Cognitive performance during exposure to moderate normobaric hypoxia after sleep restriction: relationship to physiological and stress biomarkers.

INTRODUCTION: Exposure to moderate levels of simulated hypoxia has subtle cognitive effects relative to ground level, in healthy individuals. However, there are few data on the cognitive consequences of the combination of hypoxia and partial sleep deprivation, which is a classic military or civilian operational context. In this study, we tested the hypothesis that exposure to moderate hypoxia while sleep-restricted impairs several domains of cognition, and we also assessed physiological parameters and salivary concentrations of cortisol and alpha-amylase. METHOD: Seventeen healthy males completed two sessions of cognitive tests (sustained attention using the PVT psychomotor vigilance task and executive functions using the Go-NoGo inhibition task and N-Back working memory task) after 30 minutes (T+30') and 4 hours (T+240') of exposure in a normobaric hypoxic tent (FIO2 = 13.6%, ≃ 3,500 m) (HY). This was completed after one night of sleep restriction (3 a.m. to 6 a.m. bedtime, SRHY) and one night of habitual sleep (10 p.m. to 6 a.m. bedtime, HSHY) (with cross-over randomization). The two nights sleep architecture and physiological parameters (oxygen saturation (SpO2) and heart rate (HR) during T+30' and T+240'sessions were analyzed. Salivary cortisol and alpha-amylase (sAA) concentrations were analyzed before hypoxia, after the T+30' and T+240' cognitive sessions, and after leaving the hypoxic tent. RESULTS: Sustained attention (RT and number of lapses in the PVT) and executive functions (Go-NoGo and 1-Back and 2-Back parameters, as inhibition and working memory signatures) were impaired in the SRHY condition compared to HSHY. SpO2 and HR were higher after 4 hours compared with 30 minutes of hypoxia in the HSHY condition, while only HR was statistically higher in the SRHY condition. In SRHY, salivary AA concentration was lower and cortisol was higher than in HSHY. A significant increase in sAA concentration is observed after the cognitive session at 4 hours of hypoxia exposure compared to that at 30 minutes, only in the SRHY condition. There are significant positive correlations between reaction time and the corresponding heart rate (a non-invasive marker of physiological stress) for the executive tasks in the two sleep conditions. This was not observed for salivary levels of sAA and cortisol, respective reliable indicators of the sympathoadrenomedullary system and the hypothalamic-pituitary adrenocortical system. CONCLUSION: Exposure to moderate normobaric hypoxia (≃ 3,500 m / ≃ 11,500 ft simulated) after a single night of 3-hour sleep impairs cognitive performance after 30 minutes and 4 hours of exposure. The key determinants and/or mechanism(s) responsible for cognitive impairment when exposed to moderate hypoxia with sleep restriction, particularly on the executive function, have yet to be elucidated.

In silico evidence that substitution of glycine for valine (p.G8V) in a common variant of TMPRSS2 isoform 1 increases accessibility to an endocytic signal: Implication for SARS-cov-2 entry into host cells and susceptibility to COVID-19.

The TMPRSS2 protease plays a key role in the entry of the SARS-CoV-2 into cells. The TMPRSS2 gene is highly polymorphic in humans, and some polymorphisms may affect the susceptibility to COVID-19 or disease severity. rs75603675 (c.23G > T) is a missense variant that causes the replacement of glycine with valine at position 8 (p.G8V) in the TMPRSS2 isoform 1. According to GnomAD v4.0.0 database, the allele frequency of the rs75603675 on a global scale is 38.10 %, and range from 0.92 % in East Asian to 40.77 % in non-Finnish European (NFE) population. We analyzed the occurrence of the rs75603675 in two cohorts of patients, the first with severe/critical COVID-19 enrolled in a French hospital (42 patients), and the second with predominantly asymptomatic/pauci-symptomatic/mild COVID-19 enrolled in an Italian hospital (69 patients). We found that the TMPRSS2-c.23T minor allele frequency was similar in the two cohorts, 46.43 % and 46.38 %, respectively, and higher than the frequency in the NFE population (40.77 %). Chi-square test provided significant results (p < 0.05) when the genotype data (TMPRSS2-c.23T/c.23T homozygotes + TMPRSS2-c.23G/c.23T heterozygotes vs. TMPRSS2-c.23G/c.23G homozygotes) of the two patient groups were pooled and compared to the expected data for the NFE population, suggesting a possible pathogenetic mechanism of the p.G8V substitution. We explored the possible effects of the p.G8V substitution and found that the N-terminal region of the TMPRSS2 isoform 1 contains a signal for clathrin/AP-2-dependent endocytosis. In silico analysis predicted that the p.G8V substitution may increase the accessibility to the endocytic signal, which could help SARS-CoV-2 enter cells.

