24-h passive heat and cold exposures did not modify energy intake and appetite but strongly modify food reward.

Effects of acute thermal exposures on appetite appear hypothetical in reason of very heterogeneous methodologies. The aim of this study was therefore to clearly define the effects of passive 24-h cold (16°C) and heat (32°C) exposures on appetitive responses compared to a thermo neutral condition (24°C). Twenty-three healthy, young, and active male participants realised three sessions (from 1 pm) in a laboratory conceived like an apartment dressed with the same outfit (Clo=1). Three meals composed of three or four cold or warm dishes were served ad libitum to assess energy intake (EI). Leeds Food Preference Questionnaires were used before each meal to assess food reward. Subjective appetite was regularly assessed and levels of appetitive hormones (acylated ghrelin, GLP-1, leptin, and PYY) were assessed before and after the last meal (lunch). Contrary to the literature, total EI was not modified by cold or heat exposure (p=0.120). Accordingly, hunger scores (p=0.554) were not altered. Levels of acylated ghrelin and leptin were marginally higher during the 16 (p=0.032) and 32°C (p<0.023) sessions, respectively. Interestingly, implicit wanting for cold and low-fat foods at 32°C and for warm and high-fat foods at 16°C were increased during the whole exposure (p < 0.024). Moreover, cold entrées were more consumed at 32 °C (p<0.062) and warm main dishes more consumed at 16°C (p<0.025). Thus, passive cold and hot exposures had limited effects on appetite and it seems that offering some choice based on food temperature may help individuals to express their specific food preferences and maintain EI.

Circulating microRNA levels after exercise-induced muscle damage and the repeated bout effect.

The neuromuscular system can quickly adapt to exercise-induced muscle damage (EIMD), such that it is less affected by subsequent damaging exercise, a phenomenon known as the repeated bout effect (RBE). Circulating muscle-specific microRNAs (myomiRs) may be able to potentially predict the long-lasting maximal voluntary contraction (MVC) torque deficit (>24 h), an indicator of EIMD. We aimed to investigate: 1) how plasma myomiR levels are modified by the RBE and 2) whether plasma myomiRs can predict the long-lasting MVC torque deficit. Nineteen participants performed two identical bouts of loaded downhill walking separated by 2 wk. MVC torque, creatine kinase (CK) activity, myoglobin (Mb) concentration, and myomiR levels were measured before and up to 48 h after exercise. Correlation and multiple regression analyses were performed to assess the ability of these markers to predict the largest MVC torque loss beyond 24 h postexercise. Similar to MVC torque, CK activity, and the Mb concentration, the relative abundance of certain myomiRs (hsa-miR-1-3p, and hsa-miR-133a-3p) was less affected after the second bout of exercise relative to the first bout. The CK activity, Mb concentration, and level of several myomiRs (hsa-miR-1-3p, hsa-miR-133a-3p, and hsa-miR-206) correlated with long-lasting MVC torque loss. Multiple regression showed that the best combination of markers to predict the long-lasting deficit of MVC torque included several myomiRs, Mb, and CK. Certain myomiR levels increased less after exercise bout 2 than after exercise bout 1, indicating the presence of the RBE. The measurement of myomiR levels in combination with Mb concentrations and CK activity could improve the prediction of the long-lasting MVC torque deficit.NEW & NOTEWORTHY The present study is the first to show that plasma muscle-specific microRNA (myomiR) levels can be modified by the repeated bout effect, as their levels increased less after the second exercise bout relative to the first. This study is also the first to suggest that myomiR levels could be used to partially predict maximal voluntary contraction torque loss at 24 h postexercise (i.e., the magnitude of exercise-induced muscle damage). Interestingly, the combined measurement of certain myomiR levels with those of myoglobin and creatine kinase improved the predictive value.

Contractile properties are less affected at long than short muscle length after eccentric exercise.

