Impact of blood flow-restricted bodyweight exercise on skeletal muscle adaptations.

This study ascertains the ability of bodyweight blood flow-restricted (BFR) exercise training to promote skeletal muscle adaptations of significance for muscle accretion and metabolism. Six healthy young individuals (three males and three females) performed six weeks of bodyweight BFR training. Each session consisted of five sets of sit-to-stand BFR exercise to volitional failure with 30-second inter-set recovery. Prior to, and at least 72 h after training, muscle biopsies were taken from m. vastus lateralis to assess changes in fibre type-specific cross-sectional area (CSA), satellite cell (SC) and myonuclei content and capillarization, as well as mitochondrial protein expression. Furthermore, magnetic resonance imaging was used to assess changes in whole thigh muscle CSA. Finally, isometric knee extensor muscle strength was evaluated. An increase in knee extensor whole muscle CSA was observed at middle and distal localizations after training (3·2% and 3·5%, respectively) (P<0·05), and a trend was observed towards an increase in type I fibre CSA, whereas muscle strength did not increase. Additionally, the number of SCs and myonuclei associated with type I fibres increased by 65·7% and 20%, respectively (P<0·05). No significant changes were observed in measures of muscle capillarization and mitochondrial proteins. In conclusion, six weeks of bodyweight-based BFR exercise promoted myocellular adaptations related to muscle accretion, but not metabolic properties. Moreover, the study revealed that an appropriate total training volume needs further investigation before recommending bodyweight BFR to patient populations.

Effect of protein quality on recovery after intense resistance training.

PURPOSE: The present study investigated the effects of high- versus low-quality protein supplementation on the regain of exercise performance during recovery from a period of high-intensity resistance training. METHODS: In a diet-controlled crossover study, 12 resistance-trained participants performed two identical training periods, with each training period including four sessions of high-intensity resistance exercise during 5 days, while receiving either high- or low-quality protein. Prior to and at 3, 24 and 48 h after the training periods, performance was evaluated in knee extensor and flexor isometric maximal voluntary contraction (MVC), counter-movement jumping height (CMJ), and peak and mean anaerobic power. In addition, prior to and at 48 h after the training periods, performance in time-to-exhaustion at 70 % of VO2max (TTE) was evaluated. RESULTS: After the intense training periods, decrements in the order of 4-24 % were observed for MVCext, CMJ, mean anaerobic power, and TTE. In particular for TTE, this decrement in exercise performance did not attain full recovery at 48 h post-exercise. The regain of exercise performance was not dictated by type of protein supplement. CONCLUSION: The regain of muscle strength as well as anaerobic or aerobic performances were not markedly influenced by the type of protein supplement.

Acute and chronic cytokine responses to resistance exercise and training in people with multiple sclerosis.

Exercise is a well-established part of rehabilitation for people with multiple sclerosis (PwMS), and it has been hypothesized to stimulate an anti-inflammatory environment that might be disease modifying. Yet, investigations on exercise-induced immune responses are scarce and generally not paying attention to the medical treatments of the patient. At present, PwMS are routinely enrolled in immunosuppressive medication, but exercise-induced immunomodulatory effects have not been investigated under these circumstances. The objective of this study was to investigate the acute and chronic cytokines responses to resistance exercise training in medicated PwMS. Thirty-five people with relapsing-remitting multiple sclerosis (MS) treated with interferon (IFN)-ß, were randomized to a 24-week progressive resistance training (PRT) or control group. Plasma interleukin (IL)-1ß, IL-4, IL-10, IL-17F, IL-23, tumor necrosis factor-α and IFN-γ were measured before and after 24 weeks of PRT. The acute effect was evaluated following standardized single-bout resistance exercise in the untrained and the trained state. No changes were observed in resting cytokine levels after PRT. However, an indication of reduced IL-17F secretion following resistance exercise was observed in the trained compared with the untrained state. This study suggests little acute and chronic effect of PRT on cytokine levels in IFN-treated PwMS.

Associated decrements in rate of force development and neural drive after maximal eccentric exercise.

