with negative health consequences, including an increased risk of developing metabolic disease and the loss of independence. Athletes adopt numerous nutritional strategies to maximize the benefits of exercise training and enhance recovery in pursuit of improving skeletal muscle quality, mass, or function. Importantly, many of the principles applied to enhance skeletal muscle health in athletes may be applicable to support active aging and prevent sarcopenia in the healthy (non-clinical) aging population. Here, we discuss the anabolic properties of protein supplementation in addition to ingredients that may enhance the anabolic effects of protein (e.g. omega 3 s, creatine, inorganic nitrate) in older persons. We conclude that nutritional strategies used in pursuit of performance enhancement in athletes are often applicable to improve skeletal muscle health in the healthy older population when implemented as part of a healthy active lifestyle. Further research is required to elucidate the mechanisms by which these nutrients may induce favourable changes in skeletal muscle and to determine the appropriate dosing and timing of nutrient intakes to support active aging.

Supplemental digital content is available in the text. ABSTRACT Purpose There is a lack of knowledge as to how different exercise-based cardiac rehabilitation programming affects skeletal muscle adaptations in coronary artery disease (CAD) patients. We first characterized the skeletal muscle from adults with CAD compared with a group of age- and sex-matched healthy adults. We then determined the effects of a traditional moderate-intensity continuous exercise program (TRAD) or a stair climbing–based high-intensity interval training program (STAIR) on skeletal muscle metabolism in CAD. Methods Sixteen adults (n = 16, 61 ± 7 yr), who had undergone recent treatment for CAD, were randomized to perform (3 d·wk−1) either TRAD (n = 7, 30 min at 60%–80% of peak heart rate) or STAIR (n = 9, 3 × 6 flights) for 12 wk. Muscle biopsies were collected at baseline in both CAD and healthy controls (n = 9), and at 4 and 12 wk after exercise training in CAD patients undertaking TRAD or STAIR. Results We found that CAD had a lower capillary-to-fiber ratio (C/Fi, 35% ± 25%, P = 0.06) and capillary-to-fiber perimeter exchange (CFPE) index (23% ± 29%, P = 0.034) in Type II fibers compared with healthy controls. However, 12 wk of cardiac rehabilitation with either TRAD or STAIR increased C/Fi (Type II, 23% ± 14%, P < 0.001) and CFPE (Type I, 10% ± 23%, P < 0.01; Type II, 18% ± 22%, P = 0.002). Conclusion Cardiac rehabilitation via TRAD or STAIR exercise training improved the compromised skeletal muscle microvascular phenotype observed in CAD patients.

Magnetic resonance imaging (MRI) is the current gold standard for measuring changes in muscle size (cross-sectional area [CSA] and volume) but can be cost-prohibitive and resource-intensive. We evaluated the validity of B-mode ultrasonography (US) as a low-cost alternative to MRI for measuring muscle hypertrophy and atrophy in response to resistance training and immobilization, respectively. Fourteen young men performed 10wk of unilateral resistance training (RT) to induce muscle hypertrophy. In the final two weeks of the 10wk, the subjects' contralateral leg was immobilized (IMB). The cross-sectional area of the vastus lateralis (VLCSA) was measured at the mid-thigh before and after each intervention using MRI (VLCSAMRI ) and US (VLCSAUS ). The relationship and agreement between methods were assessed. Reliability of US measurements ranged from good to excellent in all comparisons (ICC >0.67). VLCSA significantly increased after 10 weeks of RT (VLCSAUS : 7.9 ± 3.8%; VLCSAMRI : 7.8 ± 4.5%) and decreased after 2 weeks of IMB (VLCSAUS : -8.2%±5.8%; VLCSAMRI : -8.7 ± 6.1%). Significant correlations were identified between MRI and US at each time point measured (all r > 0.85) and, importantly, between MRI- and US-derived changes in VLCSA. Bland-Altman analysis revealed minimal bias in US measurements relative to the MRI (-0.5 ± 3.0%) and all measurements were within the upper and lower limits of agreement. Our data suggest that B-mode ultrasonography can be a suitable alternative to MRI for measuring changes in muscle size in response to increased and decreased muscle loading in young men.