PURPOSE: The aim of the present study was to investigate whether the electrically evoked muscle responses are differently affected over time by the knee joint angle after an exercise-induced muscle damage (EIMD). We hypothesized that low-frequency-evoked responses would be less affected at long than short muscle length, and that mechanisms located within the muscle and tendinous tissues would be involved. METHODS: Fifteen males performed 45 min loaded downhill walking (DW) exercise. Maximal voluntary contraction torque (MVC), optimal angle for torque production, voluntary activation level (VAL), twitch, doublet at 10 and 100 Hz (Db10 and Db100, respectively), rate of torque development (RTD), post-activation potentiation (PAP), muscle shear elastic modulus (µ) and aponeurosis stiffness were assessed before, after, and 4, 24, 48, 72 and 168 h after the exercise at a knee angle of 40°, 90° and 120° (0°: full extension). RESULTS: MVC, VAL and Db100 were similarly decreased across joint angles after the DW and optimal angle was not affected. Twitch, Db10, Db10/Db100, PAP and RTD were less affected and muscle µ more increased at long than short muscle lengths (p < 0.05), especially during the first 24 h after the DW exercise. CONCLUSION: Low-frequency-evoked responses were more preserved at long than short muscle length the first 24 h after the DW exercise, suggesting that joint angle should be taken into account to assess muscular alterations after EIMD. This length-dependence could be associated to the higher sensitivity to Ca2+ and the higher increase in muscle stiffness at long than short muscle length.

Dietary- but not exercise-induced acute iso-energetic deficit result in short-term appetitive compensatory responses in adolescents with obesity.

BACKGROUND: Producing negative energy balance rests on the creation of energy deficits that have been shown, depending on their modality, to induce potential appetitive compensatory responses. The aim of this study was to compare energy intake (EI), appetite feelings, and the hedonic responses to equivalent acute energy deficits induced by exercise versus energy restriction in adolescents with obesity. METHODS: In a within-participants design, seventeen adolescents with obesity (12-16 years, Tanner stage 3-5, 9 males) randomly completed three conditions: i) control (CON); ii) deficit induced by diet only (Def-EI); and iii) deficit induced by exercise only (Def-EX). Lunch was calibrated to generate a 400-kcal deficit in Def-EI and remained similar in CON and Def-EX. A 400-kcal deficit was created through a cycling bout set at 65% VO2peak in Def-EX. Ad libitum EI, macronutrient intake and relative EI (REI) were assessed at dinner, subjective appetite sensations taken at regular intervals, and food reward measured before dinner. RESULTS: Food intake at dinner was greater in Def-EI (1112 ± 265 kcal) compared to CON (983 ± 277 kcal; p = 0.005) and Def-EX (1009 ± 281 kcal; p = 0.025). Absolute protein and lipid intake were significantly higher in Def-EI (52.4 ± 9.5 g and 36.8 ± 8.9 g respectively) compared with both CON (44.9 ± 12.6 g; p = 0.001 and 33.8 ± 10.1 g; p = 0.002 respectively) and Def-EX (47.3 ± 11.8 g, p = 0.018, 35.4 ± 10.1 g, p = 0.036 respectively). Area under the curve (AUC) for hunger, desire to eat and prospective food consumption were significantly higher in Def-EI compared with both CON (p = 0.0001) and Def-EX (p = 0.0001). AUC for fullness was significantly lower on Def-EI compared with CON and Def-EX (p = 0.0001). Implicit wanting for sweet food was significantly lower on Def-EX (p = 0.031), relative to CON. CONCLUSION: Appetitive compensatory responses that are observed after iso-caloric energy restriction in adolescents with obesity are absent with acute exercise, which could contribute to optimize our impact on short-term energy balance.

Brain injury pathophysiology study by a multimodal approach in children with sickle cell anemia with no intra or extra cranial arteriopathy.

Despite its high prevalence in children with sickle cell anemia (SCA), the pathophysiology of silent cerebral infarcts (SCI) remains elusive. The main objective of this study was to explore the respective roles of major determinants of brain perfusion in SCA children with no past or current history of intracranial or extracranial vasculopathy. We used a multimodal approach based notably on perfusion imaging arterial spin labeling (ASL) magnetic resonance imaging (MRI) and near infra-red spectroscopy (NIRS), as well as biomarkers reflecting blood rheology and endothelial activation. Out of 59 SCA patients (mean age 11.4±3.9 yrs), eight (13%) had a total of 12 SCI. Children with SCI had a distinctive profile characterized by decreased blood pressure, impaired blood rheology, increased P-selectin levels, and marked anemia. Although ASL perfusion and oximetry values did not differ between groups, comparison of biological and clinical parameters according to the level of perfusion categorized in terciles showed an independent association between high perfusion and increased sP-selectin, decreased red blood cell deformability, low hemoglobin F level, increased blood viscosity and no a-thalassemia deletion. NIRS measurements did not yield additional novel results. Altogether, these findings argue for early MRI detection of SCI in children with no identified vasculopathy and suggest a potential role for ASL as an additional screening tool. Early treatment targeting hemolysis, anemia and endothelial dysfunction should reduce the risk of this under diagnosed and serious complication.

