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International Society for Mountain Medicine - VIWCMM Abstracts (Page 8)

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International Society for Mountain Medicine - VIWCMM Abstracts
16.
EFFECTS OF HYPOXIA AND EXERCISE ON MITOCHONDRIAL UCP
2
OF RAT MUSCLE
. Mingchun Cai
1
, Qingyuan Huang
1
, Yuqi Gao
1
, Wenxiang Gao
1
. Department of Pathophysiology
and High Altitude Physiology, Third Military Medical University, Chong
1
.
Uncoupling proteins (UCP1, UCP2 and UCP3) have been proposed as very important in the
regulation of basal metabolism and energy balance. UCP2 is widely expressed in different tissues.
This study was designed to investigate the effects of hypoxia alone or combined with exercise on
expression of UCP2 in rat heart and skeletal muscle mitochondria. Methods: Wistar rats were
divided into 4 groups: I normoxic control; II hypoxia; III exercise and IV hypoxia and exercise.
Rats of II and IV groups were subjected to hypobaric hypoxia for 5 weeks (23h/day). They were
first brought to simulated 4000m altitude, where rats of the IV group were forced to swim for
1h/day (6 days/week). Then the animals were taken to 5000m. Mitochondria from rat heart and
rat hind leg muscle were isolated by homogenizing tissue and following centrifuging program.
Mitochondrial uncoupling protein-2 (UCP2) was quantified by western blot. Results: Heart and
skeletal muscle UCP2 in hypoxia-combined exercise were significantly lower than control and
hypoxia (p<0.05). Compared with exercise group, hypoxia-combined exercise showed no
statistical difference. No significant difference was found between hypoxia and control.
Conclusions: During acclimatization to hypoxia, moderate exercise can down-regulate the UCP2,
which may be advantageous by increasing phosphorylation efficiency and may be favorable for
promoting acclimation to high altitude.
17.
CEREBRAL HYPOXIA AT HIGH ALTITUDE - OLFACTORY SYSTEM REGULATES.
Vidyasagar Casikar
1
, Savitha Nagabushan
2
, Venkatesh Tuppil
2
. Nepean Hospital Sydney
University
1
, St Johns Medical College Hospital, Bangalore
2
.
The present study was an attempt to understand the relationship between the olfactory system
and acute mountain sickness. Albino rats whose olfactory lobes were removed were subjected to
high altitude states under laboratory conditions. Blood and urine samples were collected at
various stages to measure biochemical parameters. Histological examinations of the brains were
done. Rats whose olfactory systems were intact were used as controls. The results suggested that
the olfactory system regulated pituitary function, and 2. hypoxic brain damage occurred in rats
whose olfactory lobes were removed. Conclusion: Olfactory system regulates physiology at high
altitudes. The importance of median forebrain bundle, the release of free radicals as a possible
cause of cerebral damage and the role of regulated breathing are discussed.
18.
HYPERGLYCAEMIA INDUCES OXIDATIVE STRESS IN SEA LEVEL RESIDENTS BUT
NOT IN RESIDENTS FROM HIGH ALTITUDE LANDS. Oscar Castillo
1
, Raquel Oré
2
, Rubén
Valdivieso
2
, Rosa Oriondo
2
, Orison Woolcott
1
, Miguel Sandoval
2
, Jorge Durand
2
. Instituto
Nacional de Biología Andina
1
, Centro de Bioquímica y Nutrición
2
.
Objectives: To determine and to compare the response of markers of oxidative stress against
hyperglycaemia during glucose clamp in people from sea level and from high altitude. Material
and Methods: Twelve healthy volunteer men from sea level (Lima, 150 m) and 6 from high
altitude (Huancayo, 3250 m) were included in the study. We used hyperglycaemic glucose clamp
at 125 mg/dL above individual basal blood glucose to induce oxidative stress. We assessed
lipoperoxidation (LPO) and superoxide dismutase (SOD) as markers of oxidative stress. Three
samples were taken: basal and 60 and 120 minutes during glucose infusion. Results: The mean
age was 28.6 ± 6.9 years and 26.0 ± 7.9 years and the BMI was 23.6 ± 0.9 and 25.5 ± 4.9 kg/m2,
in sea level (SL) and high altitude (HA) residents, respectively. The basal LPO was 2.55 ± 0.51
mol/L and 2.67 ± 0.73 mol/L, in SL and HA residents, respectively (P0.05). SOD was 730.1 ±
408.5 IU/mL and 686.9 ± 98.8 IU/mL, in SL and HA residents, respectively (P0.05). After
glucose clamp there was an increase of LPO only in SL dwellers at minute 60 (P=0.007), but no
change was found in SOD in any group. Conclusions: Hyperglycaemia induces oxidative stress in
residents from SL by increasing LPO. However, there is no induction of oxidative stress at HA, at

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