Twenty four-hour 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 with a thermoneutral condition (24°C). Twenty-three healthy, young and active male participants realised three sessions (from 13.00) 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, glucagon-like peptite-1, leptin and peptide YY) 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.

Neuromuscular and Metabolic Responses during Repeated Bouts of Loaded Downhill Walking.

INTRODUCTION: The aim of this study was to compare vastus lateralis (VL) and rectus femoris (RF) muscles for their nervous and mechanical adaptations during two bouts of downhill walking (DW) with load carriage performed 2 wk apart. Moreover, we investigated cardiometabolic and perceived exertion responses during both DW bouts. METHODS: Seventeen participants performed two 45-min sessions of loaded DW (30% of body mass; slope, -25%; speed, 4.5 km·h -1 ) separated by 2 wk. Rating of perceived exertion, cost of walking, heart rate, and EMG activity of thigh muscles were assessed during the DW. Muscle shear elastic modulus ( µ ) of RF and VL were assessed before each exercise bout. Maximal voluntary contraction torque was assessed before (PRE), immediately after (POST), and 24 and 48 h after the two exercise bouts. RESULTS: Maximal voluntary contraction torque decreased from POST (-23.7% ± 9.2%) to 48 h (-19.2% ± 11.9%) after the first exercise (Ex1), whereas it was significantly reduced only at POST (-14.6% ± 11.0%) after the second exercise (Ex2; P < 0.001). Rating of perceived exertion (Ex1: 12.3 ± 1.9; Ex2: 10.8 ± 2.0), heart rate (Ex1: 156 ± 23 bpm; Ex2: 145 ± 25 bpm), cost of walking (Ex1: 4.5 ± 0.9 J·m -1 ·kg -1 ; Ex2: 4.1 ± 0.7 J·m -1 ·kg -1 ), and RF EMG activity (Ex1: 0.071 ± 0.028 mV; Ex2: 0.041 ± 0.014 mV) were significantly decreased during Ex2 compared with Ex1 ( P < 0.01). RF µ was significantly greater in Ex2 (0.44 ± 0.18) compared with Ex1 (0.56 ± 0.27; P < 0.001). CONCLUSIONS: The RF muscle displayed specific mechanical and nervous adaptations to repeated DW bouts as compared with VL. Moreover, the muscle adaptations conferred by the first bout of DW could have induced greater exercise efficiency, inducing lesser perceived exertion and cardiometabolic demand when the same exercise was repeated 2 wk later.

Sleep loss effects on physiological and cognitive responses to systemic environmental hypoxia.

In the course of their missions or training, alpinists, but also mountain combat forces and mountain security services, professional miners, aircrew, aircraft and glider pilots and helicopter crews are regularly exposed to altitude without oxygen supplementation. At altitude, humans are exposed to systemic environmental hypoxia induced by the decrease in barometric pressure (<1,013 hPa) which decreases the inspired partial pressure of oxygen (PIO2), while the oxygen fraction is constant (equal to approximately 20.9%). Effects of altitude on humans occur gradually and depend on the duration of exposure and the altitude level. From 1,500 m altitude (response threshold), several adaptive responses offset the effects of hypoxia, involving the respiratory and the cardiovascular systems, and the oxygen transport capacity of the blood. Fatigue and cognitive and sensory disorders are usually observed from 2,500 m (threshold of prolonged hypoxia). Above 3,500 m (the threshold for disorders), the effects are not completely compensated and maladaptive responses occur and individuals develop altitude headache or acute altitude illness [Acute Mountain Sickness (AMS)]. The magnitude of effects varies considerably between different physiological systems and exhibits significant inter-individual variability. In addition to comorbidities, the factors of vulnerability are still little known. They can be constitutive (genetic) or circumstantial (sleep deprivation, fatigue, speed of ascent.). In particular, sleep loss, a condition that is often encountered in real-life settings, could have an impact on the physiological and cognitive responses to hypoxia. In this review, we report the current state of knowledge on the impact of sleep loss on responses to environmental hypoxia in humans, with the aim of identifying possible consequences for AMS risk and cognition, as well as the value of behavioral and non-pharmacological countermeasures.

