Rebecca V. Vince

Exercise-induced dehydration with and without environmental heat stress results in increased oxidative stress

While in vitro work has revealed that dehydration and hyperthermia can elicit increased cellular and oxidative stress, in vivo research linking dehydration, hyperthermia, and oxidative stress is limited. The purpose of this study was to investigate the effects of exercise-induced dehydration with and without hyperthermia on oxidative stress. Seven healthy male, trained cyclists (power output (W) at lactate threshold (LT): 199 ± 19 W) completed 90 min of cycling exercise at 95% LT followed by a 5-km time trial (TT) in 4 trials: (i) euhydration in a warm environment (EU-W, control), (ii) dehydration in a warm environment (DE-W), (iii) euhydration in a thermoneutral environment (EU-T), and (iv) dehydration in a thermoneutral environment (DE-T) (W: 33.9 ± 0.9 °C; T: 23.0 ± 1.0 °C). Oxidized glutathione (GSSG) increased significantly postexercise in dehydration trials only (DE-W: p < 0.01, DE-T: p = 0.03), and while not significant, total glutathione (TGSH) and thiobarbituric acid reactive substances (TBARS) tended to increase postexercise in dehydration trials (p = 0.08 for both). Monocyte heat shock protein 72 (HSP72) concentration was increased (p = 0.01) while lymphocyte HSP32 concentration was decreased for all trials (p = 0.02). Exercise-induced dehydration led to an increase in GSSG concentration while maintenance of euhydration attenuated these increases regardless of environmental condition. Additionally, we found evidence of increased cellular stress (measured via HSP) during all trials independent of hydration status and environment. Finally, both 90-min and 5-km TT performances were reduced during only the DE-W trial, likely a result of combined cellular stress, hyperthermia, and dehydration. These findings highlight the importance of fluid consumption during exercise to attenuate thermal and oxidative stress during prolonged exercise in the heat.

Practical Recommendations for Coaches and Athletes: A Meta-Analysis of Sodium Bicarbonate Use for Athletic Performance

Abstract Peart, DJ, Siegler, JC, and Vince, RV. Practical recommendations for coaches and athletes: A meta-analysis of sodium bicarbonate use for athletic performance. J Strength Cond Res 26(7): 1975–1983, 2012—Sodium bicarbonate (NaHCO3) is a buffering agent that is suggested to improve performance by promoting the efflux of hydrogen ions from working cells and tissues. Research surrounding its efficacy as an ergogenic aid is conflicting, making it difficult to draw conclusions as to its effectiveness for training and competition. This study performed a meta-analysis of relevant research articles to allow the development of concise practical recommendations for coaches and athletes. The overall effect size for the influence of NaHCO3 on performance was moderate, and was significantly lower for specifically trained as opposed to recreationally trained participants.

Endothelial function and stress response after simulated dives to 18 msw breathing air or oxygen.

INTRODUCTION Decompression sickness is caused by gas bubbles released upon decompression. These bubbles have the potential to occlude blood vessels and damage the vascular endothelium. The aim of this study was to quantify damage to the vascular endothelium resulting from decompression by measuring endothelial microparticles (MP) and endothelial function. METHODS Five healthy male volunteers undertook a simulated (hyperbaric chamber) air dive and 1 wk later a second dive breathing 100% oxygen at 283 kPa (18 msw) for 60 min bottom time, decompressed with 5-min stops at 161 kPa (6 msw) and 131 kPa (3 msw). Endothelial function was tested pre- and postdive by reactive hyperemia peripheral artery tonometry (RH-PAT) and CD105 (Endoglin) positive MP were quantified by flow cytometry. Plasma E- and P-selectin, interleukin-6, and serum cortisol were also quantified. RESULTS RH-PAT showed a significantly decreased endothelial function post-decompression after breathing air when compared to oxygen (-0.33 +/- 0.27 vs. +0.18 +/- 0.14). CD105 MP pre- and postdive showed no change on the oxygen dive (460 +/- 370 to 360 +/- 163), however, they increased after breathing air (440 +/- 70 to 1306 +/- 359). There was no change in expression of CD105 on MP. Furthermore no changes were observed in plasma E- or P-selectin, IL-6, or serum cortisol. CONCLUSION From the data, at least in the time frame involved, there appears to be no detectable physiological/stress response to decompression, rather decompression from breathing air probably caused mechanical damage to the endothelium, resulting in both MP release and a reduction in endothelial function.

