Based on the present data, maximum muscle strength may be optimized by specific training methods (i.e., HL-RT) while both HL- and BFR-RT seem equally effective in increasing muscle mass. Importantly, BFR-RT is a valid and effective approach for increasing muscle strength in a wide spectrum of ages and physical capacity, although it may seem particularly of interest for those individuals with physical limitations to engage in HL-RT.

Key pointsr Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown.r 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.r Muscle damage (Z-band streaming) was the highest during post-RE recovery at T1, lower at T2 and minimal at T3.r 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.r We conclude that muscle hypertrophy is the result of accumulated intermittent increases in MyoPS mainly after a progressive attenuation of muscle damage.Abstract Skeletal muscle hypertrophy is one of the main outcomes of resistance training (RT), but how hypertrophy is modulated and the mechanisms regulating it are still unknown. To investigate how muscle hypertrophy is modulated through RT, we measured day-to-day integrated myofibrillar protein synthesis (MyoPS) using deuterium oxide and assessed muscle damage at the beginning (T1), at 3 weeks (T2) and at 10 weeks of RT (T3). Ten young men (27 (1) years, mean (SEM)) had muscle biopsies (vastus lateralis) taken to measure integrated MyoPS and muscle damage (Z-band streaming and indirect parameters) before, and 24 h and 48 h post resistance exercise (post-RE) at T1, T2 and T3. Fibre cross-sectional area (fCSA) was evaluated using biopsies at T1, T2 and T3. Increases in fCSA were observed only at T3 (P = 0.017). Changes in MyoPS post-RE at T1, T2 and T3 were greater at T1 (P < 0.03) than at T2 and T3 (similar values between T2 and T3). Muscle damage was the highest during post-RE recovery at T1, attenuated at T2 and further attenuated at T3. The change in MyoPS post-RE at both T2 and T3, but not at T1, was strongly correlated (r 0.9, P < 0.04) with muscle hypertrophy. Initial MyoPS response post-RE in an RT programme is not directed to support muscle hypertrophy, coinciding with the greatest muscle damage. However, integrated MyoPS is quickly 'refined' by 3 weeks of RT, and is related to muscle hypertrophy. We conclude that muscle hypertrophy is the result of accumulated intermittent changes in MyoPS post-RE in RT, which coincides with progressive attenuation of muscle damage.

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.

We propose that early RT-induced increases in muscle CSA in untrained young individuals are not purely hypertrophy, since there is concomitant edema-induced muscle swelling, probably due to muscle damage, which may account for a large proportion of the increase. Therefore, muscle CSA increases (particularly early in an RT program) should not be labeled as hypertrophy without some concomitant measure of muscle edema/damage.

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.