Characterizing the Exponential Profile of W' Recovery Following Partial Depletion.

PURPOSE: The aim of this study was to characterize W' recovery kinetics in response to a partial W' depletion. We hypothesized that W' recovery following partial depletion would be better described by a biexponential than by a monoexponential model. METHODS: Nine healthy men performed a ramp incremental exercise test, three to five constant load trials to determine critical power and W', and ten experimental trials to quantify W' depletion. Each experimental trial consisted of two constant load work bouts (WB1 + WB2) interspersed by a recovery interval. WB1 was designed to evoke a 25% or 75% W' depletion (DEP25% + DEP75%). Subsequently, participants recovered for 30, 60, 120, 300 or 600 s, and then performed WB2 to exhaustion in order to calculate the observed W' recovery (W'OBS). W'OBS data were fitted using monoexponential and biexponential models, both with a variable and a fixed model amplitude. Root mean square error (RMSE) and Akaike information criterion (AICc) were calculated to evaluate the models' goodness-of-fit. RESULTS: The biexponential model fits were associated with overall lower RMSE values (0.4-5.0%) compared to the monoexponential models (2.9-8.0%). However, ΔAICc resulted in negative values (-15.5 and -23.3) for the model fits where the amplitude was free, thereby favoring the use of a monoexponential model for both depletion conditions. For the model fits where the amplitude was fixed at 100%, ΔAICc was negative for DEP25% (-15.0), but positive for DEP75% (11.2). W'OBS values were strongly correlated between both depletion conditions (r = 0.92), and positively associated with V̇O2peak, CP and GET (r = 0.67-0.77). CONCLUSIONS: The present study results did not provide evidence in favor of a biexponential modeling technique to characterize W' recovery following partial depletion. Moreover, we demonstrated that fixed t values were insufficient to model W' recovery across different depletion levels, and that W' recovery was positively associated with aerobic fitness. These findings underline the importance of employing variable and individualized t values in future predictive W' models.

Effect of acute heat exposure on the determination of critical power and W' in women and men.

The goal of this study was to investigate to what extent acute heat exposure would affect the parameters of the power-duration relationship, i.e. CP and W', using multiple constant workload tests to task failure, in women and men. Twenty four young physically active participants (12 men, 12 women) performed 3-5 constant load tests to determine CP and W', both in temperate (TEMP; 18°C) and hot (HOT; 36°C) environmental conditions. A repeated-measures ANOVA was executed to find differences between TEMP and HOT, and between women and men. In HOT, CP was reduced by 6.5% (227 ± 50 vs. 212 ± 47 W), while W' increased 12.4% (16.4 ± 4.4 vs. 18.5 ± 5.6 kJ). No significant two-way sex × temperature interactions were observed, indicating that the environmental conditions did not have a different effect in men compared with women. The intersection of the average curvatures in TEMP and HOT occurred at 137 s and 280 W in women, and 153 s and 397 W in men. Acute heat exposure had an impact on the parameters CP and W', i.e. CP decreased whereas W' increased. The increase in W' might be a consequence of the mathematical modelling for the used test methodology, rather than a physiological accurate value of W' in HOT. No differences induced by heat exposure were observed between women and men.

The determination of CP and W' was done using multiple constant workload tests to task failure and acute heat exposure induced changes in CP (decrease) and W' (increase).The increase in W' with acute heat exposure might be a consequence of the mathematical modelling for the used test methodology, rather than a physiological accurate value of W'.Acute heat exposure had a similar effect on performance parameters in women and men.

Critical power, W' and W' reconstitution in women and men.