The impact of 16-h heat exposure on appetite and food reward in adults.

Heat exposure is thought to reduce energy intake (EI) but studies are sparse and results not always concordant. The aim of this study was to examine whether a 16-h exposure to 32 °C leads to reduced EI compared to a control session (22 °C) and whether modifications in appetite sensations or food reward are implied. Sixteen healthy, lean, and active participants (9 women and 7 men, 25 ± 5 yo, body mass index: 22.0 ± 2.4 kg m-2) were passively exposed to two different thermal temperatures from 4:00 p.m. to 8:00 a.m. under controlled conditions. Hunger and thirst scores were regularly assessed using visual analogue scales. A fixed dinner meal (3670 ± 255 kJ) was consumed at 7:30 p.m. and an ad libitum breakfast buffet (20 foods/drinks varying in temperature, fat, and carbohydrate content) at 7:30 a.m. Components of reward (explicit liking [EL] and implicit wanting [EI]) for fat and sweet properties of food were assessed before each meal using the Leeds Food Preference Questionnaire (LFPQ). Ad libitum EI at breakfast did not differ between sessions (2319 ± 1108 vs 2329 ± 1141 kJ, in 22 and 32 °C sessions, respectively; p = 0.955). While thirst scores were higher in the 32 than the 22 °C session (p < 0.001), hunger scores did not differ (p = 0.580). EL and IW for high fat foods relative to low fat foods were decreased in 32 compared to 22 °C before dinner and breakfast (p < 0.001 for all). Although EI and hunger were not affected by a 16-h exposure to heat, modifications in food reward suggested a reduction in the preference of high-fat foods. Future research should investigate whether reduced EI in response to heat exposure is due to spontaneous selection of low-fat foods rather than altered appetite sensations.

Circulating microRNAs after a 24-h ultramarathon run in relation to muscle damage markers in elite athletes.

Ultra-endurance sports are growing in popularity but can be associated with adverse health effects, such as exercise-induced muscle damage (EIMD), which can lead to exertional rhabdomyolysis. Circulating microRNAs (miRNAs) may be useful to approach the degree of EIMD. We aimed to (1) investigate the relevance of circulating miRNAs as biomarkers of muscle damage and (2) examine the acute response of skeletal/cardiac muscle and kidney biomarkers to a 24-h run in elite athletes. Eleven elite athletes participated in the 24-h run World Championships. Counter-movement jump (CMJ), creatine kinase (CK), myoglobin (Mb), creatinine (Cr), high-sensitive cardiac troponin T (hs-cTnT), and muscle-specific miRNA (myomiR) levels were measured before, immediately after, and 24 and 48h after the race. CMJ height was reduced immediately after the race (-84.0 ± 25.2%, p < 0.001) and remained low at 24 h (-43.6 ± 20.4%, p = 0.002). We observed high CK activity (53 239 ± 63 608 U/L, p < 0.001) immediately after the race, and it remained elevated 24h after (p < 0.01). Circulating myomiR levels (miR-1-3p, miR-133a-3p, miR-133b, miR-208a-3p, miR-208b-3p, and miR-499a-5p) were elevated immediately after the 24-h run (fold changes: 18-124,723, p<0.001) and significantly (p < 0.05) correlated or tended to significantly (p < 0.07) correlate with the reduction in CMJ height at 24 h. We found no significant correlation between CMJ height loss at 24 h and CK (p = 0.23) or Mb (p = 0.41) values. All elite ultramarathon runners included in our study were diagnosed with exertional rhabdomyolysis after the 24-h ultramarathon race. MyomiR levels may be useful to approach the degree of muscle damage.

