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.

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.

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.

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.

Quantification of Neuropeptide Y and Four of Its Metabolites in Human Plasma by Micro-UHPLC-MS/MS.

Neuropeptide Y (NPY) is a 36-amino acid peptide circulating at a subpicomolar concentration participating in multiple physiological and pathological processes. NPY is prone to peptidolysis, generating metabolites with modified affinity for the five known receptors of NPY that mediate distinct effects. It is, therefore, crucial to distinguish each metabolite to understand the multiple functions of NPY. Since immunoassays are not able to distinguish NPY from its metabolites, we have validated a microliquid chromatography tandem mass spectrometry (micro-LC-MS/MS) assay for the quantification of endogenous NPY, NPY2-36, NPY3-36, NPY1-35, and NPY3-35 in human plasma. Sample preparation relies on immunoextraction in 96-well plates, followed by solid-phase extraction prior to micro-LC-MS/MS. The LLOQ ranged from 0.03 to 0.16 pM, intra- and inter-assay precision were <27% and trueness <22%. We determined reference intervals in 155 healthy volunteers and 40 hypertensive patients. We found that NPY3-36 is the main circulating peptide in resting conditions and that NPY and catecholamines are simultaneously increased during orthostasis. We also showed that the concentrations of NPY and its metabolites are similar in healthy volunteers and hypertensive patients. NPY is the prototype peptide that circulates in concentrations expected to be beyond instrumental capacities. We have been successful in developing a high-throughput specific and sensitive assay by including a deep knowledge of the physicochemical properties of these peptides to an efficient multistep sample preparation, and a micro-LC chromatography. We believe that our methodological approach opens the possibility to selectively quantify other endogenous peptides cleaved by peptidases whose concentrations are below 1 pM.

Toxic doses of caffeine are needed to increase skeletal muscle contractility.

Discrepant results have been reported regarding an intramuscular mechanism underlying the ergogenic effect of caffeine on neuromuscular function in humans. Here, we reevaluated the effect of caffeine on muscular force production in humans and combined this with measurements of the caffeine dose-response relationship on force and cytosolic free [Ca2+] ([Ca2+]i) in isolated mouse muscle fibers. Twenty-one healthy and physically active men (29 ± 9 yr, 178 ± 6 cm, 73 ± 10 kg, mean ± SD) took part in the present study. Nine participants were involved in two experimental sessions during which supramaximal single and paired electrical stimulations (at 10 and 100 Hz) were applied to the femoral nerve to record evoked forces. Evoked forces were recorded before and 1 h after ingestion of 1) 6 mg caffeine/kg body mass or 2) placebo. Caffeine plasma concentration was measured in 12 participants. In addition, submaximal tetanic force and [Ca2+]i were measured in single mouse flexor digitorum brevis (FDB) muscle fibers exposed to 100 nM up to 5 mM caffeine. Six milligrams of caffeine per kilogram body mass (plasma concentration ~40 µM) did not increase electrically evoked forces in humans. In superfused FDB single fibers, millimolar caffeine concentrations (i.e., 15- to 35-fold above usual concentrations observed in humans) were required to increase tetanic force and [Ca2+]i. Our results suggest that toxic doses of caffeine are required to increase muscle contractility, questioning the purported intramuscular ergogenic effect of caffeine in humans.

Positive expiratory pressure improves arterial and cerebral oxygenation in acute normobaric and hypobaric hypoxia.