PURPOSE: The aim of this study was to compare critical power (CP) and work capacity W', and W' reconstitution (W'REC) following repeated maximal exercise between women and men. METHODS: Twelve women ([Formula: see text]O2PEAK: 2.53 ± 0.37 L·min-1) and 12 men ([Formula: see text]O2PEAK: 4.26 ± 0.30 L·min-1) performed a minimum of 3 constant workload tests, to determine CP and W', and 1 maximal exercise repetition test with three work bouts (WB) to failure, to quantify W'REC during 2 recovery periods, i.e., W'REC1 and W'REC2. An independent samples t test was used to compare CP and W' values between women and men, and a repeated-measures ANOVA was used to compare W'REC as fraction of W' expended during the first WB, absolute W'REC, and normalized to lean body mass (LBM). RESULTS: CP normalized to LBM was not different between women and men, respectively, 3.7 ± 0.5 vs. 4.1 ± 0.4 W·kgLBM-1, while W' normalized to LBM was lower in women 256 ± 29 vs. 305 ± 45 J·kgLBM-1. Fractional W'REC1 was higher in women than in men, respectively, 74.0 ± 12.0% vs. 56.8 ± 9.5%. Women reconstituted less W' than men in absolute terms (8.7 ± 1.2 vs. 10.9 ± 2.0 kJ) during W'REC1, while normalized to LBM no difference was observed between women and men (174 ± 23 vs. 167 ± 31 J·kgLBM-1). W'REC2 was lower than W'REC1 both in women and men. CONCLUSION: Sex differences in W'REC (absolute women < men; fractional women > men) are eliminated when LBM is accounted for. Prediction models of W'REC might benefit from including LBM as a biological variable in the equation. This study confirms the occurrence of a slowing of W'REC during repeated maximal exercise.

Acute balenine supplementation in humans as a natural carnosinase-resistant alternative to carnosine.

Balenine possesses some of carnosine's and anserine's functions, yet it appears more resistant to the hydrolysing CN1 enzyme. The aim of this study was to elucidate the stability of balenine in the systemic circulation and its bioavailability in humans following acute supplementation. Two experiments were conducted in which (in vitro) carnosine, anserine and balenine were added to plasma to compare degradation profiles and (in vivo) three increasing doses (1-4-10 mg/kg) of balenine were acutely administered to 6 human volunteers. Half-life of balenine (34.9 ± 14.6 min) was respectively 29.1 and 16.3 times longer than that of carnosine (1.20 ± 0.36 min, p = 0.0044) and anserine (2.14 ± 0.58 min, p = 0.0044). In vivo, 10 mg/kg of balenine elicited a peak plasma concentration (Cmax) of 28 µM, which was 4 and 18 times higher than with 4 (p = 0.0034) and 1 mg/kg (p = 0.0017), respectively. CN1 activity showed strong negative correlations with half-life (ρ = - 0.829; p = 0.0583), Cmax (r = - 0.938; p = 0.0372) and incremental area under the curve (r = - 0.825; p = 0.0433). Overall, balenine seems more resistant to CN1 hydrolysis resulting in better in vivo bioavailability, yet its degradation remains dependent on enzyme activity. Although a similar functionality as carnosine and anserine remains to be demonstrated, opportunities arise for balenine as nutraceutical or ergogenic aid.

Can We Accurately Predict Critical Power and W' from a Single Ramp Incremental Exercise Test?

PURPOSE: The purpose of this study was to examine the suitability of a single ramp incremental test to predict critical power (CP) and W' . We hypothesized that CP would correspond to the corrected power output (PO) at the respiratory compensation point (RCP) and W' would be calculable from the work done above RCP. METHODS: One hundred fifty-three healthy young people (26 ± 4 yr, 51.4 ± 7.6 mL·min -1 ·kg -1 ) performed a maximal ramp test (20, 25, or 30 W·min -1 ), followed by three to five constant load trials to determine CP and W' . CP and W' were estimated using a "best individual fit" approach, selecting the mathematical model with the smallest total error. The RCP was identified by means of gas exchange analysis and then translated into its appropriate PO by applying a correction strategy in order to account for the gap in the V̇O 2 /PO relationship between ramp and constant load exercise. We evaluated the agreement between CP and the PO at RCP, and between W' and the total work done above CP ( W'RAMP > CP ) and above RCP ( W'RAMP > RCP ) during the ramp test. RESULTS: The CP was significantly higher than the PO at RCP (Δ = 8 ± 16 W, P < 0.001). W'RAMP > CP was significantly lower than W' (Δ = 1.9 ± 3.3 kJ, P < 0.001), whereas W'RAMP > RCP and W' did not differ from each other (Δ = -0.6 ± 5.8 kJ, P = 0.21). CONCLUSIONS: Despite the fact that CP and RCP occurred in close proximity, the estimation of W' from ramp exercise may be problematic given the likelihood of underestimation and considering the large variability. Therefore, we do not recommend the interchangeable use of CP and W' values derived from constant load versus ramp exercise, in particular, when the goal is to obtain accurate estimates or to predict performance capacity.

