Healthy active older adults have enhanced K+ channel-dependent endothelial vasodilatory mechanisms.

Microvascular endothelial dysfunction, a precursor to atherosclerotic cardiovascular disease, increases with aging. Endothelium-derived hyperpolarizing factors (EDHFs), which act through K+ channels, regulate blood flow and are important to vascular health. It is unclear how EDHFs change with healthy aging. To evaluate microvascular endothelial reliance on K+ channel-mediated dilation as a function of age in healthy humans. Microvascular function was assessed using intradermal microdialysis in healthy younger (Y; n = 7; 3 M/4 W; 26 ± 1 yr) and older adults (O; n = 12; 5 M/7 W; 64 ± 2 yr) matched for V̇o2peak (Y: 39.0 ± 3.8, O: 37.6 ± 3.1 mL·kg-1·min-1). Participants underwent graded local infusions of: the K+ channel activator Na2S (10-6 to 10-1 M), acetylcholine (ACh, 10-10 to 10-1 M), ACh + the K+ channel inhibitor tetraethylammonium (TEA; 25 or 50 mM), and ACh + the nitric oxide synthase-inhibitor l-NAME (15 mM). Red blood cell flux was measured with laser-Doppler flowmetry and used to calculate cutaneous vascular conductance (CVC; flux/mean arterial pressure) as a percentage of each site-specific maximum (%CVCmax, 43°C+28 mM sodium nitroprusside). The %CVCmax response to Na2S was higher in older adults (mean, O: 51.7 ± 3.9% vs. Y: 36.1 ± 5.3%; P = 0.03). %CVCmax was lower in the ACh+TEA vs. the ACh site starting at 10-5 M (ACh: 34.0 ± 5.7% vs. ACh+TEA: 19.4 ± 4.5%; P = 0.002) in older and at 10-4 M (ACh: 54.5 ± 9.4% vs. ACh+TEA: 31.2 ± 6.7%; P = 0.0002) in younger adults. %CVCmax was lower in the ACh+l-NAME vs. the ACh site in both groups starting at 10-4 M ACh (Y: P < 0.001; O: P = 0.02). Healthy active older adults have enhanced K+ channel-dependent endothelial vasodilatory mechanisms, suggesting increased responsiveness to EDHFs with age.

Sunscreen or simulated sweat minimizes the impact of acute ultraviolet radiation on cutaneous microvascular function in healthy humans.

NEW FINDINGS: What is the central question of this study? Are ultraviolet radiation (UVR)-induced increases in skin blood flow independent of skin erythema? Does broad-spectrum UVR exposure attenuate NO-mediated cutaneous vasodilatation, and does sunscreen or sweat modulate this response? What are the main findings and their importance? Erythema and vascular responses to UVR are temporally distinct, and sunscreen prevents both responses. Exposure to UVR attenuates NO-mediated vasodilatation in the cutaneous microvasculature; sunscreen or simulated sweat on the skin attenuates this response. Sun over-exposure may elicit deleterious effects on human skin that are separate from sunburn, and sunscreen or sweat on the skin may provide protection. ABSTRACT: Exposure to ultraviolet radiation (UVR) may result in cutaneous vascular dysfunction independent of erythema (skin reddening). Two studies were designed to differentiate changes in erythema from skin vasodilatation throughout the 8 h after acute broad-spectrum UVR exposure with (+SS) or without SPF-50 sunscreen (study 1) and to examine NO-mediated cutaneous vasodilatation after acute broad-spectrum UVR exposure with or without +SS or simulated sweat (+SW) on the skin (study 2). In both studies, laser-Doppler flowmetry was used to measure red cell flux, and cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure). In study 1, in 14 healthy adults (24 ± 4 years old; seven men and seven women), the skin erythema index and CVC were measured over two forearm sites (UVR only and UVR+SS) before, immediately after and every 2 h for 8 h post-exposure (750 mJ cm-2 ). The erythema index began to increase immediately post-UVR (P < 0.05 at 4, 6 and 8 h), but CVC did not increase above baseline for the first 4-6 h (P ≤ 0.01 at 6 and 8 h); +SS prevented both responses. In study 2, in 13 healthy adults (24 ± 4 years old; six men and seven women), three intradermal microdialysis fibres were placed in the ventral skin of the forearm [randomly assigned to UVR (450 mJ cm-2 ), UVR+SS or UVR+SW], and one fibre (non-exposed control; CON) was placed in the contralateral forearm. After UVR, a standardized local heating (42°C) protocol quantified the percentage of NO-mediated vasodilatation (%NO). The UVR attenuated %NO compared with CON (P = 0.01). The diminished %NO was prevented by +SS (P < 0.01) and +SW (P < 0.01). Acute broad-spectrum UVR attenuates NO-dependent dilatation in the cutaneous microvasculature, independent of erythema. Sunscreen protects against both inflammatory and heating-induced endothelial dysfunction, and sweat might prevent UVR-induced reductions in NO-dependent dilatation.

