Many intensive care unit (ICU) patients do not achieve target protein intakes particularly in the early days following admittance. This period of iatrogenic protein undernutrition contributes to a rapid loss of lean, in particular muscle, mass in the ICU. The loss of muscle in older (aged >60 years) patients in the ICU may be particularly rapid due to a perfect storm of increased catabolic factors, including systemic inflammation, disuse, protein malnutrition, and reduced anabolic stimuli. This loss of muscle mass has marked consequences. It is likely that the older patient is already experiencing muscle loss due to sarcopenia; however, the period of stay in the ICU represents a greatly accelerated period of muscle loss. Thus, on discharge, the older ICU patient is now on a steeper downward trajectory of muscle loss, more likely to have ICU-acquired muscle weakness, and at risk of becoming sarcopenic and/or frail. One practice that has been shown to have benefit during ICU stays is early ambulation and physical therapy (PT), and it is likely that both are potent stimuli to induce a sensitivity of protein anabolism. Thus, recommendations for the older ICU patient would be provision of at least 1.2-1.5 g protein/kg usual body weight/d, regular and early utilization of ambulation (if possible) and/or PT, and follow-up rehabilitation for the older discharged ICU patient that includes rehabilitation, physical activity, and higher habitual dietary protein to change the trajectory of ICU-mediated muscle mass loss and weakness.
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The capacity to utilize ingested protein for optimal support of protein synthesis and lean body mass is described within the paradigm of anabolic competence. Protein synthesis can be stimulated by physical exercise, however, it is not known if physical exercise affects post-exercise protein oxidation. Characterization of the driving forces behind protein oxidation, such as exercise, can contribute to improved understanding of whole body protein metabolism. The purpose of this study is to determine the effect of two levels of aerobic exercise intensity on immediate post-exercise exogenous protein oxidation. Sixteen healthy males with a mean (SD) age of 24 (4) years participated. The subjects' VO2-max was estimated with the Åstrand cycling test. Habitual dietary intake was assessed with a three-day food diary. Exogenous protein oxidation was measured by isotope ratio mass spectrometry. These measurements were initiated after the ingestion of a 30 g 13C-milk protein test drink that was followed by 330 minutes breath sample collection. On three different days with at least one week in between, exogenous protein oxidation was measured: 1) during rest, 2) after 15 minutes of aerobic exercise at 30% of VO2-max (moderate intensity), and 3) after 15 minutes of aerobic exercise at 60% of VO2-max (vigorous intensity). After vigorous intensity aerobic exercise, 31.8%±8.0 of the 30 g 13C-milk protein was oxidized compared to 26.2%±7.1 during resting condition (p = 0.012), and 25.4%±7.6 after moderate intensity aerobic exercise compared to resting (p = 0.711). In conclusion, exogenous protein oxidation is increased after vigorous intensity aerobic exercise which could be the result of an increased protein turnover rate.
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Purpose of reviewSkeletal muscle mass with aging, during critical care, and following critical care is a determinant of quality of life and survival. In this review, we discuss the mechanisms that underpin skeletal muscle atrophy and recommendations to offset skeletal muscle atrophy with aging and during, as well as following, critical care.Recent findingsAnabolic resistance is responsible, in part, for skeletal muscle atrophy with aging, muscle disuse, and during disease states. Anabolic resistance describes the reduced stimulation of muscle protein synthesis to a given dose of protein/amino acids and contributes to declines in skeletal muscle mass. Physical inactivity induces: anabolic resistance (that is likely exacerbated with aging), insulin resistance, systemic inflammation, decreased satellite cell content, and decreased capillary density. Critical illness results in rapid skeletal muscle atrophy that is a result of both anabolic resistance and enhanced skeletal muscle breakdown.SummaryInsofar as atrophic loss of skeletal muscle mass is concerned, anabolic resistance is a principal determinant of age-induced losses and appears to be a contributor to critical illness-induced skeletal muscle atrophy. Older individuals should perform exercise using both heavy and light loads three times per week, ingest at least 1.2 g of protein/kg/day, evenly distribute their meals into protein boluses of 0.40 g/kg, and consume protein within 2 h of retiring for sleep. During critical care, early, frequent, and multimodal physical therapies in combination with early, enteral, hypocaloric energy (ﰅ10–15kcal/kg/day), and high-protein (>1.2 g/kg/day) provision is recommended.
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