No Effect of Acute Balenine Supplementation on Maximal and Submaximal Exercise Performance in Recreational Cyclists.

Carnosine (ß-alanyl-L-histidine) and its methylated analogues anserine and balenine are highly concentrated endogenous dipeptides in mammalian skeletal muscle that are implicated in exercise performance. Balenine has a much better bioavailability and stability in human circulation upon acute ingestion, compared to carnosine and anserine. Therefore, ergogenic effects observed with acute carnosine and anserine supplementation may be even more pronounced with balenine. This study investigated whether acute balenine supplementation improves physical performance in four maximal and submaximal exercise modalities. A total of 20 healthy, active volunteers (14 males; six females) performed cycling sprints, maximal isometric contractions, a 4-km TT and 20-km TT following either preexercise placebo or 10 mg/kg of balenine ingestion. Physical, as well as mental performance, along with acid-base balance and glucose concentration were assessed. Balenine was unable to augment peak power (p = .3553), peak torque (p = .3169), time to complete the 4 km (p = .8566), nor 20 km time trial (p = .2660). None of the performances were correlated with plasma balenine or CN1 enzyme activity. In addition, no effect on pH, bicarbonate, and lactate was observed. Also, the supplement did not affect mental performance. In contrast, glucose remained higher during and after the 20 km time trial following balenine ingestion. In conclusion, these results overall indicate that the functionality of balenine does not fully resemble that of carnosine and anserine, since it was unable to elicit performance improvements with similar and even higher plasma concentrations.

Training Load and Acute Performance Decrements Following Different Training Sessions.

PURPOSE: To examine the differences in training load (TL) metrics when quantifying training sessions differing in intensity and duration. The relationship between the TL metrics and the acute performance decrement measured immediately after the sessions was also assessed. METHODS: Eleven male recreational cyclists performed 4 training sessions in a random order, immediately followed by a 3-km time trial (TT). Before this period, participants performed the time TT in order to obtain a baseline performance. The difference in the average power output for the TTs following the training sessions was then expressed relative to the best baseline performance. The training sessions were quantified using 7 different TL metrics, 4 using heart rate as input, 2 using power output, and 1 using the rating of perceived exertion. RESULTS: The load of the sessions was estimated differently depending on the TL metrics used. Also, within the metrics using the same input (heart rate and power), differences were found. TL using the rating of perceived exertion was the only metric showing a response that was consistent with the acute performance decrements found for the different training sessions. The Training Stress Score and the individualized training impulse demonstrated similar patterns but overexpressed the intensity of the training sessions. The total work done resulted in an overrepresentation of the duration of training. CONCLUSION: TL metrics provide dissimilar results as to which training sessions have higher loads. The load based on TL using the rating of perceived exertion was the only one in line with the acute performance decrements found in this study.

The effect of acute heat exposure on the determination of exercise thresholds from ramp and step incremental exercise.

