Riki Ogasawara

Effects of low‐intensity bench press training with restricted arm muscle blood flow on chest muscle hypertrophy: a pilot study

Single‐joint resistance training with blood flow restriction (BFR) results in significant increases in arm or leg muscle size and single‐joint strength. However, the effect of multijoint BFR training on both blood flow restricted limb and non‐restricted trunk muscles remain poorly understood. To examine the impact of BFR bench press training on hypertrophic response to non‐restricted (chest) and restricted (upper‐arm) muscles and multi‐joint strength, 10 young men were randomly divided into either BFR training (BFR‐T) or non‐BFR training (CON‐T) groups. They performed 30% of one repetition maximal (1‐RM) bench press exercise (four sets, total 75 reps) twice daily, 6 days week−1 for 2 weeks. During the exercise session, subjects in the BFR‐T group placed elastic cuffs proximally on both arms, with incremental increases in external compression starting at 100 mmHg and ending at 160 mmHg. Before and after the training, triceps brachii and pectoralis major muscle thickness (MTH), bench press 1‐RM and serum anabolic hormones were measured. Two weeks of training led to a significant increase (P<0.05) in 1‐RM bench press strength in BFR‐T (6%) but not in CON‐T (−2%). Triceps and pectoralis major MTH increased 8% and 16% (P<0.01), respectively, in BFR‐T, but not in CON‐T (−1% and 2%, respectively). There were no changes in baseline concentrations of anabolic hormones in either group. These results suggest that BFR bench press training leads to significant increases in muscle size for upper arm and chest muscles and 1‐RM strength.

Increases in Thigh Muscle Volume and Strength by Walk Training with Leg Blood Flow Reduction in Older Participants

We examined the effects of walk training combined with leg blood flow reduction (BFR) on muscle hypertrophy as well as on peak oxygen uptake (VO₂ peak) in older individuals. Both the BFR walk training (BFR-Walk, n = 10, age; 64 ± 1 years, body mass index [BMI]; 22.5 ± 0.9 kg/m²) and control walk training (CON-Walk, n = 8, age; 68 ± 1 years, BMI; 23.2 ± 1.0 kg/m²) groups performed 20 minutes of treadmill walking at an exercise intensity of 45% of heart rate reserve, 4 days per week, for 10 weeks. The BFR-Walk group wore pressure belts (160-200 mm Hg) on both legs during training. After the training, magnetic resonance imaging-measured thigh muscle cross-sectional area (3.1%, p < .01) and muscle volume (3.7%, p < .01) as well as maximal isometric (5.9%, p < .05) and isokinetic (up to 22%, p < .01) strength increased in the BFR-Walk group, but not in the CON-Walk group. Estimated VO₂ peak during a bicycle graded exercise test increased (p < .05) and correlated with oxygen pulse in both groups. In conclusion, BFR walk training improves both muscle volume and strength in older women.

mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle.

Resistance training-induced muscle anabolism and subsequent hypertrophy occur most rapidly during the early phase of training and become progressively slower over time. Currently, little is known about the intracellular signaling mechanisms underlying changes in the sensitivity of muscles to training stimuli. We investigated the changes in the exercise-induced phosphorylation of hypertrophic signaling proteins during chronic resistance training and subsequent detraining. Male rats were divided into four groups: 1 bout (1B), 12 bouts (12B), 18 bouts (18B), and detraining (DT). In the DT group, rats were subjected to 12 exercise sessions, detrained for 12 days, and then were subjected to 1 exercise session before being killed. Isometric training consisted of maximum isometric contraction, which was produced by percutaneous electrical stimulation of the gastrocnemius muscle every other day. Muscles were removed 24 h after the final exercise session. Levels of total and phosphorylated p70S6K, 4E-BP1, rpS6, and p90RSK levels were measured, and phosphorylation of p70S6K, rpS6, and p90RSK was elevated in the 1B group compared with control muscle (CON) after acute resistance exercise, whereas repeated bouts of exercise suppressed those phosphorylation in both 12B and 18B groups. Interestingly, these phosphorylation levels were restored after 12 days of detraining in the DT group. On the contrary, phosphorylation of 4E-BP1 was not altered with chronic training and detraining, indicating that, with chronic resistance training, anabolic signaling becomes less sensitive to resistance exercise stimuli but is restored after a short detraining period.