Background: Cardiac rehabilitation exercise reduces the risk of secondary cardiovascular disease. Interval training is a time-efficient alternative to traditional cardiac rehabilitation exercise and stair climbing is an accessible means. We aimed to assess the effectiveness of a high-intensity interval stair climbing intervention on improving cardiorespiratory fitness (V˙O2peak) compared to standard cardiac rehabilitation care. Methods: Twenty participants with coronary artery disease (61 ± 7 years, 18 males, two females) were randomly assigned to either traditional moderate-intensity exercise (TRAD) or high-intensity interval stair climbing (STAIR). V˙O2peak was assessed at baseline, following 4 weeks of six supervised exercise sessions and after 8 weeks of ~24 unsupervised exercise sessions. TRAD involved a minimum of 30 min at 60–80%HRpeak, and STAIR consisted of three bouts of six flights of 12 stairs at a self-selected vigorous intensity (~90 s/bout) separated by recovery periods of walking (~90 s). This study was registered as a clinical trial at clinicaltrials.gov (NCT03235674). Results: Two participants could not complete the trial due to the time commitment of the testing visits, leaving n = 9 in each group who completed the interventions without any adverse events. V˙O2peak increased after supervised and unsupervised training in comparison to baseline for both TRAD [baseline: 22.9 ± 2.5, 4 weeks (supervised): 25.3 ± 4.4, and 12 weeks (unsupervised): 26.5 ± 4.8 mL/kg/min] and STAIR [baseline: 21.4 ± 4.5, 4 weeks (supervised): 23.4 ± 5.6, and 12 weeks (unsupervised): 25 ± 6.2 mL/kg/min; p (time) = 0.03]. During the first 4 weeks of training (supervised) the STAIR vs. TRAD group had a higher %HRpeak (101 ± 1 vs. 89 ± 1%; p ≤ 0.001), across a shorter total exercise time (7.1 ± 0.1 vs. 36.7 ± 1.1 min; p = 0.009). During the subsequent 8 weeks of unsupervised training, %HRpeak was not different (87 ± 8 vs. 96 ± 8%; p = 0.055, mean ± SD) between groups, however, the STAIR group continued to exercise for less time per session (10.0 ± 3.2 vs. 24.2 ± 17.0 min; p = 0.036). Conclusions: Both brief, vigorous stair climbing, and traditional moderate-intensity exercise are effective in increasing V˙O2peak, in cardiac rehabilitation exercise programmes.

Skeletal muscle mass losses with age are associated with negative health consequences, including an increased risk of developing metabolic disease and the loss of independence. Athletes adopt numerous nutritional strategies to maximize the benefits of exercise training and enhance recovery in pursuit of improving skeletal muscle quality, mass, or function. Importantly, many of the principles applied to enhance skeletal muscle health in athletes may be applicable to support active aging and prevent sarcopenia in the healthy (non-clinical) aging population. Here, we discuss the anabolic properties of protein supplementation in addition to ingredients that may enhance the anabolic effects of protein (e.g. omega 3 s, creatine, inorganic nitrate) in older persons. We conclude that nutritional strategies used in pursuit of performance enhancement in athletes are often applicable to improve skeletal muscle health in the healthy older population when implemented as part of a healthy active lifestyle. Further research is required to elucidate the mechanisms by which these nutrients may induce favourable changes in skeletal muscle and to determine the appropriate dosing and timing of nutrient intakes to support active aging.

Basketball players face multiple challenges to in-season recovery. The purpose of this article is to review the literature on recovery modalities and nutritional strategies for basketball players and practical applications that can be incorporated throughout the season at various levels of competition. Sleep, protein, carbohydrate, and fluids should be the foundational components emphasized throughout the season for home and away games to promote recovery. Travel, whether by air or bus, poses nutritional and sleep challenges, therefore teams should be strategic about packing snacks and fluid options while on the road. Practitioners should also plan for meals at hotels and during air travel for their players. Basketball players should aim for a minimum of 8 h of sleep per night and be encouraged to get extra sleep during congested schedules since back-to back games, high workloads, and travel may negatively influence night-time sleep. Regular sleep monitoring, education, and feedback may aid in optimizing sleep in basketball players. In addition, incorporating consistent training times may be beneficial to reduce bed and wake time variability. Hydrotherapy, compression garments, and massage may also provide an effective recovery modality to incorporate post-competition. Future research, however, is warranted to understand the influence these modalities have on enhancing recovery in basketball players. Overall, a strategic well-rounded approach, encompassing both nutrition and recovery modality strategies, should be carefully considered and implemented with teams to support basketball players' recovery for training and competition throughout the season.

