Noninvasive Pulmonary Hemodynamic Evaluation in Athletes With Exercise-Induced Hypoxemia.

BACKGROUND: Pulmonary capillary stress failure is potentially involved in exercise-induced hypoxemia (ie, a significant fall in hemoglobin oxygen saturation [Spo2]) during sea level exercise in endurance-trained athletes. It is unknown whether there are specific properties of pulmonary vascular function in athletes exhibiting oxygen desaturation. METHODS: Ten endurance-trained athletes with exercise-induced hypoxemia (EIH), nine endurance-trained athletes with no exercise-induced hypoxemia (NEIH), and 10 untrained control subjects underwent an incremental exercise stress echocardiography coupled with lung diffusion capacity for carbon monoxide (Dlco) and lung diffusion capacity for nitric oxide (Dlno) testing. Functional adaptation of the pulmonary circulation was evaluated with measurements of mean pulmonary arterial pressure (mPAP), pulmonary capillary pressure, pulmonary vascular resistance (PVR), cardiac output (Qc), and pulmonary vascular distensibility (alpha) mathematically determined from the curvilinearity of the multi-point mPAP/Qc relation. RESULTS: EIH athletes exhibited a lower exercise-induced PVR decrease compared with the untrained and NEIH groups (P < .001). EIH athletes showed higher maximal mPAP compared with NEIH athletes (45.4 ± 0.9 mm Hg vs 41.6 ± 0.9 mm Hg, respectively; P = .003); there was no difference between the NEIH and untrained subjects. Alpha was lower in the EIH group compared with the NEIH group (P < .05). Maximal mPAP, Pcap, and alpha were correlated with the fall of Spo2 during exercise (P < .01, P < .01, and P < .05). Dlno and Dlco increased with exercise in all groups, with no differences between groups. Dlno/Qc was correlated to the exercise-induced Spo2 changes (P < .05). CONCLUSIONS: EIH athletes exhibit higher maximal pulmonary vascular pressures, lower vascular distensibility, or exercise-induced changes in PVR compared with NEIH subjects, in keeping with pulmonary capillary stress failure or intrapulmonary shunting hypotheses.

Pulmonary Vascular Function and Aerobic Exercise Capacity at Moderate Altitude.

PURPOSE: There has been suggestion that a greater "pulmonary vascular reserve" defined by a low pulmonary vascular resistance (PVR) and a high lung diffusing capacity (DL) allow for a superior aerobic exercise capacity. How pulmonary vascular reserve might affect exercise capacity at moderate altitude is not known. METHODS: Thirty-eight healthy subjects underwent an exercise stress echocardiography of the pulmonary circulation, combined with measurements of DL for nitric oxide (NO) and carbon monoxide (CO) and a cardiopulmonary exercise test at sea level and at an altitude of 2250 m. RESULTS: At rest, moderate altitude decreased arterial oxygen content (CaO2) from 19.1 ± 1.6 to 18.4 ± 1.7 mL·dL, P < 0.001, and slightly increased PVR, DLNO, and DLCO. Exercise at moderate altitude was associated with decreases in maximum O2 uptake (V˙O2max), from 51 ± 9 to 43 ± 8 mL·kg⋅min, P < 0.001, and CaO2 to 16.5 ± 1.7 mL·dL, P < 0.001, but no different cardiac output, PVR, and pulmonary vascular distensibility. DLNO was inversely correlated to the ventilatory equivalent of CO2 (V˙E/V˙CO2) at sea level and at moderate altitude. Independent determinants of V˙O2max as determined by a multivariable analysis were the slope of mean pulmonary artery pressure-cardiac output relationship, resting stroke volume, and resting DLNO at sea level as well as at moderate altitude. The magnitude of the decrease in V˙O2max at moderate altitude was independently predicted by more pronounced exercise-induced decrease in CaO2 at moderate altitude. CONCLUSION: Aerobic exercise capacity is similarly modulated by pulmonary vascular reserve at moderate altitude and at sea level. Decreased aerobic exercise capacity at moderate altitude is mainly explained by exercise-induced decrease in arterial oxygenation.

