Kinematics but not kinetics alterations to single-leg drop jump movements following a subject-tailored fatiguing protocol suggest an increased risk of ACL injury.

Introduction: Neuromuscular fatigue causes a transient reduction of muscle force, and alters the mechanisms of motor control. Whether these alterations increase the risk of anterior cruciate ligament (ACL) injury is still debated. Here we compare the biomechanics of single-leg drop jumps before and after the execution of a fatiguing exercise, evaluating whether this exercise causes biomechanical alterations typically associated with an increased risk of ACL lesion. The intensity of the fatiguing protocol was tailored to the aerobic capacity of each participant, minimizing potential differential effects due to inter-individual variability in fitness. Methods: Twenty-four healthy male volunteers performed single leg drop jumps, before and after a single-set fatiguing session on a cycle ergometer until exhaustion (cadence: 65-70 revolutions per minute). For each participant, the intensity of the fatiguing exercise was set to 110% of the power achieved at their anaerobic threshold, previously identified by means of a cardiopulmonary exercise test. Joint angles and moments, as well as ground reaction forces (GRF) before and after the fatiguing exercise were compared for both the dominant and the non-dominant leg. Results: Following the fatiguing exercise, the hip joint was more extended (landing: Δ=-2.17°, p = 0.005; propulsion: Δ=-1.83°, p = 0.032) and more abducted (landing: Δ=-0.72°, p = 0.01; propulsion: Δ=-1.12°, p = 0.009). Similarly, the knee joint was more extended at landing (non-dominant leg: Δ=-2.67°, p < 0.001; dominant: Δ=-1.4°, p = 0.023), and more abducted at propulsion (both legs: Δ=-0.99°, p < 0.001) and stabilization (both legs: Δ=-1.71°, p < 0.001) hence increasing knee valgus. Fatigue also caused a significant reduction of vertical GRF upon landing (Δ=-0.21 N/kg, p = 0.003), but not during propulsion. Fatigue did not affect joint moments significantly. Conclusion: The increased hip and knee extension, as well as the increased knee abduction we observed after the execution of the fatiguing exercise have been previously identified as risk factors for ACL injury. These results therefore suggest an increased risk of ACL injury after the execution of the participant-tailored fatiguing protocol proposed here. However, the reduced vertical GRF upon landing and the preservation of joint moments are intriguing, as they may suggest the adoption of protective strategies in the fatigued condition to be evaluated in future studied.

The eSports Medicine: Pre-Participation Screening and Injuries Management-An Update.

Recently, electronic sports (eSports) became one of the growing forms of new media due to the wide diffusion of games and online technologies. Even if there is still a debate about the definition and characterization of eSports, eAthletes train heavily, compete in tournaments, must abide by competition, association, and governing body rules, just like all other athletes. Furthermore, as in any other competitive discipline, there can be injuries. Aberrant sitting posture, repetitive movements, screen vision, prolonged playing hours, and a sedentary lifestyle can lead to several medical hazards in musculoskeletal, ophthalmology, neurological, and metabolic systems. Moreover, several cardiovascular changes occur in eAthletes. This paper aims to explore the different injuries that can occur in a professional eAthlete, suggesting how every high-level gamer could benefit from a pre-participation evaluation and a correct injury prevention strategy.

Role of the Air-Blood Barrier Phenotype in Lung Oxygen Uptake and Control of Extravascular Water.

The air blood barrier phenotype can be reasonably described by the ratio of lung capillary blood volume to the diffusion capacity of the alveolar membrane (Vc/Dm), which can be determined at rest in normoxia. The distribution of the Vc/Dm ratio in the population is normal; Vc/Dm shifts from ∼1, reflecting a higher number of alveoli of smaller radius, providing a high alveolar surface and a limited extension of the capillary network, to just opposite features on increasing Vc/Dm up to ∼6. We studied the kinetics of alveolar-capillary equilibration on exposure to edemagenic conditions (work at ∼60% maximum aerobic power) in hypoxia (HA) (PIO2 90 mmHg), based on an estimate of time constant of equilibration (τ) and blood capillary transit time (Tt). A shunt-like effect was described for subjects having a high Vc/Dm ratio, reflecting a longer τ (>0.5 s) and a shorter Tt (<0.8 s) due to pulmonary vasoconstriction and a larger increase in cardiac output (>3-fold). The tendency to develop lung edema in edemagenic conditions (work in HA) was found to be directly proportional to the value of Vc/Dm as suggested by an estimate of the mechanical properties of the respiratory system with the forced frequency oscillation technique.

Impact of Hanging Motionless in Harness on Respiratory and Blood Pressure Reflex Modulation in Mountain Climbers.

