Background: The role of trunk muscle training (TMT) for physical fitness (e.g., muscle power) and sport-specific performance measures (e.g., swimming time) in athletic populations has been extensively examined over the last decades. However, a recent systematic review and meta-analysis on the effects of TMT on measures of physical fitness and sport-specific performance in young and adult athletes is lacking.Objective: To aggregate the effects of TMT on measures of physical fitness and sport-specific performance in young and adult athletes and identify potential subject-related moderator variables (e.g., age, sex, expertise level) and training-related programming parameters (e.g., frequency, study length, session duration, and number of training sessions) for TMT effects.Data Sources: A systematic literature search was conducted with PubMed, Web of Science, and SPORTDiscus, with no date restrictions, up to June 2021.Study Eligibility Criteria: Only controlled trials with baseline and follow-up measures were included if they examined the effects of TMT on at least one measure of physical fitness (e.g., maximal muscle strength, change-of-direction speed (CODS)/agility, linear sprint speed) and sport-specific performance (e.g., throwing velocity, swimming time) in young or adult competitive athletes at a regional, national, or international level. The expertise level was classified as either elite (competing at national and/or international level) or regional (i.e., recreational and sub-elite).Study Appraisal and Synthesis Methods: The methodological quality of TMT studies was assessed using the Physiotherapy Evidence Database (PEDro) scale. A random-effects model was used to calculate weighted standardized mean differences (SMDs) between intervention and active control groups. Additionally, univariate sub-group analyses were independently computed for subject-related moderator variables and training-related programming parameters.Results: Overall, 31 studies with 693 participants aged 11–37 years were eligible for inclusion. The methodological quality of the included studies was 5 on the PEDro scale. In terms of physical fitness, there were significant, small-to-large effects of TMT on maximal muscle strength (SMD = 0.39), local muscular endurance (SMD = 1.29), lower limb muscle power (SMD = 0.30), linear sprint speed (SMD = 0.66), and CODS/agility (SMD = 0.70). Furthermore, a significant and moderate TMT effect was found for sport-specific performance (SMD = 0.64). Univariate sub-group analyses for subject-related moderator variables revealed significant effects of age on CODS/agility (p = 0.04), with significantly large effects for children (SMD = 1.53,p = 0.002). Further, there was a significant effect of number of training sessions on muscle power and linear sprint speed (p ≤ 0.03), with significant, small-to-large effects of TMT for > 18 sessions compared to ≤ 18 sessions (0.45 ≤ SMD ≤ 0.84,p ≤ 0.003). Additionally, session duration significantly modulated TMT effects on linear sprint speed, CODS/agility, and sport-specific performance (p ≤ 0.05). TMT with session durations ≤ 30 min resulted in significant, large effects on linear sprint speed and CODS/agility (1.66 ≤ SMD ≤ 2.42,p ≤ 0.002), whereas session durations > 30 min resulted in significant, large effects on sport-specific performance (SMD = 1.22,p = 0.008).Conclusions: Our findings indicate that TMT is an effective means to improve selected measures of physical fitness and sport-specific performance in young and adult athletes. Independent sub-group analyses suggest that TMT has the potential to improve CODS/agility, but only in children. Additionally, more (> 18) and/or shorter duration (≤ 30 min) TMT sessions appear to be more effective for improving lower limb muscle power, linear sprint speed, and CODS/agility in young or adult competitive athletes.

