Prognostic value of basal high-sensitive cardiac troponin levels on mortality in the general population: A meta-analysis.

Interest in the use of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) has expanded from diagnosis of acute myocardial infarction to risk assessment for morbidity and mortality. Although cTnT and cTnI were shown to have equivalent diagnostic performance in the setting of suspected acute myocardial infarction, potential prognostic differences are largely unexplored.The aim of this study is to quantify and compare the relationship between cTnT and cTnI, and cardiovascular and all-cause mortality in the general population.Medline, Embase, and the Cochrane Library (from inception through October 2016) were searched for prospective observational cohort studies reporting on the prognostic value of basal high-sensitive cTnT and/or cTnI levels on cardiovascular and all-cause mortality in the general population. Data on study characteristics, participants' characteristics, outcome parameters, and quality [according to the Effective Public Health Practice Project (EPHPP) "Quality Assessment Tool For Quantitative Studies] were retrieved. Hazard ratios per standard deviation increase in basal cardiac troponin level (HR per 1-SD; retrieved from the included articles or estimated) were pooled using a random-effects model.On a total of 2585 reviewed citations, 11 studies, with data on 65,019 participants, were included in the meta-analysis. Random effects pooling showed significant associations between basal cardiac troponin levels and HR for cardiovascular and all-cause mortality [HR per 1-SD 1.29 (95% confidence interval, 95% CI, 1.20-1.38) and HR per 1-SD 1.18 (95% CI, 1.11-1.26), respectively]. Stratified analyses showed higher HRs for cTnT than cTnI [cardiovascular mortality: cTnT HR per 1-SD 1.37 (95% CI, 1.23-1.52); and cTnI HR per 1-SD 1.21 (95% CI, 1.16-1.26); all-cause mortality: cTnT HR per 1-SD 1.31 (955 CI, 1.13-1.53); and cTnI HR per 1-SD 1.14 (95% CI, 1.06-1.22)]. These differences were significant (P < 0.01) in meta-regression analyses for cardiovascular mortality but did not reach statistical significance for all-cause mortality.Elevated, basal cTnT, and cTnI show robust associations with an increased risk of cardiovascular and all-cause mortality during follow-up in the general population.Systematic review registration number PROSPERO CRD42014006964.

Impact of caffeine and protein on postexercise muscle glycogen synthesis.

BACKGROUND: Both protein and caffeine coingestion with CHO have been suggested to represent effective dietary strategies to further accelerate postexercise muscle glycogen synthesis in athletes. PURPOSE: This study aimed to assess the effect of protein or caffeine coingestion on postexercise muscle glycogen synthesis rates when optimal amounts of CHO are ingested. METHODS: Fourteen male cyclists were studied on three different test days. Each test day started with a glycogen-depleting exercise session. This was followed by a 6-h recovery period, during which subjects received 1.2 g·kg⁻¹·h⁻¹ CHO, the same amount of CHO with 0.3 g·kg⁻¹·h⁻¹ of a protein plus leucine mixture (CHO + PRO), or 1.7 mg·kg⁻¹·h⁻¹ caffeine (CHO + CAF). All drinks were enriched with [U-¹³C6]-labeled glucose to assess potential differences in the appearance rate of ingested glucose from the gut. Muscle biopsies were collected immediately after cessation of exercise and after 6 h of postexercise recovery. RESULTS: The plasma insulin response was higher in CHO + PRO compared with CHO and CHO + CAF (P < 0.01). Plasma glucose responses and glucose appearance rates did not differ between experiments. Muscle glycogen synthesis rates averaged 31 ± 4, 34 ± 4, and 31 ± 4 mmol·kg⁻¹ dry weight·h⁻¹ in CHO, CHO + PRO, and CHO + CAF, respectively (P = NS). In accordance, histochemical analyses did not show any differences between net changes in Type I and Type II muscle fiber glycogen content between experiments. CONCLUSIONS: Coingestion of protein or caffeine does not further accelerate postexercise muscle glycogen synthesis when ample amounts of CHO (1.2 g·kg⁻¹·h⁻¹) are ingested.