The present study investigated the changes in contractile rate of force development (RFD) and the neural drive following a single bout of eccentric exercise. Twenty-four subjects performed 15 × 10 maximal isokinetic eccentric knee extensor contractions. Prior to and at 24, 48, 72, 96, and 168 h during post-exercise recovery, isometric RFD (30, 50 100, and 200 ms), normalized RFD [1/6,1/2, and 2/3 of maximal voluntary contraction (MVC)] and rate of electromyography rise (RER; 30, 50, and 75 ms) were measured. RFD decreased by 28-42% peaking at 48 h (P < 0.01-P < 0.001) and remained depressed at 168 h (P < 0.05). Normalized RFD at 2/3 of MVC decreased by 22-39% (P < 0.01), peaked at 72 h and returned to baseline at 168 h. These changes in RFD were associated with a decrease in RER at 48 h-96 h (P < 0.05-P < 0.001). Accumulated changes (area under curve) revealed a greater relative decrease in accumulated RFD at 100 ms by -2727 ± 309 (%h; P < 0.05) and 200 ms by -3035 ± 271 (%h; P < 0.001) compared with MVC, which decreased, by -1956 ± 234 (%h). In conclusion, RFD and RER are both markedly reduced following a bout of maximal eccentric exercise. This association suggests that exercise-induced decrements in RFD can, in part, be explained decrements in neural drive.

Blood flow restricted and traditional resistance training performed to fatigue produce equal muscle hypertrophy.

This study investigated the hypertrophic potential of load-matched blood-flow restricted resistance training (BFR) vs free-flow traditional resistance training (low-load TRT) performed to fatigue. Ten healthy young subjects performed unilateral BFR and contralateral low-load TRT elbow flexor dumbbell curl with 40% of one repetition maximum until volitional concentric failure 3 days per week for 6 weeks. Prior to and at 3 (post-3) and 10 (post-10) days post-training, magnetic resonance imaging (MRI) was used to estimate elbow flexor muscle volume and muscle water content accumulation through training. Acute changes in muscle thickness following an early vs a late exercise bout were measured with ultrasound to determine muscle swelling during the immediate 0-48 h post-exercise. Total work was threefold lower for BFR compared with low-load TRT (P < 0.001). Both BRF and low-load TRT increased muscle volume by approximately 12% at post-3 and post-10 (P < 0.01) with no changes in MRI-determined water content. Training increased muscle thickness during the immediate 48 h post-exercise (P < 0.001) and to greater extent with BRF (P < 0.05) in the early training phase. In conclusion, BFR and low-load TRT, when performed to fatigue, produce equal muscle hypertrophy, which may partly rely on transient exercise-induced increases in muscle water content.

Whey protein hydrolysate augments tendon and muscle hypertrophy independent of resistance exercise contraction mode.

In a comparative study, we investigated the effects of maximal eccentric or concentric resistance training combined with whey protein or placebo on muscle and tendon hypertrophy. 22 subjects were allocated into either a high-leucine whey protein hydrolysate + carbohydrate group (WHD) or a carbohydrate group (PLA). Subjects completed 12 weeks maximal knee extensor training with one leg using eccentric contractions and the other using concentric contractions. Before and after training cross-sectional area (CSA) of m. quadriceps and patellar tendon CSA was quantified with magnetic resonance imaging and a isometric strength test was used to assess maximal voluntary contraction (MVC) and rate of force development (RFD). Quadriceps CSA increased by 7.3 ± 1.0% (P < 0.001) in WHD and 3.4 ± 0.8% (P < 0.01) in PLA, with a greater increase in WHD compared to PLA (P < 0.01). Proximal patellar tendon CSA increased by 14.9 ± 3.1% (P < 0.001) and 8.1 ± 3.2% (P = 0.054) for WHD and PLA, respectively, with a greater increase in WHD compared to PLA (P < 0.05), with no effect of contraction mode. MVC and RFD increased by 15.6 ± 3.5% (P < 0.001) and 12-63% (P < 0.05), respectively, with no group or contraction mode effects. In conclusion, high-leucine whey protein hydrolysate augments muscle and tendon hypertrophy following 12 weeks of resistance training - irrespective of contraction mode.

Concomitant changes in cross-sectional area and water content in skeletal muscle after resistance exercise.