We examined the association between genotype and resistance training-induced changes (12 wk) in dual x-ray energy absorptiometry (DXA)-derived lean soft tissue mass (LSTM) as well as muscle fiber cross-sectional area (fCSA; vastus lateralis; n = 109; age = 22 ± 2 y, BMI = 24.7 ± 3.1 kg/m2 ). Over 315 000 genetic polymorphisms were interrogated from muscle using DNA microarrays. First, a targeted investigation was performed where single nucleotide polymorphisms (SNP) identified from a systematic literature review were related to changes in LSTM and fCSA. Next, genome-wide association (GWA) studies were performed to reveal associations between novel SNP targets with pre- to post-training change scores in mean fCSA and LSTM. Our targeted investigation revealed no genotype-by-time interactions for 12 common polymorphisms regarding the change in mean fCSA or change in LSTM. Our first GWA study indicated no SNP were associated with the change in LSTM. However, the second GWA study indicated two SNP exceeded the significance level with the change in mean fCSA (P = 6.9 × 10-7 for rs4675569, 1.7 × 10-6 for rs10263647). While the former target is not annotated (chr2:205936846 (GRCh38.p12)), the latter target (chr7:41971865 (GRCh38.p12)) is an intron variant of the GLI Family Zinc Finger 3 (GLI3) gene. Follow-up analyses indicated fCSA increases were greater in the T/C and C/C GLI3 genotypes than the T/T GLI3 genotype (P < .05). Data from the Auburn cohort also revealed participants with the T/C and C/C genotypes exhibited increases in satellite cell number with training (P < .05), whereas T/T participants did not. Additionally, those with the T/C and C/C genotypes achieved myonuclear addition in response to training (P < .05), whereas the T/T participants did not. In summary, this is the first GWA study to examine how polymorphisms associate with the change in hypertrophy measures following resistance training. Future studies are needed to determine if the GLI3 variant differentiates hypertrophic responses to resistance training given the potential link between this gene and satellite cell physiology.

Engagement in exercise-based cardiac rehabilitation following cardiac procedures reduces the risk of secondary coronary artery disease (CAD) events. Interval training can be a time-efficient and effective alternative to traditional moderate-intensity exercise in cardiac rehabilitation programming, and an accessible way to deliver interval training is through stair climbing. PURPOSE: To assess the feasibility and effectiveness of high-intensity interval training intervention, using stair climbing as the modality, in standard cardiac rehabilitation care. METHODS: Twenty participants with CAD (61±7 y, 18M/2W) were randomly assigned to one of two exercise programs: traditional moderate-intensity exercise (TRAD) or high-intensity interval stair climbing (STAIR). VO2peak was assessed at baseline, one month and three months after exercise initiation. Exercise was completed two times/week for one month under clinical supervision, and three times/week for two months unsupervised. Each participant completed sessions of either an accumulation of 45 min at 80 %HRpeak (TRAD) or 3 bouts of 6 flights of 12 stairs at a self-selected vigorous intensity (~90s/bout) separated by recovery periods of walking (~90s) (STAIR). RESULTS: Eighteen participants (90%) completed the intervention without any adverse events. Following one month of supervised exercise, the STAIR versus TRAD group achieved a higher peak HR 131±9 vs.111±13bpm (p=0.002, means±SD), and exercise intensity 106±11 vs.89±1%HRpeak, across a shorter time 3.1±0.8 vs. 36.7±5.5 min (p<0.001). Peak VO2 increased in both TRAD and STAIR, (23±3 to 25±4 and 21±5 to 24±6 mL/kg/min) respectively (p=0.03). Additional unsupervised training (2mo), the STAIR group achieved a higher peak HR, 126±13 vs.111±9 bpm (p=0.018) and less time at prescribed intensity 6.5±3.9 vs. 24.2±17 min (p=0.012), when compared to the TRAD group. There was no difference in exercise intensity 96±8 vs. 87±8 %HRpeak (p=0.055) or adherence 3.0±3.2 vs. 3.2±2.2 (p=0.70) exercise sessions/week, between the STAIR and TRAD groups. CONCLUSIONS: High-intensity interval training using stair climbing as the modality, is safe and effective within cardiac rehabilitation programming.

