Nutritional Strategies to Mitigate Muscle Loss During Rehabilitation After Sports Injuries: A Narrative Review

Article information

Exerc Sci. 2026;35(3):239-255
Publication date (electronic) : 2026 August 19
doi : https://doi.org/10.15857/ksep.2026.00101
1Data Convergence Team, Office of Hospital Information, Seoul National University Bundang Hospital, Seongnam, Korea
2Department of Health Care Exercise, Seowon University, Cheongju, Korea
Corresponding author: Jooyoung Kim Tel +82-43-299-8799 E-mail jykim1125@seowon.ac.kr
Received 2026 March 30; Revised 2026 June 28; Accepted 2026 July 4.

Abstract

Sports injuries frequently involve periods of reduced activity, immobilization, or unloading that accelerate skeletal muscle loss and delay functional recovery. This narrative review synthesizes current evidence on nutritional strategies to attenuate muscle loss during sports injury rehabilitation using a muscle-centered, phase-informed, and evidence-hierarchical perspective. Current evidence regarding energy availability, protein and amino acid strategies, creatine, and omega-3 fatty acids was qualitatively synthesized alongside current understanding of disuse atrophy, anabolic resistance, injury-related metabolic alterations, and progressive rehabilitation loading. Current evidence suggests that adequate energy availability and sufficient total protein intake represent the primary nutritional priorities for preserving skeletal muscle during rehabilitation. Within this foundation, optimized protein distribution, timing, and selective use of essential amino acids or leucine-enriched approaches may provide additional benefit, whereas creatine and omega-3 fatty acids should be considered context-dependent adjunctive strategies. Because direct evidence in injured athletic populations remains limited, practical recommendations require integration of rehabilitation studies, translational disuse models, and mechanistic evidence. Overall, effective rehabilitation nutrition should be individualized according to rehabilitation phase and integrated with progressive mechanical loading to support muscle preservation, neuromuscular recovery, functional performance, and return-to-sport readiness. The proposed phase-informed and evidence-hierarchical framework provides practical guidance for clinicians while identifying priorities for future rehabilitation nutrition research.

INTRODUCTION

Sports injuries are frequently accompanied by periods of reduced physical activity, immobilization, or unloading, each of which can induce rapid losses of skeletal muscle mass and function [1-4]. Even brief disuse after injury can lead to clinically meaningful reductions in muscle cross-sectional area, maximal force output, and neuromuscular performance [1-5]. These early deficits are not merely transient changes in physical condition; rather, they can alter the trajectory of rehabilitation by reducing tolerance to progressive loading, impairing movement quality, and delaying restoration of sport-specific capacity [6,7]. In high-performance settings, where return-to-sport timelines are tightly constrained and performance margins are small, even modest muscle loss may have disproportionate consequences for readiness, reinjury risk, and long-term competitive outcomes [6,7]. Beyond reductions in muscle quantity, deterioration in muscle quality and neuromuscular function may further compromise rehabilitation progression and ultimately influence successful return-to-sport.

From a mechanistic perspective, post-injury atrophy is driven by an interacting network of physiological disturbances, including reduced mechanical loading, suppressed muscle protein synthesis, anabolic resistance, and injury-related inflammatory and metabolic perturbations [3,8-10]. Importantly, these mechanisms do not operate in isolation [8-10]. Reduced contractile activity diminishes anabolic signaling; concomitantly, anabolic resistance can blunt the muscle protein synthetic response to feeding and rehabilitation exercise; and inflammatory/metabolic stress may further compromise nutrient utilization and tissue remodeling [3,8,9,11,12]. These disturbances are often most pronounced in early rehabilitation, when loading progression must remain conservative to protect healing tissues and restore basic joint or movement function [6,7]. Consequently, rehabilitation models that rely primarily on exercise stimuli may be insufficient to preserve muscle tissue during this vulnerable period, especially when nutritional support is suboptimal [13-16].

Nutrition is therefore a critical and modifiable determinant of muscle outcomes during rehabilitation [13-16]. Evidence from immobilization and rehabilitation-related studies suggests that muscle-preserving care should be built on several interdependent pillars: maintenance of adequate energy availability, optimization of protein dose/quality/distribution, and selective use of adjunctive nutritional strategies where contextually appropriate [13-16]. This hierarchy is clinically important because inadequate energy availability can reduce the effectiveness of downstream protein-based interventions, while poor protein patterning may limit anabolic support even when total intake appears acceptable [13,17-20]. In other words, the success of any single nutritional intervention depends on the broader metabolic environment in which it is applied [13-16].

Despite the recognized importance of nutrition in supporting recovery, its integration into sports injury rehabilitation remains inconsistent and often lacks structured, phase-specific guidance [13-16]. In many applied settings, reduced training load is frequently interpreted as a reduced nutritional requirement, and nutritional decisions are commonly made without explicit consideration of the altered physiological environment associated with disuse, anabolic resistance, and injury-related metabolic perturbations [3,8-16]. Furthermore, a substantial proportion of current recommendations is extrapolated from studies in healthy, physically active, or clinical populations, which may not adequately reflect the specific demands of individuals undergoing sports injury rehabilitation progressing through staged rehabilitation and return-to-sport progression [15,16,21]. Importantly, translating these findings into sports injury rehabilitation is not straightforward. Unlike healthy immobilization models, injured athletes experience concurrent tissue healing, pain, inflammation, progressive mechanical loading, sport-specific performance demands, and pressure to return to competition within restricted timelines. These interacting factors may substantially influence both nutritional requirements and responsiveness to nutritional interventions. Consequently, nutritional recommendations based solely on experimental disuse physiology may not fully capture the complexity of real-world sports injury rehabilitation. This translational gap highlights the need for rehabilitation-specific nutritional frameworks that integrate mechanistic evidence with athlete-centered clinical practice.

Although previous reviews have examined disuse atrophy or nutritional modulation of muscle metabolism, relatively few have provided a phase-oriented and muscle-centered synthesis specifically tailored to sports injury rehabilitation [13,15,16,21,22]. In addition, existing literature often combines heterogeneous populations, intervention contexts, and outcome domains, which can limit direct applicability for clinicians working in sports injury rehabilitation environments [15,16,21,22]. Importantly, the current evidence base is characterized by varying levels of directness, ranging from studies in rehabilitation settings to translational findings from disuse models and mechanistic investigations [1-5,8- 12,21,22]. As a result, practical recommendations in this field frequently rely on the integration of multiple levels of evidence rather than on a single homogeneous body of data [13,15,16,21,22]. Moreover, existing reviews have largely emphasized preservation of muscle mass or attenuation of disuse atrophy, whereas comparatively less attention has been directed toward rehabilitation-phase progression, neuromuscular recovery, functional performance, return-to-sport readiness, and reinjury prevention.

Accordingly, the purpose of this review is to provide a structured, phase-informed synthesis of nutritional strategies that may help attenuate muscle loss during post-injury rehabilitation in sports injury settings [13-16,22-24]. Specifically, this review aims to integrate current evidence within a rehabilitation-phase framework, distinguish between direct evidence from injured or rehabilitation populations and indirect or mechanistic evidence derived from disuse models and broader exercise nutrition literature [1-5,8-12,21,22], and translate these findings into practical considerations aligned with real-world rehabilitation progression [6,7,13-16,21,22]. By explicitly linking physiological mechanisms, levels of evidence, and phase-specific application, this review seeks to enhance the clinical interpretability and practical relevance of nutrition strategies for supporting muscle preservation during sports injury rehabilitation [13-16,21,22]. Rather than proposing isolated nutritional interventions, this review presents an evidence-hierarchical and phase-informed framework that integrates molecular mechanisms, levels of evidence, progressive rehabilitation loading, and clinically meaningful recovery outcomes. Few previous reviews have simultaneously integrated rehabilitation phase, evidence hierarchy, mechanistic rationale, and practical nutritional priorities into a unified framework specifically designed for sports injury rehabilitation.

METHODS

This review was conducted as a structured narrative synthesis to examine nutritional strategies that may attenuate muscle loss and support muscle preservation during post-injury rehabilitation, with a specific focus on sports injury rehabilitation contexts. A narrative review design was selected because the available literature is heterogeneous in terms of injury type, rehabilitation setting, participant characteristics, intervention design, and outcome measures. In addition, the current evidence base includes a combination of direct studies in injured or rehabilitation populations, translational studies using human disuse models such as immobilization, unloading, or bed rest, and mechanistic studies examining anabolic resistance, inflammation, and metabolic alterations during reduced loading. Given this heterogeneity, a quantitative meta-analysis was not considered appropriate. Instead, a structured qualitative synthesis was undertaken to emphasize mechanistic coherence, translational relevance, and practical applicability across rehabilitation phases.