Exercise-Induced Hypoxaemia Developed at Sea-Level Influences Responses to Exercise at Moderate Altitude.

PURPOSE: The aim of this study was to investigate the impact of exercise-induced hypoxaemia (EIH) developed at sea-level on exercise responses at moderate acute altitude. METHODS: Twenty three subjects divided in three groups of individuals: highly trained with EIH (n = 7); highly trained without EIH (n = 8) and untrained participants (n = 8) performed two maximal incremental tests at sea-level and at 2,150 m. Haemoglobin O2 saturation (SpO2), heart rate, oxygen uptake (VO2) and several ventilatory parameters were measured continuously during the tests. RESULTS: EIH athletes had a drop in SpO2 from 99 ± 0.8% to 91 ± 1.2% from rest to maximal exercise at sea-level, while the other groups did not exhibit a similar decrease. EIH athletes had a greater decrease in VO2max at altitude compared to non-EIH and untrained groups (-22 ± 7.9%, -16 ± 5.3% and -13 ± 9.4%, respectively). At altitude, non-EIH athletes had a similar drop in SpO2 as EIH athletes (13 ± 0.8%) but greater than untrained participants (6 ± 1.0%). EIH athletes showed greater decrease in maximal heart rate than non-EIH athletes at altitude (8 ± 3.3 bpm and 5 ± 2.9 bpm, respectively). CONCLUSION: EIH athletes demonstrated specific cardiorespiratory response to exercise at moderate altitude compared to non-EIH athletes with a higher decrease in VO2max certainly due to the lower ventilator and HRmax responses. Thus EIH phenomenon developed at sea-level negatively impact performance and cardiorespiratory responses at acute moderate altitude despite no potentiated O2 desaturation.

Acute, Exercise Dose-Dependent Impairment in Atrial Performance During an Endurance Race: 2D Ultrasound Speckle-Tracking Strain Analysis.

OBJECTIVES: This study sought to understand and characterize the acute atrial response to endurance exercise and the influence of the amount of exercise performed. BACKGROUND: Endurance exercise seems to be recognized as a risk factor for developing atrial arrhythmia. Atrial geometrical and functional remodeling may be the underlying substrate. METHODS: Echocardiography was performed in 55 healthy adults at baseline and after a 3-stage trail race: a short race (S) (14 km), n = 17; a medium race (M) (35 km), n = 21; and a long race (L) (56 km), n = 17. Analysis consisted of standard, speckle-tracking assessment of both the left ventricle (LV) and right ventricle (RV) and both the left atrium (LA) and the right atrium (RA): a-wave strain (Sa) and strain rate (Ra) as a surrogate for atrial contractile function and s-wave strain (St) and strain rate (SR) as reservoir function. RESULTS: After the race, RA reservoir function decreased in group M (Δ% SRs: -12.5) and further in group L (Δ% SRs: -15.4), with no changes in group S. RA contractile function decreased in group L (Δ% SRa: -9.3), showed no changes in group M (Δ% SRa: +0.7), and increased in group S (Δ% SRa: +14.8). A similar trend was documented in LA reservoir and contractile function but with less pronounced changes. The decrease in RA reservoir after the race correlated with the decrease in RV global longitudinal strain (GLS) (Δ% RVGLS vs. RASt and RASRs: +0.44; p < 0.05 and +0.41, respectively; p < 0.05). CONCLUSIONS: During a trail-running race, an acute exercise-dose dependent impairment in atrial function was observed, mostly in the RA, which was related to RV systolic dysfunction. The impact on atrial function of long-term endurance training might lead to atrial remodeling, favoring arrhythmia development.

Inter-individual variability in right ventricle adaptation after an endurance race.