Harness hang syncope (HHS) is a risk that specifically affects safety of harness users in mountain climbing. Aims: To evaluate individual patterns of breathing resulting from deranged cardiovascular reflexes triggering a syncopal event when a mismatch between cerebral O2 demand and supply is present. Results: Forty healthy participants [aged 39.1 (8.2) years] were enrolled in a motionless suspension test while hanging in harness. Respiratory gas exchange values were analyzed to assess the pattern of breathing (EpInWel, respiratory elastic power) and cardiovascular parameters were monitored (BP, blood pressure). Four participants experienced HHS after 30.0 (7.6) minutes, with an early manifestation of loss of control of both a sustainable EpInWel and BP, starting after 10-12 minutes. Among the other participants, two different reactions were observed during suspension: (1) group G1 tolerated 32.7 (11.4) minutes of suspension by a favorable adaptation of the EpInWel and BP parameters and (2) group G2 showed significantly shorter time of suspension 24.0 (10.4) minutes with unfavorable increase in EpInWel and BP. Conclusions: Greater resistance to HHS occurs in people developing less marked fluctuations of both respiratory and cardiovascular reflex responses. Conversely, wider fluctuations both in control of EpInWel and BP were observed in the event of decreased suspension tolerance or in syncopal events.

The Elusive Path of Brain Tissue Oxygenation and Cerebral Perfusion in Harness Hang Syncope in Mountain Climbers.

Lanfranconi, Francesca, Luca Pollastri, Giovanni Corna, Manuela Bartesaghi, Massimiliano Novarina, Alessandra Ferri, and Giuseppe Andrea Miserocchi. The elusive path of brain tissue oxygenation and cerebral perfusion in harness hang syncope in mountain climbers. High Alt Med Biol. 18:363-371, 2017. AIM: Harness hang syncope (HHS) is a risk that specifically affects wide ranges of situations requiring safety harnesses in mountains. An irreversible orthostatic stasis could lead to death if a prompt rescue is not performed. We aimed at evaluating the risk of developing HHS and at identifying the characteristics related to the pathogenesis of HHS. RESULTS: Forty adults (aged 39.1 [8.2] years) were enrolled in a suspension test lasting about 28.7 (11.4) minutes. We measured cardiovascular parameters, and near infrared spectroscopy (NIRS) was used to assess cerebral hypoxia by changes in the concentration of oxyhemoglobin (Δ[HbO2]) and de-oxyhemoglobin (Δ[HHb]). In the four participants who developed HHS: (1) systolic and diastolic blood pressure showed ample oscillations with a final abrupt drop (∼30 mmHg); (2) Δ[HbO2] increased after 8-12 minutes of suspension and reached a plateau before HHS; and (3) Δ[HHb] decreased with a final abrupt increase before syncope. CONCLUSIONS: Participants who developed HHS failed to activate cardiovascular reflexes that usually safeguard O2 availability to match the metabolic needs of the brain tissue. Since cerebral hypoxia was detected as an early phenomenon by Δ[HbO2] and Δ[HHb] changes, NIRS measurement appears to be the most important parameter to monitor the onset of HHS.

Air blood barrier phenotype correlates with alveolo-capillary O2 equilibration in hypobaric hypoxia.

The O2 diffusion limitation across the air blood barrier (DO2 and subcomponents Dm and Vc) was evaluated in 17 healthy participants exposed to hypobaric hypoxia (HA, 3840m, PIO2 ∼90mmHg). A 10% decrease in alveolar volume (VA) in all participants suggested the development of sub-clinical interstitial lung edema. In >80% of participants DO2/VA increased, reflecting an individual strategy to cope with the hypoxia stimulus by remodulating Vc or Dm. Opposite changes in Dm/Vc ratio were observed and participants decreasing Vc showed reduced alveolar blood capillary transit time. The interplay between diffusion and perfusion (cardiac output) was estimated in order to investigate the individual adaptive response to hypoxia. It appears remarkable that despite individual differences in the adaptive response to HA, diffusion limitation did not exceed ∼11% of the alveolar-venous PO2 gradient, revealing an admirable functional design of the air-blood barrier to defend the O2 diffusion/perfusion function when facing hypobaric hypoxia corresponding to 50mmHg decreased PAO2.

Reappraisal of DLCO adjustment to interpret the adaptive response of the air-blood barrier to hypoxia.

DLCO measured in hypoxia must be corrected due to the higher affinity (increase in coefficient θ) of CO with Hb. We propose an adjustment accounting for individual changes in the equation relating DLCO to subcomponents Dm (membrane diffusive capacity) and Vc (lung capillary volume): 1/DLCO=1/Dm+1/θVc. We adjusted the individual DLCO measured in hypoxia (HA, 3269m) by interpolating the 1/DLCO to the sea level (SL) 1/θ value. Nineteen healthy subjects were studied at SL and HA. Based on the proposed adjustment, DLCO increased in HA in 53% of subjects, reflecting the increase in Dm that largely overruled the decrease in Vc. We hypothesize that a decrease in Vc (buffering microvascular filtration) and the increase in Dm (possibly resulting from a decrease in thickness of the air-blood barrier) represent the anti-edemagenic adaptation of the lung to hypoxia exposure. The efficiency of this adaptation varied among subjects as DLCO did not change in 31% of subjects and decreased in 16%.

