No abstract

Dietary protein may be a modifiable risk factor for sarcopenia in older adults and should be studied further to determine its effects on preserving LM in this population.

Usual gait speed of less than 1 m/s identifies persons at high risk of health-related outcomes in well-functioning older people. Provision of a clinically meaningful cutpoint for usual gait speed may facilitate its use in clinical and research settings.

Background— Inflammation plays an important role in cardiovascular disease. The aim of this study is to investigate the predictive value of several inflammatory markers on the incidence of cardiovascular events in well-functioning older persons. Methods and Results— The subjects were 2225 participants 70 to 79 years old, without baseline cardiovascular disease, who were enrolled in the Health, Aging, and Body Composition study. Incident coronary heart disease (CHD), stroke, and congestive heart failure (CHF) events were detected during an average follow-up of 3.6 years. Blood levels of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) were assessed. After adjustment for potential confounders, IL-6 was significantly associated with all outcomes (CHD events, per IL-6 SD increase: RR, 1.27; 95% CI, 1.10 to 1.48; stroke events, per IL-6 SD increase: RR, 1.45; 95% CI, 1.12 to 1.86; CHF events, per IL-6 SD increase: RR, 1.72; 95% CI, 1.40 to 2.12). TNF-α showed significant associations with CHD (per TNF-α SD increase: RR, 1.22; 95% CI, 1.04 to 1.43) and CHF (per TNF-α SD increase: RR, 1.59; 95% CI, 1.30 to 1.95) events. CRP was significantly associated with CHF events (per CRP SD increase: RR, 1.48; 95% CI, 1.23 to 1.78). A composite summary indicator of inflammation showed a strong association with incident cardiovascular events, with an especially high risk if all 3 inflammatory markers were in the highest tertile. Conclusions— Findings suggest that inflammatory markers are independent predictors of cardiovascular events in older persons.

Importance More than 80% of patients with heart failure with preserved ejection fraction (HFPEF), the most common form of HF among older persons, are overweight/obese. Exercise intolerance is the primary symptom of chronic HFPEF and a major determinant of reduced quality-of-life (QOL). Objective To determine whether caloric restriction (Diet), or aerobic exercise training (Exercise), improves exercise capacity and QOL in obese older HFPEF patients. Design Randomized, attention-controlled, 2x2 factorial trial conducted from February 2009 November 2014. Setting Urban academic medical center. Participants 100 older (67±5 years) obese (BMI=39.3±5.6kg/m2) women (n=81) and men (n=19) with chronic, stable HFPEF enrolled from 577 patients initially screened (366 excluded by inclusion / exclusion criteria, 31 for other reasons, 80 declined participation). Twenty-six participants were randomized to Exercise alone, 24 to Diet alone, 25 to Diet+Exercise, and 25 to Control; 92 completed the trial. Interventions 20 weeks of Diet and/or Exercise; Attention Control consisted of telephone calls every 2 weeks. Main Outcomes and Measures Exercise capacity measured as peak oxygen consumption (VO2, ml/kg/min; primary outcome) and QOL measured by the Minnesota Living with HF Questionnaire (MLHF) total score (co-primary outcome; score range: 0–105, higher scores indicate worse HF-related QOL). Results By main effects analysis, peak VO2 was increased significantly by both interventions: Exercise main effect 1.2 ml/kg/min (95%CI: 0.7,1.7; p<0.001); Diet main effect 1.3 ml/kg/min (95%CI: 0.8,1.8; p<0.001). The combination of Exercise+Diet was additive (complementary) for peak VO2 (joint effect 2.5 ml/kg/min). The change in MLHF total score was non-significant with Exercise (main effect −1 unit; 95%CI: −8,5; p=0.70) and with Diet (main effect −6 units; 95%CI: −12,1; p=0.078). The change in peak VO2 was positively correlated with the change in percent lean body mass (r=0.32; p=0.003) and the change in thigh muscle/intermuscular fat ratio (r=0.27; p=0.02). There were no study-related serious adverse events. Exercise attendance was 84±14%; Diet compliance was 99±1%. Body weight decreased by 7±1 kg (7%) in Diet, 4±1 kg (3%) in Exercise, 11±1 kg (10%) in Exercise+Diet, and 1±1 kg (1%) in Control. Conclusion and Relevance Among obese older patients with clinically stable heart failure and preserved ejection fraction, caloric restriction diet or aerobic exercise training increased peak oxygen consumption, and the effects may be additive. Neither intervention had a significant effect on quality of life as measured by the Minnesota Living with Heart Failure Questionnaire, Clinical Trial Registration Clinicaltrials.gov, NCT00959660; https://clinicaltrials.gov/ct2/show/NCT00959660

