Certain commercial carbohydrate replacement products include slowly absorbed carbohydrates such as isomaltulose. Few studies have investigated the metabolic effects of ingesting isomaltulose during exercise and none have evaluated exercise performance and gastrointestinal comfort. Nine male cyclists participated postprandially during three trials of 2-h steady-state (S-S) exercise (60% W_max) followed by a 16 km time trial (TT) while ingesting 63 g∙h^-1 of either, 0.8:1 fructose: maltodextrin (F:M) or isomaltulose (ISO) or placebo-flavored water (PL). Data were analyzed by magnitude-based inferences. During S-S exercise, ISO and PL similarly increased plasma nonesterified fatty acid (NEFA) concentration (mean change ISO versus F:M: 0.18, 90%CI ± 0.21 mmol∙L^-1, 88% likelihood) and fat oxidation (10, 90%CI ± 9 g, 89% likelihood) while decreasing carbohydrate oxidation (-36, 90%CI ± 30.2 g, 91% likelihood) compared with F:M, despite equal elevations in blood glucose concentration with ISO and F:M. Rating of stomach cramps and bloating increased progressively with ISO (rating: 0-90 min S-S, weak; 120 min S-S, moderate; TT, strong) compared with F:M and PL (0-120 min S-S and TT, very weak). TT performance was substantially slower with ISO (mean change: 1.5, 90%CI ± 1.4 min, 94% likely harmful) compared with F:M. The metabolic response of ISO ingestion during moderate exercise to increase NEFA availability and fat oxidation despite elevating blood glucose concentration is anomalous for a carbohydrate supplement. However, ingesting isomaltulose at a continuous high frequency to meet the recommended carbohydrate replacement dose, results in severe gastrointestinal symptoms during prolonged or high intensity exercise and negatively affects exercise performance compared with fructose-maltodextrin supplementation.

Aims: To determine whether brachial blood pressure (BP)-independent relations between aortic pressure and cardiovascular damage are better explained by reflected (backward) (Pb) or forward (Pf) wave pressure effects. Methods: In 1174 participants from a community of African ancestry, we assessed central aortic pulse pressure (PPc), Pb, and Pf (radial applanation tonometry, SphygmoCor) as well as left ventricular mass index (LVMI) (n = 786), aortic pulse wave velocity (PWV) (n = 1019), carotid intima-media thickness (IMT) (n = 578), transmitral early-to-late left ventricular diastolic velocity (E/A) (n = 779) and estimated glomerular filtration rate (eGFR) (n = 1174). Results: Independent of mean arterial pressure and confounders, PPc, and both Pb and Pf were associated with end-organ measures or damage (P < 0.05 to P < 0.0001). With adjustments for brachial PP and confounders, Pb remained directly associated with LVMI (partial r = 0.09, P < 0.01), PWV (partial r = 0.28, P < 0.0001), and IMT (partial r = 0.28, P < 0.0001), and inversely associated with E/A (partial r = −0.31, P < 0.0001) and eGFR (partial r = −0.14, P < 0.0001). Similar relations were noted with the presence of end-organ damage (P < 0.05 to P < 0.0001). In contrast, with adjustments for brachial PP and confounders, Pf no longer retained direct relations with LVMI, PWV, and IMT or inverse relations with E/A and eGFR. Adjustments for Pb, but not Pf, diminished brachial PP-independent relationships between PPc and end-organ measures. Independent relations between Pb, but not Pf and end-organ measures, were largely attributed to Pb accounting for most of the variation in brachial-to-aortic PP amplification. Conclusions: In communities of African ancestry, brachial BP-independent relations between aortic pressure and end-organ changes are largely attributed to an impact of reflected rather than forward wave pressures.

In the present study, we examined the potential impact of adiponectin on carotid ultrasound determined atherosclerosis in 210 (119 black and 91 white) RA patients in mixed regression models. Total adiponectin concentrations were smaller in patients with compared to those without the metabolic syndrome (MetS) defined waist criterion (median (range) = 6.47 (1.23–34.54) versus 8.38 (0.82–85.30) ng/mL,P=0.02, resp.); both total and high molecular weight (HMW) adiponectin concentrations were larger in patients with compared to those without joint deformities (7.97 (0.82–85.30) and 3.51 (0.01–35.40) versus 5.36 (1.29–19.49) and 2.34 (0.01–19.49) ng/mL,P=0.003and 0.02, resp.). Total and HMW adiponectin concentrations were associated with carotid artery plaque in patients with MetS waist (odds ratio (95% CI) = 0.87 (0.76–0.99) and 0.92 (0.85–0.99) per 1-standard deviation increment,P=0.02for both) and those without joint deformities (odds ratio (95% CI) = 0.94 (0.88–0.99) and 0.94 (0.89–0.99),P=0.03for both). Plaque prevalence was lower in patients without compared to those with joint deformities (23.4% versus 42.6,P=0.004in multivariable analysis). In RA patients with abdominal obesity or no clinically evident joint damage, adiponectin concentrations are reduced but nevertheless associated with decreased carotid atherosclerosis.

To determine whether kidney function independently relates to endothelial activation and ultrasound determined carotid atherosclerosis in black and white Africans with rheumatoid arthritis (RA). We calculated the Jelliffe, 5 Cockcroft-Gault equations, Salazar-Corcoran, Modification of Diet in Renal Disease (MDRD) and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) estimated glomerular filtration rate (EGFR) equations in 233 (112 black) RA patients. The CKD-EPI eGFR was 0.1 for comparisons of AUC (SE)) for the other 8 equations. Based on optimal eGFR cutoff values with sensitivities and specificities ranging from 42 to 60% and 70 to 91% respectively, as determined in ROC curve analysis, a low eGFR increased the odds ratio for plaque 2.2 to 4.0 fold. Reduced kidney function is independently associated with atherosclerosis and endothelial activation in black and white Africans with RA, respectively. CKD is highly prevalent in black Africans with RA. Apart from the MDRD, eGFR equations are useful in predicting carotid plaque presence, a coronary heart disease equivalent, amongst black African RA patients.