Repeated sprint training in hypoxia induces specific skeletal muscle adaptations through S100A protein signaling.

Athletes increasingly engage in repeated sprint training consisting in repeated short all-out efforts interspersed by short recoveries. When performed in hypoxia (RSH), it may lead to greater training effects than in normoxia (RSN); however, the underlying molecular mechanisms remain unclear. This study aimed at elucidating the effects of RSH on skeletal muscle metabolic adaptations as compared to RSN. Sixteen healthy young men performed nine repeated sprint training sessions in either normoxia (FIO2 = 0.209, RSN, n = 7) or normobaric hypoxia (FIO2 = 0.136, RSH, n = 9). Before and after the training period, exercise performance was assessed by using repeated sprint ability (RSA) and Wingate tests. Vastus lateralis muscle biopsies were performed to investigate muscle metabolic adaptations using proteomics combined with western blot analysis. Similar improvements were observed in RSA and Wingate tests in both RSN and RSH groups. At the muscle level, RSN and RSH reduced oxidative phosphorylation protein content but triggered an increase in mitochondrial biogenesis proteins. Proteomics showed an increase in several S100A family proteins in the RSH group, among which S100A13 most strongly. We confirmed a significant increase in S100A13 protein by western blot in RSH, which was associated with increased Akt phosphorylation and its downstream targets regulating protein synthesis. Altogether our data indicate that RSH may activate an S100A/Akt pathway to trigger specific adaptations as compared to RSN.

Age and sex differences in microvascular responses during reactive hyperaemia.

Microvascular impairments are typical of several cardiovascular diseases. Near-infrared spectroscopy (NIRS) combined with a vascular occlusion test provides non-invasive insights into microvascular responses by monitoring skeletal muscle oxygenation changes during reactive hyperaemia. Despite increasing interest in the effects of sex and ageing on microvascular responses, evidence remains inconsistent. Therefore, the present study aimed to investigate the effects of sex and age on microvascular responsiveness. Twenty-seven participants (seven young men and seven young women; seven older men and six older women; aged 26 ± 1, 26 ± 4, 67 ± 3 and 69 ± 4 years, respectively) completed a vascular occlusion test consisting of 5 min of arterial occlusion followed by 5 min reperfusion. Oxygenation changes in the vastus lateralis were monitored by near-infrared spectroscopy. The findings revealed that both women (referring to young and older women) and older participants (referring to both men and women) exhibited lower microvascular responsiveness. Notably, both women and older participants demonstrated reduced desaturation (-38% and -59%, respectively) and reperfusion rates (-24% and -40%, respectively) along with a narrower range of tissue oxygenation (-39% and -39%, respectively) and higher minimal tissue oxygenation levels (+34% and +21%, respectively). Women additionally displayed higher values in resting (+12%) and time-to-peak (+15%) tissue oxygenation levels. In conclusion, this study confirmed decreased microvascular responses in women and older individuals. These results emphasize the importance of considering sex and age when studying microvascular responses. Further research is needed to uncover the underlying mechanisms and clinical relevance of these findings, enabling the development of tailored strategies for preserving vascular health in diverse populations.

Hot water immersion: Maintaining core body temperature above 38.5°C mitigates muscle fatigue.

