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Purpose : To examine data reporting characteristics in sports nutrition. Methods : We examined 236 papers from ten journals published in 2016. The primary outcome was statistical variance associated with treatment (SD (correct) vs. SEM or CI). Secondary outcomes included the reporting of: (a) effect sizes (Y/N); (b) outcome prioritization (Y/N; primary, secondary, etc.) and (c) statistical variance relative to change from baseline (CI (correct) vs. SD or SEM). As tertiary/exploratory outcome, we examined whether authors stated a directed hypothesis. Statistical evaluation was performed using chi-square analyses. Results : We observed significant trends for all analyses ( p < 0.001) and between category comparisons ( p < 0.002). For the primary outcome, 128 (59%) articles correctly used SD to denote treatment variance, while 79 (36%) and 11 (5%) used SEM and CI, respectively. For secondary outcomes, 63 articles (29%) reported effect sizes, while 155 (71%) did not. Additionally, 188 articles (86%) did not prioritize outcomes, 134 articles (61%) stated no hypotheses and 40 (19%, out of 100) articles used CI to denote change scores vs. SD (19%, n = 41) and SEM ( n = 10, 5%). Eight articles (4%) reported no variance terms. Conclusions : Overall, there are gaps regarding reporting in sports nutrition. Editors, journal publishers, and the field of exercise science alike should consider these outcomes and provide editorial staff, reviewers and authors with more concrete guidelines.

Reductions in hydrogen sulfide (H 2 S) production have been implicated in the pathogenesis of vascular dysfunction in animal models of hypertension; however, no studies have examined a functional role for H 2 S in contributing to microvascular dysfunction in hypertensive (HTN) adults. We hypothesized that endogenous production of H 2 S would be reduced, impaired endothelium-dependent vasodilation would be mediated by reductions in H 2 S-dependent vasodilation, and vascular responsiveness to exogenous H 2 S (sodium sulfide) would be attenuated in HTN compared to normotensive adults. Fifteen normotensive (51±2 years; blood pressure, 116±3/76±3 mm Hg) and 14 HTN adults (57±2 years; blood pressure 140±3/89±2 mm Hg) participated. H 2 S biosynthetic enzyme expression (Western blot) and substrate-dependent H 2 S production (amperometric probe) were measured in cutaneous tissue homogenates. Red cell flux (laser Doppler flowmetry) was measured during graded perfusions of acetylcholine (ACh; 10 -6 -10 -1 mol/L) and sodium sulfide (10 -5 -10 1 mol/L) using intradermal microdialysis; the functional role of H 2 S was determined using pharmacological inhibition with aminooxyacetic acid (0.5 mmol/L). H 2 S biosynthetic enzyme expression and substrate-dependent H 2 S production were reduced in HTN adults (all P <0.05). ACh-induced endothelium-dependent vasodilation was blunted in HTN adults ( P =0.012). Aminooxyacetic acid attenuated ACh-induced vasodilation in normotensive adults (ACh, 1.31±0.13 versus ACh+aminooxyacetic acid, 1.07±0.09 flux/mm Hg; P =0.025) but had no effect on vasodilation in HTN adults (ACh, 1.16±0.10 versus ACh+aminooxyacetic acid, 1.37±0.11 flux/mm Hg; P =0.47). Sodium sulfide-induced vasodilation was not different between groups. Collectively, these findings indicate that while the microvasculature maintains the ability to vasodilate in response to exogenous H 2 S, reductions in endogenous synthesis and H 2 S-dependent vasodilation contribute to endothelial dysfunction in human hypertension., (© 2017 American Heart Association, Inc.)

