BACKGROUND: High-altitude exposure changes the electrical conduction of the heart. However, reports on electrocardiogram (ECG) characteristics and potent prophylactic agents during high-altitude acclimatization and de-acclimatization are inadequate. This study aimed to investigate the effects of ubiquinol on electrophysiology after high-altitude hypoxia and reoxygenation.
METHODS: The study was a prospective, randomized, double-blind, placebo-controlled trial. Forty-one participants were randomly divided into two groups receiving ubiquinol 200 mg daily or placebo orally 14 days before flying to high altitude (3900 m) until the end of the study. Cardiopulmonary exercise testing was performed at baseline (300 m), on the third day after reaching high altitude, and on the seventh day after returning to baseline.
RESULTS: Acute high-altitude exposure prolonged resting ventricular repolarization, represented by increased corrected QT interval (455.9 ± 23.4 vs. 427.1 ± 19.1 ms, P < 0.001) and corrected Tpeak-Tend interval (155.5 ± 27.4 vs. 125.3 ± 21.1 ms, P < 0.001), which recovered after returning to low altitude. Ubiquinol supplementation shortened the hypoxia-induced extended Tpeak-Tend interval (-7.7 ms, [95% confidence interval (CI), -13.8 to -1.6], P = 0.014), Tpeak-Tend /QT interval (-0.014 [95% CI, -0.027 to -0.002], P = 0.028), and reserved maximal heart rate (11.9 bpm [95% CI, 3.2 to 20.6], P = 0.013) during exercise at high altitude. Furthermore, the decreased resting amplitude of the ST-segment in the V3 lead was correlated with decreased peak oxygen pulse (R = 0.713, P < 0.001) and maximum oxygen consumption (R = 0.595, P < 0.001).
CONCLUSIONS: Our results illustrated the electrophysiology changes during high-altitude acclimatization and de-acclimatization. Similarly, ubiquinol supplementation shortened the prolonged Tpeak-Tend interval and reserved maximal heart rate during exercise at high altitude.
BACKGROUND: URL: www.chictr.org.cn; Unique identifier: ChiCTR2200059900.

BACKGROUND: The performance of young swimmers is the result of a multifactorial process that is influenced by anthropometric characteristics and biological maturation. The purpose of our study was to investigate the effect of stages of biological maturation and body surface area on cardiopulmonary fitness indicators in preadolescent female swimmers, for whom menstruation has not started.
METHODS: Thirty female preadolescent swimmers (age 13.4 ± 1.0 years) participated in this study. We recorded anthropometric and morphological characteristics, stages of biological maturation, and pulmonary function parameters, and the swimmers underwent cardiopulmonary exercise testing.
RESULTS: The cut-off was set for body surface area (BSA) at 1.6 m2 and for biological maturation stages at score 3. The BSA results showed differences in variabilities in maximal effort oxygen pulse (p < 0.001), oxygen uptake (p < 0.001), ventilation (p = 0.041), tidal volume (p < 0.001), and oxygen breath (p < 0.001). Tanner stage score results showed differences in variabilities in maximal effort breath frequency (p < 0.001), tidal volume (p = 0.013), and oxygen breath (p = 0.045). Biological maturation stages and BSA were correlated during maximal effort with oxygen breath (p < 0.001; p < 0.001), oxygen uptake (p = 0.002; p < 0.001), and oxygen pulse (p < 0.001; p < 0.001).
CONCLUSIONS: In conclusion, the findings of our study showed that the girls who had a smaller body surface area and biological maturation stage presented lower values in maximal oxygen uptake and greater respiratory work.

