224 1. INTRODUCTION With the rapid improvement in transport and communication systems, an increasingly large number of people are going to high altitude for adventure and challenges such as touring, mountaineering, trekking and different mountain sports. Moreover lowland residents are also moving to high altitude for employment. Due to strategic reasons swift deployment of sea level or low altitude military personnel to high mountain regions has also become necessary for combat defence purposes. High altitude exposure affects human body because of low partial pressure of oxygen (hypoxia), severe cold, high wind and intense solar radiation. Due to acute hypobaric hypoxia in otherwise previously healthy individuals who visited high altitude may suffer from high altitude illness (HAI). High altitude induced pulmonary edema (HAPE) is one of the most ominous type of HAI. It is a kind of non-cardiogenic type of pulmonary oedema that develops in non-acclimatised persons after rapid ascent to 1 and/ or extreme physical exertion at an altitude above 2500 m. The primary causative factors for the development of HAPE are the altitude attained, speed and mode of ascent, amount of physical activity and above all degree of individual susceptibility 2,3 . Increased sympathetic activity via α-adrenergic efferent pathways 4 endothelial dysfunction, hypoxemia from a poor ventilatory response to hypoxia, uneven exaggerated hypoxia related pulmonary vasoconstriction 5 along with excessive-perfusion of certain regions of the pulmonary vascular bed and excessively elevated pressure in pulmonary artery and capillary are considered as crucial pathogenic factors for the development of this type of hydrostatic pulmonary oedema 6,7 . The excessively elevated pulmonary artery systolic pressure while exercising in both normoxic and hypoxic conditions 8 leads to mechanical injury or ‘stress failure’ of pulmonary capillaries 9 , causing extravasation of high-molecular-weight proteins, erythrocytes, leukocytes (mostly alveolar macrophages) and infammatory markers into the alveoli 10 . This stress failure causes vascular leakage in the lungs either by altering the structure of the capillary endothelium and alveolar epithelium by relaxing tight junctions between the cells and/ or by forming transcellular passage through vesicular channels 11 . It has been reported that decreased bioavailability of nitric oxide contributes hypoxia induced endothelial dysfunction in HAPE susceptible volunteers which in turn contributes enhanced hypoxic pulmonary vasoconstriction and fnally development of HAPE 12 . Plenty of research articles are available on resting and exercise induced physiological function of HAPE susceptible (HAPE-s) and HAPE resistance (HAPE-r) volunteers at sea level and high altitude both 3,14,15 . But a systemic study concerning the metabolic functions of HAPE-s volunteers to whom HAPE had developed in spite of proper 6 day acclimatization is still limited to the best of our knowledge. The present study was therefore designed for a comprehensive Received : 05 September 2017, Revised : 19 March 2018 Accepted : 28 March 2018, Online published : 25 June 2018 Exercise Responses to Metabolic Function on High Altitude Pulmonary Edema Susceptible Individuals Kaushik Halder, R.K. Gupta, Anjana Pathak, and M. Saha * DRDO-Defence Institute of Physiology and Allied Sciences, Delhi–110 054, India * E-mail: msaha1234@yahoo.com ABSTRACT The study was aimed to evaluate and compare resting and exercise induced metabolic responses between acclimatised high altitude pulmonary edema (HAPE) susceptible (HAPE-s) and HAPE resistance (HAPE-r) volunteers at sea level. A group of 14 Indian soldiers volunteered for this study, divided into two groups, (i) HAPE-s, with past history of HAPE [n 1 = 7; age = 33.3 ± 4.5 (M ± SD)] and (ii) HAPE-r, with prior history of repeated exposure to high altitude and without suffering HAPE [n 2 = 7; age = 31.9 ± 4.2 (M ± SD)]. Respiratory frequency (f R ), tidal volume ( V  T ), minute ventilation ( V  E ), oxygen consumption ( V  O 2 ), carbon dioxide output ( V  CO 2 ), heart rate (HR) and respiratory quotient (RQ) were recorded on all the volunteers during resting and exercise conditions. Ventilatory equivalent for oxygen (EqO 2 ) and oxygen pulse (O 2 P) were calculated. Signifcant differences were observed between HAPE-s and HAPE-r volunteers in f Rrest (25.3 % higher), O 2 P rest (23.7 % lower), V  Emax (50.9% lower) (all P<0.05), f Rmax (55.7 % lower), V  O 2max (55.5 % lower), O 2 P max (34.2 % lower) (all P<0.01) and V  CO 2max (42.1 % lower, P<0.001). Rest of the parameters did not show any signifcant differences between the study groups. The study revealed that resting and exercise induced metabolic responses of HAPE-r volunteers was better as compared to acclimatised HAPE-s volunteers at sea level. Keywords: High altitude; Hypoxia; High altitude illness; HAPE; Exercise; Ventilatory function Defence Life Science Journal, Vol. 3, No. 3, July 2018, pp. 224-230, DOI : 10.14429/dlsj.3.12908  2018, DESIDOC