Relationship between limb and trunk muscle hypertrophy following high-intensity resistance training and blood flow-restricted low-intensity resistance training

We examined the relationship between training‐induced limb and trunk muscle hypertrophy in high‐intensity resistance training (HIT) or blood flow–restricted low‐intensity resistance training (LI‐BFR) programmes. Thirty young men were divided into three groups: HIT (n = 10), LI‐BFR (n = 10) and non‐training control (CON, n = 10). The HIT and LI‐BFR groups performed 75% and 30%, respectively, of one‐repetition maximal (1‐RM) bench press exercise, 3 days per week for 6 weeks. During the training sessions, the LI‐BFR group wore elastic cuffs around the most proximal region of both arms. Muscle cross‐sectional area (CSA) and 1‐RM bench press strength were measured before and 3 days after the final training session. Total training volumes (lifting weight × number of repetitions) for all of the sessions were similar between the two training groups. The training led to a significant increase (P < 0·05) in bench press 1‐RM in the two training groups, but not in the CON group. Triceps brachii and pectoralis major muscle CSA increased 8·8% and 15·8% (P < 0·01), respectively, in the HIT group and 4·9% (P < 0·05) and 8·3% (P < 0·01), respectively, in the LI‐BFR group, but not in the CON group (−1·1% and 0·0%, respectively). There was significant correlation (r = 0·70, P < 0·05) between increases in triceps brachii and pectoralis major muscle CSA in the HIT group; however, the correlation was lower and non‐significant in the LI‐BFR group (r = 0·54). Our results suggest that limb and trunk muscle hypertrophy occurs simultaneously during HIT but not during LI‐BFR, possibly owing to individual differences in activation of the arm and chest muscles during the training sessions.

Effect of very low-intensity resistance training with slow movement on muscle size and strength in healthy older adults

We previously reported that low‐intensity [50% of one repetition maximum (1RM)] resistance training with slow movement and tonic force generation (LST) causes muscle hypertrophy and strength gain in older participants. The aim of this study was to determine whether resistance training with slow movement and much more reduced intensity (30%1RM) increases muscle size and strength in older adults. Eighteen participants (60–77 years) were randomly assigned to two groups. One group performed very low‐intensity (30% 1RM) knee extension exercise with continuous muscle contraction (LST: 3‐s eccentric, 3‐s concentric, and 1‐s isometric actions with no rest between each repetition) twice a week for 12 weeks. The other group underwent intermitted muscle contraction (CON: 1‐s concentric and 1‐s eccentric actions with 1‐s rest between each repetition) for the same time period. The 1RM, isometric and isokinetic strengths, and cross‐sectional image of the mid‐thigh obtained by magnetic resonance imaging were examined before and after the intervention. LST significantly increased the cross‐sectional area of the quadriceps muscle (5·0%, P<0·001) and isometric and isokinetic knee extension strengths (P<0·05). CON failed to increase muscle size (1·1%, P = 0·12), but significantly improved its strength (P<0·05). These results indicate that even if the intensity is as low as 30% 1RM, LST can increase muscle size and strength in healthy older adults. The large total contraction time may be related to muscle hypertrophy and strength gain. LST would be useful for preventing sarcopenia in older individuals.

Ursolic acid stimulates mTORC1 signaling after resistance exercise in rat skeletal muscle

A recent study identified ursolic acid (UA) as a potent stimulator of muscle protein anabolism via PI3K/Akt signaling, thereby suggesting that UA can increase Akt-independent mTOR complex 1 (mTORC1) activation induced by resistance exercise via Akt signaling. The purpose of the present study was to investigate the effect of UA on resistance exercise-induced mTORC1 activation. The right gastrocnemius muscle of male Sprague-Dawley rats aged 11 wk was isometrically exercised via percutaneous electrical stimulation (stimulating ten 3-s contractions per set for 5 sets), while the left gastrocnemius muscle served as the control. UA or placebo (PLA; corn oil only) was injected intraperitoneally immediately after exercise. The rats were killed 1 or 6 h after the completion of exercise and the target tissues removed immediately. With placebo injection, the phosphorylation of p70(S6K) at Thr(389) increased 1 h after resistance exercise but attenuated to the control levels 6 h after the exercise. On the other hand, the augmented phosphorylation of p70(S6K) was maintained even 6 h after exercise when UA was injected immediately after exercise. A similar trend of prolonged phosphorylation was observed in PRAS40 Thr(246), whereas UA alone or resistance exercise alone did not alter its phosphorylation level at 6 h after intervention. These results indicate that UA is able to sustain resistance exercise-induced mTORC1 activity.