PURPOSE: Hot water immersion (HWI) has gained popularity to promote muscle recovery, despite limited data on the optimal heat dose. The purpose of this study was to compare the responses of two exogenous heat strains on core body temperature, hemodynamic adjustments, and key functional markers of muscle recovery following exercise-induced muscle damage (EIMD). METHODS: Twenty-eight physically active males completed an individually tailored EIMD protocol immediately followed by one of the following recovery interventions: HWI (40°C, HWI40 ), HWI (41°C, HWI41 ) or warm water immersion (36°C, CON36 ). Gastrointestinal temperature (Tgi ), hemodynamic adjustments (cardiac output [CO], mean arterial pressure [MAP], and systemic vascular resistance [SVR]), pre-frontal cortex deoxyhemoglobin (HHb), ECG-derived respiratory frequency, and subjective perceptual measures were tracked throughout immersion. In addition, functional markers of muscle fatigue (maximal concentric peak torque [Tpeak ]) and muscle damage (late-phase rate of force development [RFD100-200 ]) were measured prior to EIMD (pre-), 24 h (post-24 h), and 48 h (post-48 h) post-EIMD. RESULTS: By the end of immersion, HWI41 led to significantly higher Tgi values than HWI40 (38.8 ± 0.1 vs. 38.0°C ± 0.6°C, p < 0.001). While MAP was well maintained throughout immersion, only HWI41 led to increased (HHb) (+4.2 ± 1.47 µM; p = 0.005) and respiratory frequency (+4.0 ± 1.21 breath.min-1 ; p = 0.032). Only HWI41 mitigated the decline in RFD100-200 at post-24 h (-7.1 ± 31.8%; p = 0.63) and Tpeak at post-48 h (-3.1 ± 4.3%, p = 1). CONCLUSION: In physically active males, maintaining a core body temperature of ~25 min within the range of 38.5°C-39°C has been found to be effective in improving muscle recovery, while minimizing the risk of excessive physiological heat strain.

The International Olympic Committee framework on fairness, inclusion and nondiscrimination on the basis of gender identity and sex variations does not protect fairness for female athletes.

The International Olympic Committee (IOC) recently published a framework on fairness, inclusion, and nondiscrimination on the basis of gender identity and sex variations. Although we appreciate the IOC's recognition of the role of sports science and medicine in policy development, we disagree with the assertion that the IOC framework is consistent with existing scientific and medical evidence and question its recommendations for implementation. Testosterone exposure during male development results in physical differences between male and female bodies; this process underpins male athletic advantage in muscle mass, strength and power, and endurance and aerobic capacity. The IOC's "no presumption of advantage" principle disregards this reality. Studies show that transgender women (male-born individuals who identify as women) with suppressed testosterone retain muscle mass, strength, and other physical advantages compared to females; male performance advantage cannot be eliminated with testosterone suppression. The IOC's concept of "meaningful competition" is flawed because fairness of category does not hinge on closely matched performances. The female category ensures fair competition for female athletes by excluding male advantages. Case-by-case testing for transgender women may lead to stigmatization and cannot be robustly managed in practice. We argue that eligibility criteria for female competition must consider male development rather than relying on current testosterone levels. Female athletes should be recognized as the key stakeholders in the consultation and decision-making processes. We urge the IOC to reevaluate the recommendations of their Framework to include a comprehensive understanding of the biological advantages of male development to ensure fairness and safety in female sports.

Hypoxia Sensing and Responses in Parkinson's Disease.

Parkinson's disease (PD) is associated with various deficits in sensing and responding to reductions in oxygen availability (hypoxia). Here we summarize the evidence pointing to a central role of hypoxia in PD, discuss the relation of hypoxia and oxygen dependence with pathological hallmarks of PD, including mitochondrial dysfunction, dopaminergic vulnerability, and alpha-synuclein-related pathology, and highlight the link with cellular and systemic oxygen sensing. We describe cases suggesting that hypoxia may trigger Parkinsonian symptoms but also emphasize that the endogenous systems that protect from hypoxia can be harnessed to protect from PD. Finally, we provide examples of preclinical and clinical research substantiating this potential.

Ventilatory responses to independent and combined hypoxia, hypercapnia and hypobaria in healthy pre-term-born adults.