The HMOX2 polymorphism contributes to the carotid body chemoreflex in European sea-level residents by regulating hypoxic ventilatory responses.

This study investigates whether a functional single nucleotide polymorphism of HMOX2 (heme oxygenase-2) (rs4786504 T>C) is involved in individual chemosensitivity to acute hypoxia, as assessed by ventilatory responses, in European individuals. These responses were obtained at rest and during submaximal exercise, using a standardized and validated protocol for exposure to acute normobaric hypoxia. Carriers of the ancestral T allele (n = 44) have significantly lower resting and exercise hypoxic ventilatory responses than C/C homozygous carriers (n = 40). In the literature, a hypoxic ventilatory response threshold to exercise has been identified as an independent predictor of severe high altitude-illness (SHAI). Our study shows that carriers of the T allele have a higher risk of SHAI than carriers of the mutated C/C genotype. Secondarily, we were also interested in COMT (rs4680 G > A) polymorphism, which may be indirectly involved in the chemoreflex response through modulation of autonomic nervous system activity. Significant differences are present between COMT genotypes for oxygen saturation and ventilatory responses to hypoxia at rest. In conclusion, this study adds information on genetic factors involved in individual vulnerability to acute hypoxia and supports the critical role of the ≪ O2 sensor ≫ - heme oxygenase-2 - in the chemosensitivity of carotid bodies in Humans.

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.

Lower Muscle and Blood Lactate Accumulation in Sickle Cell Trait Carriers in Response to Short High-Intensity Exercise.

It remains unclear whether sickle cell trait (SCT) should be considered a risk factor during intense physical activity. By triggering the polymerization-sickling-vaso-occlusion cascade, lactate accumulation-associated acidosis in response to high-intensity exercise is believed to be one of the causes of complications. However, our understanding of lactate metabolism in response to high-intensity exercise in SCT carriers is incomplete. Thirty male SCT carriers (n = 15) and healthy subjects (n = 15) with and without α-thalassemia performed a 2-min high-intensity exercise. Blood and muscle lactate concentrations were measured at exercise completion. Time courses of blood lactate and glucose concentrations were followed during the subsequent recovery. Additional biochemical analyses were performed on biopsies of the vastus lateralis muscle. SCT was associated with lower blood and muscle lactate concentrations in response to the short high-intensity exercise. Compared to controls, the muscle content among SCT carriers of lactate transporter MCT4 and ß2-adrenergic receptor were higher and lower, respectively. During recovery, the lactate removal ability was higher in SCT carriers. In the present study, no effect of α-thalassemia was observed. The lower blood and muscle lactate accumulations in SCT carriers may, to some extent, act as protective mechanisms: (i) against exercise-related acidosis and subsequent sickling, that may explain the relatively rare complications observed in exercising SCT carriers; and (ii) against the deleterious effects of intracellular lactate and associated acidosis on muscle function, that might explain the elevated presence of SCT carriers among the best sprinters.

Effects of Acute Heat and Cold Exposures at Rest or during Exercise on Subsequent Energy Intake: A Systematic Review and Meta-Analysis.

The objective of this meta-analysis was to assess the effect of acute heat/cold exposure on subsequent energy intake (EI) in adults. We searched the following sources for publications on this topic: PubMed, Ovid Medline, Science Direct and SPORTDiscus. The eligibility criteria for study selection were: randomized controlled trials performed in adults (169 men and 30 women; 20-52 years old) comparing EI at one or more meals taken ad libitum, during and/or after exposure to heat/cold and thermoneutral conditions. One of several exercise sessions could be realized before or during thermal exposures. Two of the thirteen studies included examined the effect of heat (one during exercise and one during exercise and at rest), eight investigated the effect of cold (six during exercise and two at rest), and three the effect of both heat and cold (two during exercise and one at rest). The meta-analysis revealed a small increase in EI in cold conditions (g = 0.44; p = 0.019) and a small decrease in hot conditions (g = -0.39, p = 0.022) for exposure during both rest and exercise. Exposures to heat and cold altered EI in opposite ways, with heat decreasing EI and cold increasing it. The effect of exercise remains unclear.

Effect of heat acclimation on metabolic adaptations induced by endurance training in soleus rat muscle.

