Felipe Damas

The placebo effect is a psychobiological response capable of influencing physical performance. Although its impact in sports settings is well documented, few studies have investigated whether a placebo effect exists for resistance training (RT)-induced muscle strength and mass changes. This study examined whether strategies involving external motivational feedback can affect the effectiveness of RT potentiating muscle strength and lean mass gains in untrained individuals. Thirty-one volunteers (25.9 ± 4.4 years, 13 women) were assigned to either a PLACEBO group (with external motivational feedback strategies) or a N-PLACEBO group (no external motivational feedback strategies). Both groups followed the same 14-week RT protocol, but with individual load progression. Muscle strength was assessed via one-repetition maximum (1 RM), and changes in lean mass of the thigh and hip via dual-energy x-ray absorptiometry (DEXA), before (pre) and after (post) RT. A two-way repeated measures ANOVA showed significant pre-to-post increases in 1 RM and lean mass in both groups (main effect of time, p < 0.001), but no significant group-by-time interaction for muscle strength or lean mass ( p > 0.05). We conclude that external motivational feedback strategies did not yield additional gains in muscle strength or lean mass of the thigh and hip in untrained individuals. Therefore, no placebo effect was observed for the analyzed outcomes.

Background: Skeletal muscle adaptations are affected by resistance training (RT)-induced acute and chronic transcriptional responses. An under-explored gene target involved in mechanotransduction is the expression of the G protein-coupled receptor 56 (GPR56). However, studies investigating the acute and chronic effects of RT manipulations on GPR56 mRNA are scarce. Methods: Twenty subjects had each leg randomly assigned to a standard ((CON) no specific manipulation) or a variable RT (manipulations in load, volume, muscle action, and pause in a session-by-session fashion (VAR)). GPR56 mRNA expression was assessed before and after 16 training sessions (chronic effect) and 24 h after a 17th session (acute effect). Results: Acute GPR56 mRNA expression increased at 24 h (p < 0.01) without differences between CON and VAR (p > 0.05). No differences were found in GPR56 mRNA expression when comparing each VAR condition (load vs. sets vs. eccentric actions vs. pause) nor with CON at 24 h (p > 0.05). Chronic GPR56 mRNA expression increased at Post compared with Pre (p < 0.02) for VAR only, with a tendency (p = 0.058) toward higher expression for VAR as compared with CON. Conclusion: GPR56 mRNA expression is acutely and chronically modulated by RT. Additionally, chronic GPR56 mRNA expression is modulated by RT variable manipulations.

The current study examined the acute effects of a lower body resistance training (RT) session on physiological and thermoregulatory measures during a sub-maximal running protocol in the heat in heat-acclimatized men. Ten resistance-untrained men (age 27.4 ± 4.1 years; height 1.78 ± 0.06 m; body mass 76.8 ± 9.9 kg; peak oxygen uptake 48.2 ± 7.0 mL kg−1 min−1) undertook a high-intensity RT session at six-repetition maximum. Indirect muscle damage markers (i.e., creatine kinase [CK], delayed-onset muscle soreness [DOMS], and countermovement jump [CMJ]) were collected prior to, immediately post and 24 and 48 h after the RT session. The sub-maximal running protocol was performed at 70% of the ventilatory threshold, which was conducted prior to and 24 and 48 h following the RT session to obtain physiological and thermoregulatory measures. The RT session exhibited significant increases in DOMS (p < 0.05; effect size [ES]: 1.41–10.53), whilst reduced CMJ (p < 0.05; ES: − 0.79–1.41) for 48 h post-exercise. There were no differences in CK (p > 0.05), although increased with moderate to large ES (0.71–1.12) for 48 h post-exercise. The physiological cost of running was increased for up to 48 h post-exercise (p < 0.05) with moderate to large ES (0.50–0.84), although no differences were shown in thermoregulatory measures (p > 0.05) with small ES (0.33). These results demonstrate that a RT session impairs sub-maximal running performance for several days post-exercise, although thermoregulatory measures are unperturbed despite elevated muscle damage indicators in heat-acclimatized, resistance untrained men. Accordingly, whilst a RT session may not increase susceptibility to heat-related injuries in heat-acclimatized men during sub-maximal running in the heat, endurance sessions should be undertaken with caution for at least 48 h post-exercise following the initial RT session in resistance untrained men.

