A pilot test of the effect of mild-hypoxia on unrealistically optimistic risk judgements

Although hypoxia is believed to occur above altitudes of 10,000 ft, some have suggested that effects may occur at lower altitudes. This pilot study explored risk judgments under conditions of mild hypoxia (simulated altitude of 8,000 ft). Some evidence of an increased optimism was found at this level, suggesting the need for a larger scale study with more experimental power

Human cardiac autonomic responses to head up tilting during 72-h starvation

Starvation may change autonomic nervous system activity and sensitivity such that a greater vagal withdrawal may occur during a sympathetic challenge. Six healthy humans endured a 3-day, water-only fast, during which participants were subjected to passive 80° head-up tilt testing twice on each day (a.m. and p.m.). Heart rate, heart rate variability (HRV), ventilation (V′E), and respiration ( V′O2 and V′CO2) were recorded during supine rest and head-up tilting. On Day 1 (a.m.), supine heart rate was 46.0 ± 3.3 beats min−1, increasing to 51.6 ± 7.4 beats min−1 on Day 3 (p.m.). On Day 1 (a.m.), supine high frequency HRV was 57.9 ± 31.6NU, increasing to 69.5 ± 21.3NU on Day 3 (p.m.). Tilt-induced increases in heart rate were greater following starvation (10.5 ± 7.8 vs. 16.1 ± 8.6 beats min−1), and tilt-induced decreases in high frequency HRV were greater following starvation (−4.1 ± 27.7 vs. −28.0 ± 20.8NU). Supine V′CO2 remained unchanged, whereas V′O2 increased and respiratory exchange ratio decreased (0.91 ± 0.10 vs. 0.80 ± 0.05). Greater vagal withdrawal and elevated heart rate induced by head-up tilting during starvation may indicate increased autonomic sensitivity

Effect of New Zealand blueberry consumption on recovery from eccentric exercise-induced muscle damage

Abstract Background Exercise-induced muscle damage (EIMD) is accompanied by localized oxidative stress / inflammation which, in the short-term at least, is associated with impaired muscular performance. Dietary antioxidants have been shown to reduce excessive oxidative stress; however, their effectiveness in facilitating recovery following EIMD is not clear. Blueberries demonstrate antioxidant and anti-inflammatory properties. In this study we examine the effect of New Zealand blueberries on EIMD after strenuous eccentric exercise. Methods In a randomized cross-over design, 10 females consumed a blueberry smoothie or placebo of a similar antioxidant capacity 5 and 10 hours prior to and then immediately, 12 and 36 hours after EIMD induced by 300 strenuous eccentric contractions of the quadriceps. Absolute peak and average peak torque across the knee, during concentric, isometric, and eccentric actions were measured. Blood biomarkers of oxidative stress, antioxidant capacity, and inflammation were assessed at 12, 36 and 60 hours post exercise. Data were analyzed using a two-way ANOVA. Results A significant (p p = 0.047) interaction effect was seen for peak isometric tension suggesting a faster rate of recovery in the blueberry intervention group. A similar trend was observed for concentric and eccentric strength. An increase in oxidative stress and inflammatory biomarkers was also observed in both treatment groups following EIMD. Although a faster rate of decrease in oxidative stress was observed in the blueberry group, it was not significant (p  Conclusions This study demonstrates that the ingestion of a blueberry smoothie prior to and after EIMD accelerates recovery of muscle peak isometric strength. This effect, although independent of the beverage’s inherent antioxidant capacity, appears to involve an up-regulation of adaptive processes, i.e. endogenous antioxidant processes, activated by the combined actions of the eccentric exercise and blueberry consumption. These findings may benefit the sporting community who should consider dietary interventions that specifically target health and performance adaptation.</p

The effect of seasonal acclimatization on whole body heat loss response during exercise in a hot humid environment with different air velocity

Seasonal acclimatization from winter to summer is known to enhance thermoeffector responses in hot-dry environments during exercise whereas its impact on sweat evaporation and core temperature (Tcore) responses in hot-humid environments remains unknown. We, therefore, sought to determine whether seasonal acclimatization is able to modulate whole body sweat rate (WBSR), evaporated sweat rate, sweating efficiency, and thermoregulatory function during cycling exercise in a hot-humid environment (32 °C, 75% RH). We also determined whether the increase in air velocity could enhance evaporated sweat rate and sweating efficiency before and after seasonal acclimatization. Twelve males cycled for 1 h at 40% V-O2max in winter (preacclimatization) and repeated the trial again in summer (after acclimatization). For the last 20 min of cycling at a steady-state of Tcore, air velocity increased from 0.2 (0.04) m/s to 1.1 (0.02) m/s by using an electric fan located in front of the participant. Seasonal acclimatization enhanced WBSR, unevaporated sweat rate, local sweat rate and mean skin temperature compared with preacclimatization state (all P 0.70). In conclusion, seasonal acclimatization enhances thermoeffector responses but does not attenuate Tcore during exercise in a hot-humid environment. Furthermore, increasing air velocity enhances evaporated sweat rate and sweating efficiency irrespective of acclimated state. NEW & NOTEWORTHY Seasonal acclimatization to humid heat enhances eccrine sweat gland function and thus results in a higher local and whole body sweat rate but does not attenuate Tcore during exercise in a hot-humid environment. Sweating efficiency is lower after seasonal acclimatization to humid heat compared with preacclimatization with and without the increase of air velocity. However, having a lower sweating efficiency does not mitigate the Tcore response during exercise in a hot-humid environment

