Dietary proteins and amino acids in the control of the muscle mass during immobilization and aging: role of the MPS response

Abstract

Dietary proteins/essential amino acids (EAAs) are nutrients with anabolic properties that may increase muscle mass or attenuate muscle loss during immobilization and aging via the stimulation of muscle protein synthesis (MPS). An EAA's anabolic threshold, capable to maximize the stimulation of MPS has been hypothesized, but during certain conditions associated with muscle loss, this anabolic threshold seems to increase which reduces the efficacy of dietary EAAs to stimulate MPS. Preliminary studies have demonstrated that acute ingestion of dietary proteins/EAA (with a sufficient amount of leucine) was capable to restore the postprandial MPS during bed rest, immobilization or aging; however, whether these improvements translate into chronic increases (or attenuates loss) of muscle mass is equivocal. For example, although free leucine supplementation acutely increases MPS and muscle mass in some chronic studies, other studies have reported no increases in muscle mass following chronic leucine supplementation. In contrast, chronically increasing leucine intake via the consumption of an overall increase in dietary protein appears to be the most effective dietary intervention toward increasing or attenuating lean mass during aging; however, more research investigating the optimal dose and timing of protein ingestion is necessary. Several studies have demonstrated that decreases in postprandial MPS as a result of increased circulating oxidative and inflammatory are more responsible than muscle protein breakdown for the decreases in muscle mass during disuse and health aging. Therefore, nutritional interventions that reduce oxidation or inflammation in conjunction with higher protein intakes that overcome the anabolic resistance may enhance the MPS response to feeding and either increase muscle mass or attenuate loss. In preliminary studies, antioxidant vitamins and amino acids with antioxidant or anti-inflammatory properties show potential to restore the anabolic response associated with protein ingestion. More research, however, is required to investigate if these nutrients translate to increases in MPS and, ultimately, increased lean mass in aging humans. The purpose of the present review is to discuss the role of protein/EAA intake to enhance postprandial MPS during conditions associated with muscle loss, and bring new perspectives and challenges associated nutritional interventions aimed to optimize the anabolic effects of dietary protein/EAAs ingestion.

Utilization of Hydroxyl-Methyl Butyrate, Leucine, Glutamine and Arginine Supplementation in Nutritional Management of Sarcopenia—Implications and Clinical Considerations for Type 2 Diabetes Mellitus Risk Modulation

“…Even though free Leu supplementation acutely increases muscle protein synthesis, and muscle mass in some long-term studies, other studies have reported no increases in muscle mass following prolonged Leu supplementation [50]. Therefore, it appears that chronically increasing Leu intake via the consumption of an overall increase in dietary protein appears to be the most effective dietary intervention toward increasing or attenuating lean mass during aging.…”

Targeting Inflammation and Downstream Protein Metabolism in Sarcopenia: A Brief Up-Dated Description of Concurrent Exercise and Leucine-Based Multimodal Intervention

“…In healthy elderly subjects, the net loss of muscle mass seems to be the result of decreased rates of post-prandial muscle protein synthesis without alterations in the basal muscle protein synthesis (Volpi et al, 2001; D'Antona and Nisoli, 2010; Cholewa et al, 2017; Table 1), whereas in sarcopenic individuals (exhibiting a state of skeletal muscle atrophy), the progression toward sarcopenia ultimately involves alterations in skeletal muscle protein turnover, whereby rates of muscle protein breakdown (MPB) chronically exceed MPS (Trappe et al, 2004; Churchward-Venne et al, 2014). Presently, accurate methodologies have been utilized to measure protein synthesis in vivo , but when measuring protein degradation these methods have presented important limitations, especially when related to MPB (Zanchi et al, 2008).…”

“…The reason why increased MPB is the major determinant of muscle mass loss during sarcopenia seems to be linked to metabolic/endocrine alterations generated by co-morbidities which accompany sarcopenia. For example, co-morbidities (cancer, sepsis, heart failure) often lead to increased secretion of catabolic hormones such as cortisol, pro-inflammatory molecules such as cytokines, and increased ROS (reactive oxygen species) formation, which may result in increased muscle proteolysis (Crossland et al, 2008, 2010; Brocca et al, 2012; Santilli et al, 2015; Cholewa et al, 2017). …”

“…This suggests that regular exercise is necessary to avoid the occurrence and development of sarcopenia, but exercise alone may not be effective enough to completely prevent and/or delay sarcopenia. As previously discussed, healthy elderly subjects usually exhibit decreased post-prandial MPS (termed anabolic resistance) with no major signs of increased MPB (Dardevet et al, 2012; Cholewa et al, 2017). On the other hand, sarcopenic individuals usually show increased MPB rates (together with decreased MPS rates), dictating the majority of muscle atrophy that occurs (Cholewa et al, 2017).…”

“…As previously discussed, healthy elderly subjects usually exhibit decreased post-prandial MPS (termed anabolic resistance) with no major signs of increased MPB (Dardevet et al, 2012; Cholewa et al, 2017). On the other hand, sarcopenic individuals usually show increased MPB rates (together with decreased MPS rates), dictating the majority of muscle atrophy that occurs (Cholewa et al, 2017). With these concepts in mind, it is becoming clear that treatment of sarcopenia must involve multi-modal strategies aiming neutralizing the low-grade inflammation but also promoting increased post-prandial MPS.…”