Pre-term birth is associated with physiological sequelae that persist into adulthood. In particular, modulated ventilatory responsiveness to hypoxia and hypercapnia has been observed in this population. Whether pre-term birth per se causes these effects remains unclear. Therefore, we aimed to assess pulmonary ventilation and blood gases under various environmental conditions, comparing 17 healthy prematurely born individuals (mean ± SD; gestational age, 28 ± 2 weeks; age, 21 ± 4 years; peak oxygen uptake, 48.1 ± 11.2 ml kg-1  min-1 ) with 16 well-matched adults born at term (gestational age, 40 ± 1 weeks; age, 22 ± 2 years; peak oxygen uptake, 51.2 ± 7.7 ml kg-1  min-1 ). Participants were exposed to seven combinations of hypoxia/hypobaria (equivalent to ∼3375 m) and/or hypercapnia (3% CO2 ), at rest for 6 min. Pulmonary ventilation, pulse oxygen saturation and the arterial partial pressures of O2 and CO2 were similar in pre-term and full-term individuals under all conditions. Higher ventilation in hypoxia compared to normoxia was only observed at terrestrial altitude, despite an equivalent (normobaric) hypoxic stimulus administered at sea level (0.138 F i O 2 ${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ). Assessment of oscillations in key variables revealed that combined hypoxic hypercapnia induced greater underlying fluctuations in ventilation in pre-term individuals only. In general, higher pulse oxygen saturation fluctuations were observed with hypoxia, and lower fluctuations in end-tidal CO2 with hypercapnia, despite similar ventilatory oscillations observed between conditions. These findings suggest that healthy prematurely born adults display similar overall ventilation to their term-born counterparts under various environmental stressors, but that combined ventilatory stimuli could induce an irregular underlying ventilatory pattern. Moreover, barometric pressure may be an important factor when assessing ventilatory responsiveness to moderate hypoxic stimuli. KEY POINTS: Evidence exists for unique pulmonary and respiratory function under hypoxic conditions in adult survivors of pre-term birth. Whether pre-term birth per se causes these differences requires a comparison of conventionally healthy prematurely born adults with an appropriately matched sample of term-born individuals. According to the present data, there is no difference between healthy pre-term and well-matched term-born individuals in the magnitude of pulmonary ventilation or arterial blood gases during independent and combined hypobaria, hypoxia and hypercapnia. Terrestrial altitude (hypobaria) was necessary to induce differences in ventilation between normoxia and a hypoxic stimulus equivalent to ∼3375 m of altitude. Furthermore, peak power in pulse oxygen saturation was similar between hypobaric normoxia and normobaric hypoxia. The observed similarities between groups suggest that ventilatory regulation under various environmental stimuli is not impaired by pre-term birth per se. Instead, an integrated combination of neonatal treatment strategies and cardiorespiratory fitness/disease status might underlie previously observed chemosensitivity impairments.

Impaired cerebrovascular CO2 reactivity at high altitude in prematurely born adults.

Premature birth impairs cardiac and ventilatory responses to both hypoxia and hypercapnia, but little is known about cerebrovascular responses. Both at sea level and after 2 days at high altitude (3375 m), 16 young preterm-born (gestational age, 29 ± 1 weeks) and 15 age-matched term-born (40 ± 0 weeks) adults were exposed to two consecutive 4 min bouts of hyperoxic hypercapnic conditions (3% CO2 -97% O2 ; 6% CO2 -94% O2 ), followed by two periods of voluntary hyperventilation-induced hypocapnia. We measured middle cerebral artery blood velocity, end-tidal CO2 , pulmonary ventilation, beat-by-beat mean arterial pressure and arterialized capillary blood gases. Baseline middle cerebral artery blood velocity increased at high altitude compared with sea level in term-born (+24 ± 39%, P = 0.036), but not in preterm-born (-4 ± 27%, P = 0.278) adults. The end-tidal CO2 , pulmonary ventilation and mean arterial pressure were similar between groups at sea level and high altitude. Hypocapnic cerebrovascular reactivity was higher at high altitude compared with sea level in term-born adults (+173 ± 326%, P = 0.026) but not in preterm-born adults (-21 ± 107%, P = 0.572). Hypercapnic reactivity was altered at altitude only in preterm-born adults (+125 ± 144%, P < 0.001). Collectively, at high altitude, term-born participants showed higher hypocapnic (P = 0.012) and lower hypercapnic (P = 0.020) CO2 reactivity compared with their preterm-born peers. In conclusion, exposure to high altitude revealed different cerebrovascular responses in preterm- compared with term-born adults, despite similar ventilatory responses. These findings suggest a blunted cerebrovascular response at high altitude in preterm-born adults, which might predispose these individuals to an increased risk of high-altitude illnesses. KEY POINTS: Cerebral haemodynamics and cerebrovascular reactivity in normoxia are known to be similar between term-born and prematurely born adults. In contrast, acute exposure to high altitude unveiled different cerebrovascular responses to hypoxia, hypercapnia and hypocapnia. In particular, cerebral vasodilatation was impaired in prematurely born adults, leading to an exaggerated cerebral vasoconstriction. Cardiovascular and ventilatory responses to both hypo- and hypercapnia at sea level and at high altitude were similar between control subjects and prematurely born adults. Other mechanisms might therefore underlie the observed blunted cerebral vasodilatory responses in preterm-born adults at high altitude.

