High-Altitude Exposure Reduces Inspiratory Muscle Strength

Abstract

It was the aim of the study to assess the maximal pressure generated by the inspiratory muscles (MIP) during exposure to different levels of altitude (i.e., hypobaric hypoxia). Eight lowlanders (2 females and 6 males), aged 27 - 46 years, participated in the study. After being evaluated at sea level, the subjects spent seven days at altitudes of more than 3000 metres. On the first day, they rode in a cable car from 1200 to 3200 metres and performed the first test after 45 - 60 minutes rest; they then walked for two hours to a mountain refuge at 3600 metres, where they spent three nights (days 2 - 3); on day 4, they walked for four hours over a glacier to reach Capanna Regina Margherita (4559 m), where they spent days 5 - 7. MIP, flow-volume curve and SpO (2) % were measured at each altitude, and acute mountain sickness (Lake Louise score) was recorded. Increasing altitude led to a significant decrease in resting SpO (2) % (from 98 % to 80 %) and MIP (from 134 to 111 cmH (2)O) (baseline to day 4: p < 0.05); there was an improvement in SpO (2) % and a slight increase in MIP during the subsequent days at the same altitude. Expiratory (but not inspiratory) flows increased, and forced vital capacity and FEF (75) decreased at higher altitudes. We conclude that exposure to high altitude hypoxia reduces the strength of the respiratory muscles, as demonstrated by the reduction in MIP and the lack of an increase in peak inspiratory flows. This reduction is more marked during the first days of exposure to the same altitude, and tends to recover during the acclimatisation process.

The influence of thoracic gas compression and airflow density dependence on the assessment of pulmonary function at high altitude

“…; Fasano et al. ). The decline in FVC while sojourning at Barafu camp may have been due to: (1) expiratory muscle weakness limiting the ability to voluntarily reduce lung volume, thereby raising residual volume (Deboeck et al.…”

“…Early work by Paul Bert in a hypobaric chamber (4500 m; Bert 1878), and by Angelo Mosso at Capanna Regina Margherita (4559 m;Mosso 1897), revealed that vital capacity acutely declines with increasing elevation above sea level. This observation has become so pervasive in the literature that one may consider it a "hallmark" of the acute pulmonary response to sojourning at high altitude (Shields et al 1968;Dramise et al 1976;Coates et al 1979;Jaeger et al 1979;Stockley and Green 1979;Gautier et al 1982;Welsh et al 1993;Saldias et al 1995;Pollard et al 1996Pollard et al , 1997Cogo et al 1997a,b;Hashimoto et al 1997;Dillard et al 1998;Mason et al 2000Mason et al , 2003Deboeck et al 2005;Fischer et al 2005;Meysman et al 2005;Senn et al 2006;Basu et al 2007;Fasano et al 2007)also see Cremona et al (2002) and Dehnert et al (2010). On the contrary, the effect of high-altitude exposure on the forced expiratory flows (FEFs) is less certain.…”

“…On the contrary, the effect of high-altitude exposure on the forced expiratory flows (FEFs) is less certain. For example, one may find evidence in the literature that FEFs are augmented (Shields et al 1968;Mansell et al 1980;Gautier et al 1982;Welsh et al 1993;Saldias et al 1995;Pollard et al 1996;Wolf et al 1996;Cogo et al 1997b;Cremona et al 2002;Deboeck et al 2005;Meysman et al 2005;Fasano et al 2007;Dehnert et al 2010;Lalande et al 2011;Bouzat et al 2013), unchanged (Wolf et al 1996;Pollard et al 1997;Meysman et al 2005;Basu et al 2007;Pellegrino et al 2010;Lalande et al 2011) or decreased at high altitude (Stockley and Green 1979;Saldias et al 1995;Cogo et al 1997a,b;Hashimoto et al 1997;Basu et al 2007) depending on the lung volume considered (i.e., peak vs. mid-expiratory flows, etc.). It is relevant to note that these studies differed on the bases of altitude exposure, subject demographics and history of high-altitude pulmonary edema, baseline pulmonary disease status, and location (i.e., hypobaric chamber vs. field-based expeditions).…”

“…In so doing, one facilitates the comparison between what was observed at altitude and what was expected simply due to the air-density dependence of FEFs. However, as with thoracic gas compression, few investigators have addressed the issue of air-density dependence on FEFs obtained at high altitude (Deboeck et al 2005;Basu et al 2007;Fasano et al 2007;Pellegrino et al 2010). Therefore, the literature is presently lacking a clear demonstration of how air-density dependence, and thoracic gas compression, may impact on the interpretation of changes in pulmonary function at high altitude.…”

Changes in contractile properties of skinned single rat soleus and diaphragm fibres after chronic hypoxia

“…This necessarily requires an enhanced activity of the respiratory muscles such as the diaphragm [49]. Yet, highaltitude exposure is accompanied by reduced respiratory muscle strength [18]. Interestingly, the diaphragm contractile function in hypobaric hypoxic rats was more severely affected than that of the limb muscles [44], similar to the situation in patients with chronic heart failure [33] or COPD [38].…”