Negative energy balance during military training: The role of contextual limitations.

During multiday training exercises, soldiers almost systematically face a moderate-to-large energy deficit, affecting their body mass and composition and potentially their physical and cognitive performance. Such energy deficits are explained by their inability to increase their energy intake during these highly demanding periods. With the exception of certain scenarios in which rations are voluntarily undersized to maximize the constraints, the energy content of the rations are often sufficient to maintain a neutral energy balance, suggesting that other limitations are responsible for such voluntary and/or spontaneous underconsumption. In this review, the overall aim was to present an overview of the impact of military training on energy balance, a context that stands out by its summation of specific limitations that interfere with energy intake. We first explore the impact of military training on the various components of energy balance (intake and expenditure) and body mass loss. Then, the role of the dimensioning of the rations (total energy content above or below energy expenditure) on energy deficits are addressed. Finally, the potential limitations inherent to military training (training characteristics, food characteristics, timing and context of eating, and the soldiers' attitude) are discussed to identify potential strategies to spontaneously increase energy intake and thus limit the energy deficit.

Metabolic response to oral glucose tolerance test performed in neutral and warm environmental temperature.

Objective: Hot environments are associated with impaired glucose metabolism at rest in healthy humans. The purpose of this study was to explore the contribution of key glucoregulatory hormones and biomarkers to this altered glucose tolerance. Methods: The effects of ambient temperature on glucose tolerance and its determinants were assessed with a 3-hr oral glucose tolerance test (OGTT) administered to 19 healthy young men and women at 22 °C and 31 °C. Results: The glucose response amplitude was greater in warm environment (AUC 904 ± 151 vs. 721 ± 89 mmol/l·180 min at 31 °C and 22 °C, respectively, p < .001). There was no significant effect of environmental temperature on insulin, growth hormone or pancreatic polypeptide concentrations (all p > .17). The cortisol response to the glucose load was reduced 30, 60, 90 and 120 minutes postload at 31 °C compared with 22 °C (p = .001). The interleukin-6 concentration was also lower in the session at 31 °C (p = .043). Conclusion: We conclude that the effects of environmental temperature on the glucoregulatory hormones and biomarkers reported in this study do not explain the exaggerated increase in blood glucose after a glucose load taken in a warm environmental temperature. Precis statement: This work demonstrates in healthy men and women that the ingestion of glucose elicits an exaggerated increase in blood glucose when the environmental temperature is warm.

Uncoupling psychological from physiological markers of heat acclimatization in a military context.

Heat acclimatization may help personnel who travel to areas with a hot climate (WBGT > 27 °C), making them operationally more efficient and performant through improvements in physiological and psychological parameters. Their work-related physical activities may aid active heat acclimatization. However, it is unknown whether adding physical training to improve adaptation is effective, particularly if there is sufficient time for full acclimatization, classically reached after 15 days. Thirty French soldiers (Training group, T) performed a progressive and moderate (from three to five 8-min running sets at 50-60% of their speed at VO2max with 4-min periods of active recovery in between) aerobic training program upon arriving at their base in United Arab Emirates (~40 °C and 20% RH). A control group (30 soldiers; No Training, NT) continued to perform only their usual outdoor military activities (~5 h d-1). A field heat stress test (HST: three 8-min running sets at 50% of the speed at VO2max) was performed before (D0), during (D10), and after (D15) the heat acclimatization period to assess physiological and psychological changes. An 8-km trial in battledress was then performed at D17. Although physiological modifications were mostly similar (p < 0.001 for all) for both groups (rectal temperature at the end of the HST: -0.58 ±â€¯0.51 vs -0.53 ±â€¯0.40 °C, HR at the end of the HST: -21 ±â€¯12 vs -19 ±â€¯9 bpm, and sweat osmolality: -47 ±â€¯30 vs -26 ±â€¯32 mOsmol.l-1 between D15 and D0 for T and NT groups, respectively), thermal discomfort (-31 ±â€¯4 vs -11 ±â€¯5 mm between D15 and D0, p = 0.001) and rates of perceived exertion (-3.0 ±â€¯0.4 vs -1.4 ±â€¯0.3 D15 and D0, p = 0.001) were much lower in the T than NT group during the HST. HST-induced modifications in facial temperature only decreased in the T group (-1.08 ±â€¯0.28 between D15 and D0, p < 0.001). Moreover, there was a difference in perceived thermal discomfort during the 8-km trial (40 ±â€¯20 vs 55 ±â€¯22 mm for the T and NT groups, respectively, p = 0.010). Thus, a 15-day, low-volume training regimen during a mission in a hot and dry environment has a modest impact on physiological adaptation but strongly decreases the perceived strain of exertion and climate potentially via greater reductions in facial temperature, even during a classical operational physical task in a military context.

