Felipe Damas

Resistance training‐induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage

Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown. We show that changes in myofibrillar protein synthesis (MyoPS) after an initial resistance exercise (RE) bout in the first week of RT (T1) were greater than those seen post‐RE at the third (T2) and tenth week (T3) of RT, with values being similar at T2 and T3. Muscle damage (Z‐band streaming) was the highest during post‐RE recovery at T1, lower at T2 and minimal at T3. When muscle damage was the highest, so was the integrated MyoPS (at T1), but neither were related to hypertrophy; however, integrated MyoPS at T2 and T3 were correlated with hypertrophy. We conclude that muscle hypertrophy is the result of accumulated intermittent increases in MyoPS mainly after a progressive attenuation of muscle damage.

A Review of Resistance Training-Induced Changes in Skeletal Muscle Protein Synthesis and Their Contribution to Hypertrophy

Muscle protein synthesis (MPS) is stimulated by resistance exercise (RE) and is further stimulated by protein ingestion. The summation of periods of RE-induced increases in MPS can induce hypertrophy chronically. As such, studying the response of MPS with resistance training (RT) is informative, as adaptations in this process can modulate muscle mass gain. Previous studies have shown that the amplitude and duration of increases in MPS after an acute bout of RE are modulated by an individual’s training status. Nevertheless, it has been shown that the initial responses of MPS to RE and nutrition are not correlated with subsequent hypertrophy. Thus, early acute responses of MPS in the hours after RE, in an untrained state, do not capture how MPS can affect RE-induced muscle hypertrophy. The purpose of this review is provide an in-depth understanding of the dynamic process of muscle hypertrophy throughout RT by examining all of the available data on MPS after RE and in different phases of an RT programme. Analysis of the time course and the overall response of MPS is critical to determine the potential protein accretion after an RE bout. Exercise-induced increases in MPS are shorter lived and peak earlier in the trained state than in the untrained state, resulting in a smaller overall muscle protein synthetic response in the trained state. Thus, RT induces a dampening of the MPS response, potentially limiting protein accretion, but when this occurs remains unknown.

Comparisons Between Low-intensity Resistance Training With Blood Flow Restriction and High-intensity Resistance Training on Quadriceps Muscle Mass and Strength in Elderly

Abstract Vechin, FC, Libardi, CA, Conceição, MS, Damas, FR, Lixandrão, ME, Berton, RPB, Tricoli, VAA, Roschel, HA, Cavaglieri, CR, Chacon-Mikahil, MPT, and Ugrinowitsch, C. Comparisons between low-intensity resistance training with blood flow restriction and high-intensity resistance training on quadriceps muscle mass and strength in elderly. J Strength Cond Res 29(4): 1071–1076, 2015—High-intensity resistance training (HRT) has been recommended to offset age-related loss in muscle strength and mass. However, part of the elderly population is often unable to exercise at high intensities. Alternatively, low-intensity resistance training with blood flow restriction (LRT-BFR) has emerged. The purpose of this study was to compare the effects of LRT-BFR and HRT on quadriceps muscle strength and mass in elderly. Twenty-three elderly individuals, 14 men and 9 women (age, 64.04 ± 3.81 years; weight, 72.55 ± 16.52 kg; height, 163 ± 11 cm), undertook 12 weeks of training. Subjects were ranked according to their pretraining quadriceps cross-sectional area (CSA) values and then randomly allocated into one of the following groups: (a) control group, (b) HRT: 4 × 10 repetitions, 70–80% one repetition maximum (1RM), and (c) LRT-BFR: 4 sets (1 × 30 and 3 × 15 repetitions), 20–30% 1RM. The occlusion pressure was set at 50% of maximum tibial arterial pressure and sustained during the whole training session. Leg press 1RM and quadriceps CSA were evaluated at before and after training. A mixed-model analysis was performed, and the significance level was set at p ⩽ 0.05. Both training regimes were effective in increasing pre- to post-training leg press 1RM (HRT: ∼54%, p < 0.001; LRT-BFR: ∼17%, p = 0.067) and quadriceps CSA (HRT: 7.9%, p < 0.001; LRT-BFR: 6.6%, p < 0.001); however, HRT seems to induce greater strength gains. In summary, LRT-BFR constitutes an important surrogate approach to HRT as an effective training method to induce gains in muscle strength and mass in elderly.