This study investigated how one bout (1EX) and three bouts (3EX) of strenuous resistance exercise affected the cross-sectional area (CSA) and water content (WC) of the quadriceps muscle and patella tendon (PT), 4 h and 52 h after the last exercise bout. Ten healthy untrained male subjects performed 1EX with one leg and 3EX with the other leg. CSA and WC were measured with magnetic resonance imaging 10, 20 and 30 cm proximal to the tibia plateau (TP) for the muscle, and at the proximal, central and distal site for the PT prior to exercise, and 4 h and 52 h after the last exercise bout. Ten centimeter above the TP, muscle CSA was significantly increased at 4 h (1EX: 13 ± 5%; 3EX: 13 ± 4%) and 52 h (1EX: 16 ± 5%; 3EX: 16 ± 5%) compared with baseline. Muscle WC was significantly increased at 4 h (1EX: 7 ± 1%; 3EX: 6 ± 2%) and 52 h (1EX: 8 ± 2%; 3EX: 8 ± 3%) compared to baseline. PT central CSA was significantly reduced at 52 h (3EX: 14 ± 2%) compared with baseline and (3EX: 13 ± 1%) compared with 4 h. Present data demonstrate that strenuous resistance exercise results in an acute increase in muscle WC and underlines the importance of ensuring sufficient time between the last exercise bout and the determination of anatomical dimensions in muscles.

Differentiated mTOR but not AMPK signaling after strength vs endurance exercise in training-accustomed individuals.

The influence of adenosine mono phosphate (AMP)-activated protein kinase (AMPK) vs Akt-mammalian target of rapamycin C1 (mTORC1) protein signaling mechanisms on converting differentiated exercise into training specific adaptations is not well-established. To investigate this, human subjects were divided into endurance, strength, and non-exercise control groups. Data were obtained before and during post-exercise recovery from single-bout exercise, conducted with an exercise mode to which the exercise subjects were accustomed through 10 weeks of prior training. Blood and muscle samples were analyzed for plasma substrates and hormones and for muscle markers of AMPK and Akt-mTORC1 protein signaling. Increases in plasma glucose, insulin, growth hormone (GH), and insulin-like growth factor (IGF)-1, and in phosphorylated muscle phospho-Akt substrate (PAS) of 160 kDa, mTOR, 70 kDa ribosomal protein S6 kinase, eukaryotic initiation factor 4E, and glycogen synthase kinase 3a were observed after strength exercise. Increased phosphorylation of AMPK, histone deacetylase5 (HDAC5), cAMP response element-binding protein, and acetyl-CoA carboxylase (ACC) was observed after endurance exercise, but not differently from after strength exercise. No changes in protein phosphorylation were observed in non-exercise controls. Endurance training produced an increase in maximal oxygen uptake and a decrease in submaximal exercise heart rate, while strength training produced increases in muscle cross-sectional area and strength. No changes in basal levels of signaling proteins were observed in response to training. The results support that in training-accustomed individuals, mTORC1 signaling is preferentially activated after hypertrophy-inducing exercise, while AMPK signaling is less specific for differentiated exercise.

Multiple sclerosis and progressive resistance training: a systematic review.

Recently progressive resistance training (PRT) has been recognised as an effective tool in the rehabilitation of persons with multiple sclerosis (MS). The objective of this study was to systematically review the literature of PRT studies for persons with MS. A comprehensive literature search (PubMed, SveMed+, Embase, Cochrane, PEDro, SPORTDiscus and Bibliotek.dk) was conducted. Identified papers were rated according to the PEDro-scale. Sixteen studies were included and scored between 3 and 8 of 11 total points on the PEDro-scale, showing a general lack of blinding. Strong evidence regarding the beneficial effect of PRT on muscle strength was observed. Regarding functional capacity, balance and self-reported measures (fatigue, quality of life and mood) evidence is less strong, but the tendency is overall positive. Indications of an effect on underlying mechanisms such as muscle morphological changes, neural adaptations and cytokines also exist, but the studies investigating these aspects are few and inconclusive. PRT has a positive effect on muscle strength for persons with MS. Heterogeneous results exist regarding the effect on functional capacity and self-reported measures probably because of differences in training protocols, samples sizes, type and severity of MS. The area of underlying mechanisms deserves more attention in future research.

Heat shock protein translocation and expression response is attenuated in response to repeated eccentric exercise.

