Sleep disorders are associated with inflammation and sympathetic activation, which are suspected to induce endothelial dysfunction, a key factor in the increased risk of cardiovascular disease. Less is known about the early effects of acute sleep deprivation on vascular function. We evaluated microvascular reactivity and biological markers of endothelial activation during continuous 40 h of total sleep deprivation (TSD) in 12 healthy men (29 +/- 3 yr). The days before [day 1 (D1)] and during TSD (D3), at 1200 and 1800, endothelium-dependent and -independent cutaneous vascular conductance was assessed by iontophoresis of acetylcholine and sodium nitroprusside, respectively, coupled to laser-Doppler flowmetry. At 0900, 1200, 1500, and 1800, heart rate (HR) and instantaneous blood pressure (BP) were recorded in the supine position. At D1, D3, and the day after one night of sleep recovery (D4), markers of vascular endothelial cell activation, including soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, and interleukin-6 were measured from blood samples at 0800. Compared with D1, plasma levels of E-selectin were raised at D3, whereas intercellular adhesion molecule-1 and interleukin-6 were raised at D4 (P< 0.05). The endothelium-dependent and -independent CVC were significantly decreased after 29 h of TSD (P < 0.05). By contrast, HR, systolic BP, and the normalized low-frequency component of HR variability (0.04-0.15 Hz), a marker of the sympathetic activity, increased significantly within 32 h of TSD (P < 0.05). In conclusion, acute exposure to 40 h of TSD appears to cause vascular dysfunction before the increase in sympathetic activity and systolic BP.

Here, we studied muscle-specific and muscle-related miRNAs in plasma of exercising humans. Our aim was to determine whether they are affected by eccentric and/or concentric exercise modes and could be biomarkers of muscle injuries or possible signaling molecules. On two separate days, nine healthy subjects randomly performed two 30-min walking exercises, one downhill (high eccentric component) and one uphill (high concentric component). Perceived exertion and heart rate were higher during the uphill exercise, while subjective pain and ankle plantar flexor strength losses within the first 48-h were higher following the downhill exercise. Both exercises increased serum creatine kinase and myoglobin with no significant differences between conditions. Plasma levels of circulating miRNAs assessed before, immediately after, and at 2-, 6-, 24-, 48-, and 72-h recovery showed that 1) hsa-mir-1, 133a, 133b, and 208b were not affected by concentric exercise but significantly increased during early recovery of eccentric exercise (2 to 6 h); 2) hsa-mir-181b and 214 significantly and transiently increased immediately after the uphill, but not downhill, exercise. The muscle-specific hsa-mir-206 was not reliably quantified and cardiac-specific hsa-mir-208a remained undetectable. In conclusion, changes in circulating miRNAs were dependent on the exercise mode. Circulating muscle-specific miRNAs primarily responded to a downhill exercise (high eccentric component) and could potentially be alternative biomarkers of muscle damage. Two muscle-related miRNAs primarily responded to an uphill exercise (high exercise intensity), suggesting they could be markers or mediators of physiological adaptations.

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The Ramadan fasting (RF) period is associated with changes in sleep habits and increased sleepiness, which may affect physical performance in athletes, and may induce metabolic, hormonal, and inflammatory disturbances. In 8 middle-distance athletes (25.0 +/- 1.3 years), a maximal aerobic velocity (MAV) test was performed 5 days before RF (day -5), and on days 7 and 21 of RF. The same days, saliva samples were collected to determine cortisol and testosterone concentrations before and after the MAV test. Blood samples were collected before RF (P1), at the end of RF (P2), and 1 week post RF (P3). Plasma levels of interleukin (IL)-6, a mediator of sleepiness and energy availability, were determined. We also evaluated changes in metabolic and hormonal parameters, mood state, and nutritional and sleep profiles. During RF, mean body mass and body fat did not statistically change. Compared with day -5, MAV values decreased at days 7 and 21 (p < 0.05, respectively), while testosterone/cortisol ratio values did not change significantly. Nocturnal sleep time and energy intake were lower at day 21 than before RF (day 0/P1) (p < 0.05). At the end of RF (day 31), the fatigue score on the Profile of Mood States questionnaire was increased (p < 0.001). For P2 vs. P1, IL-6 was increased (1.19 +/- 0.25 vs. 0.51 +/- 0.13 pg.mL-1; p < 0.05), melatonin levels were decreased (p < 0.05), and adrenalin and noradrenalin were increased (p < 0.01 and p < 0.001, respectively). At 7 days post RF, all parameters recovered to pre-RF values. In conclusion, RF is accompanied by significant metabolic, hormonal, and inflammatory changes. Sleep disturbances, energy deficiency, and fatigue during RF may decrease physical performance in Muslim athletes who maintain training. Reduction of work load and (or) daytime napping may represent adequate strategies to counteract RF effects for Muslim athletes.