| Summary: | This thesis examined the metabolic effects of acute and intermediate hypoxic exposure in humans, specifically, physiological mechanisms associated with weight loss. Namely; increased metabolic rate, changes in substrate oxidation, altered lipid metabolism and changes in taste. Study one assessed the validity and reproducibility of an online gas analyser in normobaric hypoxia [Fraction of inspired oxygen: 0.12 (FiO2:0.12) equivalent to approximately 4,500m] (n=nine; two females, seven males). The MetaMax3x demonstrates good reproducibility between repeated trials. Differences exist between the system and the gold standard Douglas Bag method for measures of oxygen uptake (percent differences of V̇O2; 21%), carbon dioxide production (V̇CO2; 10%) and minute ventilation (V̇E; 5%). The second study investigated the free fatty acid (FFA) and triglyceride (TAG) response to an acute (45 minutes) hypoxic exposure (FiO2: 0.12) (n=10; five females, five males). A greater resting metabolic rate (RMR) (+28 ± 6 kcal.hr-1 ) was observed, through increased carbohydrate (CHO) and fat oxidation. Increased plasma FFA (+54%) and TAG (+26%) were observed, highlighting metabolic perturbations from acute exposure. Study three investigated the metabolic responses to an acute (60 minute) hypoxic exposure (FiO2: 0.12) at rest and a subsequent bout of moderate exercise in normoxia following a high fat meal (n=eight males). Experimental trials included a lipid ingestion prior to a rest period at hypoxia or normoxia followed by moderate intensity exercise (60% heart rate reserve). Control trials consisted of the same protocol without lipid ingestion. Acute, severe hypoxia increased energy expenditure (EE), (+22 ± 11 kcal.hr-1 ) CHO and fat oxidation following exposure. A prior acute bout of severe hypoxia did not alter EE and substrate use during subsequent moderate intensity exercise. An exercise bout, postlipid ingestion, resulted in lower triglyceride concentration. No changes in Meteorin-like were observed throughout trials. These findings suggest that an increase in RMR occurs following a single resting hypoxic exposure and independently to Meteorin-like protein. The fourth study observed reductions in body mass (-2.36 ± 1.41 kg) and increases in CHO oxidation during an altitude stay in Peru (18 days, 3400 m) (n=10; five females, five males). The reduction in body mass (-1.89 ± 1.31 kg) was sustained four weeks post-return to sea-level. Salt, sweet and bitter taste sensations were reduced at 3,400 m compared to sea-level. No changes in self-reported appetite were observed throughout the testing period. Furthermore no changes in circulating Meteorin-like protein were observed upon return to sea-level at one and four weeks post-altitude stay. Study five investigated the blood lipid response to a high lipid meal consumed one and four weeks post-return to sea-level following an altitude stay (18 days, 3400 m) (n=10; five females, five males). No lasting postprandial effects were observed. It is likely that a time dependent effect of hypoxia exists with regards to postprandial blood lipid responses. Taken together acute and intermediate exposure to hypoxic conditions alter substrate oxidation with the potential to induce losses in body mass, independently to changes in Meteorin-like protein and self-reported appetite. Specifically, prolonged stay at moderate altitude results in a greater dependency on CHO use. Increases in RMR were observed during an acute severe bout of hypoxia, although this was not a consistent effect throughout prolonged exposure and should be further investigated. Altered taste during an altitude stay may influence food preferences, energy intake and subsequent changes in body mass and should be considered an area of future investigation. Higher circulating levels of FFA and TAG, demonstrates a metabolic perturbation from a single, acute severe hypoxic exposure.
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