PURPOSE: The aim of this study was to examine how respiratory (RT) and lactate thresholds (LT) are affected by acute heat exposure in the two most commonly used incremental exercise test protocols (RAMP and STEP) for functional evaluation of aerobic fitness, exercise prescription and monitoring training intensities. METHODS: Eleven physically active male participants performed four incremental exercise tests, two RAMP (30 W·min-1) and two STEP (40 W·3 min-1), both in 18 °C (TEMP) and 36 °C (HOT) with 40% relative humidity to determine 2 RT and 16 LT, respectively. Distinction was made within LT, taking into account the individual lactate kinetics (LTIND) and fixed value lactate concentrations (LTFIX). RESULTS: A decrease in mean power output (PO) was observed in HOT at LT (-6.2 ± 1.9%), more specific LTIND (-5.4 ± 1.4%) and LTFIX (-7.5 ± 2.4%), compared to TEMP, however not at RT (-1.0 ± 2.7%). The individual PO difference in HOT compared to TEMP over all threshold methods ranged from -53 W to +26 W. Mean heart rate (HR) did not differ in LT, while it was increased at RT in HOT (+10 ± 8 bpm). CONCLUSION: This study showed that exercise thresholds were affected when ambient air temperature was increased. However, a considerable degree of variability in the sensitivity of the different threshold concepts to acute heat exposure was found and a large individual variation was noticed. Test design and procedures should be taken into account when interpreting exercise test outcomes.

Physical Preparation of a World-Class Lightweight Men's Double Sculls Team for the Tokyo 2020 Olympics.

PURPOSE: To analyze the physical profile and training program of a world-class lightweight double sculls rowing crew toward the Tokyo 2020 Olympics. METHOD: A case study in which both rowers performed physical testing in November 2020 and April 2021 (anthropometrics, incremental rowing test, and power profiling). The training program (38 wk) in the buildup to the Olympics was analyzed, providing insight into training characteristics (volume; contribution of rowing, alternative, and strength training; prescribed and recorded [heart rate] training-intensity distribution). The entire period was split into 3 phases: preparation period (8 wk), competition period 1 (11 wk), and competition period 2 (9 wk), and training characteristics were compared. RESULTS: In the April 2021 testing, rower A (1.89 m, 74.6 kg, 4.4% body fat) had a peak oxygen uptake of 5.8 L·min-1 (77.8 mL·min-1·kg-1) and a peak power output of 491 W. Rower B (1.82 m, 70.6 kg, 7.8% body fat) had a peak oxygen uptake of 5.5 L·min-1 (77.9 mL·min-1·kg-1) and a peak power output of 482 W. The mean weekly training volume was 14 hours 47 minutes (4 h 5 min), of which 58.5% (14.6%) consisted of rowing, 13.4% (6.8%) strength training, and 28.1% (2.6%) alternative training. Heart-rate training-intensity distribution was 77.8% (4.2%) in zone 1, 16.6% (3.7%) in zone 2, and 5.6% (2.8%) in zone 3 with a lower contribution of zone 1 in competition period 1 (P = .029) and competition period 2 (P = .023) compared with the preparation period, and a higher contribution of zone 3 in competition period 1 (P = .018) and competition period 2 (P = .011) compared with the preparation period. CONCLUSION: The crew combined a high volume of rowing, alternative, and strength training in a pyramidal heart-rate training-intensity distribution throughout the year.

The ergogenic effect of acute carnosine and anserine supplementation: dosing, timing, and underlying mechanism.