Relevant literature was identified through electronic searches of PubMed/MEDLINE, SPORTDiscus, and Scopus from database inception to January 2026. Searches were conducted using combinations of terms related to sports injury rehabilitation, disuse physiology, and nutrition-based muscle preservation. Search terms included, but were not limited to, sports injury rehabilitation, musculoskeletal injury, immobilization, unloading, bed rest, disuse atrophy, energy availability, protein, essential amino acids, leucine, creatine, omega-3 fatty acids, muscle mass, muscle strength, muscle protein synthesis, and functional recovery. In addition to database searching, backward citation tracking was performed by screening the reference lists of relevant reviews, consensus statements, and primary studies to reduce the risk of omitting conceptually important literature. Only articles published in English were considered.

Study selection was guided by conceptual relevance to muscle-preserving nutrition during injury-related rehabilitation rather than by a predefined systematic review protocol. Priority was given to human studies conducted in sports injury or rehabilitation settings, as well as to human disuse models with clear translational relevance to injury-related muscle loss. Studies addressing energy availability, protein and amino acid strategies, creatine supplementation, and omega-3 fatty acids were prioritized because these represent the most commonly discussed nutritional approaches for preserving skeletal muscle during reduced loading and rehabilitation. Outcomes of interest included skeletal muscle mass, cross-sectional area, muscle strength, muscle protein synthesis, anabolic responsiveness, and functional recovery indicators. Mechanistic studies were also incorporated when they contributed meaningfully to interpretation of applied recommendations, particularly in relation to anabolic resistance, inflammatory responses, and metabolic alterations associated with disuse. Evidence with limited relevance to muscle-related rehabilitation outcomes, such as studies focused primarily on non-muscle endpoints without clear translational linkage, was deprioritized.

For interpretive clarity, the evidence was synthesized using a phase-informed framework reflecting the progression of sports injury rehabilitation. Rehabilitation was conceptually divided into four sequential phases: (i) the acute inflammatory phase, (ii) the immobilization or minimal-loading phase, (iii) the progressive reloading phase, and (iv) the return-to-sport phase. This structure was used to align nutritional priorities with evolving physiological mechanisms, mechanical loading status, and functional rehabilitation goals. In parallel, the literature was interpreted according to its directness and translational relevance, distinguishing between direct evidence from injured athletic populations, indirect evidence from non-athlete or disuse-based human models, and mechanistic evidence supporting biological plausibility. This approach was adopted because athlete-specific rehabilitation evidence remains limited, and many practical recommendations in this area necessarily rely on integration of different levels of evidence rather than on a single homogeneous body of literature.

The synthesis was qualitative rather than quantitative. Instead of pooling outcomes across studies, emphasis was placed on the direction and consistency of findings, biological plausibility, and applicability to rehabilitation practice. Nutritional strategies were interpreted within a practical hierarchy, with energy availability and total protein intake considered foundational strategies; protein distribution, protein timing, and amino acid composition considered optimization strategies; and creatine and omega-3 fatty acids considered adjunctive, context-dependent strategies. This hierarchical interpretation was chosen to reflect the applied reality that the effectiveness of adjunctive interventions depends heavily on the adequacy of core nutritional support and the presence of progressive mechanical loading during rehabilitation.

No formal risk-of-bias assessment or evidence-grading procedure was performed because this article was designed as a structured narrative review rather than a systematic review or meta-analysis. Nevertheless, greater interpretive weight was assigned to human intervention studies, systematic reviews, and consensus or position statements than to isolated mechanistic reports or indirect evidence from non-athlete populations. Accordingly, this review should be interpreted as an evidence-informed and practice-oriented synthesis intended to integrate mechanistic, translational, and applied perspectives, rather than as an exhaustive systematic review designed to provide definitive clinical guidelines.

MECHANISMS OF MUSCLE LOSS DURING REHABILITATION AFTER SPORTS INJURIES

Muscle loss after sports injury is primarily driven by disruption of skeletal muscle protein balance, typically characterized by reduced muscle protein synthesis (MPS) and, in some contexts, elevated muscle protein breakdown (MPB) [3,8-10]. In practice, these disturbances are initiated by injury-related reductions in mechanical loading and physical activity and are further shaped by inflammatory and metabolic changes that emerge during recovery [1-5,11,12]. Importantly, this is a dynamic process rather than a single acute event: the relative contribution of each mechanism can shift across rehabilitation phases depending on tissue status, loading progression, nutritional adequacy, and training reintroduction [6,7,13-16].

From a translational perspective, understanding how these mechanisms interact is critical because early deficits in muscle quantity and quality can persist even after pain and joint symptoms improve [6,7]. This mismatch between symptom relief and muscle recovery may delay functional restoration and affect return-to-sport readiness. Therefore, mechanism-aware rehabilitation should include not only progressive exercise exposure but also nutritional strategies tailored to phase-specific physiological constraints (Fig. 1 and Table 1) [13-16].

Fig. 1.

Evidence-hierarchical and phase-informed nutritional framework for preserving skeletal muscle during sports injury rehabilitation. The framework summarizes the progression of rehabilitation from the acute inflammatory phase through immobilization, progressive reloading, and return-to-sport. Across each phase, key physiological mechanisms, evidence-informed nutritional priorities, and primary clinical objectives are integrated to support muscle preservation and functional recovery. Because direct intervention studies in injured athletic populations remain limited, the proposed framework synthesizes evidence from rehabilitation research, human disuse models, mechanistic investigations, and broader sports nutrition literature.

Proposed phase-informed and evidence-hierarchical nutritional strategies for mitigating muscle loss during rehabilitation after sports injuries (muscle-centered focus)

1. Reduced mechanical loading and disuse atrophy

Mechanical loading is a central regulator of muscle mass and function through its influence on neuromuscular activation and anabolic signaling [8,9]. After sports injury, restrictions in weight-bearing activity, joint range of motion, and training participation reduce contractile activity and mechanical stimuli required to maintain muscle protein turnover [1-5]. As a result, muscle tissue rapidly shifts toward a disuse phenotype, with measurable declines in cross-sectional area, force-generating capacity, and neuromuscular performance occurring within days to weeks in immobilization/unloading models [1-5].

These findings are highly relevant to individuals undergoing sports injury rehabilitation because early rehabilitation often includes unavoidable periods of reduced loading to protect healing tissues [6,7]. Even when global physical activity is maintained (e.g., through compensatory upper-body or contralateral training), the injured limb or region may still experience local unloading sufficient to trigger atrophy [1-4]. In addition to size loss, disuse can alter muscle architecture and contractile efficiency, potentially reducing force transmission and delaying recovery of high-velocity, sport-specific actions [9]. Accordingly, disuse atrophy should be viewed as both a quantitative (mass) and qualitative (function) problem that requires early preventive management [1-5].

2. Impaired muscle protein synthesis and anabolic resistance

Beyond reduced loading, injured muscle frequently demonstrates anabolic resistance—an attenuated MPS response to protein feeding and exercise stimuli [3,8-10]. During periods of reduced activity, even nutritionally adequate protein intake may elicit a smaller anabolic response than expected under normal training conditions [3,8-10]. Mechanistically, anabolic resistance is characterized by impaired activation of anabolic signaling pathways, particularly the mechanistic target of rapamycin complex 1 (mTORC1), which plays a central role in regulating muscle protein synthesis. During immobilization and reduced mechanical loading, the sensitivity of skeletal muscle to both amino acid availability and contractile stimuli is diminished, resulting in a blunted muscle protein synthetic response despite adequate protein intake. Consequently, the normal synergistic interaction between mechanical loading and nutrient availability becomes attenuated during early rehabilitation. This phenomenon can reduce the effectiveness of habitual dietary patterns and increase the risk of cumulative net muscle loss across the rehabilitation timeline [13-16].

Anabolic resistance is particularly important in early rehabilitation, when therapeutic exercise intensity and volume are intentionally constrained [6,7]. Under these conditions, the usual synergy between feeding and mechanical stimuli is weakened, and muscle may require more deliberate nutritional structuring (e.g., protein quality/distribution/timing) to sustain anabolic signaling [23]. If unaddressed, blunted anabolic responsiveness can prolong deficits into mid-to-late rehabilitation, where inadequate muscle restoration may limit progression to high-load, high-velocity retraining [6,7]. Thus, anabolic resistance is not only a mechanistic concept but a practical barrier to efficient return-to-performance [10]. In addition to impaired mTORC1-related anabolic signaling, reduced physical activity and immobilization may also contribute to insulin resistance and impaired nutrient handling. Decreased insulin sensitivity may reduce glucose disposal, alter amino acid utilization, and diminish the efficiency with which ingested nutrients support muscle remodeling. These metabolic alterations further reinforce the importance of integrating nutritional support with progressive rehabilitation loading rather than considering dietary protein as an isolated intervention. Practical implementation of muscle-preserving nutritional strategies across different rehabilitation phases is summarized in Table 2.