Microparticle-associated vascular adhesion molecule-1 and tissue factor follow a circadian rhythm in healthy human subjects

An increased risk of death or severe injury due to late-morning thrombotic events is well established. Tissue factor (TF) is the initiator of the coagulation cascade, and endothelial stresses, coupled with production of pro-coagulant microparticles (MP) are also important factors in loss of haemostasis. TF and vascular cell adhesion molecule-1 (VCAM-1) -positive cell microparticles were assessed periodically over a 24-hour (h) period in healthy human subjects to ascertain if they followed a circadian rhythm. Eleven healthy male subjects were assessed in a temperature-controlled environment with dietary intake consistent between subjects. Blood samples were taken every 4 h by venipuncture, and TF and VCAM-1 positive microparticles were quantified by flow cytometry. A significant circadian rhythm was observed in VCAM-1 MP (p=or<0.0001), and a trend was shown, although not statistically significant (p=0.065) in TF microparticles. A peak was observed at 9 a.m. for VCAM-1 positive MP, followed by a decrease and subsequent peak at 9 p.m. and a minimum at 5 a.m. TF-positive MP followed a strikingly similar trend in both variation and absolute numbers with a delay. A circadian rhythm was observed in VCAM-1 and less so TF-positive MP. This has significant implications in terms of the well known increased risk of cardiovascular thrombotic events matching this data. To our knowledge this is the first such report of quantified measurements of these MP over a 24-h period and the only measurement of a 24-h variation of in-vivo blood-borne TF.

Polycystic ovary syndrome has no independent effect on vascular, inflammatory or thrombotic markers when matched for obesity

Previous studies investigating cardiovascular (CV) risk in obese women with polycystic ovary syndrome (PCOS) have been potentially confounded by not adequately accounting for body weight.

High versus low glycemic index 3-h recovery diets following glycogen-depleting exercise has no effect on subsequent 5-km cycling time trial performance

OBJECTIVES Some athletes train/compete multiple times in a single day and rapid restoration of muscle and hepatic glycogen stores is therefore important for athletic performance. DESIGN Randomised, counterbalanced, crossover, single blinded study investigated the effects of low/high glycaemic index (GI) meals on the physiological responses to a 3-h recovery period and subsequent 5-km cycling time trial (TT). METHODS Seven male cyclists completed glycogen-depleting exercise followed by a 3-h recovery period, when participants consumed either a high or low GI meal providing 2gkg(-1) BM of carbohydrate. Participants then performed a 5-km cycling TT. Blood samples were analysed for glucose insulin, free fatty acid (FFA) and triglyceride. RESULTS There was no significant difference between the median (IQR) cycling TT time of 8.5 (3.0) min in the LGI condition and 8.4 (1.8) min in the HGI condition (p=0.45). Serum insulin was significantly higher in the HGI condition throughout the 3-h recovery period (p=0.025), FFA concentrations were higher in the HGI condition only at 30min into recovery (p=0.008). The respiratory exchange ratio (p=0.028) and carbohydrate oxidation rate (p=0.015) increased over time in the HGI condition, whereas the rate of fat oxidation demonstrated the opposite response (p=0.001). No significant differences between conditions were observed for any physiological variables at the end of the 5-km TT. CONCLUSIONS Although the GI of the two meals indicated important metabolic differences during the recovery period, there was no evidence suggesting these differences influenced subsequent 5-km TT performance.

A comparison of cardiovascular risk indices in patients with polycystic ovary syndrome with and without coexisting nonalcoholic fatty liver disease

Women with polycystic ovary syndrome (PCOS) have an adverse cardiovascular risk profile and an increased prevalence of nonalcoholic fatty liver disease (NAFLD), which is also associated with an adverse cardiovascular risk profile.

The effect of acute hyperoxia in vivo on NF kappa B expression in human PBMC.