We aimed to investigate the mechanisms underlying muscle growth after 12 weeks of resistance training performed with blood flow restriction (RT–BFR) and high-intensity resistance training (HRT) in older individuals. Participants were allocated into the following groups: HRT, RT–BFR, or a control group. High-throughput transcriptome sequencing was performed by the Illumina HiSeq 2500 platform. HRT and RT–BFR presented similar increases in the quadriceps femoris cross-sectional area, and few genes were differently expressed between interventions. The small differences in gene expression between interventions suggest that similar mechanisms may underpin training-induced muscle growth.

Background Gene expression is an important process underpinning the acute and chronic adaptive response to resistance exercise (RE) training. Purpose To investigate the effect of training status on vastus lateralis muscle global transcriptome at rest and following acute RE. Methods Muscle biopsies of nine young men (age: 26(2) years; body mass: 69(9) kg; height 172(6) cm) who undertook RE training for 10 weeks were collected pre and 24 h post-RE in the untrained (W1) and trained (W10) states and analysed using microarray. Tests of differential expression were conducted for rested and after RE contrasts in both training states. To control for false discovery rate (FDR), multiple testing correction was performed at a cut-off of FDR < 0.05. Results Unaccustomed RE (at W1) upregulated muscle gene transcripts related to stress (e.g., heat shock proteins), damage and inflammation, structural remodelling, protein turnover and increased translational capacity. Trained muscles (at W10) showed changes in the transcriptome signature regarding the regulation of energy metabolism, favouring a more oxidative one, upregulated antioxidant- and immune-related genes/terms, and gene transcripts related to the cytoskeleton and extracellular matrix, muscle contraction, development and growth. Conclusions These results highlight that chronic repetition of RE changes muscle transcriptome response towards a more refined response to RE-induced stress.

Introduction: The myonuclear domain theory postulates that myonuclei are added to muscle fibers when increases in fiber cross-sectional area (i.e., hypertrophy) are ≥26%. However, recent studies have reported increased myonuclear content with lower levels (e.g., 12%) of muscle fiber hypertrophy.Purpose: This study aimed to determine whether a muscle fiber hypertrophy “threshold” is required to drive the addition of new myonuclei to existing muscle fibers.Methods: Studies of resistance training endurance training with or without nutrient (i.e., protein) supplementation and steroid administration with measures of muscle fiber hypertrophy and myonuclei number as primary or secondary outcomes were considered. Twenty-seven studies incorporating 62 treatment groups and 903 subjects fulfilled the inclusion criteria and were included in the analyses.Results: Muscle fiber hypertrophy of ≤10% induces increases in myonuclear content, although a significantly higher number of myonuclei are observed when muscle hypertrophy is ~22%. Additional analyses showed that age, sex, and muscle fiber type do not influence muscle fiber hypertrophy or myonuclei addition.Conclusions: Although a more consistent myonuclei addition occurs when muscle fiber hypertrophy is >22%, our results challenge the concept of a muscle hypertrophy threshold as significant myonuclei addition occurs with lower muscle hypertrophy (i.e., <10%).