Long-term monitoring of oxygen saturation at altitude can be useful in predicting the subsequent development of moderate-to-severe acute mountain sickness.

OBJECTIVE: The use of pulse oximetry (Spo2) to identify subjects susceptible to acute mountain sickness (AMS) is the subject of debate. To obtain more reliable data, we monitored Spo2 for 24 hours at altitude to investigate the ability to predict impending AMS. METHODS: The study was conducted during the climb from Alagna (1154 m) to Capanna Regina Margherita (4559 m), with an overnight stay in Capanna Gnifetti (3647 m). Sixty subjects (11 women) were recruited. Each subject was fitted with a 24-hour recording finger pulse oximeter. The subjects rode a cable car to 3275 m and climbed to 3647 m, where they spent the night. RESULTS: In the morning, 24 subjects (6 women) had a Lake Louise Questionnaire score (LLS) ≥ 3 (AMS(+)), and 15 subjects (4 women) exhibited moderate-to-severe disease (LLS ≥ 5 = AMS(++)). At Alagna, Spo2 did not differ between the AMS(-) and AMS(+) subjects. At higher stations, all AMS(+) subjects exhibited a significantly lower Spo2 than did the AMS(-) subjects: at 3275 m, 85.4% vs 87.7%; resting at 3647 m, 84.5% vs 86.4%. The receiver operating characteristics curve analysis resulted in a rather poor discrimination between the AMS(-) subjects and all of the AMS(+) subjects. With the cutoff LLS ≥ 5, the sensitivity was 86.67%, the specificity was 82.25%, and the area under the curve was 0.88 (P < .0001) for Spo2 ≤ 84% at 3647 m. CONCLUSIONS: We conclude that AMS(+) subjects exhibit a more severe and prolonged oxygen desaturation than do AMS(-) subjects starting from the beginning of altitude exposure, but the predictive power of Spo2 is accurate only for AMS(++).

Regional differences in bronchial reactivity assessed by respiratory impedance.

We used the Impulse Oscillometric System (IOS) to gain information concerning the distribution of hyper-reactivity along the bronchial tree during methacholine challenge test (MCT). 37 subjects underwent MCT until reaching the provocative dose (PD20). At each dose, we estimated respiratory resistance at 5 and 20Hz (R5, R20), and reactance at 5Hz (X5). In non-responsive subjects (N=14) no changes in R5, R20, and X5 were observed during MCT. In responsive subjects, a wide spectrum of responses was found concerning frequency dependence and PD20. We describe two phenotypes representing the extremes of response. For PD20>400µg (N=13), MCT caused equal changes of resistance/reactance on varying oscillation frequencies, suggesting a homogeneous bronchoconstriction along the bronchial tree. For PD20<200µg (N=10), a remarkable frequency dependence was observed, with increase in R5, no change in R20, and decrease in X5, suggesting hyper-responsiveness of the distal airways paralleled by a change in visco-elastic properties of lung parenchyma.

Inter-individual differences in control of alveolar capillary blood volume in exercise and hypoxia.

We compared by non-invasive technique the adaptive response of alveolar capillary network to edemagenic conditions (exercise and high altitude [HA, PIO2 107mmHg] in subjects with different resting sea level (SL) capillary blood volume (normalized to alveolar volume, Vc/Va): Group 1 (N=10, Vc/Va=16.1±6.8ml/L- mean±SD) and Group 2 (N=10, Vc/Va=25±7.7). In Group 1 Vc/Va remained unchanged in HA at rest and increased during exercise at SL (26.3±8.6) and HA (28.75±10.2); in Group 2 Vc/Va significantly decreased in HA (19±6) and did not increase in exercise at SL and HA. We hypothesize that Group2 exerts a tight control on Vc/Va being more exposed to the risk of lung edema due to inborn greater microvascular permeability. Conversely, Group 1 appears more resistant to lung edema given the large capillary recruitment in the most edemagenic condition. The 4-fold increase in frequency dependence of respiratory resistance in Group2 in HA stems for greater proneness for lung water perturbation compared to Group 1.

Pathophysiological alterations in oxygen delivery to the tissues.

This paper reviews co-factors that impact on oxygen delivery and uptake, in the attempt to unravel the mechanisms underlying the correlation between the decrease in oxygen delivery and oxygen consumption. In sequence, the following factors are analyzed that, besides a decrease in haemoglobin concentration, impair tissue metabolism: (1) lung diffusion and perfusion limitation in oxygen transport, (2) decrease in cardiac output, (3) impairment of peripheral microvascular perfusion and (4) reduced ability of cells to extract oxygen. The contribution of the various factors is modeled aiming to present a decisional flow chart for the functional evaluation of the efficiency of the oxygen transport system.