ABSTRACT
Background:The combined supplementation of vitamins C and E potentially can mitigate oxidative stress (OS) and accelerate recovery following exercise. However, there is little evidence and a lack of consensus on the effects of these vitamins for this purpose. The objective of this systematic review was to summarize the evidence on the effects of the combined supplementation of vitamins C and E in OS, inflammatory markers, muscle damage, muscle soreness, and musculoskeletal functionality following acute exercise. Methods: The search was carried out from inception until March 2021, on MEDLINE, EMBASE, Cochrane CENTRAL, Web of Science, and SPORT Discus. We included placebo-controlled randomized clinical trials (RCTs) that evaluated the effects of combined supplementation of vitamins C and E in OS, inflammatory markers, muscle damage, muscle soreness, and muscle strength following a single bout of exercise. Random-effect meta-analyses were used to compare pre to post-exercise mean changes in subjects who received supplementation with vitamins C and E or placebo versus controls. Data are presented as standard mean difference (SMD) and 95% confidence interval (95% CI). Results: Eighteen RCTs, accounting for data from 322 individuals, were included. The use of vitamins attenuated lipid peroxidation (SMD= -0.703; 95% CI= -1.035 to -0.372; p < 0.001), IL-6 (SMD= -0.576; 95%CI= -1.036 to -0.117; p = 0.014), and cortisol levels (SMD= -0.918; 95%CI= -1.475 to -0.361; p = 0.001) immediately, and creatine kinase levels 48 h following exercise (SMD= -0.991; 95%CI= -1.611 to -0.372; p = 0.002). Supplementing the combination of vitamins had no effects on protein carbonyls, reduced/oxidized glutathione ratio, catalase, interleukin-1Ra, C-reactive protein, lactate dehydrogenase, muscle soreness, and muscle strength. Conclusion: Prior supplementation of the combination of vitamins C and E attenuates OS (lipid peroxidation), the inflammatory response (interleukin-6), cortisol levels, and muscle damage (creatine kinase) following a session of exercise.
Subject(s)
Ascorbic Acid , Myalgia , Humans , Ascorbic Acid/pharmacology , Hydrocortisone/pharmacology , Dietary Supplements , Muscle, Skeletal , Randomized Controlled Trials as Topic , Vitamins/pharmacology , Oxidative Stress , Inflammation/drug therapy , Exercise/physiology , Muscle Strength , Creatine Kinase/pharmacologyABSTRACT
Background Emotional disorders are risk factors for atherosclerosis and consequent cardiovascular disease. However, it is not clear whether emotional symptoms (ESs) have direct effects on cardiovascular disease. The aim of the present study is to investigate the effects of early ESs on carotid atherosclerosis in young adults. Methods and Results We tested the association between expression of ESs at 11 and 15 years of age and carotid intima-media thickness at 18 years of age in the 1993 Pelotas Birth Cohort (N=5249, n=4336 with complete mental health data). ES s were assessed using the Strengths and Difficulties Questionnaire. Propensity score weighting procedure was run using generalized boosted regression model to adjust for potential confounding between exposure and outcome. We also tested whether traditional cardiovascular risk factors could mediate this relationship. Adjusted high expression of ESs , both at 11 and 15 years of age, led to mean increases in carotid intima-media thickness of 1.84 and 2.58 µm, respectively, at 18 years of age (both P<0.001). Longitudinal effects of ESs on atherosclerosis were direct and not significantly mediated by traditional cardiovascular risk factors. Male sex at age 15 years significantly enhanced the effects of ESs on carotid intima-media thickness at age 18 years ( P<0.001 for interaction): although high expression of ESs led to mean increases of 1.14 µm in females ( P<0.05), it led to mean increases of 5.83 µm in males ( P<0.001). Conclusions In this large birth cohort, expression of ESs in adolescence was longitudinally associated with a higher carotid intima-media thickness in young adults. The association is direct and not mediated by traditional cardiovascular risk factors. Interactions by sex might have important implications for designing future interventions.