Key Points: Hydrogen sulphide (H2 S) is vasoprotective, attenuates inflammation and modulates blood pressure in animal models; however, its specific mechanistic role in the human vasculature remains unclear. In the present study, we report the novel finding that the enzymes responsible for endogenous H2 S production, cystathionine-γ-lyase and 3-mercaptopyruvate sulphurtransferase, are expressed in the human cutaneous circulation. Functionally, we show that H2 S-induced cutaneous vasodilatation is mediated, in part, by tetraethylammonium-sensitive calcium-dependent potassium channels and not by ATP-sensitive potassium channels. In addition, nitric oxide and cyclo-oxygenase-derived byproducts are required for full expression of exogenous H2 S-mediated cutaneous vasodilatation. Future investigations of the potential role for H2 S with respect to modulating vascular function in humans may have important clinical implications for understanding the mechanisms underlying vascular dysfunction characteristic of multiple cardiovascular pathologies., Abstract: The present study aimed to identify the presence of cystathionine-γ-lyase (CSE) and 3-mercaptopyruvate sulphurtransferase (3-MST), which endogenously produce hydrogen sulphide (H2 S), and to functionally examine the mechanisms of H2 S-induced vasodilatation in the human cutaneous microcirculation. CSE and 3-MST were quantified in forearm skin samples from 5 healthy adults (24 ± 3 years) using western blot analysis. For functional studies, microdialysis fibres were placed in the forearm skin of 12 healthy adults (25 ± 3 years) for graded infusions (0.01-100 mm) of sodium sulphide (Na2 S) and sodium hydrogen sulphide (NaHS). To define the mechanisms mediating H2 S-induced vasodilatation, microdialysis fibres were perfused with Ringer solution (control), a ATP-sensitive potassium channel (KATP ) inhibitor, an intermediate calcium-dependent potassium channel (KCa ) inhibitor, a non-specific KCa channel inhibitor or triple blockade. To determine the interaction of H2 S-mediated vasodilatation with nitric oxide (NO) and cyclo-oxygenase (COX) signalling pathways, microdialysis fibres were perfused with Ringer solution (control), a non-specific NO synthase inhibitor, a non-selective COX inhibitor or combined inhibition during perfusion of increasing doses of Na2 S. CSE and 3-MST were expressed in all skin samples. Na2 S and NaHS elicited dose-dependent vasodilatation. Non-specific KCa channel inhibition and triple blockade blunted Na2 S-induced vasodilatation (P < 0.05), whereas KATP and intermediate KCa channel inhibition had no effect (P > 0.05). Separate and combined inhibition of NO and COX attenuated H2 S-induced vasodilatation (all P < 0.05). CSE and 3-MST are expressed in the human microvasculature. Exogenous H2 S elicits cutaneous vasodilatation mediated by KCa channels and has a functional interaction with both NO and COX vasodilatatory signalling pathways., (© 2015 The Authors. The Journal of Physiology © 2015 The Physiological Society.)

Localized exogenous R-tetrahydrobiopterin (R-BH(4)) corrects the deficit in local heat-induced vasodilation (VD) in hypercholesterolemic (HC) human skin through one of two plausible mechanisms: by serving as an essential cofactor to stabilizing endothelial nitric oxide (NO) synthase (eNOS) or through generalized antioxidant effects. We used the stereoisomer S-BH(4), which has the same antioxidant properties but does not function as an essential NOS cofactor, to elucidate the mechanism by which R-BH(4) restores cutaneous VD in HC humans. Intradermal microdialysis fibers were placed in 20 normocholesterolemic (NC), 13 midrange cholesterolemic (MC), and 18 HC (LDL: 94 ± 3, 124 ± 3 and 179 ± 6 mg/dl, respectively) men and women to perfuse Ringer (control site) and R-BH(4). In 10 NC, 13 MC, and 9 HC subjects (LDL: 94 ± 3, 124 ± 3, 180 ± 10 mg/dl), S-BH(4) was perfused at a third microdialysis site. Skin blood flow was measured during a standardized local heating protocol to elicit eNOS-dependent VD. After cutaneous vascular conductance (CVC = LDF/MAP) plateaued, NO-dependent VD was quantified by perfusing N(G)-nitro-l-arginine methyl ester (l-NAME). Data were normalized as %CVC(max). Fully expressed VD (NC: 97.9 ± 2.3 vs. MC: 85.4 ± 5.4, HC: 79.9 ± 4.2%CVC(max)) and the NO-dependent portion (NC: 62.1 ± 3 vs. MC: 45.8 ± 3.9, HC: 35.7 ± 2.8%CVC(max)) were reduced in HC (both P < 0.01 vs. NC), but only the fully expressed VD was reduced in MC (P < 0.01 vs. NC). R-BH(4) increased the fully expressed (93.9 ± 3.4%CVC(max); P < 0.01) and NO-dependent VD (52.1 ± 5.1%CVC(max); P < 0.01) in HC but not in NC or MC. S-BH(4) increased full-expressed VD in HC (P < 0.01) but did not affect NO-dependent VD in HC or MC. In contrast S-BH(4) attenuated NO-dependent VD in NC (control: 62.1 ± 3 vs. S-BH(4): 41.6 ± 7%CVC(max); P < 0.001). Exogenous R-BH(4) restores NO-dependent VD in HC human skin predominantly through NOS coupling mechanisms but increases full expression of the local heating response through generalized antioxidant properties.