Mechanisms underlying the health benefits of intermittent hypoxia conditioning.

Intermittent hypoxia (IH) is commonly associated with pathological conditions, particularly obstructive sleep apnoea. However, IH is also increasingly used to enhance health and performance and is emerging as a potent non-pharmacological intervention against numerous diseases. Whether IH is detrimental or beneficial for health is largely determined by the intensity, duration, number and frequency of the hypoxic exposures and by the specific responses they engender. Adaptive responses to hypoxia protect from future hypoxic or ischaemic insults, improve cellular resilience and functions, and boost mental and physical performance. The cellular and systemic mechanisms producing these benefits are highly complex, and the failure of different components can shift long-term adaptation to maladaptation and the development of pathologies. Rather than discussing in detail the well-characterized individual responses and adaptations to IH, we here aim to summarize and integrate hypoxia-activated mechanisms into a holistic picture of the body's adaptive responses to hypoxia and specifically IH, and demonstrate how these mechanisms might be mobilized for their health benefits while minimizing the risks of hypoxia exposure.

Test-retest reliability of ski-specific aerobic, sprint, and neuromuscular performance tests in highly trained cross-country skiers.

PURPOSE: Laboratory tests are commonly performed by cross-country (XC) skiers due to the challenges of obtaining reliable performance indicators on snow. However, only a few studies have reported reliability data for ski-specific test protocols. Therefore, this study examined the test-retest reliability of ski-specific aerobic, sprint, and neuromuscular performance tests. METHODS: Thirty-nine highly trained XC skiers (26 men and 13 women, age: 22 ± 4 years, V̇O2max : 70.1 ± 4.5 and 58.8 ± 4.4 mL·kg-1 ·min-1 , respectively) performed two test trials within 6 days of a diagonal V̇O2max test, n = 27; skating graded exercise test to assess the second lactate threshold (LT2 ), n = 27; 24-min double poling time trial (24-min DP, n = 25), double poling sprint test (SprintDP1 , n = 27), and 1-min self-paced skating sprint test (Sprint1-min , n = 26) using roller skis on a treadmill, and an upper-body strength test (UB-ST, n = 27) to assess peak power (Ppeak ) with light, medium, and heavy loads. For each test, the coefficient of variation (CV), intraclass correlation coefficient (ICC), and minimal detectable change (MDC) were calculated. RESULTS: V̇O2max demonstrated good-to-excellent reliability (CV = 1.4%; ICC = 0.99; MDC = 112 mL·min-1 ), whereas moderate-to-excellent reliability was found for LT2 (CV = 3.1%; ICC = 0.95). Performance during 24-min DP, SprintDP1 , and Sprint1-min showed good-to-excellent reliability (CV = 1.0%-2.3%; ICC = 0.96-0.99). Absolute reliability for UB-ST Ppeak was poor (CV = 4.9%-7.8%), while relative reliability was excellent (ICC = 0.93-0.97) across the loads. CONCLUSION: In highly trained XC skiers, sport-specific aerobic and sprint performance tests demonstrated high test-retest reliability, while neuromuscular performance for the upper body was less reliable. Using the presented protocols, practitioners can assess within- and between-season changes in relevant performance indicators.

Vertical and Leg Stiffness Modeling During Running: Effect of Speed and Incline.

