How does prolonged tennis playing affect lower limb muscles' activity during first and second tennis serves?

We examined the effect of prolonged tennis playing on lower limb muscles' activity during the execution of first and second tennis serves. Ten male competitive tennis players executed five first and second serves before (pretest) and after (posttest) a 3-h tennis match. Surface electromyographic (EMG) activity of four lower limb muscles (vastus lateralis, rectus femoris, gastrocnemius lateralis, and soleus muscles) on each leg was recorded along with maximum ball velocity measured by a radar gun and peak vertical forces recorded by a force platform. For the vastus lateralis, gastrocnemius lateralis, and soleus muscles of the left leg as well as the vastus lateralis muscle of the right leg, EMG amplitude decreased from pre- to posttests (p ≤ 0.033). These reductions in the EMG signal were generally more pronounced in the first serve (i.e., ranging from -10% to -40%) compared to the second serve (0% to -25%). Maximum ball velocity for both first (159 ± 12 vs. 154 ± 12 km/h) and second (126 ± 20 vs. 125 ± 15 km/h) serves remained unchanged from pre- to posttests (p = 0.638) Similarly, peak vertical forces did not differ between pretest and posttest for both first (1.78 ± 0.30 vs. 1.72 ± 0.29 body weight) and second (1.62 ± 0.25 vs. 1.75 ± 0.23 body weight) serves (p = 0.730). In conclusion, a 3-h tennis match led to decreased activation levels in various leg muscles during serves, particularly in first serves compared to second serves. Despite consistent maximum ball velocity and peak vertical forces, these reductions in EMG signals suggest that skilled tennis players may adopt compensatory strategies after prolonged play.

Difference in expiratory flow limitations development in normoxia and hypoxia in healthy individuals.

The present study investigated the maintenance/repeatability of expiratory flow limitation (EFL) between normoxia and hypoxia. Fifty-one healthy active individuals (27 men and 24 women) performed a lung function test and a maximal incremental cycling test in both normoxia and hypoxia (inspired oxygen fraction = 0.14) on two separate visits. During exercise in normoxia, 28 participants exhibited EFL (55 %). In hypoxia, another cohort of 28 participants exhibited EFL. The two groups only partly overlapped. Individuals with EFL only in normoxia reported lower maximal ventilation values in hypoxia than in normoxia (n=5; -13.5 ± 7.8 %) compared to their counterparts with EFL only in hypoxia (n=5; +6.7 ± 6.3 %) or without EFL (n=18; +5.1 ± 10.3 %) (p=0.004 and p<0.001, respectively). EFL development may be induced by different mechanisms in hypoxia vs. normoxia since the individuals who exhibited flow limitation were not the same between the two environmental conditions. This change seems influenced by the magnitude of the maximal ventilation change.

Hot But Not Cold Water Immersion Mitigates the Decline in Rate of Force Development following Exercise-Induced Muscle Damage.

PURPOSE: In recent years, there has been significant advancement in the guidelines for recovery protocols involving heat or cold water immersion. Yet, comparison between the effects of hot and cold water immersion on key markers of neuromuscular recovery following exercise-induced muscle damage (EIMD) is lacking. METHODS: Thirty physically active males completed an individualized and tailored EIMD protocol immediately followed by one of the following recovery interventions: cold water immersion (11 °C, CWI11), hot water immersion (41 °C, HWI41) or warm-bath control (36 °C, CON36). Gastrointestinal temperature was tracked throughout HWI41. Knee extensors' maximal isokinetic strength [peak torque (Tpeak)] and explosive strength [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. In addition, pressure pain threshold (PPT) was measured to quantify the recovery from muscle soreness. Surface electromyography signals (sEMG) from the vastus lateralis were captured to extract the rates of electromyography rise (REMGR) and the spectral power in the low-frequency band. RESULTS: At post-48 h, Tpeak returned to baseline values following both CWI11 (-8.3 ± 6.8 %, p = 0.079) and HWI41 (-1.4 ± 4.1%, p = 1). In contrast, RFD100-200 (-2.3 ± 29.3%, p = 1) and PPT (+5.6 ± 14.6%, p = 1) returned to baseline values at post-48 h only following HWI41. Spectral analysis of the sEMG signal revealed that the low-frequency band was significantly increased following CWI11 (+9.0 ± 0.52%, p = 0.012). REMGR was unchanged regardless of the condition (all p > 0.05). CONCLUSIONS: A single session of HWI41, rather than CWI11, improved the recovery of the late-phase rate of force development following EIMD in physically active males. This suggests that in athletic contexts where a rapid force development is a key performance determinant, hot bath should be preferred over cold bath.