We tested the hypothesis that presleep consumption of α-lactalbumin (LA), a fraction of whey with a high abundance of tryptophan, would improve indices of sleep quality and time-trial (TT) performance in cyclists relative to an isonitrogenous collagen peptide (CP) supplement lacking tryptophan. Using randomized, double-blind, crossover designs, cyclists consumed either 40 g of LA or CP 2 hr prior to sleep. In Study 1, six elite male endurance track cyclists (age 23 ± 6 years, V˙O2peak 70.2 ± 4.4 ml·kg-1·min-1) consumed a supplement for three consecutive evenings before each 4-km TT on a velodrome track, whereas in Study 2, six well-trained cyclists (one female; age 24 ± 5 years, V˙O2peak 66.9 ± 8.3 ml·kg-1·min-1) consumed a supplement the evening before each 4-km TT on a stationary cycle ergometer. Indices of sleep quality were assessed with wrist-based actigraphy. There were no differences between the CP and LA supplements in terms of total time in bed, total sleep time, or sleep efficiency in Study 1 (LA: 568 ± 71 min, 503 ± 67 min, 88.3% ± 3.4%; CP: 546 ± 30 min, 479 ± 35 min, 87.8% ± 3.1%; p = .41, p = .32, p = .74, respectively) or Study 2 (LA: 519 ± 90 min, 450 ± 78 min, 87.2% ± 7.6%; CP: 536 ± 62 min, 467 ± 57 min, 87.3% ± 6.4%; p = .43, p = .44, p = .97, respectively). Similarly, time to complete the 4-km TT was unaffected by supplementation in Study 1 (LA: 274.9 ± 7.6 s; CP: 275.5 ± 7.2 s; p = .62) and Study 2 (LA: 344.3 ± 22.3 s; CP: 343.3 ± 23.0 s; p = .50). Thus, relative to CP, consuming LA 2 hr prior to sleep over 1-3 days did not improve actigraphy-based indices of sleep quality or 4-km TT performance in cyclists.

Exercise-based cardiac rehabilitation is associated with reduced secondary events in coronary artery disease (CAD) patients. Despite this evidence, the rate of participation in cardiac rehabilitation exercise is low. There is a lack of information evaluating how both traditional and time-reduced higher intensity protocols affect muscle metabolism in this population, even though CAD exacerbates skeletal muscle defects that contribute to the poor metabolic phenotype. PURPOSE: To determine the effect of a traditional cardiac rehabilitation exercise program and an alternative stair climbing-based high-intensity interval training program on the skeletal muscle phenotype in CAD patients. METHODS: 16 participants (15M, 1F) were randomly assigned to either traditional moderate-intensity exercise (7M, TRAD) or brief but higher-intensity interval stair climbing exercise (8M, 1F, STAIR). Both programs were 12 weeks (3d/w) in duration, each TRAD exercise session consisted of 45 minutes of moderate-intensity aerobic exercise, and each STAIR session consisted of 3 bouts x 6 flights of high-intensity stair climbing. Muscle biopsies were collected from the vastus lateralis at baseline and after 12 weeks of training. Immunofluorescent staining of muscle cross sections was completed to determine fiber size, capillarization, satellite cell (SC) and myonuclear content. RESULTS: There were no differences in the cross-sectional area and myonuclear domain of type I or II fibers following 12 weeks of either TRAD or STAIR training (p>0.05). Following 12 weeks, both exercise programs resulted in increases in, myonuclear content (type I: TRAD Δ0.4±0.5, STAIR Δ0.3±0.6, p=0.012; type II: TRAD Δ0.8±0.7, STAIR Δ0.4±0.7, p=0.006), capillary contacts (type I: TRAD Δ0.5±0.5, STAIR Δ0.2±0.7, p=0.038; type II: TRAD Δ1.2±0.6, STAIR Δ0.7±0.4, p<0.001), capillary-to-fiber perimeter exchange index (type I: TRAD Δ1.6±1.8, STAIR Δ0.4±0.8, p=0.011; type II: TRAD Δ1.8±1.7, STAIR Δ0.7±0.8, p=0.002), and capillary to fiber ratio (type II: TRAD Δ0.5±0.3, STAIR: Δ0.3±0.2, p<0.001). CONCLUSION: Both brief stair climbing-based high-intensity interval training and traditional cardiac rehabilitation exercise result in improvements in variables associated with skeletal muscle health in CAD patients.