Association between oxidative stress and vascular reactivity in children with sickle cell anaemia and sickle haemoglobin C disease.

Oxidative stress and haemolysis-associated nitric oxide (NO) depletion plays a crucial role in the development of vasculopathy in sickle cell anaemia (SS). However it remains unknown whether oxidative stress and haemolysis levels influence vascular function in patients with sickle haemoglobin C disease (SC). Microvascular response to heat (using Laser Doppler flowmetry on finger), oxidative stress biomarkers, NO metabolites, endothelin-1 and haematological parameters were compared between patients with SS and SC. Vascular function, oxidative and nitrosative markers were also measured in healthy (AA) children. SS and SC had increased plasma advanced oxidation protein products (AOPP), malondialdehyde, plasma antioxidant activities and NO end products, compared to AA. SC had lower catalase activity compared to AA and SS. Haemolytic rate, glutathione peroxidase and nitrotyrosine concentrations were significantly increased in children with SS compared to SC and AA. SS and SC had impaired microvascular reactivity compared to AA. In SS, the plateau phase of the response to local thermal heating was negatively associated with nitrotyrosine and AOPP. No association between vascular function parameters and oxidative stress markers was observed in SC. Mild haemolysis in SC, compared to SS, may limit oxidative and nitrosative stress and could explain the better preserved microvascular function in this group.

Exacerbation of oxidative stress during sickle vaso-occlusive crisis is associated with decreased anti-band 3 autoantibodies rate and increased red blood cell-derived microparticle level: a prospective study.

Painful vaso-occlusive crisis, a hallmark of sickle cell anaemia, results from complex, incompletely understood mechanisms. Red blood cell (RBC) damage caused by continuous endogenous and exogenous oxidative stress may precipitate the occurrence of vaso-occlusive crises. In order to gain insight into the relevance of oxidative stress in vaso-occlusive crisis occurrence, we prospectively compared the expression levels of various oxidative markers in 32 adults with sickle cell anaemia during vaso-occlusive crisis and steady-state conditions. Compared to steady-state condition, plasma levels of free haem, advanced oxidation protein products and myeloperoxidase, RBC caspase-3 activity, as well as the concentrations of total, neutrophil- and RBC-derived microparticles were increased during vaso-occlusive crises, whereas the reduced glutathione content was decreased in RBCs. In addition, natural anti-band 3 autoantibodies levels decreased during crisis and were negatively correlated with the rise in plasma advanced oxidation protein products and RBC caspase-3 activity. These data showed an exacerbation of the oxidative stress during vaso-occlusive crises in sickle cell anaemia patients and strongly suggest that the higher concentration of harmful circulating RBC-derived microparticles and the reduced anti-band 3 autoantibodies levels may be both related to the recruitment of oxidized band 3 into membrane aggregates.

Micro- and macrovascular function in children with sickle cell anaemia and sickle cell haemoglobin C disease.

It is unclear whether vascular function is affected similarly in children with sickle cell anaemia (SS) and children with sickle haemoglobin C (SC) disease. Therefore, we compared micro and macrovascular functions in healthy (AA) children, children with SS and SC disease, and assessed their association with physical activity. Participants (24 SS, 22 SC and 16 AA), were compared in terms of 1) thermal hyperaemic response (finger pad warming to 42°C) measured by Laser Doppler techniques, 2) arterial stiffness determined by pulse wave velocity, 3) daily energy expenditure related to moderate and intense physical activities estimated by questionnaire and 4) fitness level, evaluated by the six-minute walk test. Response to heating differed between SS, SC and controls. Peripheral microvascular reactivity was lower and pulse wave velocity higher in SS compared to AA. SC had blunted microvascular reactivity in response to heating compared to AA but pulse wave velocity was not different within the two groups. Physical activity and fitness levels were markedly lower in sickle cell patients compared to healthy controls but no association was observed with vascular function. Microvasodilatory reserve is decreased in both SS and SC patients but only SS patients were also characterised by impaired macrovascular function.