BACKGROUND: Right ventricle (RV) dysfunction has been described in athletes after endurance races. We aimed to understand and characterize the RV response to endurance exercise, the impact of individual variability and the effects of the amount of exercise. METHODS AND RESULTS: Echocardiography was performed in 55 healthy adults at baseline and after a three-stage trail race: short (14 km; n = 17); medium (35 km; n = 21); and long (56 km; n = 17). Standard and speckle tracking echocardiographic assessment of the RV was performed with global and separate analysis of the RV basal (inflow) and apical regions. Although no change was observed in the short distance runners, the RV systolic deformation decreased significantly (p < 0.05) after both the medium length and long races (Δ% RV global strain -7.6 ± 20.1 and -8.7 ± 21.8, respectively) with significant RV dilatation (Δ% RV volume +10.6 ± 9.9 and +15.3 ± 12.8, respectively). The RV basal segment made a major contribution to stroke volume during exercise, showing larger increases in size and strain compared with the apex. Various patterns of RV adaptation to exercise, ranging from increases in both RV segmental strains and sizes to an insufficient increase in size and a decrease in strain, were identified; this individual variability was not correlated with prior training. CONCLUSION: An acute RV impairment was demonstrated after a trail-running race and was related to the amount of exercise. A high inter-individual variability was observed. Differences in RV adaptation patterns were independent of prior training, suggesting the influence was due to other individual factors.

Epidemiological and medical aspects of canyoning rescue operations.

AIM: To describe the characteristics of canyoning rescue operations (CRO), type and severity of injuries or illnesses, and on-site medical procedures. PATIENTS AND METHODS: A retrospective analysis of all CRO data from an emergency medical rescue team in Aragon, Spain, between 1 August 1999 and 31 July 2009. RESULTS: A total of 520 patients were identified, with a male to female ratio of 1.4. The median age was 32 years (range 10-73 years). The median time from the emergency call to admission to an acute care facility (or evacuation for uninjured patients) was 90 min (range 10-860 min). In 329 (63.3%) cases technical skills or ability in the terrain with some grade of difficulty was required. Accessibility of the incident site was associated with type of rescue (p<0.0001), where patients in incident sites with moderate to extremely difficult access were more often rescued by ground rescue alone or supported by air rescue than by air rescue alone. 419 (80.6%) patients had trauma-related injuries. The most common injuries involved the lower extremities (74%). The percentage of patients with a NACA score ≥4 was higher for medical/environmental illnesses than traumatic injuries (p<0.0001), despite that the total number was smaller. 175 (33.7%) patients received analgesics. 370 (71.2%) patients required splinting/immobilization. Major life-saving medical interventions were rarely performed on-site. CONCLUSIONS: The length and exposure to environmental factors validates the importance of emergency physicians and paramedics in CRO. Physicians and paramedics should be familiar with Pre-hospital Trauma Life Support, medical procedures related to environmental, topographical and logistical conditions, and helicopter rescue operations including winch operations.

Apo A-I promoter polymorphism influences basal HDL-cholesterol and its response to pravastatin therapy.

Statins decrease cardiovascular morbidity and mortality, essentially, by reducing LDL-cholesterol levels and, additionally, by increasing HDL-cholesterol concentrations. Environmental and genetic factors are known to affect LDL-C response to statins but less is known regarding HDL-C. We have evaluated the lipid and lipoprotein response to 20 mg/day of pravastatin for 16 weeks in relation to the G/A polymorphism in the promoter region of the apo A-I gene in 397 hypercholesterolaemic subjects followed-up on an out-patient basis. In the study population, 61.7% were homozygous for the G allele and 36% were heterozygous. The A allele carriers had an HDL-C 6.5% higher than the G allele homozygotes (P=0.021 in univariate analysis; P=0.009 in multivariate analysis). However, on segregation by gender and smoking status the effect was significant only in non-smoking males. The A allele carriers did not increase their HDL-C concentrations after treatment (-0.3, 95%CI -3.3 to 2.7%) while G allele homozygotes had a 4.9% increase (95%CI 2.5-7.3%). Differences in the response between both groups were significant before (P=0.008) and after adjustment for confounding variables such as age and baseline HDL-C concentration (P=0.046). We conclude that the G/A polymorphism of the apo A-I promoter region affects not only baseline HDL-C concentrations but also its response to pravastatin treatment.