Example phase-informed implementation of muscle-preserving nutritional strategies during sports injury rehabilitation

3. Injury-related inflammation and metabolic alterations

Sports injury is often accompanied by local—and in some cases systemic—inflammatory responses that influence muscle remodeling and recovery kinetics [11,12]. Beyond their essential role in tissue repair, inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) may impair anabolic signaling by suppressing mTORC1 activity and promoting catabolic pathways. Although activation of the inflammatory response is necessary for initiating tissue repair, excessive or prolonged inflammation may attenuate muscle protein synthesis, reduce anabolic sensitivity, and delay recovery of muscle function. Inflammatory mediators and stress-related signaling can modulate anabolic pathways, substrate utilization, and tissue turnover [11,12]. While inflammation is necessary for repair, excessive or prolonged inflammatory burden may suppress effective anabolic signaling and contribute to delayed restoration of muscle function [22].

In parallel, injury-related inactivity and altered movement patterns can induce metabolic disturbances, including reduced insulin sensitivity, altered nutrient partitioning, and impaired substrate handling [2]. These changes may further compromise protein balance by reducing the efficiency with which nutrients support repair and adaptation [2,20]. Clinically, this means that muscle loss during rehabilitation is not explained by unloading alone; rather, it reflects a multi-system recovery environment in which inflammatory and metabolic states can amplify or attenuate the impact of nutrition and exercise interventions [13-16]. This helps explain inter-individual variability in recovery trajectories, even among athletes with similar injuries. Emerging evidence also suggests that short-term disuse and immobilization may impair mitochondrial function, reducing metabolic flexibility and the capacity of skeletal muscle to efficiently utilize nutrients during recovery. Although these alterations remain incompletely understood in injured athletes, mitochondrial dysfunction may represent an additional mechanism contributing to anabolic resistance and delayed rehabilitation.

4. Persistence of muscle loss during rehabilitation

Although progressive loading and therapeutic exercise are core components of sports rehabilitation, restoration of muscle mass and function frequently lags behind improvements in pain, swelling, and joint-specific clinical signs [6,7]. In early and transitional phases, priorities such as tissue protection, movement control, and joint stability may limit exposure to hypertrophic or high-tension stimuli [6,7]. Consequently, muscle deficits initiated during immobilization/disuse may persist into later phases unless deliberately targeted [1-5].

This persistence has important practical implications. Individuals may appear clinically improved yet retain unresolved deficits in strength, power, inter-limb symmetry, or neuromuscular control—factors associated with reduced performance quality and potentially increased reinjury vulnerability [6,7]. Therefore, recovery should not be interpreted solely through symptom resolution; muscle-centered endpoints should be tracked across phases [6,7]. The temporal mismatch between structural/functional muscle recovery and symptom improvement supports integrating adjunctive, phase-specific nutritional strategies with exercise-based rehabilitation to improve the quality and durability of return-tosport outcomes [13-16]. Collectively, these interacting mechanisms indicate that muscle loss during rehabilitation is not solely a consequence of reduced mechanical loading. Rather, impaired anabolic signaling, inflammation-mediated metabolic alterations, insulin resistance, and mitochondrial dysfunction collectively create a physiological environment in which nutritional interventions become both more necessary and more challenging. Accordingly, effective rehabilitation nutrition should be designed to complement progressive mechanical loading while addressing these phase-specific physiological constraints, as summarized in Fig. 1.

ENERGY AVAILABILITY AND MUSCLE PRESERVATION

Adequate energy availability is a foundational prerequisite for preserving skeletal muscle during post-injury rehabilitation [13-16]. Although total daily energy expenditure often declines when sport participation and habitual training loads are reduced, this should not be interpreted as a proportional reduction in nutritional need [13-16]. Individuals undergoing sports injury rehabilitation continue to face meaningful energetic demands related to tissue repair, immune activity, pain-related stress responses, and rehabilitation training [13-16]. Accordingly, excessive energy restriction—whether intentional, for example because of body composition concerns, or unintentional, for example because of reduced appetite or disrupted daily structure—may create a metabolic environment that accelerates muscle loss rather than supports recovery [17-20,25,26].

From a mechanistic perspective, low energy availability may impair muscle preservation through several interacting pathways [17-20,25,26]. Insufficient energy intake can suppress anabolic signaling, increase amino acid oxidation, and reduce the efficiency with which ingested protein is used to support muscle remodeling and repair [17-20]. Under such conditions, dietary amino acids may be diverted away from tissue accretion toward energy provision, thereby attenuating the expected anabolic benefit of otherwise adequate protein intake [17-20]. This interaction is particularly important during rehabilitation, because nutritional strategies are not implemented in isolation; rather, their effectiveness depends on the metabolic context in which they are applied [13-16]. In practical terms, protein-based interventions are unlikely to achieve their full muscle-preserving effect when energy availability is chronically insufficient [13-20].

These considerations are especially relevant during phases of minimal loading or restricted activity, when exercise-derived anabolic stimulation is reduced and disuse-related anabolic resistance may be more pronounced [3,8-10,13-16]. In this context, adequate energy availability serves as the physiological foundation upon which other nutrition strategies are layered [13-16]. If energy intake is not sufficient to support recovery demands, early losses of muscle mass and function may be amplified and may persist into later phases of rehabilitation, ultimately delaying restoration of strength, power, and sport-specific capacity [1-7]. Thus, energy availability should be interpreted not simply as a background dietary consideration, but as a primary determinant of whether muscle-preserving rehabilitation nutrition can be effective [13-16].

Beyond its role in muscle protein balance, energy availability also has broader implications for rehabilitation quality and progression [17-20]. Sustained under-fueling may adversely affect endocrine and metabolic function, reduce perceived readiness, impair tolerance to rehabilitation loading, and compromise progression toward return-to-sport goals [18-20]. This is particularly important in sport or rehabilitation populations, in whom pressure to maintain body composition or minimize weight gain during injury may increase the risk of inadequate intake [15,16]. In such cases, the consequences of low energy availability extend beyond muscle preservation alone and may negatively affect the overall efficiency and quality of the rehabilitation process [13-16].

From an applied perspective, energy planning during rehabilitation should be individualized and phase-informed rather than based on a single fixed caloric prescription [13-16]. Practical implementation should focus first on avoiding clinically low energy availability and establishing minimum adequacy, then adjusting intake according to injury severity, current loading status, body-mass trajectory, appetite, and functional progression [17-20]. Monitoring indicators such as unintended body-mass loss, persistent fatigue, poor session quality, reduced appetite, or delayed progression through rehabilitation milestones may help identify athletes at risk of under-fueling [13-16]. Early correction is important, because cumulative energy deficits may compound disuse-related muscle loss and become difficult to reverse later in the recovery process [13-20].

Energy availability should also be integrated with daily meal structure and rehabilitation scheduling [13-16]. Consistent eating patterns, appropriate intake on both rehabilitation and non-rehabilitation days, and adequate support around training or therapy sessions may help maintain a more stable anabolic environment across the rehabilitation continuum [13-16]. This stable nutritional foundation increases the likelihood that downstream strategies—such as optimized protein intake, amino acid support, and selected adjunctive supplementation—will exert meaningful effects [13-16,22-24].

Overall, current evidence supports energy availability as the most fundamental nutritional priority for attenuating muscle loss during post-injury rehabilitation [13-20,25,26]. However, injury-specific dose-response data remain limited, and practical recommendations are still derived largely from broader athlete nutrition and RED-S frameworks rather than from direct rehabilitation trials [18-20,25,26]. From an evidence-translation perspective, it should be emphasized that energy availability recommendations during sports injury rehabilitation are derived primarily from broader athlete nutrition and RED-S literature rather than from injury-specific intervention trials. Therefore, the practical application of energy availability targets during rehabilitation should be individualized according to injury severity, rehabilitation phase, body-composition goals, appetite, and progression of mechanical loading. Future research should therefore clarify phase-specific energy needs across injury types and determine how energy availability interacts with loading progression to influence muscle retention, functional recovery, and return-to-sport outcomes [13-16,22,25,26].

PROTEIN AND AMINO ACID-BASED STRATEGIES

Protein- and amino acid-based strategies represent a central component of muscle-preserving nutrition during post-injury rehabilitation [13-16,23]. Their importance is amplified in this context because injury-related unloading and reduced training exposure alter the physiological environment in which dietary protein exerts its effects [3,8-10]. Specifically, reduced mechanical stimulation and the presence of anabolic resistance attenuate the muscle protein synthetic response to feeding, such that habitual protein intake patterns that are sufficient during normal training may be inadequate during rehabilitation [3,8-10,23]. Accordingly, protein provision during rehabilitation should be considered a structured and dynamic intervention rather than a fixed dietary target, with coordinated attention to total intake, distribution, amino acid composition, and timing relative to rehabilitation stimuli [23].

