The present study investigated the contribution of myofibrillar protein synthesis (MyoPS) and associated gene signaling to recovery from 300 muscle-damaging, eccentric contractions. Measured with D2O, MyoPS rates were elevated during recovery and observed alongside expression of inflammatory and regenerative signaling pathways. A nutritional intervention accelerated recovery; however, MyoPS and gene signaling were unchanged compared with placebo. These data indicate that MyoPS and associated signaling do not explain accelerated recovery from muscle damage.

Context The early events regulating the remodelling programme following skeletal muscle damage are poorly understood. Objective The objective of this study was to determine the association between myofibrillar protein synthesis (myoPS) and nuclear factor-kappa B (NF-κB) signalling by nutritionally accelerating recovery of muscle function following damage. Design, setting, participants, and interventions Healthy males and females consumed daily post-exercise and pre-bed protein-polyphenol (PP; n=9; 4 females) or isocaloric maltodextrin placebo (PLA; n=9; 3 females) drinks (parallel design), 6 days before and 3 days after 300 unilateral eccentric quadriceps contractions (EC) during complete dietary control. Main outcome measures Muscle function was assessed daily, and skeletal muscle biopsies were taken after 24, 27 and 36 h for measurements of myoPS rates using deuterated water, and gene ontology and NF-κB signalling analysis using an RT-qPCR gene array. Results EC impaired muscle function for 48 h in PLA, but for just 24 h in PP (P=0.047). EC increased myoPS compared to the control leg during post-exercise (24–27 h; 0.14±0.01 vs 0.11±0.01%·h -1, respectively; P=0.075) and overnight periods (27–36 h; 0.10±0.01 vs 0.07±0.01%·h -1, respectively; P=0.020), but was not further increased by PP (P>0.05). PP decreased post-exercise and overnight muscle IL1R1 (PLA=2.8±0.4, PP=1.1±0.4 and PLA=1.9±0.4, PP=0.3±0.4 log2 fold change, respectively) and IL1RL1 (PLA=4.9±0.7, PP=1.6±0.8 and PLA=3.7±0.6, PP=0.7±0.7 log2 fold change, respectively) mRNA expression (P<0.05) and downstream NF-κB signalling compared to PLA. Conclusion PP ingestion likely accelerates recovery of muscle function by attenuating inflammatory NF-κB transcriptional signalling, possibly to reduce aberrant tissue degradation rather than increase myoPS rates.

Introduction: Short-term disuse leads to muscle loss driven by lowered daily myofibrillar protein synthesis (MyoPS). However, disuse commonly results from muscle damage, and its influence on muscle deconditioning during disuse is unknown. Methods: 21 males (20±1 y, BMI=24±1 kg·m-2 (±SEM)) underwent 7 days of unilateral leg immobilization immediately preceded by 300 bilateral, maximal, muscle-damaging eccentric quadriceps contractions (DAM; n=10) or no exercise (CON; n=11). Participants ingested deuterated water and underwent temporal bilateral thigh MRI scans and vastus lateralis muscle biopsies of immobilized (IMM) and non-immobilized (N-IMM) legs. Results: N-IMM quadriceps muscle volume remained unchanged throughout in both groups. IMM quadriceps muscle volume declined after 2 days by 1.7±0.5% in CON (P=0.031; and by 1.3±0.6% when corrected to N-IMM; P=0.06) but did not change in DAM, and declined equivalently in CON (by 6.4±1.1% [5.0±1.6% when corrected to N-IMM]) and DAM (by 2.6±1.8% [4.0±1.9% when corrected to N-IMM]) after 7 days. Immobilization began to decrease MyoPS compared with N-IMM in both groups after 2 days (P=0.109), albeit with higher MyoPS rates in DAM compared with CON (P=0.035). Frank suppression of MyoPS was observed between days 2-7 in CON (IMM=1.04±0.12, N-IMM=1.86±0.10%·d-1; P=0.002) but not DAM (IMM=1.49±0.29, N-IMM=1.90±0.30%·d-1; P>0.05). Declines in MyoPS and quadriceps volume after 7 days correlated positively in CON (R2=0.403; P=0.035) but negatively in DAM (R2=0.483; P=0.037). Quadriceps strength declined following immobilization in both groups, but to a greater extent in DAM. Conclusion: Prior muscle damaging eccentric exercise increases MyoPS and prevents loss of quadriceps muscle volume after 2 (but not 7) days of disuse.

Background Pre-exercise supplements containing low doses of caffeine improve endurance exercise performance, but the most efficacious time for consumption before intense endurance exercise remains unclear, as does the contribution of caffeine metabolism. Methods This study assessed the timing of a commercially available supplement containing 200 mg of caffeine, 1600 mg of β-alanine and 1000 mg of quercetin [Beachbody Performance Energize, Beachbody LLC, USA] on exercise performance, perception of effort and plasma caffeine metabolites. Thirteen cyclists (V̇O2max 64.5 ± 1.4 ml kg− 1 min− 1 (± SEM)) completed four experimental visits consisting of 30 min of steady-state exercise on a cycle ergometer at 83 ± 1% V̇O2max followed by a 15-min time trial, with perceived exertion measured regularly. On three of the visits, participants consumed caffeine either 35 min before steady-state exercise (PRE), at the onset of steady-state (ONS) or immediately before the time trial (DUR) phases, with a placebo consumed at the other two time points (i.e. three drinks per visit). The other visit (PLA) consisted of consuming the placebo supplement at all three time points. The placebo was taste-, colour- and calorie-matched. Results Total work performed during the time trial in PRE was 5% greater than PLA (3.53 ± 0.14 vs. 3.36 ± 0.13 kJ kg− 1 body mass; P = 0.0025), but not ONS (3.44 ± 0.13 kJ kg− 1; P = 0.3619) or DUR (3.39 ± 0.13 kJ kg− 1; P = 0.925), which were similar to PLA. Perceived exertion was lowest during steady-state exercise in the PRE condition (P < 0.05), which coincided with elevated plasma paraxanthine in PRE only (P < 0.05). Conclusion In summary, ingestion of a pre-exercise supplement containing 200 mg caffeine 35 min before exercise appeared optimal for improved performance in a subsequent fatiguing time trial, possibly by reducing the perception of effort. Whether this was due to increased circulating paraxanthine requires further investigation. Trial registration ClinicalTrials.Gov,NCT02985606; 10/26/2016.

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