Cerebral and muscle microvascular oxygenation in children with sickle cell disease: Influence of hematology, hemorheology and vasomotion.

The present study investigated cerebral and muscle hemoglobin oxygen saturation (tissue oxygen index, TOI) in children with sickle cell anemia (SS), sickle cell hemoglobin C disease (SC) and healthy children (AA). TOI was measured by near-infrared spectroscopy (NIRS) and spectral analysis of the TOI variability was used to assess flowmotion and vasomotion. Arterial oxyhemoglobin saturation (SpO2), hemorheological and hematological parameters were also measured in SS and SC children. Both TOI were lower in SS compared to both AA and SC children, with SC exhibiting lower values than AA children. Cerebral vasomotion expressed in absolute values was enhanced in SS compared to AA and SC children. Muscle vasomotion did not differ between the three groups. Hematocrit, SpO2 and red blood cell deformability were positively associated with cerebral TOI in SS children. We demonstrated that 1) cerebral and muscle TOI were markedly decreased in SS children while the decrease of TOI was milder in SC children, 2) cerebral TOI level was associated with several biological markers in SS children only and 3) cerebral vasomotion was enhanced in SS, possibly to counterbalance the effects of chronic cerebral hypoxia.

Which side of the balance determines the frequency of vaso-occlusive crises in children with sickle cell anemia: Blood viscosity or microvascular dysfunction?

Vascular resistance and tissue perfusion may be both affected by impaired vascular function and increased blood viscosity. Little is known about the effects of vascular function on the occurrence of painful vaso-occlusive crises (VOC) in children with sickle cell anemia (SCA). The aim of the present study was to determine which side of the balance (blood viscosity or vascular function) is the most deleterious in SCA and increases the risk for frequent hospitalized VOC. Microvascular function, microcirculatory oxygenation and blood viscosity were determined in a group of 22 SCA children/adolescents at steady state and a group of 13 healthy children/adolescents. Univariate analyses demonstrated blunted microvascular reactivity during local thermal heating test and decreased microcirculatory oxygenation in SCA children compared to controls. Multivariate analysis revealed that increased blood viscosity and decreased microcirculatory oxygenation were independent risk factors of frequent VOC in SCA. In contrast, the level of microvascular dysfunction does not predict VOC rate. In conclusion, increased blood viscosity is usually well supported in healthy individuals where vascular function is not impaired. However, in the context of SCA, microvascular function is impaired and any increase of blood viscosity or decrease in microcirculatory oxygenation would increase the risks for frequent VOC.

Impaired glucose tolerance after brief heat exposure: a randomized crossover study in healthy young men.

A high demand on thermoregulatory processes may challenge homoeostasis, particularly regarding glucose regulation. This has been understudied, although it might concern millions of humans. The objective of this project was to examine the isolated and combined effects of experimental short-term mild heat exposure and metabolic level on glucoregulation. Two experimental randomized crossover studies were conducted. Ten healthy young men participated in study A, which comprises four sessions in a fasting state at two metabolic levels [rest and exercise at 60% of maximal oxygen uptake (O2) for 40 min] in two environmental temperatures (warm: 31°C and control: 22°C). Each session ended with an ad libitum meal, resulting in similar energy intake across sessions. In study B, 12 healthy young men underwent two 3 h oral glucose tolerance tests (OGTTs) in warm and control environmental temperatures. Venous blood was sampled at several time points. In study A, repeated measure ANOVAs revealed higher postprandial serum glucose and insulin levels with heat exposure. Glycaemia following the OGTT was higher in the warm temperature compared with control. The kinetics of the serum glucose response to the glucose load was also affected by the environmental temperature (temperature-by-time interaction, P=0.030), with differences between the warm and control conditions observed up to 90 min after the glucose load (all P<0.033). These studies provide evidence that heat exposure alters short-term glucoregulation. The implication of this environmental factor in the physiopathology of Type 2 diabetes has yet to be investigated.