Carotid artery longitudinal wall motion (CALM) exhibits reduced magnitude in older adults and in individuals with chronic diseases, although longitudinal data are lacking to indicate how changes in CALM might develop over time. Therefore, the aim of this study was to investigate the effect of exercise training in healthy men on CALM using a retrospective design. Carotid ultrasound data were analysed from two previous studies in which men performed 12 wk of moderate-intensity continuous exercise training (n = 9), sprint-interval training (n = 7), higher-repetition resistance exercise training (n = 15) or lower-repetition resistance exercise training (n = 15). The CALM pattern was unaltered after 12 wk of exercise training, regardless of exercise mode, with no differences in systolic or diastolic CALM magnitudes (p > 0.05), similar to carotid intima-media thickness (p > 0.05). Our findings suggest that CALM is resistant to transient changes in lifestyle factors, similar to wall thickness in otherwise healthy populations.

Loading of skeletal muscle changes the tissue phenotype reflecting altered metabolic and functional demands. In humans, heterogeneous adaptation to loading complicates the identification of the underpinning molecular regulators. A within-person differential loading and analysis strategy reduces heterogeneity for changes in muscle mass by ∼40% and uses a genome-wide transcriptome method that models each mRNA from coding exons and 3' and 5' untranslated regions (UTRs). Our strategy detects ∼3-4 times more regulated genes than similarly sized studies, including substantial UTR-selective regulation undetected by other methods. We discover a core of 141 genes correlated to muscle growth, which we validate from newly analyzed independent samples (n = 100). Further validating these identified genes via RNAi in primary muscle cells, we demonstrate that members of the core genes were regulators of protein synthesis. Using proteome-constrained networks and pathway analysis reveals notable relationships with the molecular characteristics of human muscle aging and insulin sensitivity, as well as potential drug therapies.

Skeletal muscle myofibrillar protein synthesis (MPS) increases in response to protein feeding and to resistance exercise (RE), where each stimuli acts synergistically when combined. The efficacy of plant proteins such as potato protein (PP) isolate to stimulate MPS is unknown. We aimed to determine the effects of PP ingestion on daily MPS with and without RE in healthy women. In a single blind, parallel-group design, 24 young women (21 ± 3 years, n = 12/group) consumed a weight-maintaining baseline diet containing 0.8 g/kg/d of protein before being randomized to consume either 25 g of PP twice daily (1.6 g/kg/d total protein) or a control diet (CON) (0.8 g/kg/d total protein) for 2 wks. Unilateral RE (~30% of maximal strength to failure) was performed thrice weekly with the opposite limb serving as a non-exercised control (Rest). MPS was measured by deuterated water ingestion at baseline, following supplementation (Rest), and following supplementation + RE (Exercise). Ingestion of PP stimulated MPS by 0.14 ± 0.09 %/d at Rest, and by 0.32 ± 0.14 %/d in the Exercise limb. MPS was significantly elevated by 0.20 ± 0.11 %/d in the Exercise limb in CON (P = 0.008). Consuming PP to increase protein intake to levels twice the recommended dietary allowance for protein augmented rates of MPS. Performance of RE stimulated MPS regardless of protein intake. PP is a high-quality, plant-based protein supplement that augments MPS at rest and following RE in healthy young women.

