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
|Date of Award||May 2017|