Background: Recent studies suggest that acute-combined carnosine and anserine supplementation has the potential to improve the performance of certain cycling protocols. Yet, data on optimal dose, timing of ingestion, effective exercise range, and mode of action are lacking. Three studies were conducted to establish dosing and timing guidelines concerning carnosine and anserine intake and to unravel the mechanism underlying the ergogenic effects. Methods: First, a dose response study A was conducted in which 11 men randomly received placebo, 10, 20, or 30 mg.kg-1 of both carnosine and anserine. They performed 3x maximal voluntary isometric contractions (MVC), followed by a 5 x 6 s repeated cycling sprint ability test (RSA), once before the supplement and 30 and 60 minutes after. In a second study, 15 men performed 3x MVCs with femoral nerve electrical stimulation, followed by an RSA test, once before 30 mg.kg-1 carnosine and anserine and 60 minutes after. Finally, in study C, eight men performed a high intensity cycling training after randomly ingesting 30 mg.kg-1 of carnosine and anserine, a placebo or antihistamines (reduce post-exercise blood flow) to investigate effects on muscle perfusion. Results: Study A showed a 3% peak power (p = 0.0005; 95% CI = 0.07 to 0.27; ES = 0.91) and 4.5% peak torque (p = 0.0006; 95% CI = 0.12 to 0.50; ES = 0.87) improvement on RSA and MVC, with 30 mg.kg-1 carnosine + anserine ingestion 60 minutes before the performance yielding the best results. Study B found no performance improvement on group level; however, a negative correlation (r = -0.54; p = 0.0053; 95% CI = -0.77 to -0.19) was found between carnosinase enzyme activity (responsible for carnosine and anserine breakdown) and performance improvement. No effect of the supplement on neuromuscular function nor on muscle perfusion was found. Conclusions: These studies reveal that acute ingestion of 30 mg.kg-1 of both carnosine and anserine, 60 minutes before a high intensity exercise, can potentially improve performance, such as short cycling sprints or maximal muscle contractions. Subjects with lower carnosinase activity, and thus a slower breakdown of circulating dipeptides, appear to benefit more from this ergogenic effect. Finally, neither the involvement of a direct effect on neuromuscular function, nor an indirect effect on recovery through increased muscle perfusion could be confirmed as potential mechanism of action. The ergogenic mechanism therefore remains elusive.

A longitudinal study on the interchangeable use of whole-body and local exercise thresholds in cycling.

PURPOSE: This study longitudinally examined the interchangeable use of critical power (CP), the maximal lactate steady state (MLSS) and the respiratory compensation point (RCP) (i.e., whole-body thresholds), and breakpoints in muscle deoxygenation (m[HHb]BP) and muscle activity (iEMGBP) (i.e., local thresholds). METHODS: Twenty-one participants were tested on two timepoints (T1 and T2) with a 4-week period (study 1: 10 women, age = 27 ± 3 years, [Formula: see text] = 43.2 ± 7.3 mL min-1kg-1) or a 12-week period (study 2: 11 men, age = 25 ± 4 years, [Formula: see text] = 47.7 ± 5.9 mL min-1 kg-1) in between. The test battery included one ramp incremental test (to determine RCP, m[HHb]BP and iEMGBP) and a series of (sub)maximal constant load tests (to determine CP and MLSS). All thresholds were expressed as oxygen uptake ([Formula: see text]) and equivalent power output (PO) for comparison. RESULTS: None of the thresholds were significantly different in study 1 ([Formula: see text]: P = 0.143, PO: P = 0.281), but differences between whole-body and local thresholds were observed in study 2 ([Formula: see text]: P < 0.001, PO: P = 0.024). Whole-body thresholds showed better 4-week test-retest reliability (TEM = 88-125 mL min-1 or 6-10 W, ICC = 0.94-0.98) compared to local thresholds (TEM = 189-195 mL min-1 or 15-18 W, ICC = 0.58-0.89). All five thresholds were strongly associated at T1 and T2 (r = 0.75-0.99), but their changes from T1 to T2 were mostly uncorrelated (r = - 0.41-0.83). CONCLUSION: Whole-body thresholds (CP/MLSS/RCP) showed a close and consistent coherence taking into account a 3-6%-bandwidth of typical variation. In contrast, local thresholds (m[HHb]BP/iEMGBP) were characterized by higher variability and did not consistently coincide with the whole-body thresholds. In addition, we found that most thresholds evolved independently of each other over time. Together, these results do not justify the interchangeable use of whole-body and local exercise thresholds in practice.

Association between SARS-COV-2 infection and muscle strain injury occurrence in elite male football players: a prospective study of 29 weeks including three teams from the Belgian professional football league.