The mechanisms of hyperbaric oxygen (HBO) therapy have not been fully elucidated. It is presumed that breathing 100% oxygen at pressure generates free radicals and the cellular response to these may confer protection. A crucial signalling molecule, nuclear transcription factor kappa B (NFκB), translocates from the cytoplasm to the nucleus and activates a raft of pathways in response to various stimuli, and plays a role in inflammatory processes. This study focussed upon the expression of NFκB in isolated human peripheral blood mononuclear cells (PBMC) following HBO. Ten healthy male volunteers underwent a single HBO treatment, breathing 100% oxygen at a pressure of 2.8 ATA for 1 h. EDTA blood samples were taken pre‐, post‐ and 4‐h post‐HBO. PBMC were isolated, nuclear extracts prepared and assayed using a NFkBp50 transcription factor ELISA. Mean NFκB expression of 0.27 (0.20–0.34, 95%CI) absorbance units (mg protein)−1 was observed pre‐HBO and this increased to 0.29 (0.20–0.38, 95%CI) immediately post‐HBO. A significant increase in NFκB expression within PBMC was observed 4‐h post‐HBO, in comparison to pre‐HBO (mean 0.38, 0.30–0.47, 95%CI, p = 0.027). This study demonstrates that HBO induces NFκB activation in human PBMC, which could be a crucial step in the mechanism of HBO treatment. Copyright

Apolipoprotein E ε4 Allele Modulates the Immediate Impact of Acute Exercise on Prefrontal Function

The difference between Apolipoprotein E ε4 carriers and non-carriers in response to single exercise sessions was tested. Stroop and Posner tasks were administered to young untrained women immediately after walking sessions or moderately heavy exercise. Exercise had a significantly more profound impact on the Stroop effect than on the Posner effect, suggesting selective involvement of prefrontal function. A significant genotype-by-exercise interaction indicated differences in response to exercise between ε4 carriers and non-carriers. Carriers showed facilitation triggered by exercise. The transient executive down-regulation was construed as due to exercise-dependent hypofrontality. The facilitation observed in carriers was interpreted as better management of prefrontal metabolic resources, and explained within the antagonistic pleiotropy hypothesis framework. The findings have implications for the interpretation of differences between ε4 carriers and non-carriers in the benefits triggered by long-term exercise that might depend, at least partially, on mechanisms of metabolic response to physical activity.

Effect of Lactate Supplementation and Sodium Bicarbonate on 40-km Cycling Time Trial Performance

Abstract Northgraves, MJ, Peart, DJ, Jordan, CA, and Vince, RV. Effect of lactate supplementation and sodium bicarbonate on 40-km cycling time trial performance. J Strength Cond Res 28(1): 273–280, 2014—The use of nutritional supplements to improve sporting performance and increase training adaptations is commonplace among athletes and is an expanding market in terms of product choice and availability. The purpose of this study was to examine the effects of 2 ergogenic aids with extracellular blood buffering potential, namely sodium bicarbonate (NaHCO3) and a lactate supplement, during a 40-km cycling time trial. Seven recreationally active men (age, 22.3 ± 3.3 years; height, 182.5 ± 6.5 cm; body mass, 79.2 ± 6.3 kg) completed five 40-km cycling time trials, including a familiarization trial in a randomized, blind, double placebo-controlled design. Subjects ingested (a) 300 mg·kg−1 body mass NaHCO3 (BICARB), (b) 45 mg∣kg−1 body mass sodium chloride (PL-BICARB) as the placebo for the NaHCO3 trial, (c) 1115 mg lactate (LACTATE), or (d) plain flour as the placebo for the lactate trial (PL-LACTATE) 60 minutes before exercise. There was no significant difference in performance between the 4 conditions (p > 0.05). Although NaHCO3 ingestion induced significant changes in all the acid-base variables (all p < 0.05), no significant change was seen following lactate ingestion (p > 0.05). Subjects in the LACTATE condition did have a significantly higher heart rate (p < 0.05) without experiencing any greater perceived exertion (p > 0.05) than the other 3 conditions. Neither NaHCO3 nor lactate supplementation seem to improve 40-km cycling time trial performance. However, the potential benefits following LACTATE regarding perceived exertion require further research.