Time Course of Resistance Training-Induced Muscle Hypertrophy in the Elderly.

Abstract Lixandrão, ME, Damas, F, Chacon-Mikahil, MPT, Cavaglieri, CR, Ugrinowitsch, C, Bottaro, M, Vechin, FC, Conceição, MS, Berton, R, and Libardi, CA. Time course of resistance training–induced muscle hypertrophy in the elderly. J Strength Cond Res 30(1): 159–163, 2016—Extended periods of resistance training (RT) induce muscle hypertrophy. Nevertheless, to date, no study has investigated the time window necessary to observe significant changes in muscle cross-sectional area (CSA) in older adults. Therefore, this study investigated the time course of muscle hypertrophy after 10 weeks (20 sessions) of RT in the elderly. Fourteen healthy older subjects were randomly allocated in either the RT (n: 6) or control group (n: 8). The RT was composed of 4 sets × 10 repetitions (70–80% 1 repetition maximum [1RM]) in a leg press machine. The time course of vastus lateralis muscle hypertrophy (CSA) was assessed on a weekly basis by mode-B ultrasonography. Leg press muscle strength was assessed by dynamic 1RM test. Our results demonstrated that the RT group increased leg press 1RM by 42% (p ⩽ 0.05) after 10 weeks of training. Significant increases in vastus lateralis muscle CSA were observed only after 18 sessions of training (9 weeks; p ⩽ 0.05; 7.1%). In conclusion, our training protocol promoted muscle mass accrual in older subjects, and this was only observable after 18 sessions of RT (9 weeks).

Susceptibility to Exercise-Induced Muscle Damage: a Cluster Analysis with a Large Sample.

We investigated the responses of indirect markers of exercise-induced muscle damage (EIMD) among a large number of young men (N=286) stratified in clusters based on the largest decrease in maximal voluntary contraction torque (MVC) after an unaccustomed maximal eccentric exercise bout of the elbow flexors. Changes in MVC, muscle soreness (SOR), creatine kinase (CK) activity, range of motion (ROM) and upper-arm circumference (CIR) before and for several days after exercise were compared between 3 clusters established based on MVC decrease (low, moderate, and high responders; LR, MR and HR). Participants were allocated to LR (n=61), MR (n=152) and HR (n=73) clusters, which depicted significantly different cluster centers of 82%, 61% and 42% of baseline MVC, respectively. Once stratified by MVC decrease, all muscle damage markers were significantly different between clusters following the same pattern: small changes for LR, larger changes for MR, and the largest changes for HR. Stratification of individuals based on the magnitude of MVC decrease post-exercise greatly increases the precision in estimating changes in EIMD by proxy markers such as SOR, CK activity, ROM and CIR. This indicates that the most commonly used markers are valid and MVC orchestrates their responses, consolidating the role of MVC as the best EIMD indirect marker.

Pronounced energy restriction with elevated protein intake results in no change in proteolysis and reductions in skeletal muscle protein synthesis that are mitigated by resistance exercise

Preservation of lean body mass (LBM) may be important during dietary energy restriction (ER) and requires equal rates of muscle protein synthesis (MPS) and muscle protein breakdown (MPB). Currently, the relative contribution of MPS and MPB to the loss of LBM during ER in humans is unknown. We aimed to determine the impact of dietary protein intake and resistance exercise on MPS and MPB during a controlled short‐term energy deficit. Adult men (body mass index, 28.6 ± 0.6 kg/m2; age 22 ± 1 yr) underwent 10 d of 40%‐reduced energy intake while performing unilateral resistance exercise and consuming lower protein (1.2 g/kg/d, n = 12) or higher protein (2.4 g/kg/d, n = 12). Pre‐ and postintervention testing included dual‐energy X‐ray absorptiometry, primed constant infusion of ring‐[13C6]phenylalanine, and 15[N]phenylalanine to measure acute postabsorptive MPS and MPB; D2O to measure integrated MPS; and gene and protein expression. There was a decrease in acute MPS after ER (higher protein, 0.059 ± 0.006 to 0.051 ± 0.009%/h; lower protein, 0.061 ± 0.005 to 0.045 ± 0.006%/h; P < 0.05) that was attenuated with resistance exercise (higher protein, 0.067 ± 0.01%/h; lower protein, 0.061 ± 0.006%/h), and integrated MPS followed a similar pattern. There was no change in MPB (energy balance, 0.080 ± 0.01%/hr; ER rested legs, 0.078 ± 0.008%/hr; ER exercised legs, 0.079 ± 0.006%/hr). We conclude that a reduction in MPS is the main mechanism that underpins LBM loss early in ER in adult men.—Hector, A. J., McGlory, C., Damas, F., Mazara, N., Baker, S. K., Phillips, S. M. Pronounced energy restriction with elevated protein intake results in no change in proteolysis and reductions in skeletal muscle protein synthesis that are mitigated by resistance exercise. FASEB J. 32, 265‐275 (2018). www.fasebj.org