Positive expiratory pressure (PEP) has been shown to limit hypoxia-induced reduction in arterial oxygen saturation, but its effectiveness on systemic and cerebral adaptations, depending on the type of hypoxic exposure [normobaric (NH) versus hypobaric (HH)], remains unknown. Thirteen healthy volunteers completed three randomized sessions consisting of 24-h exposure to either normobaric normoxia (NN), NH (inspiratory oxygen fraction, FiO2 = 13.6%; barometric pressure, BP = 716 mmHg; inspired oxygen partial pressure, PiO2 = 90.9 ± 1.0 mmHg), or HH (3,450 m, FiO2 = 20.9%, BP = 482 mmHg, PiO2 = 91.0 ± 0.6 mmHg). After the 6th and the 22nd hours, participants breathed quietly through a facemask with a 10-cmH2O PEP for 2 × 5 min interspaced with 5 min of free breathing. Arterial (SpO2, pulse oximetry), quadriceps, and cerebral (near-infrared spectroscopy) oxygenation, middle cerebral artery blood velocity (MCAv; transcranial Doppler), ventilation, and cardiovascular responses were recorded continuously. SpO2without PEP was significantly lower in HH (87 ± 4% on average for both time points, P < 0.001) compared with NH (91 ± 3%) and NN (97 ± 1%). PEP breathing did not change SpO2 in NN but increased it similarly in NH and HH (+4.3 ± 2.5 and +4.7 ± 4.1% after 6h; +3.5 ± 2.2 and +4.1 ± 2.9% after 22h, both P < 0.001). Although MCAv was reduced by PEP (in all sessions and at all time points, -6.0 ± 4.2 cm/s on average, P < 0.001), the cerebral oxygenation was significantly improved (P < 0.05) with PEP in both NH and HH, with no difference between conditions. These data indicate that PEP could be an attractive nonpharmacological means to improve arterial and cerebral oxygenation under both normobaric and hypobaric mild hypoxic conditions in healthy participants.

Acute and chronic changes in baroreflex sensitivity in hypobaric vs. normobaric hypoxia.

Normobaric hypoxia (NH) is used as a surrogate for hypobaric hypoxia (HH). Recent studies reported physiological differences between NH and HH. Baroreflex sensitivity (BRS) decreases at altitude or following intense training. However, until now no study compared the acute and chronic changes of BRS in NH vs. HH. First, BRS was assessed in 13 healthy male subjects prior and after 20 h of exposure at 3450 m (study 1), and second in 15 well-trained athletes prior and after 18 days of "live-high train-low" (LHTL) at 2250 m (study 2) in NH vs. HH. BRS decreased (p < 0.05) to the same extent in NH and HH after 20 h of hypoxia and after LHTL. These results confirm that altitude decreases BRS but the decrease is similar between HH and NH. The persistence of this decrease after the cessation of a chronic exposure is new and does not differ between HH and NH. The previously reported physiological differences between NH and HH do not appear strong enough to induce different BRS responses.

AltitudeOmics: effect of ascent and acclimatization to 5260 m on regional cerebral oxygen delivery.

Cerebral hypoxaemia associated with rapid ascent to high altitude can be life threatening; yet, with proper acclimatization, cerebral function can be maintained well enough for humans to thrive. We investigated adjustments in global and regional cerebral oxygen delivery (DO2) as 21 healthy volunteers rapidly ascended and acclimatized to 5260 m. Ultrasound indices of cerebral blood flow in internal carotid and vertebral arteries were measured at sea level, upon arrival at 5260 m (ALT1; atmospheric pressure 409 mmHg) and after 16 days of acclimatization (ALT16). Cerebral DO2 was calculated as the product of arterial oxygen content and flow in each respective artery and summed to estimate global cerebral blood flow. Vascular resistances were calculated as the quotient of mean arterial pressure and respective flows. Global cerebral blood flow increased by ∼70% upon arrival at ALT1 (P < 0.001) and returned to sea-level values at ALT16 as a result of changes in cerebral vascular resistance. A reciprocal pattern in arterial oxygen content maintained global cerebral DO2 throughout acclimatization, although DO2 to the posterior cerebral circulation was increased by ∼25% at ALT1 (P = 0.032). We conclude that cerebral DO2 is well maintained upon acute exposure and acclimatization to hypoxia, particularly in the posterior and inferior regions of the brain associated with vital homeostatic functions. This tight regulation of cerebral DO2 was achieved through integrated adjustments in local vascular resistances to alter cerebral perfusion during both acute and chronic exposure to hypoxia.

Cerebral oxygenation during the Richalet hypoxia sensitivity test and cycling time-trial performance in severe hypoxia.

