Association of dietary protein intake, inflammation with muscle mass, physical performance and incident sarcopenia in Chinese community-dwelling older adults

Abstract

ObjectivesInflammation and impaired muscle synthesis are important factors of sarcopenia. Plant protein may reduce inflammation but may not be as efficient as animal protein in providing essential amino acids. We therefore examined the associations between dietary protein intake and changes in muscle mass and physical performance, incident sarcopenia, and the interaction effect of inflammation. DesignProspective cohort study. SettingThe Mr. OS and Ms. OS (Hong Kong) cohort. ParticipantsA total of 2,811 sarcopenia-free participants and 569 sarcopenia participants aged ≥65 years were recruited from communities. MeasurementsDietary protein intake was assessed using a validated food frequency questionnaire. Serum high-sensitivity C-reactive protein (hs-CRP) was measured. Linear regression examined the associations between dietary protein intake and 4-year changes in muscle mass and physical performance. Cox regression examined the association between dietary protein intake and incident sarcopenia. ResultsHigher plant protein intake, but not total and animal protein, was associated with less decline in muscle mass and gait speed among sarcopenia-free participants. Conversely, higher ratio of animal-to-plant protein was associated with reduced muscle mass loss among participants with sarcopenia. The highest tertile of plant protein intake was associated with lower incident sarcopenia risk (HR: 0.75, 95% CI: 0.57−0.98; P-trend = 0.034) compared to the lowest tertile. Notably, this association was observed among participants with higher serum hs-CRP levels (HR: 0.57, 95% CI: 0.34−0.95), but not in those with lower hs-CRP levels. ConclusionDietary animal and plant protein intake have differential associations with muscle mass and physical performance in older adults with and without sarcopenia. The role of plant protein in preventing sarcopenia involves modulation of inflammation.