1. Total protein intake during rehabilitation

Adequate total daily protein intake is a foundational requirement for maintaining muscle protein balance under reduced-loading conditions [23]. Evidence from immobilization and disuse models suggests that protein requirements may be functionally elevated during periods of reduced activity in order to offset declines in muscle protein synthesis and maintain sufficient substrate availability for tissue repair and remodeling [3,8-10]. In rehabilitation settings, insufficient protein intake—particularly when combined with low energy availability—may accelerate muscle loss and delay the restoration of strength and function [13-20,23].

Importantly, total protein intake should be interpreted within the context of rehabilitation phase and overall energy status rather than as a single static threshold [13-16]. During early phases characterized by limited mechanical loading, maintaining adequate substrate availability may help attenuate net catabolism despite blunted anabolic signaling. As rehabilitation progresses and loading increases, adequate protein intake remains essential to support training adaptation and reconditioning [23,27,28]. From an applied perspective, consistent daily intake is likely more important than intermittent high-protein feeding, and monitoring should focus on adherence, body-mass trends, perceived recovery, and functional progression [13-16].

2. Protein distribution and feeding frequency

Beyond total intake, the distribution of protein across the day influences integrated muscle protein synthetic responses [29,30]. Under conditions of reduced activity and anabolic resistance, skewed intake patterns—such as low protein consumption during the day followed by a large evening intake—may provide suboptimal stimulation of muscle protein synthesis [29,30]. More evenly distributed protein intake across multiple meals or feeding opportunities may enhance cumulative anabolic signaling and better support net protein balance during rehabilitation [29,30].

This strategy is particularly relevant during early-to-mid rehabilitation phases, when exercise-induced anabolic stimulation is limited or inconsistent [13-16]. Regular protein feedings may help maintain repeated anabolic signaling opportunities throughout the day, partially compensating for reduced mechanical input. In practice, distribution strategies should be individualized based on appetite, gastrointestinal tolerance, daily schedule, and rehabilitation timing, with the goal of avoiding prolonged periods of low amino acid availability [13-16].

3. Essential amino acids and leucine-enriched approaches

Essential amino acids (EAAs), particularly leucine, play a key role in initiating muscle protein synthesis through activation of anabolic signaling pathways [31,32]. During rehabilitation, when anabolic resistance is present, leucine-enriched protein or EAA strategies may help augment the anabolic response to feeding and partially mitigate disuse-related declines in muscle protein synthesis [31-33]. Mechanistically, increased leucine availability may enhance translation initiation and improve the efficiency of anabolic signaling under conditions of reduced mechanical stimulation [31,32].

However, the practical interpretation of this evidence requires caution. The effects of leucine or EAA supplementation are context-dependent, and findings are not uniformly consistent across populations and study designs [32,33]. Importantly, these strategies do not replace the need for adequate total protein and energy intake, and their effectiveness is likely dependent on the broader nutritional and rehabilitation context [13-20,22]. Therefore, EAA or leucine-enriched approaches should be considered as conditional optimization strategies, particularly when full protein targets are difficult to achieve due to reduced appetite or logistical constraints during rehabilitation [13-16].

4. Timing of protein and amino acid intake

The timing of protein and amino acid intake relative to rehabilitation exercise may provide additional support for muscle preservation and recovery [34]. Although early rehabilitation phases are characterized by reduced exercise-induced anabolic sensitivity, aligning protein intake before and/or after rehabilitation sessions may enhance amino acid availability during periods of increased anabolic potential [34]. As loading intensity and training complexity increase, timing strategies may become more relevant for supporting adaptation and recovery [13,23].

Pre-sleep protein ingestion has also been proposed as a strategy to support overnight muscle protein synthesis and recovery [35,36]. While mechanistically plausible, direct evidence in injury-specific contexts remains limited, and the practical value of this strategy likely depends on total daily intake, evening dietary patterns, and individual tolerance [35,36]. Accordingly, protein timing should be considered a secondary optimization layer that complements, but does not replace, total protein adequacy and appropriate distribution [23].

5. Practical integration and phase-specific priorities

In applied rehabilitation settings, the effectiveness of protein and amino acid strategies depends on their integration within a phase-specific framework rather than on isolated interventions [6,7,13-16]. During early phases characterized by minimal loading, priority should be placed on maintaining adequate total protein intake and consistent distribution in order to limit negative protein balance [23,29,30]. As rehabilitation progresses and loading is reintroduced, protein strategies should increasingly align with training demands, including attention to timing and potential use of targeted amino acid approaches [31-33]. During later phases, when sport-specific loading increases, protein intake should support both recovery and performance adaptation while maintaining consistency in dietary patterns [6,7].

Across all phases, monitoring and iterative adjustment are essential. Practical indicators such as dietary adherence, session quality, fatigue and recovery trends, and progression of functional performance should inform ongoing refinement of protein strategies [13-16]. When progress is suboptimal, it is important to reassess the interaction between energy availability, total protein intake, distribution, timing, and rehabilitation loading rather than modifying individual components in isolation [13-16,22].

Overall, current evidence supports total protein intake as a foundational nutritional strategy for mitigating muscle loss during rehabilitation, with distribution, timing, and amino acid composition serving as context-dependent optimization strategies [13-16,23,29-33]. However, direct evidence in injured athletic populations remains limited, and many recommendations are derived from disuse models and broader exercise nutrition literature [3,8-10,23]. Future research should clarify phase-specific protein requirements and determine how protein strategies interact with rehabilitation loading to influence muscle preservation, functional recovery, and return-to-sport outcomes [13-16,22].

CREATINE AS AN ADJUNCTIVE STRATEGY DURING REHABILITATION

Creatine is one of the most extensively studied ergogenic aids for improving lean mass and strength in resistance training contexts, and its potential role as an adjunctive strategy during post-injury rehabilitation has received increasing attention [37]. In rehabilitation settings characterized by reduced mechanical loading, temporary immobilization, and delayed return to high-intensity training, creatine may provide indirect support for muscle preservation by enhancing training capacity and improving the quality of rehabilitation exercise [38-40]. However, its effects in this context should be interpreted within the broader framework of integrated nutrition and loading, rather than as a primary intervention for preventing muscle atrophy. Importantly, the effectiveness of creatine supplementation is likely to depend on the rehabilitation phase and the degree of mechanical loading. During periods of complete immobilization or minimal muscle activation, creatine is unlikely to substantially attenuate muscle atrophy in the absence of sufficient anabolic stimuli. Conversely, as progressive resistance exercise and neuromuscular retraining are reintroduced, creatine may become increasingly relevant by enhancing training quality and supporting adaptations to rehabilitation loading.

From a mechanistic perspective, creatine supplementation increases intramuscular phosphocreatine availability, thereby enhancing the capacity for rapid adenosine triphosphate resynthesis during repeated muscular contractions [37]. This may be particularly relevant during rehabilitation sessions that involve repeated efforts, progressive resistance, or neuromuscular retraining under fatigue [37,38]. Additional proposed mechanisms include improved cellular hydration, enhanced intracellular signaling related to muscle protein synthesis, and improved training quality through reduced relative fatigue during repeated exercise bouts [37,41]. Importantly, these mechanisms are more closely linked to exercise performance and adaptation than to direct attenuation of disuse-induced anabolic suppression.

The practical relevance of creatine during rehabilitation appears to be phase-dependent. During early phases characterized by minimal loading or immobilization, when mechanical stimuli are substantially limited, the expected impact of creatine on muscle preservation is likely to be small [6,7,38]. In contrast, during progressive reloading phases, when structured rehabilitation exercise is reintroduced and loading capacity begins to increase, creatine may contribute to improved session quality, greater tolerance to progressive overload, and more effective neuromuscular retraining [38-41]. In this context, creatine may indirectly support muscle preservation by enhancing the effectiveness of the mechanical stimulus rather than by acting as a direct anti-atrophy agent.

Evidence from disuse and retraining models provides some support for this interpretation. Nevertheless, findings remain inconsistent across studies. Differences in rehabilitation protocols, immobilization duration, training status, supplementation timing, and outcome measures make direct comparison difficult. Moreover, relatively few randomized controlled trials have been conducted in injured athletic populations, limiting confidence in injury-specific recommendations. Studies involving immobilization and subsequent retraining have reported that creatine supplementation may attenuate declines in strength-related outcomes or enhance recovery of muscle performance during reloading phases [34-36]. However, findings are not entirely consistent across all models, and direct evidence in injured athletic populations remains limited. As such, creatine should be considered a context-dependent adjunct rather than a universally effective intervention for preventing muscle loss during rehabilitation.