Rescue of tropomyosin deficiency in Drosophila and human cancer cells by synaptopodin reveals a role of tropomyosin α in RhoA stabilization

Tropomyosins are widespread actin-binding proteins that influence numerous cellular functions including actin dynamics, cell migration, tumour suppression, and Drosophila oocyte development. Synaptopodin is another actin-binding protein with a more restricted expression pattern in highly dynamic cell compartments such as kidney podocyte foot processes, where it promotes RhoA signalling by blocking the Smurf1-mediated ubiquitination of RhoA. Here, we show that synaptopodin has a shorter half-life but shares functional properties with the highly stable tropomyosin. Transgenic expression of synaptopodin restores oskar mRNA localization in Drosophila oocytes mutant for TmII, thereby rescuing germline differentiation and fertility. Synaptopodin restores stress fibres in tropomyosin-deficient human MDA-MB 231 breast cancer cells and TPMα-depleted fibroblasts. Gene silencing of TPMα but not TPMβ causes loss of stress fibres by promoting Smurf1-mediated ubiquitination and proteasomal degradation of RhoA. Functionally, overexpression of synaptopodin or RhoA(K6,7R) significantly reduces MDA-MB 231 cell migration. Our findings elucidate RhoA stabilization by structurally unrelated actin-binding proteins as a conserved mechanism for regulation of stress fibre dynamics and cell motility in a cell type-specific fashion

Rescue of tropomyosin deficiency in Drosophila

Tropomyosins are widespread actin-binding proteins that influence numerous cellular functions including actin dynamics, cell migration, tumour suppression, and Drosophila oocyte development. Synaptopodin is another actin-binding protein with a more restricted expression pattern in highly dynamic cell compartments such as kidney podocyte foot processes, where it promotes RhoA signalling by blocking the Smurf1-mediated ubiquitination of RhoA. Here, we show that synaptopodin has a shorter half-life but shares functional properties with the highly stable tropomyosin. Transgenic expression of synaptopodin restores oskar mRNA localization in Drosophila oocytes mutant for TmII, thereby rescuing germline differentiation and fertility. Synaptopodin restores stress fibres in tropomyosin-deficient human MDA-MB 231 breast cancer cells and TPMα-depleted fibroblasts. Gene silencing of TPMα but not TPMβ causes loss of stress fibres by promoting Smurf1-mediated ubiquitination and proteasomal degradation of RhoA. Functionally, overexpression of synaptopodin or RhoA(K6,7R) significantly reduces MDA-MB 231 cell migration. Our findings elucidate RhoA stabilization by structurally unrelated actin-binding proteins as a conserved mechanism for regulation of stress fibre dynamics and cell motility in a cell type-specific fashion

Carbohydrate supplementation improves moderate and high-intensity exercise in the heat

The aim of the present study was to clarify the effect of carbohydrate (CHO) supplementation on moderate and high-intensity endurance exercise in the heat. Eight endurance-trained men [maximal oxygen uptake ( VO(2max)) 59.5+/-1.6 ml kg(-1) bw(-1), mean+/-SE] cycled to exhaustion twice at 60% VO(2max) and twice at 73% VO(2max) at an ambient temperature of 35 degrees C. Subjects ingested either a 6.4% maltodextrin solution (CHO) or an artificially flavoured and coloured placebo (PLA). Time to fatigue was significantly greater with CHO in both the 60% and 73% VO(2max) trials (14.5% and 13.5% improvement, respectively). Heart rate and oxygen uptake ( VO(2)) did not differ at any point between PLA and CHO. Hypoglycaemia was not seen in any condition but plasma glucose concentrations tended to be higher at both intensities when CHO was fed. CHO oxidation rates were similar at 60% VO(2max) between CHO and PLA. There were no differences between PLA and CHO in the rate of rise of rectal temperatures ( T(rec)) at either intensity but there was a trend for subjects to fatigue at a high temperature when taking CHO. Ratings of perceived exertion (RPE) tended to be lower throughout both CHO trials; this was significant at 80 min and at fatigue at 60% VO(2max). It is concluded that supplementation with CHO improves exercise performance in the heat at both moderate and high endurance intensities. In the absence of a clear metabolic explanation, a central effect involving an increased tolerance of rising deep body temperature merits further investigation

COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness

Steroid-resistant nephrotic syndrome (SRNS) is a frequent cause of end-stage renal failure. Identification of single-gene causes of SRNS has generated some insights into its pathogenesis; however, additional genes and disease mechanisms remain obscure, and SRNS continues to be treatment refractory. Here we have identified 6 different mutations in coenzyme Q10 biosynthesis monooxygenase 6 (COQ6) in 13 individuals from 7 families by homozygosity mapping. Each mutation was linked to early-onset SRNS with sensorineural deafness. The deleterious effects of these human COQ6 mutations were validated by their lack of complementation in coq6-deficient yeast. Furthermore, knockdown of Coq6 in podocyte cell lines and coq6 in zebrafish embryos caused apoptosis that was partially reversed by coenzyme Q10 treatment. In rats, COQ6 was located within cell processes and the Golgi apparatus of renal glomerular podocytes and in stria vascularis cells of the inner ear, consistent with an oto-renal disease phenotype. These data suggest that coenzyme Q10–related forms of SRNS and hearing loss can be molecularly identified and potentially treated