OBJECTIVES: The aim of this study was to investigate the association between SARS-CoV-2 infection and muscle strain injury in elite athletes. METHODS: A prospective cohort study in three Belgian professional male football teams was performed during the first half of the 2020-2021 season (June 2020-January 2021). Injury data were collected using established surveillance methods. Assessment of SARS-CoV-2 infection was performed by a PCR test before each official game. RESULTS: Of the 84 included participants, 22 were infected with SARS-CoV-2 and 14 players developed a muscle strain during the follow-up period. Cox's proportional hazards regression analyses demonstrated a significant association between SARS-CoV-2 infection and the development of muscle strain (HR 5.1; 95% CI 1.1 to 23.1; p=0.037), indicating an increased risk of developing muscle strains following SARS-CoV-2 infection. All athletes who sustained a muscle strain after infection were injured within the first month (15.71±11.74 days) after sports resumption and completed a longer time in quarantine (14.57±6.50 days) compared with the infected players who did not develop a muscle strain (11.18±5.25 days). CONCLUSION: This study reported a five times higher risk of developing a muscle strain after a SARS-CoV-2 infection in elite male football players. Although this association should be examined further, it is possible that short-term detraining effects due to quarantine, and potentially pathological effects of the SARS-CoV-2 infection are associated with a higher risk of muscle strain injury.

The Fitness-Fatigue Model: What's in the Numbers?

PURPOSE: The purpose of this commentary is to outline some of the pitfalls when using the fitness-fatigue model to unravel the interaction between training load and performance. By doing so, we encourage sport scientists and coaches to interpret the parameters from the model with some extra caution. CONCLUSIONS: Caution is needed when interpreting the fitness-fatigue model since the parameter values are influenced by the starting parameter values, the modeling technique, and the input of the model. Also, the use of general constants should be avoided since they do not account for interindividual differences and differences between training-load methods. Therefore, we advise sport scientists and coaches to use the model as a way to work more data-informed rather than working data-driven.

Six weeks of static apnea training does not affect Hbmass and exercise performance.

Acute apnea is known to induce decreases in oxyhemoglobin desaturation (SpO2) and increases in erythropoietin concentration ([EPO]). This study examined the potential of an apnea training program to induce erythropoiesis and increase hematological parameters and exercise performance. Twenty-two male subjects were randomly divided into an apnea and control group. The apnea group performed a 6-wk apnea training program consisting of a daily series of five maximal static apneas. Before and after training, subjects visited the lab on 3 test days to perform 1) a ramp incremental test measuring V̇o2peak, 2) CO-rebreathing for Hbmass determination and a 3-km time trial, and 3) an apnea test protocol with continuous finger SpO2 registration. Venous blood samples were drawn before and 180 min after the apnea test for analysis of [EPO]. Minimal SpO2 reached during the apnea test protocol was 91 ± 7% pre and 82 ± 7% post apnea training. The apnea test protocol did not elicit an acute increase in [EPO] (P = 0.685) before nor after the training program. Consequently, resting [EPO] (P = 0.170), Hbmass (P = 0.134), V̇o2peak (P = 0.796), and 3-km cycling time trial performance (P = 0.509) were not affected either. The apnea test and training protocol, consisting of five maximal static apneas, did not induce a sufficiently strong hypoxic stimulus to cause erythropoiesis and therefore did not result in an increase in resting [EPO], Hbmass, V̇o2peak, or time trial performance. Longer and/or more intense training sessions inducing a stronger hypoxic stimulus are probably needed to obtain changes in hematological and exercise parameters.NEW & NOTEWORTHY Apnea training has been suggested as a promising method to improve exercise performance for over a decade. However, to our knowledge, this study is the first to evaluate its value on both hematological parameters and exercise performance, including Hbmass and a control group. No changes in Hbmass nor exercise performance were observed. Contradicting previous research, no acute increase in [EPO] following apnea was observed either, indicating that more intense protocols are needed, at least in nonapnea-trained individuals.

Slow Wave Sleep of Elite and Nonelite Gymnasts Is Influenced by Weekly Training Hours, Not by Fitness Level.

