Key pointsr Exercise acutely increases the concentrations of metabolites and hormones such as growth hormone (GH) and, to a lesser extent, insulin-like growth factor 1 (IGF-1); however, the biological function of this response is unclear.r Pharmacological administration of these hormones stimulates collagen synthesis in muscle and tendon; however, whether the post-exercise biochemical milieu has a similar action is unknown.r Treating engineered ligaments with serum obtained from young healthy men after exercise resulted in more collagen and improved tensile strength over those treated with serum from resting men.r Further, we show that the increase in collagen induced by post-exercise serum (i) is not reproduced by treatment with recombinant GH or IGF-1, and (ii) is associated with the activation of PI3 kinase/mTORC1 and ERK1/2 signalling.Abstract Exercise stimulates a dramatic change in the concentration of circulating hormones, such as growth hormone (GH), but the biological functions of this response are unclear. Pharmacological GH administration stimulates collagen synthesis; however, whether the post-exercise systemic milieu has a similar action is unknown. We aimed to determine whether the collagen content and tensile strength of tissue-engineered ligaments is enhanced by serum obtained post-exercise. Primary cells from a human anterior cruciate ligament (ACL) were used to engineer ligament constructs in vitro. Blood obtained from 12 healthy young men 15 min after resistance exercise contained GH concentrations that were ß7-fold greater than resting serum (P < 0.001), whereas IGF-1 was not elevated at this time point (P = 0.21 vs. rest). Ligament constructs were treated for 7 days with medium supplemented with serum obtained at rest (RestTx) or 15 min post-exercise (ExTx), before tensile testing and collagen content analysis. Compared with RestTx, ExTx enhanced collagen content (+19%; 181 ± 33 vs. 215 ± 40 μg per construct P = 0.001) and ligament mechanical properties -maximal tensile load (+17%, P = 0.03 vs. RestTx) and ultimate tensile strength (+10%, P = 0.15 vs. RestTx). In a separate set of engineered ligaments, recombinant IGF-1, but not GH, enhanced collagen content and mechanics. Bioassays in 2D culture revealed that acute treatment with post-exercise serum activated mTORC1 and ERK1/2. In conclusion, the post-exercise biochemical milieu, but not recombinant GH, enhances collagen content and tensile strength of engineered ligaments, in association with mTORC1 and ERK1/2 activation.

BackgroundWe implemented a high-protein diet (2 g·kg−1·d−1) throughout 12 weeks of concurrent exercise training to determine whether interferences to adaptation in muscle hypertrophy, strength and power could be attenuated compared to resistance training alone.MethodsThirty-two recreationally active males (age: 25 ± 5 years, body mass index: 24 ± 3 kg·m−2; mean ± SD) performed 12 weeks of either isolated resistance (RES; n = 10) or endurance (END; n = 10) training (three sessions·w−1), or concurrent resistance and endurance (CET; n = 12) training (six sessions·w−1). Maximal strength (1RM), body composition and power were assessed pre- and post-intervention.ResultsLeg press 1RM increased ~ 24 ± 13% and ~ 33 ± 16% in CET and RES from PRE-to-POST (P < 0.001), with no difference between groups. Total lean mass increased ~ 4% in both CET and RES from PRE-to-POST (P < 0.001). Ultrasound estimated vastus lateralis volume increased ~ 15% in CET and ~ 11% in RES from PRE-to-POST (P < 0.001), with no difference between groups. Wingate peak power relative to body mass displayed a trend (P = 0.053) to be greater in RES (12.5 ± 1.6 W·kg BM−1) than both CET (10.8 ± 1.7 W·kg BM−1) and END (10.9 ± 1.8 W·kg BM−1) at POST. Absolute VO2peak increased 6.9% in CET and 12% in END from PRE-to-POST (P < 0.05), with no difference between groups.ConclusionDespite high protein availability, select measures of anaerobic power-based adaptations, but not muscle strength or hypertrophy, appear susceptible to ‘interference effects’ with CET and should be closely monitored throughout training macro-cycles.Trials Registry: This trial was registered with the Australian-New Zealand Clinical Trials Registry (ACTRN12617001229369).Electronic supplementary materialThe online version of this article (10.1007/s40279-018-0999-9) contains supplementary material, which is available to authorized users.