BACKGROUND: The Richalet hypoxia sensitivity test (RT), which quantifies the cardiorespiratory response to acute hypoxia during exercise at an intensity corresponding to a heart rate of ~130 bpm in normoxia, can predict susceptibility of altitude sickness. Its ability to predict exercise performance in hypoxia is unknown. OBJECTIVES: Investigate: (1) whether cerebral blood flow (CBF) and cerebral tissue oxygenation (O2Hb; oxygenated hemoglobin, HHb; deoxygenated hemoglobin) responses during RT predict time-trial cycling (TT) performance in severe hypoxia; (2) if subjects with blunted cardiorespiratory responses during RT show greater impairment of TT performance in severe hypoxia. STUDY DESIGN: Thirteen men [27 ± 7 years (mean ± SD), Wmax: 385 ± 30 W] were evaluated with RT and the results related to two 15 km TT, in normoxia and severe hypoxia (FIO2 = 0.11). RESULTS: During RT, mean middle cerebral artery blood velocity (MCAv: index of CBF) was unaltered with hypoxia at rest (p > 0.05), while it was increased during normoxic (+22 ± 12 %, p < 0.05) and hypoxic exercise (+33 ± 17 %, p < 0.05). Resting hypoxia lowered cerebral O2Hb by 2.2 ± 1.2 µmol (p < 0.05 vs. resting normoxia); hypoxic exercise further lowered it to -7.6 ± 3.1 µmol below baseline (p < 0.05). Cerebral HHb, increased by 3.5 ± 1.8 µmol in resting hypoxia (p < 0.05), and further to 8.5 ± 2.9 µmol in hypoxic exercise (p < 0.05). Changes in CBF and cerebral tissue oxygenation during RT did not correlate with TT performance loss (R = 0.4, p > 0.05 and R = 0.5, p > 0.05, respectively), while tissue oxygenation and SaO2 changes during TT did (R = -0.76, p < 0.05). Significant correlations were observed between SaO2, MCAv and HHb during RT (R = -0.77, -0.76 and 0.84 respectively, p < 0.05 in all cases). CONCLUSIONS: CBF and cerebral tissue oxygenation changes during RT do not predict performance impairment in hypoxia. Since the changes in SaO2 and brain HHb during the TT correlated with performance impairment, the hypothesis that brain oxygenation plays a limiting role for global exercise in conditions of severe hypoxia remains to be tested further.

Baroreflex sensitivity is blunted in hypoxia independently of changes in inspired carbon dioxide pressure in prematurely born male adults.

Premature birth may result in specific cardiovascular responses to hypoxia and hypercapnia, that might hamper high-altitude acclimatization. This study investigated the consequences of premature birth on baroreflex sensitivity (BRS) under hypoxic, hypobaric and hypercapnic conditions. Seventeen preterm born males (gestational age, 29 ± 1 weeks), and 17 age-matched term born adults (40 ± 0 weeks) underwent consecutive 6-min stages breathing different oxygen and carbon dioxide concentrations at both sea-level and high-altitude (3375 m). Continuous blood pressure and ventilatory parameters were recorded in normobaric normoxia (NNx), normobaric normoxic hypercapnia (NNx + CO2 ), hypobaric hypoxia (HHx), hypobaric normoxia (HNx), hypobaric normoxia hypercapnia (HNx + CO2 ), and hypobaric hypoxia with end-tidal CO2 clamped at NNx value (HHx + clamp). BRS was assessed using the sequence method. Across all conditions, BRS was lower in term born compared to preterm (13.0 ± 7.5 vs. 21.2 ± 8.8 ms⋅mmHg-1 , main group effect: p < 0.01) participants. BRS was lower in HHx compared to NNx in term born (10.5 ± 4.9 vs. 16.0 ± 6.0 ms⋅mmHg-1 , p = 0.05), but not in preterm (27.3 ± 15.7 vs. 17.6 ± 8.3 ms⋅mmHg-1 , p = 0.43) participants, leading to a lower BRS in HHx in term born compared to preterm (p < 0.01). In conclusion, this study reports a blunted response of BRS during acute high-altitude exposure without any influence of changes in inspired CO2 in healthy prematurely born adults.

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, due to 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 (V̇E) (p < 0.001), larger ΔVO2max (p = 0.019) and lower hypoxia-related V̇E 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.

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.

Women at Altitude: Sex-Related Physiological Responses to Exercise in Hypoxia.