Aerobic training leads to well-known systemic metabolic and muscular alterations. Heat acclimation may also increase mitochondrial muscle mass. We studied the effects of heat acclimation combined with endurance training on metabolic adaptations of skeletal muscle. Thirty-two rats were divided into four groups: control (C), trained (T), heat-acclimated (H), and trained with heat acclimation (H+T) for 6 weeks. Soleus muscle metabolism was studied, notably by the in situ measurement of mitochondrial respiration with pyruvate (Pyr) or palmitoyl-coenzyme A (PCoA), under phosphorylating conditions ( V˙max ) or not ( V˙0 ). Aerobic performance increased, and retroperitoneal fat mass decreased with training, independently of heat exposure (p < 0.001 and p < 0.001, respectively). Citrate synthase and hydroxyl-acyl-dehydrogenase activity increased with endurance training (p < 0.001 and p < 0.01, respectively), without any effect of heat acclimation. Training induced an increase of the V˙0 and V˙max for PCoA (p < .001 and p < .01, respectively), without interference with heat acclimation. The training-induced increase of V˙0 (p < 0.01) for pyruvate oxidation was limited when combined with heat acclimation (-23%, p < 0.01). Training and heat acclimation independently increased the V˙max for pyruvate (+60% p < 0.001 and +50% p = 0.01, respectively), without an additive effect of the combination. Heat acclimation doubled the training effect on muscle glycogen storage (p < 0.001). Heat acclimation did not improve mitochondrial adaptations induced by endurance training in the soleus muscle, possibly limiting the alteration of carbohydrate oxidation while not facilitating fatty-acid utilization. Furthermore, the increase in glycogen storage observed after HA combined with endurance training, without the improvement of pyruvate oxidation, appears to be a hypoxic metabolic phenotype.

Endurance Is Improved in Female Rats After Living High-Training High Despite Alterations in Skeletal Muscle.

Altitude camps are used during the preparation of endurance athletes to improve performance based on the stimulation of erythropoiesis by living at high altitude. In addition to such whole-body adaptations, studies have suggested that high-altitude training increases mitochondrial mass, but this has been challenged by later studies. Here, we hypothesized that living and training at high altitude (LHTH) improves mitochondrial efficiency and/or substrate utilization. Female rats were exposed and trained in hypoxia (simulated 3,200 m) for 5 weeks (LHTH) and compared to sedentary rats living in hypoxia (LH) or normoxia (LL) or those that trained in normoxia (LLTL). Maximal aerobic velocity (MAV) improved with training, independently of hypoxia, whereas the time to exhaustion, performed at 65% of MAV, increased both with training (P = 0.009) and hypoxia (P = 0.015), with an additive effect of the two conditions. The distance run was 7.98 ± 0.57 km in LHTH vs. 6.94 ± 0.51 in LLTL (+15%, ns). The hematocrit increased >20% with hypoxia (P < 0.001). The increases in mitochondrial mass and maximal oxidative capacity with endurance training were blunted by combination with hypoxia (-30% for citrate synthase, P < 0.01, and -23% for Vmax glut-succ, P < 0.001 between LHTH and LLTL). A similar reduction between the LHTH and LLTL groups was found for maximal respiration with pyruvate (-29%, P < 0.001), for acceptor-control ratio (-36%, hypoxia effect, P < 0.001), and for creatine kinase efficiency (-48%, P < 0.01). 3-hydroxyl acyl coenzyme A dehydrogenase was not altered by hypoxia, whereas maximal respiration with Palmitoyl-CoA specifically decreased. Overall, our results show that mitochondrial adaptations are not involved in the improvement of submaximal aerobic performance after LHTH, suggesting that the benefits of altitude camps in females relies essentially on other factors, such as the transitory elevation of hematocrit, and should be planned a few weeks before competition and not several months.

Cardiolipin content controls mitochondrial coupling and energetic efficiency in muscle.

Unbalanced energy partitioning participates in the rise of obesity, a major public health concern in many countries. Increasing basal energy expenditure has been proposed as a strategy to fight obesity yet raises efficiency and safety concerns. Here, we show that mice deficient for a muscle-specific enzyme of very-long-chain fatty acid synthesis display increased basal energy expenditure and protection against high-fat diet-induced obesity. Mechanistically, muscle-specific modulation of the very-long-chain fatty acid pathway was associated with a reduced content of the inner mitochondrial membrane phospholipid cardiolipin and a blunted coupling efficiency between the respiratory chain and adenosine 5'-triphosphate (ATP) synthase, which was restored by cardiolipin enrichment. Our study reveals that selective increase of lipid oxidative capacities in skeletal muscle, through the cardiolipin-dependent lowering of mitochondrial ATP production, provides an effective option against obesity at the whole-body level.

