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Toxic and Asphyxiating Hazards in Confined Spaces
Published in Neil McManus, Safety and Health in Confined Spaces, 2018
Hypoventilation exists when ventilation of the alveoli is insufficient to supply the metabolic needs of the body (Comroe et al. 1962). The term “hypoventilation syndrome” originally was applied to obese individuals who were anoxemic because of insufficient alveolar ventilation. However, hypoventilation can occur for many reasons: uneven distribution of air in the lung, impairment of diffusion, depression of respiratory centers and neural transmission, injury, disease, obesity, agerelated processes, and drugs. With each breath providing insufficient fresh air, alveolar and arterial partial pressure of oxygen decreases, arterial and alveolar partial pressures of carbon dioxide increase, and pH decreases.
Effect of swim intensity on responses to dynamic apnoea
Published in Journal of Sports Sciences, 2018
A. Guimard, K. Collomp, H. Zorgati, S. Brulaire, X. Woorons, V. Amiot, F. Prieur
In studies conducted in swimmers untrained in apnoea, the breathing pattern was often manipulated in order to induce short periods of apnoea through voluntary hypoventilation (Key et al., 2014; Lavin, Guenette, Smoliga, & Zavorsky, 2015; West, Drummond, Vanness, & Ciccolella, 2005; Woorons, Gamelin, Lamberto, Pichon, & Richalet, 2014). It appears that performing voluntary hypoventilation at high lung volume, (i.e. controlled-frequency breathing) induces hypercapnia but not hypoxemia (Holmer & Gullstrand, 1980) whereas swimming with voluntary hypoventilation at low lung volume leads to severe hypoxemia (Woorons et al., 2014). Enhancing the duration of breath holding at high lung volume should lead to a significant hypoxemia. Besides it was already observed that apnoea of longer duration, corresponding to complete apnoea over the length of a swimming pool, could lead to a significant decrease in arterial O2 saturation (Guimard et al., 2014, 2017).
Repeated-sprint training in hypoxia induced by voluntary hypoventilation improves running repeated-sprint ability in rugby players
Published in European Journal of Sport Science, 2018
Charly Fornasier-Santos, Grégoire P. Millet, Xavier Woorons
While most of the RSH studies used simulated altitude (i.e. normobaric hypoxia), two recent repeated-sprint studies induced arterial desaturation through voluntary hypoventilation at low lung volume (VHL) (Trincat, Woorons, & Millet, 2017; Woorons, Mucci, Aucouturier, Anthierens, & Millet, 2017). It has been shown that this breathing modality could lead to both a significant arterial and muscle deoxygenation during exercise (Woorons et al., 2010, 2017), leading to a hypoxic state similar to what is obtained at altitudes above 2000 m (Woorons et al., 2011). Although the hypoxic dose (i.e. scale and time spent at low arterial oxygen saturation) is low with VHL (Woorons, 2014), this kind of approach was effective for improving RSA after RSH induced by VHL (RSH-VHL) in competitive swimmers (Trincat et al., 2017). This improvement was significantly greater than in the group who performed the same repeated-sprint training in normoxia (RSN). Of interest is that the magnitude of the RSA enhancement after RSH-VHL in swimming (+ 35%) was in line with what has been previously reported after RSH in cycling (+38%; Faiss, Léger et al., 2013) and in double poling cross-country skiing (+58%; Faiss et al., 2015).
Effect of muscle distribution on lung function in young adults
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Wenbo Shu, Mengchi Chen, Zhengyi Xie, Liqian Huang, Binbin Huang, Peng Liu
The possible mechanism explaining the high correlation between the muscle tissue of male and female subjects and VC was reported. Next, we elaborate on the possible differences between male and female subjects of different body types. The present study showed that VC and TMM were more positively correlated with male and female subjects with low weight. Many muscles of the human body were directly or indirectly involved in breathing exercises at different respiratory intensities (Pilarski et al. 2019), and TMM change as lung function changes (Park et al. 2018). However, in this process, the role of fat is often negative. Obesity is related to increased work of breathing, decreased respiratory compliance, and hypoventilation (Parameswaran et al. 2006). A variety of mechanisms explain the damage caused by excessive body fat distribution to lung function. Excessive fat accumulation will increase the friction in the process of muscle contraction and affect the exertion of muscle strength (Chatrath et al. 2002). Second, too much fat in the abdominal viscera will hinder the contraction of the diaphragm and affect respiratory function (Manika et al. 2012). The increase in abdominal visceral fat reduces the functional volume of the chest cavity and reduces the respiratory reserve capacity (Paralikar et al. 2012). Moreover, the deposition of fat on the chest wall limits the expansion and displacement of the chest cavity (Poulain et al. 2006). In addition, excessive accumulation of fat will cause vasculitis markers to play a local inflammatory role in the lung tissue, reducing the diameter of the airway (Sin and Man 2003; Aronson et al. 2006; Groenewegen et al. 2008).