The order of concurrent endurance and resistance exercise modifies mTOR signaling and protein synthesis in rat skeletal muscle

Concurrent training, a combination of endurance (EE) and resistance exercise (RE) performed in succession, may compromise the muscle hypertrophic adaptations induced by RE alone. However, little is known about the molecular signaling interactions underlying the changes in skeletal muscle adaptation during concurrent training. Here, we used an animal model to investigate whether EE before or after RE affects the molecular signaling associated with muscle protein synthesis, specifically the interaction between RE-induced mammalian target of rapamycin complex 1 (mTORC1) signaling and EE-induced AMP-activated protein kinase (AMPK) signaling. Male Sprague-Dawley rats were divided into five groups: an EE group (treadmill, 25 m/min, 60 min), an RE group (maximum isometric contraction via percutaneous electrical stimulation for 3 × 10 s, 5 sets), an EE before RE group, an EE after RE group, and a nonexercise control group. Phosphorylation of p70S6K, a marker of mTORC1 activity, was significantly increased 3 h after RE in both the EE before RE and EE after RE groups, but the increase was smaller in latter. Furthermore, protein synthesis was greatly increased 6 h after RE in the EE before RE group. Increases in the phosphorylation of AMPK and Raptor were observed only in the EE after RE group. Akt and mTOR phosphorylation were increased in both groups, with no between-group differences. Our results suggest that the last bout of exercise dictates the molecular responses and that mTORC1 signaling induced by any prior bout of RE may be downregulated by a subsequent bout of EE.

Time course for arm and chest muscle thickness changes following bench press training.

The purpose of this study was to investigate the time course of hypertrophic adaptations in both the upper arm and trunk muscles following high-intensity bench press training. Seven previously untrained young men (aged 25 ± 3 years) performed free-weight bench press training 3 days (Monday, Wednesday and Friday) per week for 24 weeks. Training intensity and volume were set at 75% of one repetition maximum (1-RM) and 30 repetitions (3 sets of 10 repetitions, with 2-3 min of rest between sets), respectively. Muscle thickness (MTH) was measured using B-mode ultrasound at three sites: the biceps and triceps brachii and the pectoralis major. Measurements were taken a week prior to the start of training, before the training session on every Monday and 3 days after the final training session. Pairwise comparisons from baseline revealed that pectoralis major MTH significantly increased after week-1 (p = 0.002), triceps MTH increased after week-5 (p = 0.001) and 1-RM strength increased after week-3 (p = 0.001) while no changes were observed in the biceps MTH from baseline. Significant muscle hypertrophy was observed earlier in the chest compared to that of the triceps. Our results indicate that the time course of the muscle hypertrophic response differs between the upper arm and chest.

The role of mTOR signalling in the regulation of skeletal muscle mass in a rodent model of resistance exercise.

Resistance exercise (RE) activates signalling by the mammalian target of rapamycin (mTOR), and it has been suggested that rapamycin-sensitive mTOR signalling controls RE-induced changes in protein synthesis, ribosome biogenesis, autophagy, and the expression of peroxisome proliferator gamma coactivator 1 alpha (PGC-1α). However, direct evidence to support the aforementioned relationships is lacking. Therefore, in this study, we investigated the role of rapamycin-sensitive mTOR in the RE-induced activation of muscle protein synthesis, ribosome biogenesis, PGC-1α expression and hypertrophy. The results indicated that the inhibition of rapamycin-sensitive mTOR could prevent the induction of ribosome biogenesis by RE, but it only partially inhibited the activation of muscle protein synthesis. Likewise, the inhibition of rapamycin-sensitive mTOR only partially blocked the hypertrophic effects of chronic RE. Furthermore, both acute and chronic RE promoted an increase in PGC-1α expression and these alterations were not affected by the inhibition of rapamycin-sensitive mTOR. Combined, the results from this study not only establish that rapamycin-sensitive mTOR plays an important role in the RE-induced activation of protein synthesis and the induction of hypertrophy, but they also demonstrate that additional (rapamycin-sensitive mTOR-independent) mechanisms contribute to these fundamentally important events.

Effects of periodic and continued resistance training on muscle CSA and strength in previously untrained men.

To determine muscle adaptations to retraining after short‐term detraining, we examined the effects of continuous and interrupted resistance training on muscle size and strength in previously untrained men. Fifteen young men were divided into continuous training (CTr) or retraining (RTr) groups and performed high‐intensity bench press training. The CTr group trained continuously for 15 weeks, while the RTr group trained for 6 weeks, stopped for a 3‐week detraining period and resumed training at week 10. After the initial training phase, increases (P<0·01) in one repetition maximum (1‐RM) and magnetic resonance imaging‐measured triceps brachii and pectorals major muscle cross‐sectional areas (CSAs) were similar in both groups. Muscle CSA and 1‐RM increased (P<0·05) continuously for the CTr group, but the muscle adaptations were lower (P<0·05) after the last 6‐week training period than after the initial phase. In the RTr group, there were no significant decreases in muscle CSA and 1‐RM after the 3‐week detraining period, and increases in muscle CSA after retraining were similar to those observed after initial training. Ultimately, improvements in 1‐RM and muscle CSA in both groups were similar after the 15‐week training period. Our results suggest that compared with continuous 15‐week training, 3‐week detraining does not inhibit muscle adaptations.