Four-month operational heat acclimatization positively affects the level of heat tolerance 6 months later.

Benefits obtained after heat acclimation/acclimatization should be completely lost after an estimated period of 6 weeks. However, this estimate is still hypothetical. We evaluate the long-term effects of heat acclimatization on the level of heat tolerance. Physiological and subjective markers of heat tolerance were assessed during a heat stress test (HST: 3 × 8-min runs outdoors [~ 40 °C and 20% RH] at 50% of their estimated speed at VO2max) performed on the 2nd day upon arrival to the desert military base in the United Arab Emirates after a first day of mostly passive exposure to heat. Among the 50 male French soldiers, 25 partook in a 4-month military mission in countries characterized by a hot environment ~ 6 months prior to the study (HA). The other 25 participants were never heat acclimatized (CT). Rectal temperature (p = 0.023), heart rate (p = 0.033), and perceived exertion (p = 0.043) were lower in the HA than CT group at the end of HST. Soldiers who experienced a former 4-month period of natural heat acclimatization very likely had a higher level of heat tolerance during exercise in the heat, even 6 months after returning from the previous desert mission, than that of their non-acclimatized counterparts.

A basal heat stress test to detect military operational readiness after a 14-day operational heat acclimatization period.

A basal heat stress test (HST) to predict the magnitude of adaptive responses during heat acclimatization (HA) would be highly useful for the armed forces. The aim was to identify physiological markers assessed during a HST (three 8-min running sets at 50% of the speed at VO2max) performed just before a 14-day HA period that would identify participants still at "risk" at the end of HA. Individuals that responded poorly (large increases in rectal temperature [Trec] and heart rate [HR]) during the initial HST were more likely to respond favorably to HA (large reductions in Trec and HR). However, they were also more likely to exhibit lower tolerance to HST at D15. Basal Trec was found to efficiently discriminate participants showing a Trec > 38.5°C after HA, who are considered to be "at risk". Finally, participants were classified by quartiles based on basal Trec and HR at the end of the HST and physiological strain index (PSI). Most of the participants "at risk" were among the upper quartile (i.e. the least tolerant) of Trec and PSI (p = 0.011 for both). Overall, these results show that the individuals who are less tolerant to a basal HST are very likely to benefit the most from HA but they also remain less tolerant to heat at the end of HA than those who better tolerated the basal HST. A basal HST could therefore theoretically help the command to select the most-ready personnel in hot conditions while retaining those who are less tolerant 6.

Changes in the Viscoelastic Properties of the Vastus Lateralis Muscle With Fatigue.

We investigated the in vivo effects of voluntary fatiguing isometric contractions of the knee extensor muscles on the viscoelastic properties of the vastus lateralis (VL). Twelve young males (29.0 ± 4.5 years) performed an intermittent voluntary fatigue protocol consisting of 6 sets × 10 repetitions of 5-s voluntary maximal isometric contractions with 5-s passive recovery periods between repetitions. Voluntary and evoked torque were assessed before, immediately after, and 20 min after exercise. The shear modulus (µ) of the VL muscle was estimated at rest and during a ramped isometric contraction using a conventional elastography technique. An index of active muscle stiffness was then calculated (slope from the relationship between shear modulus and absolute torque). Resting muscle viscosity (η) was quantified using a shear-wave spectroscopy sequence to measure the shear-wave dispersion. Voluntary and evoked torque decreased by ∼37% (P < 0.01) immediately after exercise. The resting VL µ was lower at the end of the fatigue protocol (-57.9 ± 5.4%, P < 0.001), whereas the resting VL η increased (179.0 ± 123%, P < 0.01). The active muscle stiffness index also decreased with fatigue (P < 0.05). By 20 min post-fatigue, there were no significant differences from the pre-exercise values for VL η and the active muscle stiffness index, contrary to the resting VL µ. We show that the VL µ is greatly reduced and η greatly enhanced by fatigue, reflecting a more compliant and viscous muscle. The quantification of both shear µ and η moduli in vivo may contribute to a better understanding of the mechanical behavior of muscles during fatigue in sports medicine, as well as in clinical situations.