From an applied perspective, creatine supplementation should be integrated within a broader rehabilitation nutrition framework that prioritizes energy availability and adequate protein intake [13-16,23]. In the absence of sufficient energy intake, protein provision, and progressive loading, the potential benefits of creatine are likely to be attenuated [13-16]. Practical implementation should also consider individual tolerance, adherence, and clinical context. Monitoring indicators may include rehabilitation session quality, fatigue during repeated efforts, progression of strength and functional metrics, and consistency of supplement use.

Creatine is generally regarded as safe and well tolerated in athletic populations when used within established guidelines [37,42,43]. Nevertheless, as with any supplementation strategy, individual screening and context-specific considerations are warranted. Importantly, current evidence does not support the use of creatine as a stand-alone intervention for muscle preservation during rehabilitation, but rather as a supportive strategy that may enhance training adaptations once sufficient mechanical loading is reintroduced.

Overall, creatine may offer practical value as an adjunctive strategy during rehabilitation, particularly in phases characterized by progressive reloading and increasing training demands [37-41]. However, the current evidence base is largely derived from disuse and retraining models, and further research is needed to clarify its role in injured athletic populations, including phase-specific effects and impacts on clinically meaningful outcomes such as functional recovery and return-tosport readiness [22,37-41]. Accordingly, creatine should currently be viewed as a rehabilitation-supportive supplement rather than a universally indicated anti-atrophy intervention. Its greatest potential value may lie in facilitating recovery of muscle function and training capacity during progressive reloading rather than preventing muscle loss during complete unloading.

OMEGA-3 FATTY ACIDS AND ANABOLIC SENSITIVITY

Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been proposed as potential modulators of muscle anabolic sensitivity and recovery-related physiology [44-49]. In the context of post-injury rehabilitation, their relevance arises from the observation that muscle preservation is often limited not only by reduced mechanical loading, but also by impaired anabolic responsiveness to nutritional and exercise stimuli [3,8-10]. Accordingly, omega-3 fatty acids have been investigated as an adjunctive strategy that may enhance the efficiency of core anabolic inputs rather than directly prevent muscle atrophy.

From a mechanistic perspective, EPA and DHA may influence multiple pathways relevant to muscle adaptation [44-46]. Proposed mechanisms include incorporation into cell membranes with subsequent alterations in membrane fluidity and signaling environments, modulation of intracellular pathways associated with muscle protein synthesis, and regulation of inflammatory processes that may otherwise impair anabolic signaling efficiency [11,12,44-46]. These effects are biologically plausible in rehabilitation settings characterized by low-grade inflammation, altered substrate utilization, and anabolic resistance [3,8-12]. In this context, omega-3 fatty acids may contribute to a more favorable anabolic milieu, particularly when combined with adequate energy availability and sufficient protein intake [13,20,23].

The potential practical value of omega-3 supplementation appears to be context-dependent and may vary across rehabilitation phases. During phases of minimal loading or restricted activity, when exercise-induced anabolic stimuli are limited, strategies that improve anabolic sensitivity may be particularly relevant [6,7]. As rehabilitation progresses and mechanical loading increases, omega-3 fatty acids may continue to play a supportive role by complementing protein-based strategies and helping to maintain recovery quality across repeated rehabilitation sessions [44-49]. However, the magnitude and consistency of these effects remain uncertain. This uncertainty is particularly important because the proposed benefits of omega-3 fatty acids may depend on several factors, including baseline omega-3 status, habitual dietary intake, EPA and DHA dose, supplementation duration, injury type, inflammatory burden, and the extent of concurrent rehabilitation loading. Therefore, omega-3 supplementation should not be interpreted as a uniformly effective strategy across all rehabilitation contexts.

Importantly, the current evidence base has several limitations that constrain interpretation. Much of the available evidence has been derived from studies involving healthy individuals, older adults, or experimental disuse and exercise-induced muscle damage models rather than injured athletes undergoing structured rehabilitation [13,15,16,21,22]. Direct trials in injured athletic populations are scarce, and a substantial proportion of available data is derived from older adults, general populations, or experimental models of reduced activity [46-49]. In addition, considerable heterogeneity exists in study design, including differences in dosage, duration, EPA:DHA composition, and outcome measures [40-43]. As a result, findings are not entirely consistent, and clear dose-response relationships specific to rehabilitation contexts have not been established.

From an applied perspective, omega-3 fatty acids should therefore be considered a conditional adjunctive strategy rather than a primary intervention for muscle preservation [13-16]. In addition, because inflammation is required for the initiation of tissue repair, omega-3 fatty acids should be framed as a strategy to modulate or optimize the inflammatory environment rather than simply suppress inflammation. This distinction is clinically important during the early inflammatory phase of rehabilitation, when excessive anti-inflammatory approaches may theoretically interfere with normal healing processes. Their use may be most appropriate in cases where dietary intake of omega-3 is low, where inflammatory or metabolic disturbances are likely to impair recovery, or where optimization of the anabolic environment is a priority within an otherwise well-structured nutrition and rehabilitation program [13,20,23]. Importantly, omega-3 supplementation is unlikely to compensate for inadequate energy availability, insufficient protein intake, or poorly progressed rehabilitation loading.

Practical implementation should be integrated within a broader nutrition and rehabilitation framework, with attention to individual tolerance, habitual dietary intake, and potential clinical considerations such as bleeding risk or interactions with medications. Monitoring should focus on overall recovery trends, perceived muscle soreness or fatigue, and progression of functional outcomes, rather than on isolated expectations of muscle mass preservation.

Overall, omega-3 fatty acids may provide a biologically plausible and potentially beneficial adjunct for enhancing anabolic sensitivity during rehabilitation; however, current evidence remains limited and indirect, particularly in sport or rehabilitation populations [44-51]. Future research should prioritize phase-specific intervention studies in rehabilitation settings, clarify optimal dosing strategies, and determine whether omega-3 supplementation meaningfully influences clinically relevant outcomes such as functional recovery, return-to-sport readiness, and reinjury risk [22,44-49]. Until such evidence is available, omega-3 supplementation should be individualized based on dietary intake, clinical context, medication use, and rehabilitation goals rather than routinely recommended for all injured athletes.

PRACTICAL CONSIDERATIONS ACROSS REHABILITATION PHASES

Fig. 1 and Tables 1 and 2 provide complementary phase-informed frameworks for implementing muscle-preserving nutritional strategies during sports injury rehabilitation [13-16]. Fig. 1 summarizes the overall rehabilitation framework across the different stages of recovery, whereas Table 1 presents evidence-hierarchical nutritional priorities and their clinical interpretation. These recommendations should be interpreted as practical starting points rather than rigid prescriptions, as nutritional requirements during rehabilitation are highly individualized and influenced by injury characteristics, loading status, metabolic demands, and behavioral factors such as appetite and adherence [13-16,21]. In addition, much of the available evidence is derived from disuse models or non-athlete populations, and therefore requires careful translation when applied to athlete-centered rehabilitation contexts [1-5,21]. Importantly, the ultimate goal of rehabilitation nutrition is not merely preservation of muscle mass, but restoration of functional capacity that supports progressive loading, neuromuscular recovery, and safe return-to-sport. Accordingly, nutritional interventions should be evaluated according to their contribution to clinically meaningful rehabilitation outcomes rather than changes in muscle mass alone.

A key principle for practical implementation is that nutritional priorities should be aligned with the functional context of rehabilitation rather than strictly with time-based progression [6,7]. In phases characterized by minimal loading or restricted activity, the primary objective is attenuation of muscle loss rather than promotion of maximal hypertrophy [13-20]. Under these conditions, anabolic resistance may be more pronounced and exercise-induced anabolic signaling limited, increasing the relative importance of foundational nutritional strategies. Accordingly, priority should be given to maintaining adequate energy availability and ensuring sufficient total protein intake with appropriate distribution across the day [13-16,23,29,30]. In situations where full protein targets are difficult to achieve due to reduced appetite or logistical constraints, targeted use of essential amino acids or leucine-enriched strategies may be considered as a conditional optimization approach [31-33].

As rehabilitation progresses into phases of progressive reloading, nutritional strategies should shift toward supporting adaptation to increasing mechanical stimuli and improving the quality of rehabilitation exercise [6,7]. During this phase, foundational strategies remain essential, but additional emphasis may be placed on protein timing in relation to rehabilitation sessions and maintenance of consistent intake patterns across training and non-training days [13-16,23,31]. Adjunctive strategies such as creatine supplementation may also be considered in this context, particularly when the goal is to enhance training capacity, reduce fatigue during repeated efforts, and support progression toward higher loading tolerance [37-41]. Importantly, the effectiveness of such adjuncts is contingent upon adequate energy and protein availability, as well as appropriate progression of rehabilitation loading [13-16].