The objective of this work was to investigate myonuclear permanence and transcriptional regulation as mechanisms for cellular muscle memory after strength training in humans. Twelve untrained men and women performed 10 weeks of unilateral elbow‐flexor strength training followed by 16 weeks of de‐training. Thereafter, 10 weeks’ re‐training was conducted with both arms: the previously trained arm and the contralateral untrained control arm. Muscle biopsies were taken from the trained arm before and after both training periods and from the control arm before and after re‐training. Muscle biopsies were analysed for fibre cross‐sectional area (fCSA), myonuclei and global transcriptomics (RNA sequencing). During the first training period, myonuclei increased in type 1 (13 ± 17%) and type 2 (33 ± 23%) fibres together with a 30 ± 43% non‐significant increase in mixed fibre fCSA (P = 0.069). Following de‐training, fCSA decreased in both fibre types, whereas myonuclei were maintained, resulting in 33% higher myonuclear number in previously trained vs. control muscle in type 2 fibres. Furthermore, in the previously trained muscle, three differentially expressed genes (DEGs; EGR1, MYL5 and COL1A1) were observed. Following re‐training, the previously trained muscle showed larger type 2 fCSA compared to the control (P = 0.035). However, delta change in type 2 fCSA was not different between muscles. Gene expression was more dramatically changed in the control arm (1338 DEGs) than in the previously trained arm (822 DEGs). The sustained higher number of myonuclei in the previously trained muscle confirms myonuclear accretion and permanence in humans. Nevertheless, because of the unclear effect on the subsequent hypertrophy with re‐training, the physiological benefit remains to be determined. image Key points: Muscle memory is a cellular mechanism that describes the capacity of skeletal muscle fibres to respond differently to training stimuli if the stimuli have been previously encountered. This study overcomes past methodological limitations related to the choice of muscles and analytical procedures. We show that myonuclear number is increased after strength training and maintained during de‐training. Increased myonuclear number and differentially expressed genes related to muscle performance and development in the previously trained muscle did not translate into a clearly superior responses during re‐training. Because of the unclear effect on the subsequent hypertrophy and muscle strength gain with re‐training, the physiological benefit remains to be determined.

Background: The improvement in muscle strength generally exceeds the increase in muscle size following strength training in frail elderly, highlighting the complex aetiology of strength deficit in aging. The aim of this study was to investigate the effect of heavy‐load strength training on a broad number of factors related to specific strength in frail elderly.Methods: Thirty‐four frail elderly men (n = 18) and women (n = 16) aged 67 to 98 (86 ± 7 years) were randomized to either a group performing strength training twice a week for 10 weeks (ST) or a non‐exercising control group (CON). Knee extensor muscle strength was tested as one‐repetition maximum (1RM) and isometric maximal voluntary contraction (MVC) torque. Muscle activation was assessed by the interpolated twitch technique, and muscle density [mean Hounsfield units (HU)] and intermuscular adipose tissue (IMAT) by computed tomography scans of the quadriceps femoris. Muscle biopsies from the vastus lateralis were obtained to investigate changes in intramyocellular lipids and single‐fibre specific tension.Results: In ST, knee extension 1RM and MVC improved by 17 and 7%, respectively. Muscle cross‐sectional area of the quadriceps femoris increased by 7%, accompanied by a 4% increase of muscle density. No changes in IMAT, voluntary activation level, single‐fibre specific tension, or lipid content were observed.Conclusions: In contrast to several previous reports, the improvements in isometric muscle strength and muscle area were in good agreement in the present study. The training‐induced increase in muscle density was not due to changes in skeletal muscle lipid content. Instead, the increase in muscle density may reflect increased packing of contractile material or simply an increased ratio of muscle tissue relative to IMAT.