Effect of high-intensity interval training and continuous endurance training on peak oxygen uptake among seniors aged 65 or older: A meta-analysis of randomized controlled trials.

BACKGROUND: Ageing is intrinsically associated with a progressive decline in cardiorespiratory fitness (CRF) as measured by peak oxygen uptake (VO2peak ). Improving CRF through physical activity contribute to better and healthy ageing. High-intensity interval training (HIIT) is a potent method of improving CRF among seniors, yet comparisons between this type of training and traditional endurance training (ET) are equivocal especially among older adults. PURPOSE: To analyse the effects of HIIT and ET on the VO2peak of seniors aged 65 years or older when compared with controls and also when the two types of training were compared with one another. METHODS: A comprehensive, systematic database search for manuscripts was performed in Embase, Medline, PubMed Central, ScienceDirect, Scopus and Web of Science using key words. Two reviewers independently assessed interventional studies for potential inclusion. Fifteen randomized controlled trials (RCTs) were included totalling 480 seniors aged 65 years or over. Across the trials, no high risk of bias was measured. RESULTS: In pooled analysis of the RCTs, the VO2peak was significantly higher after ET sessions compared with controls (mean difference-MD = 1.35; 95% confidence interval-CI: 0.73-1.96). Furthermore, VO2peak was found significantly higher not only when compared HIIT with controls (MD = 4.61; 95% CI: 3.21-6.01), but also when compared HIIT with ET (MD = 3.76; 95% CI: 2.96-4.56). CONCLUSION: High-intensity interval training and ET both elicit large improvements in the VO2peak of older adults aged 65 or over. When compared with ET, the gain in VO2peak was greater following HIIT. Nevertheless, further RCTs are therefore needed to confirm our results in senior's population.

Beneficial effects of exercise training on cognitive performances during total sleep deprivation in healthy subjects.

OBJECTIVE: Exercise training has been shown to improve learning and memory, and to protect against the negative impact of sleep deprivation. The aim of this study was to investigate the effects of seven weeks of moderate- and high-intensity interval exercise training on vigilance/sustained attention, inhibition processes and working memory during 40-h total sleep deprivation (TSD) in 16 healthy young men. METHODS: The subjects were evaluated before (Baseline, BAS) and during TSD, and the day after a night of recovery sleep (Recovery, REC). RESULTS: Exercise training significantly decreased errors and increased speed assessed by the psychomotor vigilance task (PVT) during TSD and REC while no difference was found in executive inhibition (Go-noGo task) and working memory (2-Back task) performances. The multiple sleep latency test results were higher during BAS and REC at Post-exercise training, and no difference occurred in subjective sleepiness and daytime microsleeps over the 40-h TSD. The PVT speed was positively correlated with maximal oxygen consumption and maximal aerobic power measured before entry in the in-laboratory TSD protocol, and stage 3 sleep duration measured during the first night in the in-laboratory TSD protocol (N-1). Exercise training effects on sleep were found during the night recovery with lower stage-3 sleep and higher rapid eye movement (REM) sleep durations. An exercise training effect was also found on free insulin-like growth factor I levels with lower levels during TSD at Post-exercise training. CONCLUSIONS: In healthy young men, exercise training reduced sleep pressure at baseline and protected against sustained attention deficits induced by TSD with persistent effect after one night of recovery sleep. Nevertheless, exercise training was not effective in reducing deficits in executive inhibition and working memory induced by TSD.

Resting Muscle Shear Modulus Measured With Ultrasound Shear-Wave Elastography as an Alternative Tool to Assess Muscle Fatigue in Humans.

The aim of this study was to investigate the time course of the resting vastus lateralis (VL) muscle shear elastic modulus (µ) measured with ultrasound shear-wave elastography during repetition of isometric maximal voluntary contractions (MVCs) of the knee extensors (KE). Fifteen well-trained young males repeated 60 5-s isometric MVCs. Evoked electrical stimulations and the VLµ were measured every ten MVCs at rest. The resting VLµ significantly decreased (-34.7 ± 6.7%; P < 0.001) by the end of the fatigue protocol. There was also a 38.4 ± 12.6 % decrease in MVC after exercise (P < 0.001). The potentiated doublet and single twitch torque amplitudes and properties were significantly modified by the end of exercise (P < 0.001). This study shows the time course of the resting VLµ during the repetition of maximal voluntary fatiguing exercise of the KE muscles. The decrease of the resting VLµ could directly affect the force transmission capabilities accounting for peripheral fatigue.