During advanced reconditioning and return-to-sport preparation phases, nutritional priorities should reflect the increasing demands of sport-specific training and performance restoration [6,7]. In this context, energy intake should be adjusted to match rising training loads, and protein intake should support both recovery and adaptation to higher-intensity exercise [13-16,27,28]. Optimization strategies, including appropriate protein timing and maintenance of balanced distribution, remain relevant, while adjunctive strategies such as creatine and omega-3 fatty acids may be incorporated selectively depending on individual needs, dietary patterns, and recovery goals [37-41,44-49]. However, these strategies should be viewed as supportive rather than primary drivers of adaptation.

Across all rehabilitation phases, dynamic monitoring and iterative adjustment are essential for effective implementation [13-16]. Practical indicators may include body-mass trajectory, dietary adherence, appetite, perceived fatigue and recovery, rehabilitation session quality, and progression of strength and functional performance metrics [6,7,13-16]. When expected progress is not observed, practitioners should reassess the interaction between energy availability, total protein intake, distribution and timing, adjunctive strategies, and rehabilitation loading rather than modifying individual components in isolation [13-16,23].

Effective translation of nutritional strategies is further strengthened when integrated within a multidisciplinary rehabilitation model [52]. Coordination among sports physicians, physiotherapists or athletic trainers, strength and conditioning staff, and sports nutrition practitioners allows nutritional interventions to be aligned with tissue healing status, loading progression, and functional milestones [52]. Importantly, nutrition and progressive mechanical loading should not be considered independent therapeutic strategies but complementary anabolic stimuli. Mechanical loading provides the primary physiological signal for muscle remodeling by activating mechanosensitive anabolic pathways, whereas nutritional support ensures sufficient energy availability and amino acid provision to translate these mechanical signals into tissue repair and functional adaptation. Consequently, the effectiveness of nutritional interventions is likely to increase as rehabilitation progresses and mechanical loading is progressively restored. This concept further supports the need for phase-specific nutritional strategies because the relative contribution of nutrition and mechanical loading changes substantially from early immobilization to return-to-sport. This integrated approach enhances both the precision and practicality of nutritional support during rehabilitation.

Finally, it is important to emphasize that nutrition should be viewed as a critical enabler of rehabilitation adaptation rather than a substitute for progressive mechanical loading [6,7,13-16]. In the absence of sufficient and appropriately progressed loading stimuli, nutritional interventions alone are unlikely to fully prevent or reverse muscle loss. Conversely, when phase-specific nutrition is effectively integrated with structured rehabilitation and progressive loading, the likelihood of preserving muscle function and optimizing return-to-sport outcomes is substantially improved [6,7,13-16,52,53].

LIMITATIONS AND FUTURE DIRECTIONS

Several limitations should be considered when interpreting the current evidence base on nutritional strategies for mitigating muscle loss during post-injury rehabilitation [13-16]. First, a substantial proportion of available evidence is derived from experimental disuse models, such as immobilization, unloading, or reduced activity paradigms, which provide valuable mechanistic insight but do not fully replicate the complexity of real-world sports injury rehabilitation [1-5,54-57]. In applied settings, rehabilitation is influenced by factors such as pain, restricted joint function, progressive loading constraints, and non-linear recovery trajectories, all of which may modify both nutritional requirements and responsiveness to intervention [6,7,54-57].

Second, direct evidence in injured athletic populations remains limited. Many current recommendations are extrapolated from non-athlete cohorts, older adults, or general exercise populations, which may reduce external validity when applied to high-performance athletes [15,16,21]. Rehabilitation demands vary considerably according to sport, competition level, injury type, surgical status, and seasonal context, and these factors are not consistently represented in the existing literature [52,58].

Third, substantial heterogeneity across studies complicates interpretation and translation. Differences in intervention design, including dosage, timing, duration, and co-interventions, as well as variability in rehabilitation protocols and outcome measures, limit the ability to draw definitive conclusions or establish standardized recommendations [21,22]. In many cases, nutritional interventions are examined without adequate characterization of concurrent loading progression, despite the likelihood that mechanical loading strongly influences nutritional effectiveness [53].

Fourth, outcome selection in the current literature is often limited in scope. Many studies focus on changes in muscle mass or isolated strength measures, while fewer assess clinically meaningful endpoints such as integrated functional performance, inter-limb asymmetry, return-to-sport readiness, durability of recovery, reinjury risk, or broader metabolic outcomes such as insulin sensitivity and substrate regulation [52,53,59,60]. As a result, the practical significance of observed nutritional effects may be difficult to determine.

Fifth, participant stratification is frequently insufficient. Factors such as sex differences, sport-specific demands, injury characteristics, and baseline nutritional status—particularly low energy availability—are not consistently accounted for, potentially obscuring meaningful variability in response to nutritional strategies [25,26,48].

Future research should therefore prioritize designs that better reflect applied rehabilitation practice. Phase-specific, athlete-centered intervention studies are needed to examine how nutritional strategies interact with progressive loading across different stages of rehabilitation [52,53]. Greater standardization in reporting of nutritional interventions, including dosage, timing, duration, and adherence, would improve comparability and reproducibility [21,24]. In addition, future studies should incorporate clinically relevant outcome measures that extend beyond muscle mass, including functional performance, return-to-sport quality, and long-term injury risk [52,53].

Finally, future work should move beyond a strictly muscle-centered perspective to incorporate broader aspects of rehabilitation, including connective tissue recovery, neuromuscular control, and the management of low energy availability and RED-S risk [25-28,55]. Integrating these dimensions will support the development of more comprehensive and clinically applicable nutrition frameworks for sports injury rehabilitation.

CONCLUSION

Muscle loss during post-injury rehabilitation is a rapid and multifactorial process driven by reduced mechanical loading, suppressed muscle protein synthesis, anabolic resistance, and broader injury-related metabolic alterations. Because early rehabilitation often requires restricted loading to protect healing tissues, exercise alone may be insufficient to preserve muscle mass and function. In this context, nutrition serves as an important supportive component of muscle preservation during rehabilitation.

Current evidence suggests that adequate energy availability and sufficient total protein intake represent the primary nutritional priorities for attenuating muscle loss during rehabilitation. Within this foundation, strategies such as appropriate protein distribution, timing, and the selective use of essential amino acids or leucine-enriched approaches may provide additional benefit, although their effects appear to be context-dependent. Creatine and omega-3 fatty acids may also be considered as adjunctive strategies, with their potential value likely emerging in specific phases or conditions rather than as universal interventions.

Importantly, effective rehabilitation nutrition should extend beyond preservation of muscle mass alone. Nutritional strategies should be individualized according to rehabilitation phase, integrated with progressive mechanical loading, and evaluated using clinically meaningful outcomes including neuromuscular recovery, functional performance, return-to-sport readiness, and reinjury risk. Although direct evidence in injured athletic populations remains limited, the proposed phase-informed and evidence-hierarchical framework provides a clinically applicable approach for integrating nutritional strategies with progressive rehabilitation loading while identifying priorities for future research.

Notes

CONFLICT OF INTEREST

The authors declare no conflict of interest.

AUTHOR CONTRIBUTIONS

Conceptualization: J Kim, K Lee; Data curation: K Lee; Methodology: K Lee, J Kim; Project administration: J Kim; Visualization: K Lee, J Kim; Writing - original draft: K Lee; Writing - review & editing: J Kim, K Lee.