IntroductionWe aimed to determine if candidate genetic polymorphisms were associated with resistance training‐induced changes in skeletal muscle hypertrophy variables.MethodsTwo cohorts of predominantly Caucasian college‐aged male participants (N=109; n=66: Auburn, AL, USA; n=43: Hamilton, Ontario, Canada) performed 12 weeks of progressive full‐body resistance training (3–4 days/week). Vastus lateralis muscle biopsies and dual x‐ray absorptiometry (DXA) scans were performed prior to the intervention (Pre), and 72 hours following the last training bout (Post). Immunohistochemistry was performed to assess mean fiber cross sectional area (fCSA), DXA scans were analyzed to assess whole‐body (fat‐ and bone‐free) lean soft tissue mass (LSTM), and over 800,000 genetic polymorphisms were interrogated from muscle tissue using DNA microarrays. Select polymorphisms from a systematic literature review were examined in relation to Pre‐to‐Post changes in mean fCSA as well as changes in DXA LSTM.ResultsThere were no genotype*time interactions for ACTN3 (rs1815739), ACE (rs4343), ADRB2 (rs1042714), FTO (rs9939609, rs1421085, rs8050136), IL15RA (rs2296135), VDR (rs1544410), LEPR (rs113710182), FST (rs7229102), IGF1 (rs5742692), or MSTN (rs72909336) with regard to training‐induced changes in DXA LSTM or mean fCSA. Interestingly, when participants were clustered in tertiles according to percent changes in mean fCSA and DXA LSTM, Pre mean fCSA and Pre DXA LSTM were inversely correlated. Pre mean fCSA values were greater in the lower (5607±1195 μm2) versus middle (4673±1154 μm2, p=0.007) and upper tertiles (4558±895 μm2, p<0.001), while Pre DXA LSTM values were greater in the lower (63.3±7.0 kg) versus middle (59.6±6.9 kg, p=0.043) upper tertiles (57.5±5.8 kg, p<0.001). Stepwise linear regression was performed using baseline DXA LSTM and mean fCSA along with gene scores from the candidate polymorphisms to predict percent changes in DXA LSTM as well as mean fCSA with training, respectively. The only significant predictor of percent DXA LSTM change to training was Pre DXA LSTM (β=−0.327, model r2=0.11, p=0.001). Likewise, the only significant predictor of percent mean fCSA change to training was Pre mean fCSA (β=−0.310, model r2=0.09, p=0.001).ConclusionsCollectively, our data suggest that pre‐training DXA LSTM or fCSA values (rather than the genetic influence of select polymorphisms) are better predictors of change scores in these variables with resistance training.Support or Funding InformationFunding for this project on the Auburn Campus was provided by Hilmar Ingredients, Bionutritional Research Group, and discretionary lab funds by M.D.R. Funding for the McMaster Campus project was provided through an operating grant provided to S.M.P through the Natural Science and Engineering Research Council of Canada.Figure 1

Background: Aging appears to attenuate the response of skeletal muscle protein synthesis (MPS) to anabolic stimuli such as protein ingestion (and the ensuing hyperaminoacidemia) and resistance exercise (RE). Objectives: The purpose of this study was to determine the effects of protein quality on feeding- and feeding plus RE-induced increases of acute and longer-term MPS after ingestion of whey protein (WP) and collagen protein (CP). Methods: In a double-blind parallel-group design, 22 healthy older women (mean +/- SD age: 69 +/- 3 y, n = 11/group) were randomly assigned to consume a 30-g supplement of either WP or CP twice daily for 6 d. Participants performed unilateral RE twice during the 6-d period to determine the acute (via [C-13(6)]-phenylalanine infusion) and longer-term (ingestion of deuterated water) MPS responses, the primary outcome measures. Results: Acutely, WP increased MPS by a mean +/- SD 0.017 +/- 0.008%/h in the feeding-only leg (Rest) and 0.032 +/- 0.012%/h in the feeding plus exercise leg (Exercise) (both P < 0.01), whereas CP increased MPS only in Exercise (0.012 +/- 0.013%/h) (P < 0.01) and MPS was greater in WP than CP in both the Rest and Exercise legs (P = 0.02). Longer-term MPS increased by 0.063 +/- 0.059%/d in Rest and 0.173 +/- 0.104%/d in Exercise (P < 0.0001) with WP; however, MPS was not significantly elevated above baseline in Rest (0.011 +/- 0.042%/d) or Exercise (0.020 +/- 0.034%/d) with CP. Longer-term MPS was greater in WP than in CP in both Rest and Exercise (P < 0.001). Conclusions: Supplementation with WP elicited greater increases in both acute and longer-term MPS than CP supplementation, which is suggestive that WP is a more effective supplement to support skeletal muscle retention in older women than CP. This trial was registered at clinicaltrials.gov as NCT03281434.