Sex differences in physiological responses to various stressors, including exercise, have been well documented. However, the specific impact of these differences on exposure to hypoxia, both at rest and during exercise, has remained underexplored. Many studies on the physiological responses to hypoxia have either excluded women or included only a limited number without analyzing sex-related differences. To address this gap, this comprehensive review conducted an extensive literature search to examine changes in physiological functions related to oxygen transport and consumption in hypoxic conditions. The review encompasses various aspects, including ventilatory responses, cardiovascular adjustments, hematological alterations, muscle metabolism shifts, and autonomic function modifications. Furthermore, it delves into the influence of sex hormones, which evolve throughout life, encompassing considerations related to the menstrual cycle and menopause. Among these physiological functions, the ventilatory response to exercise emerges as one of the most sex-sensitive factors that may modify reactions to hypoxia. While no significant sex-based differences were observed in cardiac hemodynamic changes during hypoxia, there is evidence of greater vascular reactivity in women, particularly at rest or when combined with exercise. Consequently, a diffusive mechanism appears to be implicated in sex-related variations in responses to hypoxia. Despite well-established sex disparities in hematological parameters, both acute and chronic hematological responses to hypoxia do not seem to differ significantly between sexes. However, it is important to note that these responses are sensitive to fluctuations in sex hormones, and further investigation is needed to elucidate the impact of the menstrual cycle and menopause on physiological responses to hypoxia.

Hemoglobin Mass and Blood Volume in Swimming: A Comparison Between Highly Trained, Elite, and World-Class Swimmers.

PURPOSE: Total hemoglobin mass (tHbmass) and blood volume (BV) are important determinants of maximal oxygen uptake and endurance capacity. Higher-caliber endurance athletes usually possess higher tHbmass and BV values. This study aimed to compare tHbmass and BV among swimmers of diverse competitive calibers and distances. METHODS: Thirty swimmers (16 female and 14 male) participated in the study: 3 were tier 5, world class (869 [59] FINA points); 15 were tier 4, elite/international (853 [38] points); and 12 were tier 3, highly trained/national (808 [35] points). They specialized in competition distances ranging from 200 m to open-water 10 km. Between February 2019 and February 2020, all swimmers had their tHbmass and BV measured by carbon monoxide rebreathing 1 to 6 times and participated in multiple competitions and race events. RESULTS: Relative tHbmass and BV were not different (P > .05) between tiers among women or among men (pooled tHbmass values 14.5 [0.5], 12.5 [1.5], 12.6 [2.3] g/kg for tier 5, tier 4, and tier 3, respectively). No differences were observed in relative tHbmass (P = .215) and BV (P = .458) between pool and open-water swimmers or between 200-, 400-, and 1500-m specialists (P > .05). No significant correlations were found between the highest measured absolute or relative tHbmass and BV and the highest FINA points scored over the follow-up period (R = -.42-.17, P = .256-.833), irrespective of competition distance. CONCLUSION: tHbmass and BV values did not differ between swimmers of different calibers or among competition distances. Furthermore, these values did not correlate with FINA points, either in males or in females. The present results indicate that hematological characteristics may have a lesser impact on swimming performance than on land-based endurance sports.

Daily cardiac autonomic responses during the Tour de France in a male professional cyclist.

Background: Heart rate variability (HRV) is a common means of monitoring responses to training, yet in professional cycling, one may question its usefulness, particularly during multi-day competitions such as Grand Tours. Objectives: This study aims to report and analyze HRV responses in a male professional cyclist over a season, including the Tour de France. Methods: A professional cyclist recorded resting and exercise inter-beat intervals during 5 months, comprising a training period with two altitude sojourns and two competition blocks, including the Tour de France. Resting recordings lasted 5 min in the supine position and were used for computation of mean heart rate (HR), root mean square of the successive differences (RMSSDs), and power in the low- and high-frequency bands (LF and HF, respectively). Training load quantification was based on recorded HR during exercise and expressed as training impulses (TRIMPSs). Results: LF (3,319 ± 2,819 vs. 1,097 ± 1,657 ms2), HF (3,590 ± 1858 vs. 1,267 ± 1,683 ms2), and RMSSD (96 ± 26 vs. 46 ± 30 ms) were higher and HR (47 ± 4 vs. 54 ± 2 bpm) was lower during the training period when compared to the two competition blocks. The coefficient of variation (CV) was significantly lower during the training period than during the two competition blocks for RMSSD (26 vs. 72%), LF (85 vs. 160%), and HF (58 vs. 141%). Discussion: The present study confirms that monitoring daily HRV responses during training periods is valuable in professional cycling, but questions its usefulness during the Tour de France. Moreover, the previous suggestion that CV in RMSSD would help to predict poor performance was not confirmed in a professional cyclist.

Physiological Responses to Exercise in Hypoxia in Preterm Adults: Convective and Diffusive Limitations in the O 2 Transport.