References

1. Wall BT, Dirks ML, van Loon LJC. Skeletal muscle atrophy during short-term disuse: implications for age-related sarcopenia. Ageing Res Rev 2013;12(4):898–906.
2. Dirks ML, Wall BT, van de Valk B, Holloway TM, Holloway GP, et al. One week of bed rest leads to substantial muscle atrophy and induces whole-body insulin resistance in the absence of skeletal muscle lipid accumulation. Diabetes 2016;65(10):2862–75.
3. Glover EI, Phillips SM, Oates BR, Tang JE, Tarnopolsky MA, et al. Immobilization induces anabolic resistance in human myofibrillar protein synthesis with low- and high-dose amino acid infusion. J Physiol 2008;586(24):6049–61.
4. Kilroe SP, Fulford J, Holwerda AM, Jackman SR, Lee BP, et al. Short-term muscle disuse induces a rapid and sustained decline in daily myofibrillar protein synthesis rates. Am J Physiol Endocrinol Metab 2020;318(2):E117–30.
5. de Boer MD, Selby A, Atherton P, Smith K, Seynnes OR, et al. The temporal responses of protein synthesis, gene expression and cell signalling in human quadriceps muscle and patellar tendon to disuse. J Physiol 2007;585(Pt 1):241–51.
6. Taberner M, Allen T, Cohen DD. Progressing rehabilitation after injury: consider the control-chaos continuum. Br J Sports Med 2019;53(18):1132–6.
7. Buckthorpe M. Optimising the late-stage rehabilitation and return-to-sport training and testing process after ACL reconstruction. Sports Med 2019;49(7):1043–58.
8. Brook MS, Wilkinson DJ, Atherton PJ. Nutrient modulation in the management of disease-induced muscle wasting: evidence from human studies. Curr Opin Clin Nutr Metab Care 2017;20(6):433–9.
9. Narici MV, de Boer MD. Disuse of the musculo-skeletal system in space and on earth. Eur J Appl Physiol 2011;111(3):403–20.
10. Suetta C, Frandsen U, Jensen L, Jensen MM, Jespersen JG, et al. Aging affects the transcriptional regulation of human skeletal muscle disuse atrophy. PLoS One 2012;7(12):e51238.
11. Biolo G, Ciocchi B, Stulle M, Piccoli A, Lorenzon S, et al. Metabolic consequences of physical inactivity. J Ren Nutr 2005;15(1):49–53.
12. Breen L, Phillips SM. Skeletal muscle protein metabolism in the elderly: interventions to counteract the anabolic resistance of ageing. Nutr Metab (Lond) 2011;8:68.
13. Tipton KD. Nutritional support for exercise-induced injuries. Sports Med 2015;45 Suppl 1:S93–104.
14. Papadopoulou SK. Rehabilitation nutrition for injury recovery of athletes: the role of macronutrient intake. Nutrients 2020;12(8):2449.
15. Close GL, Sale C, Baar K, Bermon S. Nutrition for the prevention and treatment of injuries in track and field athletes. Int J Sport Nutr Exerc Metab 2019;29(2):189–97.
16. Smith-Ryan AE, Hirsch KR, Saylor HE, Gould LM, Blue MNM. Nutritional considerations and strategies to facilitate injury recovery and rehabilitation. J Athl Train 2020;55(9):918–30.
17. Loucks AB. Energy availability, not body fatness, regulates reproductive function in women. Exerc Sport Sci Rev 2003;31(3):144–8.
18. Mountjoy M, Sundgot-Borgen J, Burke L, Carter S, Constantini N, et al. The IOC consensus statement: beyond the Female Athlete Triad-relative energy deficiency in sport (RED-S). Br J Sports Med 2014;48(7):491–7.
19. Mountjoy M, Sundgot-Borgen JK, Burke LM, Ackerman KE, Blauwet C, et al. IOC consensus statement on relative energy deficiency in sport (RED-S): 2018 update. Br J Sports Med 2018;52(11):687–97.
20. Burke LM, Lundy B, Fahrenholtz IL, Melin AK. Pitfalls of conducting and interpreting estimates of energy availability in free-living athletes. Int J Sport Nutr Exerc Metab 2018;28(4):350–63.
21. Hughes DC, Ellefsen S, Baar K. Adaptations to endurance and strength training. Cold Spring Harb Perspect Med 2018;8(6):a029769.
22. Giraldo-Vallejo JE, Cardona-Guzmán MÁ, Rodríguez-Alcivar EJ, Kočí J, Petro JL, et al. Nutritional strategies in the rehabilitation of musculoskeletal injuries in athletes: a systematic integrative review. Nutrients 2023;15(4):819.
23. Wall BT, Morton JP, van Loon LJC. Strategies to maintain skeletal muscle mass in the injured athlete: nutritional considerations and exercise mimetics. Eur J Sport Sci 2015;15(1):53–62.
24. Howard EE, Pasiakos SM, Blesso CN, Fussell MA, Rodriguez NR. Divergent roles of inflammation in skeletal muscle recovery from injury. Front Physiol 2020;11:87.
25. Mountjoy M, Ackerman KE, Bailey DM, Burke LM, Constantini N, et al. 2023 International Olympic Committee's (IOC) consensus statement on Relative Energy Deficiency in Sport (REDs). Br J Sports Med 2023;57(17):1073–97.
26. Ackerman KE, Holtzman B, Cooper KM, Flynn EF, Bruinvels G, et al. Low energy availability surrogates correlate with health and performance consequences of relative energy deficiency in sport. Br J Sports Med 2019;53(10):628–33.
27. Burke LM, Castell LM, Casa DJ, Close GL, Costa RJS, et al. International Association of Athletics Federations consensus statement 2019: nutrition for athletics. Int J Sport Nutr Exerc Metab 2019;29(2):73–84.
28. Impey SG, Hammond KM, Shepherd SO, Sharples AP, Stewart C, et al. Fuel for the work required: a practical approach to amalgamating train-low paradigms for endurance athletes. Physiol Rep 2016;4(10):e12803.
29. Areta JL, Burke LM, Ross MLR, Camera DM, West DWD, et al. Timing and distribution of protein ingestion during prolonged recovery from resistance exercise alters myofibrillar protein synthesis. J Physiol 2013;591(9):2319–31.
30. Mamerow MM, Mettler JA, English KL, Casperson SL, Arentson-Lantz E, et al. Dietary protein distribution positively influences 24-h muscle protein synthesis in healthy adults. J Nutr 2014;144(6):876–80.
31. Norton LE, Layman DK. Leucine regulates translation initiation of protein synthesis in skeletal muscle after exercise. J Nutr 2006;136(2):533S–7S.
32. Churchward-Venne TA, Burd NA, Phillips SM. Nutritional regulation of muscle protein synthesis with resistance exercise: strategies to enhance anabolism. Nutr Metab (Lond) 2012;9:40.
33. Wilkinson DJ, Hossain T, Hill DS, Phillips BE, Crossland H, et al. Effects of leucine and its metabolite β-hydroxy-β-methylbutyrate on human skeletal muscle protein metabolism. J Physiol 2013;591(11):2911–23.
34. Tipton KD, Rasmussen BB, Miller SL, Wolf SE, Owens-Stovall SK, et al. Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol Endocrinol Metab 2001;281(2):E197–206.
35. Res PT, Groen B, Pennings B, Beelen M, Wallis GA, et al. Protein ingestion before sleep improves postexercise overnight recovery. Med Sci Sports Exerc 2012;44(8):1560–9.
36. Snijders T, Res PT, Smeets JSJ, van Vliet S, van Kranenburg J, et al. Protein ingestion before sleep increases muscle mass and strength gains during prolonged resistance-type exercise training in healthy young men. J Nutr 2015;145(6):1178–84.
37. Kreider RB, Kalman DS, Antonio J, Ziegenfuss TN, Wildman R, et al. International Society of Sports Nutrition position stand: safety and efficacy of creatine supplementation in exercise, sport, and medicine. J Int Soc Sports Nutr 2017;14:18.
38. Hespel P, Op’t Eijnde B, Van Leemputte M, Ursø B, Greenhaff PL, et al. Oral creatine supplementation facilitates the rehabilitation of disuse atrophy and alters the expression of muscle myogenic factors in humans. J Physiol 2001;536(Pt 2):625–33.
39. Op’t Eijnde B, Ursø B, Richter EA, Greenhaff PL, Hespel P. Effect of oral creatine supplementation on human muscle GLUT4 protein content after immobilization. Diabetes 2001;50(1):18–23.
40. Johnston APW, Burke DG, MacNeil LG, Candow DG. Effect of creatine supplementation during cast-induced immobilization on the preservation of muscle mass, strength, and endurance. J Strength Cond Res 2009;23(1):116–20.
41. Forbes SC, Candow DG, Ostojic SM, Roberts MD, Chilibeck PD. Meta-analysis examining the importance of creatine ingestion strategies on lean tissue mass and strength in older adults. Nutrients 2021;13(6):1912.
42. Antonio J, Candow DG, Forbes SC, Gualano B, Jagim AR, et al. Common questions and misconceptions about creatine supplementation: what does the scientific evidence really show? J Int Soc Sports Nutr 2021;18(1):13.
43. Candow DG, Forbes SC, Chilibeck PD, Cornish SM, Antonio J, et al. Variables influencing the effectiveness of creatine supplementation as a therapeutic intervention for sarcopenia. Front Nutr 2019;6:124.
44. Smith GI, Atherton P, Reeds DN, Mohammed BS, Rankin D, et al. Omega-3 polyunsaturated fatty acids augment the muscle protein anabolic response to hyperinsulinaemia-hyperaminoacidaemia in healthy young and middle-aged men and women. Clin Sci (Lond) 2011;121(6):267–78.
45. McGlory C, Galloway SDR, Hamilton DL, McClintock C, Breen L, et al. Temporal changes in human skeletal muscle and blood lipid composition with fish oil supplementation. Prostaglandins Leukot Essent Fatty Acids 2014;90(6):199–206.
46. McGlory C, Calder PC, Nunes EA. The influence of omega-3 fatty acids on skeletal muscle protein turnover in health, disuse, and disease. Front Nutr 2019;6:144.
47. Ochi E, Tsuchiya Y. Eicosapentaenoic acid (EPA) and docosahexaneoic acid (DHA) in muscle damage and function. Nutrients 2018;10(5):552.
48. Da Boit M, Sibson R, Sivasubramaniam S, Meakin JR, Greig CA, et al. Sex differences in the effect of fish-oil supplementation on the adaptive response to resistance exercise training in older people. Am J Clin Nutr 2017;105(1):151–8.
49. Philpott JD, Witard OC, Galloway SDR. Applications of omega-3 polyunsaturated fatty acid supplementation for sport performance. Res Sports Med 2019;27(2):219–37.
50. Ochi E, Tsuchiya Y, Yanagimoto K. Effect of eicosapentaenoic acids-rich fish oil supplementation on motor nerve function after eccentric contractions. J Int Soc Sports Nutr 2017;14:23.
51. Tsuchiya Y, Yanagimoto K, Nakazato K, Hayamizu K, Ochi E. Eicosapentaenoic and docosahexaenoic acids-rich fish oil supplementation attenuates strength loss and limited joint range of motion after eccentric contractions: a randomized, double-blind, placebo-controlled, parallel-group trial. Eur J Appl Physiol 2016;116(6):1179–88.
52. Ardern CL, Glasgow P, Schneiders A, Witvrouw E, Clarsen B, et al. 2016 consensus statement on return to sport from the first world congress in sports physical therapy, Bern. Br J Sports Med 2016;50(14):853–64.
53. Impellizzeri FM, McCall A, Ward P, Bornn L, Coutts AJ. Training load and its role in injury prevention, part I: back to the future. J Athl Train 2020;55(9):885–92.
54. Hortobágyi T, Dempsey L, Fraser D, Zheng D, Hamilton G, et al. Changes in muscle strength, muscle fibre size and myofibrillar gene expression after immobilization and retraining in humans. J Physiol 2000;524(Pt 1):293–304.
55. Aagaard P, Suetta C, Caserotti P, Magnusson SP, Kjaer M. Role of the nervous system in sarcopenia and muscle atrophy with aging: strength training as a countermeasure. Scand J Med Sci Sports 2010;20(1):49–64.
56. Brook MS, Wilkinson DJ, Phillips BE, Perez-Schindler J, Philp A, et al. Skeletal muscle homeostasis and plasticity in youth and ageing: impact of nutrition and exercise. Acta Physiol (Oxf) 2016;216(1):15–41.
57. Abadi A, Glover EI, Isfort RJ, Raha S, Safdar A, et al. Limb immobilization induces a coordinate down-regulation of mitochondrial and other metabolic pathways in men and women. PLoS One 2009;4(8):e6518.
58. Turnagöl HH, Koşar ŞN, Güzel Y, Aktitiz S, Atakan MM. Nutritional considerations for injury prevention and recovery in combat sports. Nutrients 2022;14(1):53.
59. Biensø RS, Ringholm S, Kiilerich K, Aachmann-Andersen NJ, Krogh-Madsen R, et al. GLUT4 and glycogen synthase are key players in bed rest-induced insulin resistance. Diabetes 2012;61(5):1090–9.
60. Krogh-Madsen R, Thyfault JP, Broholm C, Mortensen OH, Olsen RH, et al. A 2-week reduction of ambulatory activity attenuates peripheral insulin sensitivity. J Appl Physiol (1985) 2010;108(5):1034–40.