Aerobic or resistance exercise performed the previous day does not attenuate postprandial hyperglycemia-induced endothelial dysfunction in overweight/obese adults.

INTRODUCTION: Postprandial hyperglycemia (PPH) impairs vascular endothelial function (VEF). A single bout of aerobic exercise (AE) attenuates PPH-induced decreases in brachial artery flow-mediated dilation (FMD), a non-invasive measure of VEF, in healthy adults for up to 17 h post-exercise. Studies examining the effects of resistance exercise (RE) on postprandial FMD responses are lacking. PURPOSE: We hypothesized that a single bout of exercise performed the prior evening would attenuate PPH-induced decreases in FMD, independent of exercise modality. METHODS: In a randomized, cross-over design, overweight/obese adults [n = 11 (8 women); 22 ± 4 years; 32.3 ± 5.8 kg m-2] completed 3 separate trials: control (seated rest), AE (30 min at ~ 60% VO2max), or whole-body RE (30 min, 6 exercises, 3 × 10-repetition maximum). Each trial occurred 14-17 h prior to an oral glucose tolerance test (OGTT). Brachial artery FMD and plasma glucose and insulin were measured prior to and at 30-min intervals for 2 h following the OGTT. Repeated-measures ANOVA and Bonferroni post hoc tests were used to evaluate differences within and between trials. RESULTS: Trials occurred 15.3 ± 1.0 h prior to the OGTT. Relative to baseline, FMD transiently decreased (P < 0.05) at 30-60 min post-ingestion, plasma glucose increased (P < 0.01) at 30-90 min post-ingestion, and plasma insulin increased (P < 0.01) at 30-120 min post-ingestion. No between trial differences were observed for FMD, glucose, or insulin. CONCLUSIONS: Aerobic or resistance exercise performed the evening prior to an OGTT does not attenuate postprandial decreases in brachial artery FMD in overweight/obese adults.

Effects of prior aerobic exercise on sitting-induced vascular dysfunction in healthy men.

INTRODUCTION: Acute aerobic exercise prevents sitting-induced impairment of flow-mediated dilation (FMD). Further, evidence suggests that sitting-induced impairment of FMD occurs via an oxidative stress-dependent mechanism that disrupts endothelial function. PURPOSE: We hypothesized that acute aerobic exercise would prevent impairment of femoral artery FMD by limiting oxidative stress responses that increase endothelin-1 (ET-1) levels and disrupt nitric oxide (NO) status. METHODS: In a randomized, cross-over study, healthy men (n = 11; 21.2 ± 1.9 years) completed two 3 h sitting trials that were preceded by 45 min of either quiet rest (REST) or a single bout of continuous treadmill exercise (65% maximal oxygen consumption) (EX). Superficial femoral artery FMD, plasma glucose, malondialdehyde (MDA), ET-1, arginine (ARG) and its related metabolites [homoarginine (HA), asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA)] were assessed at baseline, 1 h following EX (or REST) (0 h), and at 1 h intervals during 3 h of uninterrupted sitting. Data were analyzed using repeated measures ANOVA. RESULTS: During REST, femoral artery FMD declined from baseline (2.6 ± 1.8%) at 1, 2, and 3 h of sitting and resting shear rate decreased at 3 h. In contrast, when sitting was preceded by EX, femoral artery FMD (2.7 ± 2.0%) and resting shear rate responses were unaffected. No between trial differences were detected for plasma glucose, MDA, ET-1, ARG, HA, ADMA, or SDMA. CONCLUSION: Prior aerobic exercise prevented the decline in femoral artery FMD that is otherwise induced by prolonged sitting independent of changes in oxidative stress, ET-1, and NO status.

Temperature regulation during exercise in the heat: Insights for the aging athlete.