Peak Oxygen Uptake is Slope Dependent: Insights from Ground Reaction Forces and Muscle Oxygenation in Trained Male Runners.

BACKGROUND: The aim of this study is to explore the effect of treadmill slope on ground reaction forces and local muscle oxygenation as putative limiting factors of peak oxygen uptake in graded maximal incremental running tests. Thirteen trained male runners completed five maximal incremental running tests on treadmill at - 15%, - 7.5%, 0%, 7.5% and 15% slopes while cardiorespiratory and local muscle oxygenation responses as well as ground reaction forces were continuously recorded. Blood lactate concentration and isometric knee extensor torque were measured before and after each test. RESULTS: Peak oxygen uptake was lower at - 15% slope compared to all other conditions (from - 10 to - 17% lower, p < 0.001), with no difference between - 7.5 and + 15% slope. Maximal heart rate and ventilation values were reached in all conditions. The negative external mechanical work increased from steep uphill to steep downhill slopes (from 6 to 92% of total external work) but was not correlated with the peak oxygen uptake reduction. Local muscle oxygenation remained higher in - 15% slope compared to level running (p = 0.003). CONCLUSIONS: Similar peak oxygen uptake can be reached in downhill running up to - 7.5% slope. At more severe downhill slopes (i.e., - 15%), greater negative muscle work and limited local muscle deoxygenation occurred, even in subjects familiarized to downhill running, presumably preventing the achievement of similar to other condition's peak oxygen uptake. KEY POINTS: Trained male runners can reach like level running V̇O2peak at moderate but not at severe negative slope. Negative external mechanical work increases with increasing negative slope. At maximal intensity Vastus Lateralis muscle oxygenation is higher in steep negative slope. Knee extensor isometric muscle torque is preserved after maximal level and uphill running, but reduced after downhill running, despite lower blood lactate. Progressive reduction of V̇O2 at maximal effort with increasing negative slope might be related to the metabolic consequences of increased lower limb negative external work (i.e., eccentric muscle actions).

Does "Live High-Train Low and High" Hypoxic Training Alter Stride Mechanical Pattern During Repeated Sprints in Elite Team-Sport Players?

PURPOSE: We examined changes in stride temporal parameters and spring-mass model characteristics during repeated sprints following a 3-week period of "live high-train low and high" (LHTLH) altitude training in team-sport players. METHODS: While residing under normobaric hypoxia (≥14 h/d; inspired oxygen fraction [FiO2] 14.5%-14.2%) for 14 days, elite field hockey players performed, in addition to their regular field hockey practice in normoxia, 6 sessions (4 × 5 × 5-s maximal sprints; 25-s passive recovery; 5-min rest) under either normobaric hypoxia (LHTLH; FiO2 ∼14.5%, n = 11) or normoxia (live high-train low; FiO2 20.9%, n = 12). A control group (live low-train low; FiO2 ∼20.9%, n = 9) residing in normoxia without additional repeated-sprint training was included. Before (Pre) and a few days (Post-1) and 3 weeks (Post-2) after the intervention, stride mechanics were assessed during an overground repeated-sprint test (8 × 20 m, 20-s recovery). Two-way repeated-measures analysis of variance (time [Pre, Post-1, and Post-2] × condition [LHTLH, live high-train low, and live low-train low]) were conducted. RESULTS: Peak sprinting speed increased in LHTLH from Pre to Post-1 (+2.2% [2.0%]; P = .002) and Post-2 (+2.0% [2.4%]; P = .025), with no significant changes in live high-train low and live low-train low. There was no main effect of time (all P ≥ .062), condition (all P ≥ .771), or a significant time × condition interaction (all P ≥ .230) for any stride temporal variable (contact time, flight time, stride frequency, and stride length) or spring-mass model characteristics (vertical and leg stiffness). CONCLUSIONS: Peak sprinting speed improved in elite field hockey players following LHTLH altitude training, while stride mechanical adjustments to repeated overground sprints remained unchanged for at least 3 weeks postintervention.

Effects of preterm birth on the pattern of altitude acclimatization at rest and during moderate-intensity exercise across three days at 3,375 m.

