Abstract

Increasing dietary protein intake during periods of muscle disuse may mitigate the resulting decline in muscle protein synthesis (MPS). The purpose of this randomized pilot study was to determine the effect of increased protein intake during periods of disuse before anterior cruciate ligament (ACL) reconstruction on myofibrillar protein synthesis (MyoPS), and proteolytic and myogenic gene expression. Six healthy, young males (30 ± 9 y) were randomized to consume a high-quality, optimal protein diet (OP; 1.9 g·kg−1·d−1) or adequate protein diet (AP; 1.2 g·kg−1·d−1) for two weeks before ACL reconstruction. Muscle biopsies collected during surgery were used to measure integrated MyoPS during the intervention (via daily deuterium oxide ingestion) and gene expression at the time of surgery. MyoPS tended to be higher, with a large effect size in OP compared to AP (0.71 ± 0.1 and 0.54 ± 0.1%·d−1; p = 0.076; g = 1.56). Markers of proteolysis and myogenesis were not different between groups (p > 0.05); however, participants with greater MyoPS exhibited lower levels of MuRF1 gene expression compared to those with lower MyoPS (r = −0.82, p = 0.047). The data from this pilot study reveal a potential stimulatory effect of increased daily protein intake on MyoPS during injury-mediated disuse conditions that warrants further investigation.

Highlights

  • Introduction published maps and institutional affilMuscle atrophy and weakness are well-recognized clinical outcomes of anterior cruciate ligament (ACL) injury and reconstructive surgery that can persist postoperatively despite aggressive physical rehabilitation efforts [1,2]

  • The objective of this study was to determine the effect of a high-quality, optimal protein diet (OP; 2.0 g·kg−1 ·d−1 ) compared to adequate protein diet (AP; 1.0 g·kg−1 ·d−1 ) for two weeks before ACL reconstruction on integrated myofibrillar protein synthesis (MyoPS) and proteolytic gene expression

  • This pilot study showed that patients consuming a high-quality, OP diet (1.9 g protein·kg−1 ·d−1 ) for two weeks before ACL reconstruction tended to have greater MyoPS

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Summary

Introduction

Muscle atrophy and weakness are well-recognized clinical outcomes of anterior cruciate ligament (ACL) injury and reconstructive surgery that can persist postoperatively despite aggressive physical rehabilitation efforts [1,2]. Muscle atrophy under these conditions results, in part, from knee joint trauma and associated deficits in neuromuscular signaling. Injury-related effusion, inflammation, pain, and damage to articular sensory receptors in the knee joint alter neural signaling from the injured area that restricts activation of surrounding muscle [3,4] This protective response, combined with periods of limb immobilization and declines in habitual physical activity, induces rapid muscle disuse atrophy due to unloading and reduced neural activation of muscle [5,6]. Developing interventions that mitigate disuse atrophy following ACL injury and subsequent reconstruction may accelerate and optimize recovery. iations.

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