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Fig. 1.

Evidence-hierarchical and phase-informed nutritional framework for preserving skeletal muscle during sports injury rehabilitation. The framework summarizes the progression of rehabilitation from the acute inflammatory phase through immobilization, progressive reloading, and return-to-sport. Across each phase, key physiological mechanisms, evidence-informed nutritional priorities, and primary clinical objectives are integrated to support muscle preservation and functional recovery. Because direct intervention studies in injured athletic populations remain limited, the proposed framework synthesizes evidence from rehabilitation research, human disuse models, mechanistic investigations, and broader sports nutrition literature.

Table 1.

Proposed phase-informed and evidence-hierarchical nutritional strategies for mitigating muscle loss during rehabilitation after sports injuries (muscle-centered focus)

Strategy level Strategy Practical recommendation (starting point) Mechanistic rationale Evidence level/directness Notes/cautions
Foundation Energy availability Avoid clinically low energy availability (< 30 kcal/kg FFM/day); aim toward ~40-45 kcal/kg FFM/day when feasible (individualized) Supports MPS, reduces amino acid oxidation, attenuates anabolic resistance Moderate-high (indirect sport-related evidence) [13-20,25,26] Derived largely from broader athletic/RED-S literature; not injury-specific thresholds
Foundation Total protein intake ~1.6-2.2 g/kg/day; consider higher end during reduced loading or energy restriction Maintains substrate availability, offsets reduced MPS during disuse Moderate (disuse+sport-related extrapolation) [3,8-10,23,27,28] Ensure GI tolerance; emphasize high-quality protein sources
Optimization Protein distribution 3-5 evenly distributed protein feedings/day (~0.25-0.40 g/kg/meal) Repeated stimulation of MPS across the day under reduced anabolic sensitivity Moderate (human intervention studies) [29,30] Avoid long low-protein intervals; adapt to appetite and rehab schedule
Optimization Protein timing Align protein intake before/after rehabilitation sessions; consider pre-sleep protein where appropriate Enhances amino acid availability during periods of increased anabolic signaling Low-moderate (exercise models; limited injury-specific data) [34-36] Secondary to total intake and distribution; individual tolerance varies
Optimization EAA/leucine-enriched strategies Consider EAA (10-20 g) or leucine (~2-3 g per meal) when full protein targets are difficult to achieve Augments anabolic signaling and may partially overcome anabolic resistance Low-moderate (mechanistic+mixed human evidence) [31-33] Context-dependent; not a substitute for total protein adequacy
Adjunctive Creatine monohydrate Optional loading (~0.3 g/kg/day for 5-7 days), then 3-5 g/day maintenance Increases phosphocreatine availability; may improve training quality during reloading Low-moderate (disuse/retraining models) [37-43] Limited direct injury evidence; ensure hydration and screening where appropriate
Adjunctive Omega-3 (EPA+DHA) ~2-4 g/day combined EPA+DHA (individualized) May enhance anabolic sensitivity and modulate inflammation-related signaling Low (non-athlete+indirect evidence) [44-51] Heterogeneous evidence; consider diet, bleeding risk, and context

Recommendations are intended as practical starting points derived from a combination of direct, translational, and mechanistic evidence, and should not be interpreted as injury-specific prescriptive guidelines.

Table 2.

Example phase-informed implementation of muscle-preserving nutritional strategies during sports injury rehabilitation

Rehabilitation phase (functional context) Typical characteristics Primary objective Key nutrition priorities Example practical applications Monitoring focus
Protection/minimal loading phase (early immobilization or restricted loading; typically early post-injury) Limited mechanical loading; high anabolic resistance; reduced activity; possible appetite disruption Attenuate rapid muscle loss Foundation strategies: ensure energy availability; maintain total protein intake; improve protein distribution Maintain consistent meal pattern (3-5 protein feedings/day); avoid unintentional under-fueling; consider EAA when appetite is low Body mass trend; appetite; protein intake consistency; early strength decline
Optimization (conditional): EAA/leucine when intake is insufficient
Progressive reloading phase (reintroduction of structured rehabilitation loading) Gradual increase in loading; improving anabolic responsiveness; structured rehab sessions introduced Preserve muscle while supporting neuromuscular recovery and training quality Foundation: energy + total protein Align protein intake with rehab sessions; initiate creatine if appropriate; maintain consistent intake on training and non-training days Rehab session quality; fatigue; adherence; tolerance to increasing load
Optimization: protein timing around sessions; maintain distribution
Adjunct (context-dependent): consider creatine
Advanced reconditioning/return-to-sport phase (high-load, sport-specific preparation) Increased loading intensity; sport-specific training; higher metabolic demand Restore strength, hypertrophy, and performance capacity Foundation: energy adequacy adjusted to load; maintain high protein Adjust energy intake to match increased load; maintain high-quality protein intake; consider omega-3 if dietary intake is low Strength/power recovery; functional performance; readiness; body composition changes
Optimization:integrate protein timing with training; maintain distribution
Adjunct (conditional): creatine, omega-3 depending on context

Recommendations are intended as practical starting points derived from a combination of direct, translational, and mechanistic evidence, and should not be interpreted as injury-specific prescriptive guidelines.