Preterm birth elicits long-lasting physiological effects in various organ systems, potentially modulating exercise and environmental stress responses. To establish whether prematurely-born adults respond uniquely during early high-altitude acclimatization at rest and during exercise, 17 healthy adults born preterm (gestational age < 32 wk) and 17 term-born, age- and aerobic-capacity-matched, control participants completed a three-day high-altitude sojourn (3,375 m). Oxygen uptake, pulmonary ventilation, and hemodynamic responses, as well as pulse oxygen saturation, brain tissue saturation index (TSI), and skeletal muscle TSI, were measured daily at rest and during moderate-intensity steady-state exercise bouts. In general, the prematurely-born group displayed comparable acclimatization responses at rest, with similar ventilation and cardiac output observed between groups throughout. Resting brain TSI was, however, higher in the preterm group upon arrival at high altitude (72 ± 7% vs. 68 ± 3%; d = 1.20). Absolute exercising oxygen uptake was lower in the preterm participants (P = 0.047), with this group displaying lower exercising cardiac output underpinned by reduced stroke volume (both P = 0.035). Nevertheless, exercising minute ventilation (V̇e) did not differ between groups (P = 0.237) while brain TSI (70 ± 6% vs. 66 ± 3%; d = 1.35) and pulse oxygen saturation (85 ± 3% vs. 82 ± 5%; d = 1.52) were higher with prematurity upon arrival to high altitude. These findings suggest that healthy prematurely-born adults exhibit comparable early acclimatization patterns to their term-born counterparts and better maintain cerebral oxygenation at rest. Together, these data suggest that prematurely-born adults should not be discouraged from high-altitude sojourns involving physical activity.NEW & NOTEWORTHY The acclimatization pattern across three days at 3,375 m, at rest and during moderate-intensity exercise, was similar between healthy adults born prematurely and their term-born counterparts. Preterm adults free from respiratory complications were found to better maintain brain tissue and capillary oxygen saturation at high altitudes, whereas the term-born group experienced larger altitude-induced reductions. Despite apparent cardiac limitations, preterm individuals tolerated exercise similarly to their term-born peers. These findings underscore the notion that preterm birth per se does not predispose healthy adults to decreased altitude tolerance during exercise.

Antioxidant and neurodevelopmental gene polymorphisms in prematurely born individuals influence hypoxia-related oxidative stress.

Preterm born (PTB) infants are at risk for injuries related to oxidative stress. We investigated the association between antioxidant and neurodevelopmental gene polymorphisms and oxidative stress parameters in PTB male young adults and their term-born counterparts at rest and during exercise. Healthy young PTB (N = 22) and full-term (N = 15) males underwent graded exercise tests in normobaric normoxic (FiO2 = 0.21) and hypoxic (FiO2 = 0.13) conditions. CAT rs1001179 was associated with decrease in nitrites in the whole group and in PTB individuals (P = 0.017 and P = 0.043, respectively). GPX1 rs1050450 was associated with decrease in ferric reducing antioxidant power in the whole group and in full-term individuals (P = 0.017 and P = 0.021, respectively). HIF1A rs11549465 was associated with decrease in nitrotyrosine and increase in malondialdehyde (P = 0.022 and P = 0.018, respectively). NOTCH4 rs367398 was associated with increase in advanced oxidation protein products and nitrites (P = 0.002 and P = 0.004, respectively) in hypoxia. In normoxia, NOTCH4 rs367398 was associated with increase in malondialdehyde in the whole group (P = 0.043). BDNF rs6265 was associated with decreased nitrites/nitrates in the whole group and in PTB individuals (P = 0.009 and P = 0.043, respectively). Polymorphisms in investigated genes and PTB might influence oxidative stress response after exercise in normoxic or hypoxic conditions far beyond the neonatal period in young male adults.

Baroreflex and chemoreflex interaction in high-altitude exposure: possible role on exercise performance.