OBJECTIVE: The purpose of this review is to evaluate the currently-available literature regarding the impact of both primary aging and age-related fitness on thermoregulatory function during exercise in the heat. In so doing, we aim to (1) characterize the influence of fitness in mitigating age-related declines in thermoregulation, (2) address the limitations of prior experimental approaches for investigating age-related thermoregulatory impairments, (3) examine to what extent aerobic fitness can be maintained in the aging athlete, and (4) begin to address the specific environmental conditions in which age-related impairments in thermoregulatory function may place highly active older adults at increased risk for heat-related illness and injury and/or limited performance. DESIGN: Mini-review. METHODS: Review and synthesis of available information. RESULTS: The earth's climate is warming, accompanied by a consequently greater frequency and severity of extreme heat events. At the same time, lifespan is increasing and people of all ages are staying increasingly active. Age-related impairments in thermoregulatory function are well-documented, leading to increased heat-related health risks and reduced exercise/athletic performance for older adults in hot environmental conditions. High aerobic fitness improves body temperature regulation during exercise via augmented sweating and improved cardiovascular function, including cardiac output and skin blood flow, in humans of all ages. CONCLUSIONS: The masters athlete is better suited for exercise/heat-stress compared to his or her less fit peers. However, while age and thermoregulation in general has been studied extensively, research on the most fit older adults, including highly competitive athletes, is generally lacking.

Hydration Is More Important Than Exogenous Carbohydrate Intake During Push-to-the-Finish Cycle Exercise in the Heat.

Dehydration ≥2% loss of body mass is associated with reductions in performance capacity, and carbohydrate (CHO)-electrolyte solutions (CES) are often recommended to prevent dehydration and provide a source of exogenous carbohydrate during exercise. It is also well established that performance capacity in the heat is diminished compared to cooler conditions, a response attributable to greater cardiovascular strain caused by high skin and core temperatures. Because hydration status, environmental conditions, and carbohydrate availability interact to influence performance capacity, we sought to determine how these factors affect push-to-the-finish cycling performance. Ten young trained cyclists exercised at a moderate intensity (2.5 W·kg-1) in a hot-dry condition [40°C, 20% relative humidity (RH)] until dehydration of ~2% body mass. Subjects then consumed either no fluid (NF) or enough fluid (water, WAT; Gatorade®, GAT; or GoodSport™, GS) to replace 75% of lost body mass over 30 min. After a 30-min light-intensity warm-up (1.5 W·kg-1) in a 35°C, 20% RH environment, subjects then completed a 120-kJ time trial (TT). TT time-to-completion, absolute power, and relative power were significantly improved in WAT (535 ± 214 s, 259 ± 99 W, 3.3 ± 0.9 W·kg-1), GAT (539 ± 226 s, 260 ± 110 W, 3.3 ± 1.0 W·kg-1), and GS (534 ± 238 s, 262 ± 105 W, 3.4 ± 1.0 W·kg-1) compared to NF (631 ± 310 s, 229 ± 96 W, 3.0 ± 0.9 W·kg-1) all (p < 0.01) with no differences between WAT, GAT, and GS, suggesting that hydration is more important than carbohydrate availability during exercise in the heat. A subset of four subjects returned to the laboratory to repeat the WAT, GAT, and GS treatments to determine if between-beverage differences in time-trial performance were evident with a longer TT in thermoneutral conditions. Following dehydration, the ambient conditions in the environmental chamber were reduced to 21°C and 20% RH and subjects completed a 250-kJ TT. All four subjects improved TT performance in the GS trial (919 ± 353 s, 300 ± 100 W, 3.61 ± 0.86 W·kg-1) compared to WAT (960 ± 376 s, 283 ± 91 W, 3.43 ± 0.83 W·kg-1), while three subjects improved TT performance in the GAT trial (946 ± 365 s, 293 ± 103 W, 3.60 ± 0.97 W·kg-1) compared to WAT, highlighting the importance of carbohydrate availability in cooler conditions as the length of a push-to-the-finish cycling task increases.

Hydration Efficacy of a Milk Permeate-Based Oral Hydration Solution.

Milk permeate is an electrolyte-rich, protein- and fat-free liquid with a similar carbohydrate and mineral content to that of milk. Its hydration efficacy has not been examined. The beverage hydration index (BHI) has been used to compare various beverages to water in terms of post-ingestion fluid balance and retention. Our purpose was to compare the BHI (and related physiological responses) of a novel milk permeate solution (MPS) to that of water and a traditional carbohydrate-electrolyte solution (CES). Over three visits, 12 young subjects consumed 1 L of water, CES, or MPS. Urine samples were collected immediately post-ingestion and at 60, 120, 180, and 240 min. BHI was calculated by dividing cumulative urine output after water consumption by cumulative urine output for each test beverage at each time point. The BHI for MPS was significantly higher at all time points compared to water (all p < 0.001) and CES (all p ≤ 0.01) but did not differ between CES and water at any time point. Drinking 1 L of MPS resulted in decreased cumulative urine output across the subsequent 4 h compared to water and CES, suggesting that a beverage containing milk permeate is superior to water and a traditional CES at sustaining positive fluid balance post-ingestion.