Intensity, recovery kinetics and well-being indices are not altered during an official FIFA futsal tournament in Oceanian players.

Physiological responses (intensity and recovery kinetics) and well-being indices were examined during a 4-day FIFA international tournament. Ten outfield New Caledonian players (age: 25.5 ± 3.8 years; height: 170 ± 7 cm; weight: 70.7 ± 8.6 kg) were assessed during the four matches. Players' aerobic and anaerobic capacities were measured before the tournament while heart rate (HR), intra-matches recovery and well-being indices (Hooper index) were measured throughout the tournament. HR (168 ± 8 bpm), exercise intensity (83.4 ± 2.3% of HR reserve) and recovery indices were similar throughout the tournament. Well-being indices were largely alike during the tournament while rating of perceived exertion increased throughout the tournament that was not associated with HR or well-being indices. High aerobic and anaerobic capacities were associated with high match intensities and slow recovery indices. In summary, match intensity assessed by HR, recovery kinetics and well-being of Oceanian futsal players were not modified during a 4-day FIFA futsal tournament. Assessment of aerobic and anaerobic capacities may be useful to select players for optimal performance during this type of international tournament.

High red blood cell nitric oxide synthase activation is not associated with improved vascular function and red blood cell deformability in sickle cell anaemia.

Human red blood cells (RBC) express an active and functional endothelial-like nitric oxide (NO) synthase (RBC-NOS). We report studies on RBC-NOS activity in sickle cell anaemia (SCA), a genetic disease characterized by decreased RBC deformability and vascular dysfunction. Total RBC-NOS content was not significantly different in SCA patients compared to healthy controls; however, using phosphorylated RBC-NOS-Ser(1177) as a marker, RBC-NOS activation was higher in SCA patients as a consequence of the greater activation of Akt (phosphorylated Akt-Ser(473) ). The higher RBC-NOS activation in SCA led to higher levels of S-nitrosylated α- and ß-spectrins, and greater RBC nitrite and nitrotyrosine levels compared to healthy controls. Plasma nitrite content was not different between the two groups. Laser Doppler flowmetric experiments demonstrated blunted microcirculatory NO-dependent response under hyperthermia in SCA patients. RBC deformability, measured by ektacytometry, was reduced in SCA in contrast to healthy individuals, and pre-shearing RBC in vitro did not improve deformability despite an increase of RBC-NOS activation. RBC-NOS activation is high in freshly drawn blood from SCA patients, resulting in high amounts of NO produced by RBC. However, this does not result in improved RBC deformability and vascular function: higher RBC-NO is not sufficient to counterbalance the enhanced oxidative stress in SCA.

Physical activity level is not a determinant of autonomic nervous system activity and clinical severity in children/adolescents with sickle cell anemia: A pilot study.

BACKGROUND: Autonomic nervous system (ANS) activity has been suggested to modulate the clinical severity of sickle cell anemia (SCA) by increasing the risk for vaso-occlusive events. Regular physical activity (PA) is known to improve ANS activity and health status in several cardiovascular and metabolic diseases. Whether regular PA improves the health status of SCA patients remains unknown. PROCEDURE: Twenty-two patients with SCA and 15 healthy (AA) children/adolescents participated to the study. Heart rate variability was measured in supine position and after a tilt-test to quantify the ANS activity. PA energy expenditure (PAEE) was assessed with questionnaire. RESULTS: 1) PAEE was lower in SCA compared to AA (190 ± 152 vs. 432 ± 277 kcal · d(-1), respectively, P < 0.01), 2) overall ANS activity was lower in SCA compared to AA, 3) parasympathetic withdrawal was observed in SCA with aging, 4) ANS reactivity was slightly impaired in SCA compared to AA (reduction in HFnu: -38 ± 27 vs. -58 ± 14%, respectively, P < 0.05), 5) ANS indices, PAEE, and rates of clinical events were not correlated. CONCLUSION: Both the level of PA and ANS activity are reduced in SCA compared to AA children/adolescents, particularly in those older than 15 years. Neither PAEE, nor ANS activity seem to influence the clinical severity of children/adolescents with SCA.