Subject(s)
Atherosclerosis/diagnosis , Carotid Artery Diseases/diagnosis , Emotions/physiology , Mental Health , Risk Assessment/methods , Adolescent , Age Factors , Atherosclerosis/epidemiology , Atherosclerosis/psychology , Carotid Artery Diseases/epidemiology , Carotid Artery Diseases/psychology , Carotid Intima-Media Thickness , Child , Disease Progression , Female , Follow-Up Studies , Humans , Latin America/epidemiology , Male , Propensity Score , Retrospective Studies , Risk Factors , Surveys and Questionnaires , Time FactorsABSTRACT
The purpose of this study was to determine the effects of different therapeutic 1-MHz ultrasound waveforms on endothelial function before and after cyclooxygenase (COX) inhibition. Forty-two healthy volunteers aged 27.2 ± 3.8 y underwent interventions and an evaluation for endothelial function (n = 15; with COX inhibition, n = 15; duration of the vasodilator effect, n = 12) by technique flow-mediated dilation. Continuous ultrasound therapy (0.4 W/cm(2 SATA)), pulsed ultrasound therapy (20% duty cycle, 0.08 W/cm(2 SATA)) or placebo (equipment power off) was randomly applied over the brachial artery for 5 min. COX inhibition (aspirin) was carried out 30 min before treatments. In relation to the placebo, flow-mediated dilation increased by 4.8% using continuous ultrasound and by 3.4% using pulsed ultrasound. After COX, flow-mediated dilation was enhanced by 2.1% by continuous ultrasound and 2.6% by pulsed ultrasound. This vasodilation persisted for 20 min. Continuous and pulsed therapeutic 1-MHz ultrasound waveforms improved endothelial function in humans, which provided them with anti-inflammatory vascular effects.
Subject(s)
Blood Flow Velocity/physiology , Brachial Artery/physiology , Brachial Artery/radiation effects , Endothelium, Vascular/physiology , Endothelium, Vascular/radiation effects , Ultrasonic Therapy/methods , Adult , Aspirin/administration & dosage , Blood Flow Velocity/drug effects , Blood Flow Velocity/radiation effects , Brachial Artery/drug effects , Double-Blind Method , Endothelium, Vascular/drug effects , Female , Humans , Male , Reference Values , Treatment Outcome , Ultrasonic Waves , Vasodilation/physiology , Vasodilation/radiation effects , Vasodilator Agents/administration & dosage , Young AdultSubject(s)
Anxiety/epidemiology , Anxiety/psychology , Endothelium, Vascular/physiology , Neuropsychological Tests , Panic Disorder/epidemiology , Panic Disorder/psychology , Adult , Anxiety/diagnosis , Female , Follow-Up Studies , Humans , Male , Middle Aged , Panic Disorder/diagnosis , Predictive Value of Tests , Vasodilation/physiologyABSTRACT
The aim of this study was to investigate endothelial venous function, inflammatory markers, and systemic oxidative stress after an oral lipid overload (OLO). We studied 18 healthy adults (9 men; age, 29.2 +/- 0.9 years; body mass index, 22.3 +/- 0.4 kg/m(2)). Blood samples were collected in the fasting state and 3, 4, and 5 hour after the OLO (1000 kcal, 58% fat) for metabolic variables, oxidative stress, inflammatory markers, adiponectin, and resistin. Changes in vein diameter to phenylephrine, acetylcholine, and sodium nitroprusside (dorsal hand vein technique) were measured before and after the OLO. Oral lipid overload increased triglycerides (61 +/- 6 vs 134 +/- 17 mg/dL, P < .001), insulin (7.2 +/- 0.8 vs 10.7 +/- 1.3 muU/mL, P < .05), and resistin (5.38 +/- 0.5 vs 6.81 +/- 0.7 ng/mL, P < .05) and reduced antioxidant capacity (plasma total antioxidant capacity: 186.7 +/- 56 vs 161.8 +/- 50 U Trolox per microliter plasma, P < .01), vascular reactivity (171.3 +/- 85 vs 894.4 +/- 301 ng/mL, P < .001), and maximum acetylcholine venodilation (105.9% +/- 9% vs 61.0% +/- 7%, P < .05). No changes were observed for sodium nitroprusside. Post-OLO triglycerides were positively correlated with phenylephrine dose (rho = 0.38, P < .05) and resistin (rho = 0.43, P < .01) and negatively correlated with the maximum acetylcholine venodilation (rho = -0.36, P < .05). In conclusion, an OLO impaired venoconstriction responsiveness in healthy subjects, probably because of a reduction in the antioxidant capacity.