Human skeletal muscle satellite cells are activated in response to both resistance and endurance exercise. It was initially proposed that satellite cell proliferation and differentiation were only required to support resistance exercise-induced hypertrophy. However, satellite cells may also play a role in muscle fibre remodelling after endurance-based exercise and extracellular matrix regulation. Given the importance of dietary protein, particularly branched chain amino acids, in supporting myofibrillar and mitochondrial adaptations to both resistance and endurance-based training, a greater understanding of how protein intake impacts satellite cell activity would provide further insight into the mechanisms governing skeletal muscle remodelling with exercise. While many studies have investigated the capacity for protein ingestion to increase post-exercise rates of muscle protein synthesis, few investigations have examined the role for protein ingestion to modulate satellite cell activity. Here we review the molecular mechanisms controlling the activation of satellite cells in response to mechanical stress and protein intake in both in vitro and in vivo models. We provide a mechanistic framework that describes how protein ingestion may enhance satellite activity and promote exercise adaptations in human skeletal muscle.

Concurrent exercise training has been suggested to create an ‘interference effect,’ attenuating resistance training-based skeletal muscle adaptations, including myofibre hypertrophy. Satellite cells support myofibre hypertrophy and are influenced by exercise mode. To determine whether satellite cells contribute to the ‘interference effect’ changes in satellite cell and myonuclear content were assessed following a period of training in 32 recreationally active males (age: 25 ± 5 year; body mass index: 24 ± 3 kg⋅m–2; mean ± SD) who undertook 12-week of either isolated (3 d⋅w–1) resistance (RES; n = 10), endurance (END; n = 10), or alternate day (6 d⋅w–1) concurrent (CET, n = 12) training. Skeletal muscle biopsies were obtained pre-intervention and after 2, 8, and 12 weeks of training to determine fibre type-specific cross-sectional area (CSA), satellite cell content (Pax7+DAPI+), and myonuclei (DAPI+) using immunofluorescence microscopy. After 12 weeks, myofibre CSA increased in all training conditions in type II (P = 0.0149) and mixed fibres (P = 0.0102), with no difference between conditions. Satellite cell content remained unchanged after training in both type I and type II fibres. Significant correlations were observed between increases in fibre type-specific myonuclear content and CSA of Type I (r = 0.63, P &lt; 0.0001), Type II (r = 0.69, P &lt; 0.0001), and mixed fibres (r = 0.72, P &lt; 0.0001). Resistance, endurance, and concurrent training induce similar myofibre hypertrophy in the absence of satellite cell and myonuclear pool expansion. These findings suggest that myonuclear accretion via satellite cell fusion is positively correlated with hypertrophy after 12 weeks of concurrent training, and that individuals with more myonuclear content displayed greater myofibre hypertrophy.

Purpose: To investigate strength and structural adaptations after 12 weeks of resistance, endurance cycling, and concurrent training. Methods: Thirty-two healthy males undertook 12 weeks of resistance-only (RT; n = 10), endurance-only (END; n = 10), or concurrent resistance and endurance training (CONC; n = 12). Biceps femoris long head (BFlh) architecture, strength (3-lift 1-repetition maximum), and body composition were assessed. Results: Fascicle length of the BFlh reduced 15% (6%) (P < .001) and 9% (6%) (P < .001) in the END and CONC groups postintervention, with no change in the RT group (−4% [11%], P = .476). All groups increased BFlh pennation angle (CONC: 18% [9%], RT: 14% [8%], and END: 18% [10%]). Thickness of the BFlh increased postintervention by 7% (6%) (P = .002) and 7% (7%) (P = .003) in the CONC and RT groups, respectively, but not in the END group (0% [3%], P = .994). Both the CONC and RT groups significantly increased by 27% (11%) (P < .001) and 33% (12%) (P < .001) in 3-lift totals following the intervention, with no changes in the END cohort (6% [6%], P = .166). No significant differences were found for total body (CONC: 4% [2%], RT: 4% [2%], and END: 3% [2%]) and leg (CONC: 5% [3%], RT: 6% [3%], and END: 5% [3%]) fat-free mass. Conclusions: Twelve weeks of RT, END, or CONC significantly modified BFlh architecture. This study suggests that conventional resistance training may dampen BFlh fascicle shortening from cycling training while increasing strength simultaneously in concurrent training. Furthermore, the inclusion of a cycle endurance training stimulus may result in alterations to hamstring architecture that increase the risk of future injury. Therefore, the incorporation of endurance cycling training within concurrent training paradigms should be reevaluated when trying to modulate injury risk.