AIM: This study hypothesized that heat shock protein (HSP) translocation and upregulation is more probable to occur after eccentric exercise than after concentric exercise or repeated eccentric exercise. METHODS: Fourteen young, healthy, untrained male subjects completed two bench-stepping exercise bouts with 8 weeks between bouts, and were compared with a control group (n = 6). Muscle biopsies collected from m. vastus lateralis of both legs prior to and at 3 h, 24 h and 7 days after exercise were quantified for mRNA levels and/or for HSP27, alphabeta-crystallin and inducible HSP70 content in cytosolic and cytoskeletal protein fractions. RESULTS: The first bout of exercise reduced muscle strength and increased muscle soreness predominantly in the eccentric leg (P < 0.05). These responses were attenuated after the repeated eccentric exercise bout (P < 0.05), suggesting a repeated bout adaptation. Increases in inducible HSP70 and HSP27 protein content in cytoskeletal fractions were observed exclusively after eccentric exercise (P < 0.05). For HSP27, an approx. 10-fold upregulation after first-bout eccentric exercise was attenuated to a an approximately fourfold upregulation after the repeated eccentric exercise bout. mRNA levels for HSP70, HSP27 and alphabeta-crystallin were upregulated within approximately two to fourfold ranges at time points 3 and 24 h post-exercise (P < 0.05). This upregulation was induced exclusively by eccentric exercise but with a tendency to attenuated expression 3 h after the repeated eccentric exercise bout. CONCLUSION: Our results show that HSP translocation and expression responses are induced by muscle damaging exercise, and suggest that such HSP responses are closely related to the extent of muscle damage.

Expression patterns of atrogenic and ubiquitin proteasome component genes with exercise: effect of different loading patterns and repeated exercise bouts.

Unaccustomed exercise is known to produce strength loss, soreness, and myocellular disruption. With repeated application of exercise stimuli, the appearance of these indexes of muscle damage is attenuated, the so-called "repeated bout effect." No direct connection has been established between this repeated bout effect and exercise-induced increases in protein turnover, but it appears that a degree of tolerance is developed toward exercise for both. The present study sought to investigate markers of protein degradation by determining the expression of components related to the ubiquitin-proteasome system (UPS) with repeated exercise bouts. Healthy men carried out 30 min of bench stepping, performing eccentric work with one and concentric work with the other leg (n = 14), performing a duplicate exercise bout 8 wk later. A nonexercising control group was included (n = 6). RNA was extracted from muscle biopsies representing time points preexercise, +3 h, +24 h, and +7 days, and selected mRNA species were quantified using Northern blotting. The exercise model proved sufficient to produce a repeated bout effect in terms of strength and soreness. For forkhead box O transcription factor 1 (FOXO1) and muscle RING finger protein-1 (MURF1), strong upregulations were seen exclusively with concentric loading (P < 0.001), while atrogin-1 displayed a strong downregulation exclusively in response to eccentric exercise (P < 0.001). For MURF1 transcription, the first bout produced a downregulation that persisted until the second bout (P < 0.01). In conclusion, the UPS is modulated differentially in response to varying loading modalities and with different time frames in a way that to some extent reflects changes in protein metabolism known to take place with exercise.

Caspase 3 expression correlates with skeletal muscle apoptosis in Duchenne and facioscapulo human muscular dystrophy. A potential target for pharmacological treatment?

Apoptosis was detected in different muscular diseases, including severe dystrophin deficiency, but apoptotic mechanisms are not completely described in adult skeletal muscle. Studying patients affected by Duchenne muscular dystrophy (DMD) and by facio-scapulo-humeral dystrophy (FSHD) we showed an increase of apoptotic myonuclei, bax, and bcl-2-positive myofibers. Positive correlation was detected between apoptotic nuclei and bax expression (p < 0.01). Expression of caspases was analyzed by RNase protection. Caspase transcript was not detected in normal skeletal muscles. DMD muscles expressed caspase 8, 3, 5, 2, 7 and Granzyme B mRNAs. Low levels of caspase 6, 3, and Granzyme B transcripts were detected in FSHD patients. Tissue levels of caspase 3 protein significantly correlated with apoptotic myonuclei (p < 0.05) and with bax expression (p < 0.01). In all DMD cases the activity of caspase 3 was increased, while the FSHD samples were heterogeneous. These data indicate that human skeletal muscle fibers. during the dystrophic process, modulate the expression of caspases and that caspase 3 is involved in myofiber cell death. opening new perspective in the pharmacological treatments of muscular dystrophies, such as the use of caspase inhibitors.