PURPOSE: Premature birth induces long-term sequelae on the cardiopulmonary system, leading to reduced exercise capacity. However, the mechanisms of this functional impairment during incremental exercise remain unclear. Also, a blunted hypoxic ventilatory response was found in preterm adults, suggesting an increased risk for adverse effects of hypoxia in this population. This study aimed to investigate the oxygen cascade during incremental exercise to exhaustion in both normoxia and hypobaric hypoxia in prematurely born adults with normal lung function and their term born counterparts. METHODS: Noninvasive measures of gas exchange, cardiac hemodynamics, and both muscle and cerebral oxygenation were continuously performed using metabolic cart, transthoracic impedance, and near-infrared spectroscopy, respectively, during an incremental exercise test to exhaustion performed at sea level and after 3 d of high-altitude exposure in healthy preterm ( n = 17; gestational age, 29 ± 1 wk; normal lung function) and term born ( n = 17) adults. RESULTS: At peak, power output, oxygen uptake, stroke volume indexed for body surface area, and cardiac output were lower in preterm compared with term born in normoxia ( P = 0.042, P = 0.027, P = 0.030, and P = 0.018, respectively) but not in hypoxia, whereas pulmonary ventilation, peripheral oxygen saturation, and muscle and cerebral oxygenation were similar between groups. These later parameters were modified by hypoxia ( P < 0.001). Hypoxia increased muscle oxygen extraction at submaximal and maximal intensity in term born ( P < 0.05) but not in preterm participants. Hypoxia decreased cerebral oxygen saturation in term born but not in preterm adults at rest and during exercise ( P < 0.05). Convective oxygen delivery was decreased by hypoxia in term born ( P < 0.001) but not preterm adults, whereas diffusive oxygen transport decreased similarly in both groups ( P < 0.001 and P < 0.001, respectively). CONCLUSIONS: These results suggest that exercise capacity in preterm is primarily reduced by impaired convective, rather than diffusive, oxygen transport. Moreover, healthy preterm adults may experience blunted hypoxia-induced impairments during maximal exercise compared with their term counterparts.

High-Intensity Interval Training, Performance, and Oxygen Uptake Kinetics in Highly Trained Traditional Rowers.

PURPOSE: Oxygen uptake kinetics (VO2kinetics) is a measure of an athlete's capacity to respond to variations in energy demands. Faster VO2kinetics is associated with better performance in endurance sports, but optimal training methods to improve VO2kinetics remain unclear. This study compared the effects of 2 high-intensity interval-training (HIIT) programs on traditional rowing performance and VO2kinetics. METHODS: Twelve highly trained rowers performed one of two 6-week HIIT protocols: either 3-minute repetitions at 90% (HIIT90; n = 5) of peak aerobic power (PAP) or 90-second repetitions at 100% (HIIT100; n = 7) of PAP. Before (PRE) and after (POST) the training intervention, they performed an incremental test to exhaustion to determine the individual lactate threshold, onset of blood lactate accumulation and PAP, and two 6-minute rest-to-exercise transitions to determine VO2kinetics. RESULTS: No significant changes (P > .05) were observed for rowing ergometer power output at individual lactate threshold (HIIT90 PRE 255 [12], POST 264 [13]; HIIT100 247 [24], 266 [28] W), onset of blood lactate accumulation (279 [12], 291 [16]; 269 [23], 284 [32] W), or PAP (359 [13], 381 [15]; 351 [21], 363 [29] W) or for any parameters of VO2kinetics. No differences were observed between HIIT interventions. CONCLUSION: The HIIT interventions did not induce significant performance or VO2kinetics improvements, although mean power output at individual lactate threshold, onset of blood lactate accumulation, and PAP increased by 5.7%, 5.0%, and 4.5%, respectively. This suggests that the exact intensity and duration of HIIT sessions performed in the same intensity domain may be of lesser importance than other well-established influential factors (eg, training volume progression, training intensity distribution, altitude training) to develop aerobic qualities in endurance athletes.

End-tidal carbon dioxide tension is a reliable surrogate of arterial carbon dioxide tension across different oxygen, carbon dioxide and barometric pressures.

End-tidal CO2 tension provides an accurate estimation of P aCO2 in healthy awake individuals over an extensive range of CO2 pressures induced by 17 environmental conditions combining different O2, CO2 and barometric pressures https://bit.ly/3YuKPAY.