A spring mass model is often used to describe human running, allowing to understand the concept of elastic energy storage and restitution. The stiffness of the spring is a key parameter and different methods have been developed to estimate both the vertical and the leg stiffness components. Nevertheless, the validity and the range of application of these models are still debated. The aim of the present study was to compare three methods (i. e., Temporal, Kinetic and Kinematic-Kinetic) of stiffness determination. Twenty-nine healthy participants equipped with reflective markers performed 5-min running bouts at four running speeds and eight inclines on an instrumented treadmill surrounded by a tri-dimensional motion camera system. The three methods provided valid results among the different speeds, but the reference method (i. e., Kinematic-Kinetic) provided higher vertical stiffness and lower leg stiffness than the two other methods (both p<0.001). On inclined terrain, the method using temporal parameters provided non valid outcomes and should not be used. Finally, this study highlights that both the assumption of symmetry between compression and decompression phases or the estimation of the vertical displacement and changes in leg length are the major sources of errors when comparing different speeds or different slopes.

Both Hypoxia and Hypobaria Impair Baroreflex Sensitivity but through Different Mechanisms.

Baroreflex sensitivity (BRS) is a measure of cardiovagal baroreflex and is lower in normobaric and hypobaric hypoxia compared to normobaric normoxia. The aim of this study was to assess the effects of hypobaria on BRS in normoxia and hypoxia. Continuous blood pressure and ventilation were recorded in eighteen seated participants in normobaric normoxia (NNx), hypobaric normoxia (HNx), normobaric hypoxia (NHx) and hypobaric hypoxia (HHx). Barometric pressure was matched between NNx vs. NHx (723±4 mmHg) and HNx vs. HHx (406±4 vs. 403±5 mmHg). Inspired oxygen pressure (PiO2) was matched between NNx vs. HNx (141.2±0.8 vs. 141.5±1.5 mmHg) and NHx vs. HHx (75.7±0.4 vs. 74.3±1.0 mmHg). BRS was assessed using the sequence method. BRS significantly decreased in HNx, NHx and HHx compared to NNx. Heart rate, mean systolic and diastolic blood pressures did not differ between conditions. There was the specific effect of hypobaria on BRS in normoxia (BRS was lower in HNx than in NNx). The hypoxic and hypobaric effects do not add to each other resulting in comparable BRS decreases in HNx, NHx and HHx. BRS decrease under low barometric pressure requires future studies independently controlling O2 and CO2 to identify central and peripheral chemoreceptors' roles.

Molecular Mechanisms of High-Altitude Acclimatization.

High-altitude illnesses (HAIs) result from acute exposure to high altitude/hypoxia. Numerous molecular mechanisms affect appropriate acclimatization to hypobaric and/or normobaric hypoxia and curtail the development of HAIs. The understanding of these mechanisms is essential to optimize hypoxic acclimatization for efficient prophylaxis and treatment of HAIs. This review aims to link outcomes of molecular mechanisms to either adverse effects of acute high-altitude/hypoxia exposure or the developing tolerance with acclimatization. After summarizing systemic physiological responses to acute high-altitude exposure, the associated acclimatization, and the epidemiology and pathophysiology of various HAIs, the article focuses on molecular adjustments and maladjustments during acute exposure and acclimatization to high altitude/hypoxia. Pivotal modifying mechanisms include molecular responses orchestrated by transcription factors, most notably hypoxia inducible factors, and reciprocal effects on mitochondrial functions and REDOX homeostasis. In addition, discussed are genetic factors and the resultant proteomic profiles determining these hypoxia-modifying mechanisms culminating in successful high-altitude acclimatization. Lastly, the article discusses practical considerations related to the molecular aspects of acclimatization and altitude training strategies.

Respiratory responses to hypoxia during rest and exercise in individuals born pre-term: a state-of-the-art review.