PURPOSE: This study aimed to determine the influencing factors of potential differences in sleep architecture between elite (EG) and nonelite (NEG) female artistic gymnasts. METHODS: Twelve EG (15.1 [1.5] y old) and 10 NEG (15.3 [1.8] y old) underwent a nocturnal polysomnography after a regular training day (5.8 [0.8] h vs 2.6 [0.7] h), and, on a separate test day, they performed an incremental treadmill test after a rest day in order to determine physical fitness status. A multiple linear regression assessed the predictive value of training and fitness parameters toward the different sleep phases. Total sleep time and sleep efficiency (proportion of time effectively asleep to time in bed), as well as percentage of nonrapid eye movement sleep phase 1 (NREM1) and 2 (NREM2), slow wave sleep (SWS), and rapid eye movement sleep (REM), during a single night were compared between EG and NEG using an independent-samples t test. RESULTS: Peak oxygen uptake influenced NREM1 (ß = 1.035, P = .033), while amount of weekly training hours predicted SWS (ß = 1.897, P = .032). No differences were documented between EG and NEG in total sleep time and sleep efficiency. SWS was higher in EG (36.9% [11.4%]) compared with NEG (25.9% [8.3%], P = .020), compensated by a lower proportion of NREM2 (38.7% [10.2%] vs 48.4% [6.5%], P = .017), without differences in NREM1 and REM. CONCLUSIONS: The proportion of SWS was only predicted by weekly training hours and not by training hours the day of the polysomnography or physical fitness, while NREM1 was linked with fitness level. Sleep efficiency did not differ between EG and NEG, but in EG, more SWS and less NREM2 were identified.

Heart Rate and Muscle Oxygenation Kinetics During Dynamic Constant Load Intermittent Breath-Holds.

Introduction: Acute apnea evokes bradycardia and peripheral vasoconstriction in order to conserve oxygen, which is more pronounced with face immersion. This response is contrary to the tachycardia and increased blood flow to muscle tissue related to the higher oxygen consumption during exercise. The aim of this study was to investigate cardiovascular and metabolic responses of dynamic dry apnea (DRA) and face immersed apnea (FIA). Methods: Ten female volunteers (17.1 ± 0.6 years old) naive to breath-hold-related sports, performed a series of seven dynamic 30 s breath-holds while cycling at 25% of their peak power output. This was performed in two separate conditions in a randomized order: FIA (15°C) and DRA. Heart rate and muscle tissue oxygenation through near-infrared spectroscopy were continuously measured to determine oxygenated (m[O2Hb]) and deoxygenated hemoglobin concentration (m[HHb]) and tissue oxygenation index (mTOI). Capillary blood lactate was measured 1 min after the first, third, fifth, and seventh breath-hold. Results: Average duration of the seven breath-holds did not differ between conditions (25.3 s ± 1.4 s, p = 0.231). The apnea-induced bradycardia was stronger with FIA (from 134 ± 4 to 85 ± 3 bpm) than DRA (from 134 ± 4 to 100 ± 5 bpm, p < 0.001). mTOI decreased significantly from 69.9 ± 0.9% to 63.0 ± 1.3% (p < 0.001) which is reflected in a steady decrease in m[O2Hb] (p < 0.001) and concomitant increase in m[HHb] (p = 0.001). However, this was similar in both conditions (0.121 < p < 0.542). Lactate was lower after the first apnea with FIA compared to DRA (p = 0.038), while no differences were observed in the other breath-holds. Conclusion: Our data show strong decreases in heart rate and muscle tissue oxygenation during dynamic apneas. A stronger bradycardia was observed in FIA, while muscle oxygenation was not different, suggesting that FIA did not influence muscle oxygenation. An order of mechanisms was observed in which, after an initial tachycardia, heart rate starts to decrease after muscle tissue deoxygenation occurs, suggesting a role of peripheral vasoconstriction in the apnea-induced bradycardia. The apnea-induced increase in lactate was lower in FIA during the first apnea, probably caused by the stronger bradycardia.

Metabolic instability vs fibre recruitment contribution to the [Formula: see text] slow component in different exercise intensity domains.