The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis

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.

An inability to distinguish edematous swelling from true hypertrophy still prevents a completely accurate interpretation of the time course of muscle hypertrophy.

the experimental design are important and described in the “Discussion” section of our article (Damas et al. 2015). The explanation the authors provide in the letter is already acknowledged in our manuscript: “Additionally, DeFreitas et al. (2011) speculated that the significant increase in muscle CSA that they found in the first week of RT in untrained individuals was possibly [italics added for emphasis] due to edema and could be falsely attributed to hypertrophy; thus, they considered that the increased CSA was indicative of hypertrophy only at week 3–4 (when it was different from week 1)”. Since DeFreitas et al. did not provide any measurement of edema it is not possible to estimate the degree of edema that was present at the third week of RT, and that was the main reason that we suggested they might have overestimated the degree of increase in muscle CSA. Importantly, the authors report an increase in muscle CSA of 5.95 % at week 3, leading the reader to believe that this was the actual magnitude of muscle hypertrophy. In their letter, on the other hand, they report (perhaps more appropriately and realistically, in our opinion) an increase in muscle CSA of around 2.41 % (under the assumption that an unchanged amount of edema of 3.45 % was present at this time), which was not clearly stated in their manuscript. In addition, the authors include in their original manuscript the minimal detectable statistical difference approach stating “...if an individual has a preto post-training increase in CSA that is less than 3.37 % [and estimate with an incredible degree of precision], then the change was not real. The change in that scenario could be attributed to the measurement error of the instrument. However, an increase in CSA greater than 3.37 % (in total change) should be attributed to the intervention, which is typically resistance training”. It seems then that a large assumption has been made by DeFreitas et al. that edema is a constant fraction of the CSA measurement and their Dear Editor,

Early- and later-phases satellite cell responses and myonuclear content with resistance training in young men

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 (1st-wk: high damage), early (3rd-wk: attenuated damage), and later (10th-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 1st (T1), 5th (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.

The repeated bout effect of traditional resistance exercises on running performance across three bouts

This study investigated the repeated bout effect of 3 typical lower body resistance-training sessions on maximal and submaximal effort running performance. Twelve resistance-untrained men (age, 24 ± 4 years; height, 1.81 ± 0.10 m; body mass, 79.3 ± 10.9 kg; peak oxygen uptake, 48.2 ± 6.5 mL·kg-1·min-1; 6-repetition maximum squat, 71.7 ± 12.2 kg) undertook 3 bouts of resistance-training sessions at 6-repetitions maximum. Countermovement jump (CMJ), lower-body range of motion (ROM), muscle soreness, and creatine kinase (CK) were examined prior to and immediately, 24 h (T24), and 48 h (T48) after each resistance-training bout. Submaximal (i.e., below anaerobic threshold (AT)) and maximal (i.e., above AT) running performances were also conducted at T24 and T48. Most indirect muscle damage markers (i.e., CMJ, ROM, and muscle soreness) and submaximal running performance were significantly improved (P < 0.05; 1.9%) following the third resistance-training bout compared with the second bout. Whilst maximal running performance was also improved following the third bout (P < 0.05; 9.8%) compared with other bouts, the measures were still reduced by 12%-20% versus baseline. However, the increase in CK was attenuated following the second bout (P < 0.05) with no further protection following the third bout (P > 0.05). In conclusion, the initial bout induced the greatest change in CK; however, at least 2 bouts were required to produce protective effects on other indirect muscle damage markers and submaximal running performance measures. This suggests that submaximal running sessions should be avoided for at least 48 h after resistance training until the third bout, although a greater recovery period may be required for maximal running sessions.