Purpose: The endurance training (ET)-induced increases in peak oxygen uptake ( $$\dot{V}$$V˙ O_2peak) and cardiac output ( $$\dot{Q}$$Q˙ _peak) during upright cycling are reversed to pre-ET levels after removing the training-induced increase in blood volume (BV). We hypothesised that ET-induced improvements in $$\dot{V}$$V˙ O_2peak and $$\dot{Q}$$Q˙ _peak are preserved following phlebotomy of the BV gained with ET during supine but not during upright cycling. Arteriovenous O₂ difference (a- $$\bar{\text{v}}$$v¯ O₂diff; $$\dot{V}$$V˙ O₂/ $$\dot{Q}$$Q˙ ), cardiac dimensions and muscle morphology were studied to assess their role for the $$\dot{V}$$V˙ O_2peak improvement. Methods: Twelve untrained subjects ( $$\dot{V}$$V˙ O_2peak: 44 ± 6 ml kg⁻¹ min⁻¹) completed 10 weeks of supervised ET (3 sessions/week). Echocardiography, muscle biopsies, haemoglobin mass (Hb_mass) and BV were assessed pre- and post-ET. $$\dot{V}$$V˙ O_2peak and $$\dot{Q}$$Q˙ _peak during upright and supine cycling were measured pre-ET, post-ET and immediately after Hb_mass was reversed to the individual pre-ET level by phlebotomy. Results: ET increased the Hb_mass (3.3 ± 2.9%; P = 0.005), BV (3.7 ± 5.6%; P = 0.044) and $$\dot{V}$$V˙ O_2peak during upright and supine cycling (11 ± 6% and 10 ± 8%, respectively; P ≤ 0.003). After phlebotomy, improvements in $$\dot{V}$$V˙ O_2peak compared with pre-ET were preserved in both postures (11 ± 4% and 11 ± 9%; P ≤ 0.005), as was $$\dot{Q}$$Q˙ _peak (9 ± 14% and 9 ± 10%; P ≤ 0.081). The increased $$\dot{Q}$$Q˙ _peak and a- $$\bar{\text{v}}$$v¯ O₂diff accounted for 70% and 30% of the $$\dot{V}$$V˙ O_2peak improvements, respectively. Markers of mitochondrial density (CS and COX-IV; P ≤ 0.007) and left ventricular mass (P = 0.027) increased. Conclusion: The ET-induced increase in $$\dot{V}$$V˙ O_2peak was preserved despite removing the increases in Hb_mass and BV by phlebotomy, independent of posture. $$\dot{V}$$V˙ O_2peak increased primarily through elevated $$\dot{Q}$$Q˙ _peak but also through a widened a- $$\bar{\text{v}}$$v¯ O₂diff, potentially mediated by cardiac remodelling and mitochondrial biogenesis.

Background: This study compared the muscle activity and six repetition maximum (6-RM) loads in bench press with narrow, medium, and wide grip widths with sub-group comparisons of resistance-trained (RT) and novice-trained (NT) men. Methods: After two familiarization sessions, twenty-eight subjects lifted their 6-RM loads with the different grip widths with measurement of electromyographic activity. Results: Biceps brachii activity increased with increasing grip width, whereas wide grip displayed lower triceps brachii activation than medium and narrow. In the anterior deltoid, greater activity was observed using a medium compared to narrow grip. Similar muscle activities were observed between the grip widths for the other muscles. For the RT group, greater biceps brachii activity with increasing grip width was observed, but only greater activity was observed in the NT group between narrow and wide. Comparing wide and medium grip width, the RT group showed lower triceps activation using a wide grip, whereas the NT group showed lower anterior deltoid activation using a narrow compared to medium grip. Both groups demonstrated lower 6-RM loads using a narrow grip compared to the other grips. Conclusion: Grip widths affect both 6-RM loads and triceps brachii, biceps brachii, and anterior deltoid activity especially between wide and narrow grip widths.

Purpose: Aging is associated with increased myocellular stress and loss of muscle mass and function. Heat shock proteins (HSPs) are upregulated during periods of stress as part of the cells protective system. Exercise can affect both acute HSP regulation and when repeated regularly counteract unhealthy age-related changes in the muscle. Few studies have investigated effects of exercise on HSP content in elderly. The aim of the study was to compare muscular HSP levels in young and elderly and to investigate how training affects HSP content in muscles from aged males and females. Methods: Thirty-eight elderly were randomized to 12 weeks of strength training (STG), functional strength training (FTG) or a control group (C). To compare elderly to young, 13 untrained young performed 11 weeks of strength training (Y). Muscle biopsies were collected before and after the intervention and analyzed for HSP27, αB-crystallin and HSP70. Results: Baseline HSP70 were 35% higher in elderly than in young, whereas there were no differences between young and elderly in HSP27 or αB-crystallin. After the training intervention, HSP70 were reduced in STG (− 33 ± 32%; P = 0.001) and FTG (− 28 ± 30%; P = 0.012). The decrease in HSP70 was more pronounced in the oldest. In contrast, Y increased HSP27 (134 ± 1%; P < 0.001) and αB-crystallin (84 ± 94%; P = 0.008). Conclusion: Twelve weeks of STG or FTG decreased the initial high levels of HSP70 in aged muscles. Thus, regular strength training can normalize some of the increases in cellular stress associated with normal aging, and lead to a healthier cellular environment in aged muscle cells.