The hypoxic chemoreflex and the arterial baroreflex are implicated in the ventilatory response to exercise. It is well known that long-term exercise training increases parasympathetic and decreases sympathetic tone, both processes influenced by the arterial baroreflex and hypoxic chemoreflex function. Hypobaric hypoxia (i.e., high altitude [HA]) markedly reduces exercise capacity associated with autonomic reflexes. Indeed, a reduced exercise capacity has been found, paralleled by a baroreflex-related parasympathetic withdrawal and a pronounced chemoreflex potentiation. Additionally, it is well known that the baroreflex and chemoreflex interact, and during activation by hypoxia, the chemoreflex is predominant over the baroreflex. Thus, the baroreflex function impairment may likely facilitate the exercise deterioration through the reduction of parasympathetic tone following acute HA exposure, secondary to the chemoreflex activation. Therefore, the main goal of this review is to describe the main physiological mechanisms controlling baro- and chemoreflex function and their role in exercise capacity during HA exposure.

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.

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.

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.

Fitness Level- and Sex-Related Differences in Pulmonary Limitations to Maximal Exercise in Normoxia and Hypoxia.

PURPOSE: Both maximal-intensity exercise and altitude exposure challenge the pulmonary system that may reach its maximal capacities. Expiratory flow limitation (EFL) and exercise-induced hypoxemia (EIH) are common in endurance-trained athletes. Furthermore, because of their smaller airways and lung size, women, independently of their fitness level, may be more prone to pulmonary limitations during maximal-intensity exercise, particularly when performed in hypoxic conditions. The objective of this study was to investigate the impact of sex and fitness level on pulmonary limitations during maximal exercise in normoxia and their consequences in acute hypoxia. METHODS: Fifty-one participants were distributed across four different groups according to sex and fitness level. Participants visited the laboratory on three occasions to perform maximal incremental cycling tests in normoxia and hypoxia (inspired oxygen fraction = 0.14) and two hypoxic chemosensitivity tests. Pulmonary function and ventilatory capacities were evaluated at each visit. RESULTS: EIH was more prevalent (62.5% vs 22.2%, P = 0.004) and EFL less common (37.5% vs 70.4%, P = 0.019) in women than men. EIH prevalence was different ( P = 0.004) between groups of trained men (41.7%), control men (6.7%), trained women (50.0%), and control women (75.0%). All EIH men but only 40% of EIH women exhibited EFL. EFL individuals had higher slope ratio ( P = 0.029), higher ventilation (V̇ E ) ( P < 0.001), larger ΔVO 2max ( P = 0.019), and lower hypoxia-related V̇ E increase ( P < 0.001). CONCLUSIONS: Women reported a higher EIH prevalence than men, regardless of their fitness level, despite a lower EFL prevalence. EFL seems mainly due to the imbalance between ventilatory demands and capacities. It restricts ventilation, leading to a larger performance impairment during maximal exercise in hypoxic conditions.

Constant low-to-moderate mechanical asymmetries during 800-m track running.

Introduction: Modifications in asymmetry in response to self-paced efforts have not been thoroughly documented, particularly regarding horizontally-derived ground reaction force variables. We determined the magnitude and range of gait asymmetries during 800 m track running. Methods: Eighteen physical education students completed an 800 m self-paced run on a 200 m indoor track. During the run, vertical and horizontal ground reaction forces were measured at a sampling frequency of 500 Hz using a 5 m-long force platform system, with data collected once per lap. The following mechanical variables were determined for two consecutive steps: contact time and duration of braking/push-off phases along with vertical/braking/push-off peak forces and impulses. The group mean asymmetry scores were evaluated using the "symmetry angle" (SA) formula, where scores of 0% and 100% correspond to perfect symmetry and perfect asymmetry, respectively. Results: There was no influence of distance interval on SA scores for any of the nine biomechanical variables (P ≥ 0.095). The SA scores were ∼1%-2% for contact time (1.3 ± 0.5%), peak vertical forces (1.8 ± 0.9%), and vertical impulse (1.7 ± 1.0%). The SA scores were ∼3%-8% for duration of braking (3.6 ± 1.1%) and push-off (3.2 ± 1.4%) phases, peak braking (5.0 ± 2.1%) and push-off (6.9 ± 3.1%) forces as well as braking (7.6 ± 2.3%) and push-off (7.7 ± 3.3%) impulses. The running velocity progressively decreased at 300 m and 500 m compared to that at 100 m but levelled off at 700 m (P < 0.001). Discussion: There were no modifications in gait asymmetries, as measured at 200-m distance intervals during 800-m track running in physical education students. The 800 m self-paced run did not impose greater mechanical constraints on one side of the body. Experimental procedures for characterizing the gait pattern during 800 m track running could be simplified by collecting leg mechanical data from only one side.

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.