Doma, K, Leicht, A, Sinclair, W, Schumann, M, Damas, F, Burt, D, and Woods, C. Impact of exercise-induced muscle damage on performance test outcomes in elite female basketball players. J Strength Cond Res 32(6): 1731–1738, 2018—The purpose of this study was 2-fold: first, to examine the impact of exercise-induced muscle damage (EIMD) on physical fitness qualities after a basketball-specific training session; second, to determine the reproducibility of the sport-specific performance measures in elite female basketball players. Ten elite female basketball players (age 25.6 ± 4.5 years; height 1.8 ± 0.7 m; and body mass 76.7 ± 8.3 kg) undertook a 90-minute training session involving repeated jumping, sprinting, and game-simulated training. Indirect muscle damage markers (i.e., countermovement jump, delayed onset of muscle soreness [DOMS], and creatine kinase [CK]) and sport-specific performances (i.e., change-of-direction [COD] test and suicide test [ST]) were measured before and 24 hours after training. These measures were also collected 1 week after training to determine the reproducibility of the basketball-specific performance measures. A significant reduction in lower-body power (−3.5 ± 3.6%; p ≤ 0.05), while a significant increase in DOMS (46.7 ± 26.3%; p ≤ 0.05) and CK (57.6 ± 23.1%; p ≤ 0.05) was observed 24 hours after exercise. The ST was also significantly increased (2.1 ± 1.8%; p ≤ 0.05), although no difference was observed for COD (0.1 ± 2.0%; p > 0.05). The intraclass correlation coefficient and coefficient of variation for the COD and ST were 0.81 and 0.90, respectively, and 1.9 and 1.5%, respectively. In conclusion, appropriate recovery should be considered the day after basketball-specific training sessions in elite basketball players. Furthermore, this study showed the usability of performance measures to detect changes during periods of EIMD, with acceptable reproducibility and minimal measurement error.

Satellite cells (SC) are associated with skeletal muscle remodelling after muscle damage and/or extensive hypertrophy resulting from resistance training (RT). We recently reported that early increases in muscle protein synthesis (MPS) during RT appear to be directed toward muscle damage repair, but MPS contributes to hypertrophy with progressive muscle damage attenuation. However, modulations in acute-chronic SC content with RT during the initial (1^st-wk: high damage), early (3^rd-wk: attenuated damage), and later (10^th-wk: no damage) stages is not well characterized. Ten young men (27 ± 1 y, 23.6 ± 1.0 kg·m^-2) underwent 10-wks of RT and muscle biopsies (vastus-lateralis) were taken before (Pre) and post (48h) the 1^st (T1), 5^th (T2) and final (T3) RT sessions to evaluate fibre type specific SC content, cross-sectional area (fCSA) and myonuclear number by immunohistochemistry. We observed RT-induced hypertrophy after 10-wks of RT (fCSA increased ~16% in type II, P < 0.04; ~8% in type I [ns]). SC content increased 48h post-exercise at T1 (~69% in type I [P = 0.014]; ~42% in type II [ns]), and this increase was sustained throughout RT (pre T2: ~65%, ~92%; pre T3: ~30% [ns], ~87%, for the increase in type I and II, respectively, vs. pre T1 [P < 0.05]). Increased SC content was not coupled with changes in myonuclear number. SC have a more pronounced role in muscle repair during the initial phase of RT than muscle hypertrophy resulted from 10-wks RT in young men. Chronic elevated SC pool size with RT is important providing proper environment for future stresses or larger fCSA increases.

Resistance training (RT)-induced skeletal muscle hypertrophy is a highly intricate process. Despite substantial advances, we are far from understanding exactly how muscle hypertrophy develops during RT. The aim of the present review is to discuss new insights related to the role of skeletal muscle damage and muscle protein synthesis (MPS) in mediating RT-induced hypertrophy. Specifically, the thesis that in the early phase of RT (≤ 4 previous RT sessions) increases in muscle cross-sectional area are mostly attributable to muscle damage-induced muscle swelling; then (after ~ 10 sessions), a modest magnitude of muscle hypertrophy ensues; but only during a latter phase of RT (after ~ 18 sessions) is true muscle hypertrophy observed. We argue that the initial increases in MPS post-RT are likely directed to muscle repair and remodelling due to damage, and do not correlate with eventual muscle hypertrophy induced by several RT weeks. Increases in MPS post-RT session only contribute to muscle hypertrophy after a progressive attenuation of muscle damage, and even more significantly when damage is minimal. Furthermore, RT protocols that do not promote significant muscle damage still induce similar muscle hypertrophy and strength gains compared to conditions that do promote initial muscle damage. Thus, we conclude that muscle damage is not the process that mediates or potentiates RT-induced muscle hypertrophy.

Low-load resistance training (< 50% of one-repetition maximum [1RM]) associated with blood-flow restriction (BFR-RT) has been thought to promote increases in muscle strength and mass. However, it remains unclear if the magnitude of these adaptations is similar to conventional high-load resistance training (> 65% 1RM; HL-RT).