The pre-term birth survival rate has increased considerably in recent decades, and research investigating the long-term effects of premature birth is growing. Moreover, altitude sojourns are increasing in popularity and are often accompanied by various levels of physical activity. Individuals born pre-term appear to exhibit altered acute ventilatory responses to hypoxia, potentially predisposing them to high-altitude illness. These impairments are likely due to the use of perinatal hyperoxia stunting the maturation of carotid body chemoreceptors, but may also be attributed to limited lung diffusion capacity and/or gas exchange inefficiency. Aerobic exercise capacity also appears to be reduced in this population. This may relate to the aforementioned respiratory impairments, or could be due to physiological limitations in pulmonary blood flow or at the exercising muscle (e.g. mitochondrial efficiency). However, surprisingly, the debilitative effects of exercise when performed at altitude do not seem to be exacerbated by premature birth. In fact, it is reasonable to speculate that pre-term birth could protect against the consequences of exercise combined with hypoxia. The mechanisms that underlie this assertion might relate to differences in oxidative stress responses or in cardiopulmonary morphology in pre-term individuals, compared to their full-term counterparts. Further research is required to elucidate the independent effects of neonatal treatment, sex differences and chronic lung disease, and to establish causality in some of the proposed mechanisms that could underlie the differences discussed throughout this review. A more in-depth understanding of the acclimatisation responses to chronic altitude exposures would also help to inform appropriate interventions in this clinical population.

Wales Anaerobic Test: Reliability and Fitness Profiles of International Rugby Union Players.

ABSTRACT: Beard, A, Ashby, J, Chambers, R, Millet, GP, and Brocherie, F. Wales Anaerobic Test (WAT): Reliability and fitness profiles of international rugby union players. J Strength Cond Res 36(9): 2589-2596, 2022-To provide strength and conditioning coaches a practical and evidence-based test for repeated-sprint ability (RSA) in rugby union players, this study assessed the relative and absolute test-retest reliability of the Wales Anaerobic Test (WAT) and its position-specific association with other fitness performance indices. Thirty-four players (forwards: n = 19; backs: n = 15) of the Welsh rugby union male senior national team performed the WAT (10 × 50-m distance, 25-30 seconds of passive recovery) twice within 4 days. Time for each repetition was recorded, with the best (WAT Best ) and total time (WAT TT ) retained for analysis. Relative (intraclass correlation coefficient [ICC]) and absolute ( SEM ) reliability of the WAT indices were quantified. Furthermore, association (Pearson's product-moment correlations and stepwise backward elimination procedure) with other fitness performance indices (10- and 40-m sprinting times, 30-15 intermittent fitness test [30-15 IFT ] and the Yo-Yo intermittent recovery test level 2 [YYIR2]) was investigated. Pooled values revealed "moderate" to "high" ICCs for WAT Best (ICC = 0.89, p = 0.626) and WAT TT (ICC = 0.95, p = 0.342). Good test sensitivity was reported for forwards and backs' WAT TT ( p > 0.101). Both WAT Best and WAT TT correlated with 10-m and 40-m sprinting times ( r > 0.69, p < 0.001) as well as with 30-15 IFT ( r < -0.77, p < 0.001) and YYIR2 ( r < -0.68, p < 0.001) for pooled values. The WAT proved to be a reliable and sensitive test to assess the rugby union specific RSA-related fitness of international players.

RMSSD Is More Sensitive to Artifacts Than Frequency-Domain Parameters: Implication in Athletes' Monitoring.

Easy-to-use and accurate heart rate variability (HRV) assessments are essential in athletes' follow-up, but artifacts may lead to erroneous analysis. Artifact detection and correction are the purpose of extensive literature and implemented in dedicated analysis programs. However, the effects of number and/or magnitude of artifacts on various time- or frequency-domain parameters remain unclear. The purpose of this study was to assess the effects of artifacts on HRV parameters. Root mean square of the successive differences (RMSSD), standard deviation of the normal to normal inter beat intervals (SDNN), power in the low- (LF) and high-frequency band (HF) were computed from two 4-min RR recordings in 178 participants in both supine and standing positions, respectively. RRs were modified by (1) randomly adding or subtracting 10, 30, 50 or 100 ms to the successive RRs; (2) a single artifact was manually inserted; (3) artifacts were automatically corrected from signal naturally containing artifacts. Finally, RR recordings were analyzed before and after automatic detection-correction of artifacts. Modifying each RR by 10, 30, 50 and 100 ms randomly did not significantly change HRV parameters (range -6%, +6%, supine). In contrast, by adding a single artifact, RMSSD increased by 413% and 269%, SDNN by 54% and 47% in supine and standing positions, respectively. LF and HF changed only between -3% and +8% (supine and standing) in the artifact condition. When more than 0.9% of the signal contained artifacts, RMSSD was significantly biased, whilst when more than 1.4% of the signal contained artifacts LF and HF were significantly biased. RMSSD and SDNN were more sensitive to a single artifact than LF and HF. This indicates that, when using RMSSD only, a single artifact may induce erroneous interpretation of HRV. Therefore, we recommend using both time- and frequency-domain parameters to minimize the errors in the diagnoses of health status or fatigue in athletes.

[Exercise training with blood flow restriction : mechanisms and applications]. / Entraînement avec occlusion vasculaire: mécanismes et applications.

Traditional guidelines state that substantial muscle development requires training at least 70% of the one-repetition maximum (1RM) load. However, recent evidence has proven that low load training (20-40 % 1RM) combined with moderate blood flow restriction (BFR) can also lead to improvements in muscle mass and strength. While BFR has primarily been studied in clinical populations, emerging evidence demonstrates the effectiveness of BFR in sport. This article displays the mechanisms, methods, protocols, risks, and known effects of BFR.

Les directives traditionnelles stipulent qu'un développement musculaire nécessite un entraînement avec une charge minimale correspondant à 70 % du maximum d'une répétition (1RM). Cependant, des preuves récentes suggèrent que l'entraînement à faible charge (20-40 % de 1RM), combiné à une restriction modérée du flux sanguin (Blood Flow Restriction, BFR), peut également entraîner des améliorations de la masse et de la force musculaires. Alors que le BFR a d'abord été principalement étudié sur des populations cliniques, de nouveaux travaux rapportent son efficacité en milieu sportif. Cet article présente les mécanismes, les méthodes, les protocoles, les risques ainsi que les effets connus du BFR.

Hypoxia Conditioning as a Promising Therapeutic Target in Parkinson's Disease?

Several lines of research point to a key role of low oxygen supply (hypoxia) in Parkinson's disease pathogenesis. Although severe hypoxia is detrimental for the brain, physiological adaptations to mild hypoxia are neuroprotective. Herein we discuss, how neuroprotective effects can be induced by hypoxia conditioning and how related approaches have the potential to be harnessed as therapeutic strategies in Parkinson's disease. © 2021 International Parkinson and Movement Disorder Society.

Central and peripheral muscle fatigue following repeated-sprint running in moderate and severe hypoxia.

NEW FINDINGS: What is the central question of this study? Increasing severity of arterial hypoxaemia induces a shift towards greater central, relative to peripheral, mechanisms of fatigue during exhaustive exercise. Does a similar pattern exist for 'all-out' repeated-sprint running? What is the main finding and its importance? Severe normobaric hypoxia [fraction of inspired oxygen ( FI,O2 ) = 0.13] did not induce a greater contribution from central fatigue, but indices of muscle fatigue were elevated compared with normoxia ( FI,O2  = 0.21) and moderate hypoxia ( FI,O2  = 0.17). This suggests a different fatigue response to repeated-sprint running versus other exercise modalities and, consequently, that task specificity might modulate the effect of hypoxia on the central versus peripheral contribution to fatigue. ABSTRACT: We examined the effects of increasing hypoxia severity on repeated-sprint running performance and neuromuscular fatigue. Thirteen active males completed eight sprints of 5 s (recovery = 25 s) on a motorized sprint treadmill in normoxia (sea level, SL; FI,O2  = 0.21), in moderate hypoxia (MH; FI,O2  = 0.17) and in severe hypoxia (SH; FI,O2  = 0.13). After 6 min of passive recovery, in all conditions a second set of four sprints of 5 s was conducted in normoxia. Neuromuscular function of the knee extensors was assessed at baseline (Pre-) and 1 min after set 1 (Post-set 1) and set 2 (Post-set 2). In set 1, the mean distance covered in SL (22.9 ± 1.2 m) was not different to MH (22.7 ± 1.3 m; P = 0.71) but was greater than in SH (22.3 ± 1.3 m; P = 0.04). No significant differences between conditions for mean distance occurred in set 2. There was a decrease in maximal voluntary contraction torque (Δ = -31.4 ± 18.0 N m, P < 0.001) and voluntary activation (%VA; Δ = -7.1 ± 5.1%, P = 0.001) from Pre- to Post-set 1, but there was no effect of hypoxia. No further change from Post-set 1 to Post-set 2 occurred for either maximal voluntary contraction or %VA. The decrease in potentiated twitch torque in SL (Δ = -13.3 ± 5.2 N m) was not different to MH (Δ = -13.3 ± 6.3 N m) but was lower than in SH (Δ = -16.1 ± 4 N m) from Pre- to Post-set 1 (interaction, P < 0.003). Increasing severity of normobaric hypoxia, up to an equivalent elevation of 3600 m, can increase indices of peripheral fatigue but does not impact central fatigue after 'all-out' repeated-sprint running.

Effects of Normobaric Hypoxia on Matched-severe Exercise and Power-duration Relationship.

We investigated the effects of hypoxia on matched-severe intensity exercise and on the parameters of the power-duration relationship. Fifteen trained subjects performed in both normoxia and normobaric hypoxia (FiO2=0.13, ~3000 m) a maximal incremental test, a 3 min all-out test (3AOT) and a transition from rest to an exercise performed to exhaustion (Tlim) at the same relative intensity (80%∆). Respiratory and pulmonary gas-exchange variables were continuously measured (K5, Cosmed, Italy). Tlim test's V̇O2 kinetics was calculated using a two-component exponential model. V̇O2max (44.1±5.1 vs. 58.7±6.4 ml.kg-1.min-1, p<0.001) was decreased in hypoxia. In Tlim, time-to-exhaustion sustained was similar (454±130 vs. 484±169 s) despite that V̇O2 kinetics was slower (τ1: 31.1±5.8 vs. 21.6±4.7 s, p<0.001) and the amplitude of the V̇O2 slow component lower (12.4±5.4 vs. 20.2±5.7 ml.kg-1.min-1, p<0.05) in hypoxia. CP was reduced (225±35 vs. 270±49 W, p<0.001) but W' was unchanged (11.3±2.9 vs. 11.4±2.7 kJ) in hypoxia. The changes in CP/V̇O2max were positively correlated with changes in W' (r = 0.58, p<0.05). The lower oxygen availability had an impact on aerobic related physiological parameters, but exercise tolerance is similar between hypoxia and normoxia when the relative intensity is matched despite a slower V̇O2 kinetics in hypoxia.

Continuous Analysis of Marathon Running Using Inertial Sensors: Hitting Two Walls?

Marathon running involves complex mechanisms that cannot be measured with objective metrics or laboratory equipment. The emergence of wearable sensors introduced new opportunities, allowing the continuous recording of relevant parameters. The present study aimed to assess the evolution of stride-by-stride spatio-temporal parameters, stiffness, and foot strike angle during a marathon and determine possible abrupt changes in running patterns. Twelve recreational runners were equipped with a Global Navigation Satellite System watch, and two inertial measurement units clamped on each foot during a marathon race. Data were split into eight 5-km sections and only level parts were analyzed. We observed gradual increases in contact time and duty factor as well as decreases in flight time, swing time, stride length, speed, maximal vertical force and stiffness during the race. Surprisingly, the average foot strike angle decreased during the race, but each participant maintained a rearfoot strike until the end. Two abrupt changes were also detected around km 25 and km 35. These two breaks are possibly due to the alteration of the stretch-shortening cycle combined with physiological limits. This study highlights new measurable phenomena that can only be analyzed through continuous monitoring of runners over a long period of time.