Discussion
The present study used a follow-up
method to investigate the change in perceptual organization during HA
adaptation and deadaptation. For the adaptation process, compared with
the sea level baseline, increased HR and DBP and decreased SpO2 and VC
were found when entering HA. Shorter latencies of P1 and N170 showed a
faster process of perceptual organization, as well as a larger amplitude
of complete face N170. For the deadaptation process, all physiological
parameters recovered to baseline levels one week after returning to sea
level. Compared with HA, the amplitude of the P1 component of the
incomplete face decreased after one week, while that of the complete
face decreased after one month. The right hemisphere N170 amplitude
increased after entering HA and one week after returning to sea level
but returned to baseline one month later. The changes in physiological
data and ERP components were out of sync; the perceptual organization
function recovery takes a relatively long time. These findings offer
novel insights into the neural mechanism of HA adaptation and
deadaptation on cognitive processes, especially in the nonprefrontal
domain.
After twenty-five days of HA exposure, shorter P1 and N170 latencies
were observed, consistent with previous chronic (two-year) HA exposure
study
. The results suggested that higher levels of cortical excitation within
the visual cortex leads to a faster perceptual process when entering HA.
After staying at HA for approximately four weeks, the organism is in a
state of hypoxia stress. The reduced SpO2 and VC and increased HR and
DBP revealed a decrease in the partial pressure of oxygen under a
hypoxic environment at HA, causing sympathetic nerve
excitement, which may lead to
faster perceptual processing. This acceleration is compatible with
previous studies that reported that the resting EEG of people who first
arrived at HA had enhanced β wave activity, which is a
manifestation of increased excitability and excessive alertness in the
cerebral cortex .
According to a previous study,
hypoxia results in the facilitation of perception
tasks .
The perception task involves
activating sensory cortices, which are greatly influenced by
neurotransmitter activity, including dopamine (DA), 5-hydroxytryptamine
(5-HT), and peptide corticotropin releasing factor (CRF). HA exposure
induces high concentrations of neurotransmitters, leading to massive
anoxic depolarization of neurons in cortical tissues and causing brain
hyperexcitability , which could
positively affect perceptual process speed.
Existing
studies have also suggested that cognitive performance decreased
obviously when SpO2 was 80%, but activation and increased performance
were observed when SpO2 was 90%, and this activation could have a
general stimulating effect on central nervous system (CNS) functional
adaptation to the impacts of
hypoxia , which may reflect a
mechanism attempting to restore/protect neuronal
homeostasis . Therefore, it might
be interpreted as an adaptive trait rather than a deficit, perhaps
attenuating hypoxemia effects under mild hypoxia. Further studies are
needed to provide definitive conclusions on the mechanisms relating to
the acceleration of perceptual organization processing under HA
adaptation.
The N170 amplitude was larger than that at sea level after entering HA
for twenty-five days, which was also similar to the result of two years
of exposure . The increased N170
amplitude under HA adaptation may be related to maintaining the facial
configural encoding process efficiency during hypoxic stress, as certain
cortical areas were activated to a greater extent to compensate for
decreased processing efficiency due to HA
exposure . The increased N170
amplitude may indicate a higher level of neural activity at HA
. Interestingly, similar
observations in terms of the N170 enhancement phenomenon were also found
among elderly adults, which may be due to an increase in the sensitivity
to visual stimuli or a decline in brain adaptability with
aging . A recent study revealed
that cognitive resources were insufficient under HA exposure during a
visual attention paradigm, which is similar to normal aging
. Moreover, hypoxia was found to
accompany inflammatory brain states, such as neurodegeneration
. Evidence underscores that
hypoxia triggers both the accumulation of cerebral amyloidogenesis and
tau phosphorylation, the pathological markers of Alzheimer’s disease,
which are featured cognitive aging
. