Combined effects of normobaric hypoxia and cold on respiratory system responses to high-intensity exercise.

IF 2.6 4区 医学 Q2 PHYSIOLOGY
Alexa Callovini, Alessandro Fornasiero, Aldo Savoldelli, Gianluigi Dorelli, Marco Decet, Lorenzo Bortolan, Barbara Pellegrini, Federico Schena
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Abstract

Cold temperatures (<-15°C) increase exercise-induced bronchoconstriction (EIB), while hypoxic-induced hyperventilation exacerbates respiratory muscle fatigue for a given exercising task. This study aimed to determine the individual and combined effects of cold and normobaric hypoxia on the respiratory system responses to high-intensity exercise. Fourteen trained male runners ( V ̇ O 2 max ${{\dot{V}}_{{{{\mathrm{O}}}_2}{\mathrm{max}}}}$ : 64 ± 5 mL/kg/min) randomly performed an incremental cardiopulmonary exercise test (CPET) to volitional exhaustion under four environmental conditions: normothermic (18°C) normoxia ( F I O 2 ${{F}_{{\mathrm{I}}{{{\mathrm{O}}}_2}}}$ : 20.9%) and hypoxia ( F I O 2 ${{F}_{{\mathrm{I}}{{{\mathrm{O}}}_2}}}$ : 13.5%), and cold (-20°C) normoxia and hypoxia. Ventilatory responses during exercise and lung function (LF), maximal inspiratory (MIP) and expiratory (MEP) pressure measurements before and after exercise were evaluated. Volume of air forcefully exhaled in 1 s (FEV1), FEV1/forced vital capacity (FVC), peak expiratory flow, forced expiratory flow during the mid (25-75%) portion of the FVC, and maximal expiratory flow at 50% of FVC were affected by cold exposure. No significant pre- to post-exercise change in MIP and MEP was found, independent of environmental conditions. Greater LF impairments in cold-normoxia and coldhypoxia were associated with the lowest peak ventilatory responses during exercise. Cold exposure was found to negatively impact peak ventilatory responses and post-exercise LF, further highlighting a relationship between EIB presence and the blunted ventilatory response in the cold. Respiratory muscle strength remained unchanged after exercise regardless of the environmental condition, suggesting no detrimental effect of hypoxia on this parameter when intermittent short-duration high-intensity exercises are performed. Future studies should investigate the combined cold-hypoxic effect on longer exercise durations at a sustained high intensity, accounting for differences between normobaric and hypobaric hypoxia exposures.

常压缺氧和低温对高强度运动呼吸系统反应的联合影响。
低温(v_2 max ${{\dot{V}}_{{{{\mathrm{O}} _2}{\mathrm{max}}}}$: 64±5 mL/kg/min)随机在常温(18℃)、常氧(f_2 ${{F}_{\mathrm{I}}}}_2}}}$: 20.9%)、低氧(f_2 ${{F}_{\mathrm{I}}}}}}$: 13.5%)、低温(-20℃)常氧、低氧。评估运动期间的通气反应和运动前后的肺功能(LF)、最大吸气(MIP)和呼气(MEP)压力测量。1 s内用力呼气气量(FEV1)、FEV1/用力肺活量(FVC)、呼气峰值流量、FVC中期(25-75%)用力呼气流量、FVC 50%时最大呼气流量均受冷暴露的影响。运动前后MIP和MEP没有明显的变化,独立于环境条件。在冷-常氧和冷-低氧条件下,更大的LF损伤与运动期间最低峰值通气反应有关。研究发现,冷暴露对高峰通气反应和运动后LF有负面影响,进一步强调了EIB存在与寒冷条件下通气反应减弱之间的关系。无论环境条件如何,运动后呼吸肌力量均保持不变,提示间歇性短时间高强度运动时,缺氧对该参数无不利影响。未来的研究应该调查在持续高强度下较长运动时间的低温-缺氧联合效应,并考虑常压和低压缺氧暴露之间的差异。
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来源期刊
Experimental Physiology
Experimental Physiology 医学-生理学
CiteScore
5.10
自引率
3.70%
发文量
262
审稿时长
1 months
期刊介绍: Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged. Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.
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