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.

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.

Interactions between muscle stem cells, mesenchymal-derived cells and immune cells in muscle homeostasis, regeneration and disease.

Recent evidence has revealed the importance of reciprocal functional interactions between different types of mononuclear cells in coordinating the repair of injured muscles. In particular, signals released from the inflammatory infiltrate and from mesenchymal interstitial cells (also known as fibro-adipogenic progenitors (FAPs)) appear to instruct muscle stem cells (satellite cells) to break quiescence, proliferate and differentiate. Interestingly, conditions that compromise the functional integrity of this network can bias muscle repair toward pathological outcomes that are typically observed in chronic muscular disorders, that is, fibrotic and fatty muscle degeneration as well as myofiber atrophy. In this review, we will summarize the current knowledge on the regulation of this network in physiological and pathological conditions, and anticipate the potential contribution of its cellular components to relatively unexplored conditions, such as aging and physical exercise.

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.

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.