Oxygen-pulse morphology and gas exchange analysis measured during cardiopulmonary exercise testing (CPET) has been associated with myocardial ischaemia. The aim of this analysis was to examine the relationship between CPET parameters, myocardial ischaemia and anginal symptoms in patients with chronic coronary syndrome and to determine the ability of these parameters to predict the placebo-controlled response to percutaneous coronary intervention (PCI).
Patients with severe single-vessel coronary artery disease (CAD) were randomized 1:1 to PCI or placebo in the ORBITA trial. Subjects underwent pre-randomization treadmill CPET, dobutamine stress echocardiography (DSE) and symptom assessment. These assessments were repeated at the end of a 6-week blinded follow-up period.A total of 195 patients with CPET data were randomized (102 PCI, 93 placebo). Patients in whom an oxygen-pulse plateau was observed during CPET had higher (more ischaemic) DSE score [+0.82 segments; 95% confidence interval (CI): 0.40 to 1.25, P = 0.0068] and lower fractional flow reserve (-0.07; 95% CI: -0.12 to -0.02, P = 0.011) compared with those without. At lower (more abnormal) oxygen-pulse slopes, there was a larger improvement of the placebo-controlled effect of PCI on DSE score [oxygen-pulse plateau presence (Pinteraction = 0.026) and oxygen-pulse gradient (Pinteraction = 0.023)] and Seattle angina physical-limitation score [oxygen-pulse plateau presence (Pinteraction = 0.037)]. Impaired peak VO2, VE/VCO2 slope, peak oxygen-pulse, and oxygen uptake efficacy slope was significantly associated with higher symptom burden but did not relate to severity of ischaemia or predict response to PCI.
Although selected CPET parameters relate to severity of angina symptoms and quality of life, only an oxygen-pulse plateau detects the severity of myocardial ischaemia and predicts the placebo-controlled efficacy of PCI in patients with single-vessel CAD.

The purpose of the present study was to investigate training-specific adaptations to eight weeks of moderate intensity continuous training (CT) and sprint interval training (SIT). Young healthy subjects (n = 25; 9 males and 16 females) performed either continuous training (30-60 min, 70-80% peak heart rate) or sprint interval training (5-10 near maximal 30 s sprints, 3 min recovery) three times per week for eight weeks. Maximal oxygen consumption, 20 m shuttle run test and 5·60 m sprint test were performed before and after the intervention. Furthermore, heart rate, oxygen pulse, respiratory exchange ratio, lactate and running economy were assessed at five submaximal intensities, before and after the training interventions. Maximal oxygen uptake increased after CT (before: 47.9 ± 1.5; after: 49.7 ± 1.5 mL·kg-1·min-1, p < 0.05) and SIT (before: 50.5 ± 1.6; after: 53.3 ± 1.5 mL·kg-1·min-1, p < 0.01), with no statistically significant differences between groups. Both groups increased 20 m shuttle run performance and 60 m sprint performance, but SIT performed better than CT at the 4th and 5th 60 m sprint after the intervention (p < 0.05). At submaximal intensities, CT, but not SIT, reduced heart rate (p < 0.05), whereas lactate decreased in both groups. In conclusion, both groups demonstrated similar improvements of several performance measures including VO2max, but sprint performance was better after SIT, and CT caused training-specific adaptations at submaximal intensities.

BACKGROUND: Studies suggest that acute decreases in lung hyperinflation at rest improves cardiac function and increases lung vascular perfusion from decompression of a compromised heart. In those studies, changes in resting oxygen uptake induced by medications, an alternative explanation for compensatory increased cardiac function, were not explored.
METHODS: This double-blind, multicenter, double-crossover study enrolled adults with chronic obstructive pulmonary disease, resting hyperinflation, and > 10% improvement in inspiratory capacity after 2 inhalations of budesonide/formoterol 160/4.5 μg. Metabolic, cardiac, and ventilatory function were measured 60 min pre-/post-dose at each visit. Primary endpoint was change in resting oxygen uptake for budesonide/formoterol versus placebo.
RESULTS: Fifty-one patients (median age: 63 years) received treatment. Compared with placebo, budesonide/formoterol significantly increased resting oxygen uptake (mean change from baseline: 1.25 vs 11.37 mL/min; P = 0.007) as well as tidal volume and minute ventilation. This occurred despite improvements in the inspiratory capacity, forced vital capacity, and expiratory volume in 1 s. No significant treatment differences were seen for oxygen saturation, respiratory rate, and resting dyspnea. There was a numerical increase in oxygen pulse (oxygen uptake/heart rate). Correlations between inspiratory capacity and oxygen pulse were weak.
CONCLUSIONS: Budesonide/formoterol treatment in resting hyperinflated patients with COPD results in significant deflation. The increase in oxygen uptake and minute ventilation at lower lung volumes, without changes in heart rate and with minimal improvement in oxygen pulse, suggests increased oxygen demand as a contributor to increased cardiac function.
BACKGROUND: ClinicalTrials.gov identifier: NCT02533505.