This study focused on the steady-state phase of exercise to evaluate the relative contribution of metabolic instability (measured with NIRS and haematochemical markers) and muscle activation (measured with EMG) to the oxygen consumption ([Formula: see text]) slow component ([Formula: see text]) in different intensity domains. We hypothesized that (i) after the transient phase, [Formula: see text], metabolic instability and muscle activation tend to increase differently over time depending on the relative exercise intensity and (ii) the increase in [Formula: see text] is explained by a combination of metabolic instability and muscle activation. Eight active men performed a constant work rate trial of 9 min in the moderate, heavy and severe intensity domains. [Formula: see text], root mean square by EMG (RMS), deoxyhaemoglobin by NIRS ([HHb]) and haematic markers of metabolic stability (i.e. [La-], pH, HCO3-) were measured. The physiological responses in different intensity domains were compared by two-way RM-ANOVA. The relationships between the increases of [HHb] and RMS with [Formula: see text] after the third min were compared by simple and multiple linear regressions. We found domain-dependent dynamics over time of [Formula: see text], [HHb], RMS and the haematic markers of metabolic instability. After the transient phase, the rises in [HHb] and RMS showed medium-high correlations with the rise in [Formula: see text] ([HHb] r = 0.68, p < 0.001; RMS r = 0.59, p = 0.002). Moreover, the multiple linear regression showed that both metabolic instability and muscle activation concurred to the [Formula: see text] (r = 0.75, [HHb] p = 0.005, RMS p = 0.042) with metabolic instability possibly having about threefold the relative weight compared to recruitment. Seventy-five percent of the dynamics of the [Formula: see text] was explained by [HHb] and RMS.

Effects of Regular Physical Activity on the Immune System, Vaccination and Risk of Community-Acquired Infectious Disease in the General Population: Systematic Review and Meta-Analysis.

BACKGROUND: Regular physical activity is the prime modality for the prevention of numerous non-communicable diseases and has also been advocated for resilience against COVID-19 and other infectious diseases. However, there is currently no systematic and quantitative evidence synthesis of the association between physical activity and the strength of the immune system. OBJECTIVE: To examine the association between habitual physical activity and (1) the risk of community-acquired infectious disease, (2) laboratory-assessed immune parameters, and (3) immune response to vaccination. METHODS: We conducted a systemic review and meta-analysis according to PRISMA guidelines. We searched seven databases (MEDLINE, Embase, Cochrane CENTRAL, Web of Science, CINAHL, PsycINFO, and SportDiscus) up to April 2020 for randomised controlled trials and prospective observational studies were included if they compared groups of adults with different levels of physical activity and reported immune system cell count, the concentration of antibody, risk of clinically diagnosed infections, risk of hospitalisation and mortality due to infectious disease. Studies involving elite athletes were excluded. The quality of the selected studies was critically examined following the Cochrane guidelines using ROB2 and ROBINS_E. Data were pooled using an inverse variance random-effects model. RESULTS: Higher level of habitual physical activity is associated with a 31% risk reduction (hazard ratio 0.69, 95% CI 0.61-0.78, 6 studies, N = 557,487 individuals) of community-acquired infectious disease and 37% risk reduction (hazard ratio 0.64, 95% CI 0.59-0.70, 4 studies, N = 422,813 individuals) of infectious disease mortality. Physical activity interventions resulted in increased CD4 cell counts (32 cells/µL, 95% CI 7-56 cells/µL, 24 studies, N = 1112 individuals) and salivary immunoglobulin IgA concentration (standardised mean difference 0.756, 95% CI 0.146-1.365, 7 studies, N = 435 individuals) and decreased neutrophil counts (704 cells/µL, 95% CI 68-1340, 6 studies, N = 704 individuals) compared to controls. Antibody concentration after vaccination is higher with an adjunct physical activity programme (standardised mean difference 0.142, 95% CI 0.021-0.262, 6 studies, N = 497 individuals). CONCLUSION: Regular, moderate to vigorous physical activity is associated with reduced risk of community-acquired infectious diseases and infectious disease mortality, enhances the first line of defence of the immune system, and increases the potency of vaccination. PROTOCOL REGISTRATION: The original protocol was prospectively registered with PROSPERO (CRD42020178825).