The effect of a physiological increase in temperature on mitochondrial fatty acid oxidation in rat myofibers.

We investigated the effect of temperature increase on mitochondrial fatty acid (FA) and carbohydrate oxidation in the slow-oxidative skeletal muscles (soleus) of rats. We measured mitochondrial respiration at 35°C and 40°C with the physiological substrates pyruvate + 4 mM malate (Pyr) and palmitoyl-CoA (PCoA) + 0.5 mM malate + 2 mM carnitine in permeabilized myofibers under nonphosphorylating (V˙0) or phosphorylating (V˙max) conditions. Mitochondrial efficiency was calculated by the respiratory control ratio (RCR = V˙max/V˙0). We used guanosine triphosphate (GTP), an inhibitor of uncoupling protein (UCP), to study the mechanisms responsible for alterations of mitochondrial efficiency. We measured hydrogen peroxide (H2O2) production under nonphosphorylating and phosphorylating conditions at both temperatures and substrates. We studied citrate synthase (CS) and 3-hydroxyl acyl coenzyme A dehydrogenase (3-HAD) activities at both temperatures. Elevating the temperature from 35°C to 40°C increased PCoA-V˙0 and decreased PCoA-RCR, corresponding to the uncoupling of oxidative phosphorylation (OXPHOS). GTP blocked the heat-induced increase of PCoA-V˙0. Rising temperature moved toward a Pyr-V˙0 increase, without significance. Heat did not alter H2O2 production, resulting from either PCoA or Pyr oxidation. Heat induced an increase in 3-HAD but not in CS activities. In conclusion, heat induced OXPHOS uncoupling for PCoA oxidation, which was at least partially mediated by UCP and independent of oxidative stress. The classically described heat-induced glucose shift may actually be mostly due to a less efficient FA oxidation. These findings raise questions concerning the consequences of heat-induced alterations in mitochondrial efficiency of FA metabolism on thermoregulation.NEW & NOTEWORTHY Ex vivo exposure of skeletal myofibers to heat uncouples substrate oxidation from ADP phosphorylation, decreasing the efficiency of mitochondria to produce ATP. This heat effect alters fatty acids (FAs) more than carbohydrate oxidation. Alteration of FA oxidation involves uncoupling proteins without inducing oxidative stress. This alteration in lipid metabolism may underlie the preferential use of carbohydrates in the heat and could decrease aerobic endurance.

Proposition for a shortened version of the Leeds Food Preference Questionnaire (LFPQ).

The Leeds Food Preference Questionnaire (LFPQ) assesses, among other components, food preference (FP) using a procedure that requires both time and concentration. Its use may therefore be difficult in a complex protocol. In this article, we assessed the suitability of two shorter versions: 1) the LFPQ-S2, using two instead of four foods per group, and 2) the food preference questionnaire (FPQ-S16), using the 16 same foods as the LFPQ, displayed simultaneously, that have to be ranked in order of preference. We assessed the reliability of these short versions using correlations and interchangeability (Bland and Altman) analyses. Sixty-nine healthy French adults completed the original LFPQ using foods adapted to the French context, and then the FPQ-S16 procedure before (hungry state) and after (satiated state) a classic lunch. Finally, they had to select the two foods that best depict the characteristics of each group. The two foods receiving the most votes were used to calculate FP scores with the LFPQ-S2 procedure. The FP scores were no different between the three questionnaires and were modified similarly by lunch intake. The FP scores also highly correlated between the two short versions and the LFPQ (mean r = 0.83 and 0.88 in the hungry state and r = 0.86 and 0.87 in the satiated state for LFPQ-S2 and FPQ-S16, respectively). Finally, the FPQ-S16 was considered to be a better surrogate of the LFPQ than the LFPQ-S2. Scores of specific categories (groups of foods categorized by one property; e.g. high-fat foods) showed modest-to-good agreement, whereas scores of combined categories (groups of foods categorized by combined properties, e.g. high-fat and sweet foods) showed poor-to-modest agreement. Overall, the two short versions of the LFPQ could replace it to assess FP in a protocol in which time is limited. The FPQ-S16 appears to be a better solution than the LFPQ-S2, based on interchangeability analyses.