Persistent, sub-clinical inflammation, as indicated by higher circulating levels of inflammatory mediators, is a prominent risk factor for several chronic diseases, as well as aging-related disability. As such, the inflammatory pathway is a potential therapeutic target for lifestyle interventions designed to reduce disease and disability. Physical exercise is well recognized as an important strategy for reducing the risk of chronic disease, and recent research has focused on its role in the improvement of the inflammatory profile. This review summarizes the evidence for and against the role of increasing physical activity in the reduction of chronic inflammation. Large population-based cohort studies consistently show an inverse association between markers of systemic inflammation and physical activity or fitness status, and data from several small-scale intervention studies support that exercise training diminishes inflammation. However, data from large, randomized, controlled trials designed to definitively test the effects of exercise training on inflammation are limited, and results are inconclusive. Future studies are needed to refine our understanding of the effects of exercise training on systemic low-grade inflammation, the magnitude of such an effect, and the amount of exercise necessary to elicit clinically meaningful changes in the deleterious association between inflammation and disease.

These findings provide evidence from a randomized controlled trial that a dietary intervention designed to elicit weight loss reduces overall inflammation in older, obese persons. Additional studies are needed to assess the effects of different modes and intensities of exercise on inflammation.

BackgroundObesity is associated with low-grade chronic inflammation, and serum markers of inflammation are independent risk factors for cardiovascular disease (CVD). However, the molecular and cellular mechanisms that link obesity to chronic inflammation and CVD are poorly understood.Methods and FindingsAcute-phase serum amyloid A (A-SAA) mRNA levels, and A-SAA adipose secretion and serum levels were measured in obese and nonobese individuals, obese participants who underwent weight-loss, and persons treated with the insulin sensitizer rosiglitazone. Inflammation-eliciting activity of A-SAA was investigated in human adipose stromal vascular cells, coronary vascular endothelial cells and a murine monocyte cell line. We demonstrate that A-SAA was highly and selectively expressed in human adipocytes. Moreover, A-SAA mRNA levels and A-SAA secretion from adipose tissue were significantly correlated with body mass index ( r = 0.47; p = 0.028 and r = 0.80; p = 0.0002, respectively). Serum A-SAA levels decreased significantly after weight loss in obese participants ( p = 0.006), as well as in those treated with rosiglitazone ( p = 0.033). The magnitude of the improvement in insulin sensitivity after weight loss was significantly correlated with decreases in serum A-SAA ( r = −0.74; p = 0.034). SAA treatment of vascular endothelial cells and monocytes markedly increased the production of inflammatory cytokines, e.g., interleukin (IL)-6, IL-8, tumor necrosis factor alpha, and monocyte chemoattractant protein-1. In addition, SAA increased basal lipolysis in adipose tissue culture by 47%. ConclusionsA-SAA is a proinflammatory and lipolytic adipokine in humans. The increased expression of A-SAA by adipocytes in obesity suggests that it may play a critical role in local and systemic inflammation and free fatty acid production and could be a direct link between obesity and its comorbidities, such as insulin resistance and atherosclerosis. Accordingly, improvements in systemic inflammation and insulin resistance with weight loss and rosiglitazone therapy may in part be mediated by decreases in adipocyte A-SAA production.