Effect of yelling on maximal aerobic power during an incremental test of cycling performance

Background：People experiencing strong feelings of fatigue during exercise sometimes subconsciously yell to refocus their efforts and,thus,maintain exercise performance.The present study examined the influenc of yelling during high-intensity exercise by analysing cardiorespiratory reactions and integrated electromyography（i EMG） changes in the vastus lateralis during a cycle ergometer test.Methods：A total of 23 moderately trained people were recruited.The cycling test began with a resistance of 25 W/min,which was gradually increased.During the experimental trial,the participants were required to yell at least 3 times when they felt exhausted;during the controlled trial,they were not allowed to produce any yelling sounds.The testing order was randomly assigned and the 2 trials were completed within an interval between 3–10 days.Two-way repeated measures ANOVA was applied to analyse the differences within and between the trials,and interaction of trial and time.Results：The peak power and time to exhaustion（p〈0.01） in the yelling trial were higher than those in the control trial.However,the vastus lateralis iE MG values of both trials at peak power were not significant y different.During the yelling period at 90%–100% of the maximal effort,a significan time-by-trialinteraction（p〈0.05）wasobservedinoxygenconsumption（VO2）,CO2 production,O2 pulse,ventilation,andrespiratoryrate. Alltheabove measures showed a significan between-trial difference（p〈0.02）.However,heart rate,respiratory exchange ratio,end-tidal oxygen pressure,and ventilatory equivalent for oxygen showed only significan between-trial difference（p〈0.05）,but without interaction of trial and time.Conclusion：Yelling enhances the peak O2 pulse and VO2 and maintains CO2-exclusion efficien y during high-intensity exercise.It may enable maintaining muscle activation without stronger EMG signals being required during high-intensity exercise.

Evaluation of respiratory dysfunction in a pig model of severe acute dichlorvos poisoning

Background Respiratory failure is the main cause of death in acute organophosphorus pesticide poisoning. In this study, a pulse-induced contour cardiac output monitor was used to evaluate the respiratory status in a pig model of acute dichlorvos poisoning. Methods Twenty female pigs were randomly allocated to dichlorvos （n=7）, atropine （n=7）, and control （n=6） groups. In the dichlorvos group, pigs were administered 80% emulsifiable dichlorvos （100 mg/kg） via a gastric tube. In the atropine group, pigs were similarly administered dichlorvos, and 0.5 hours later, atropine was injected to attain and maintain atropinization. The control group was administered saline solution. Arterial blood gas was measured at 0, 0.5, 1, 2, 4, and 6 hours post-injection. The extravascular lung water index and pulmonary vascular permeability index were recorded by the pulse-induced contour cardiac output monitor. At termination of the study, the animals were euthanized, the lung wet-to-dry weight ratio was determined, and histopathology was observed. Results In the dichlorvos group, the extravascular lung water index and pulmonary vascular permeability index were substantially increased from 0.5 hours and were particularly high within 1 hour. In the atropine group, these indices increased initially, but decreased from the 1-hour mark. The control group exhibited no obvious changes. In both the dichlorvos and atropine groups, the extravascular lung water index was negatively correlated with partial pressure of oxygen/fraction of inspiration oxygen （POz/FiO2） and positively correlated with the pulmonary vascular permeability index. Compared with the control group, the lung wet-to-dry weight ratio markedly increased and the histopathological findings obviously changed in the dichlorvos group, but only mildly increased and changed, respectively, in the atropine group. Conclusion The extravascular lung water index is an appropriate and valuable parameter for assessment of respiratory function in acute dichlorvos poisoning.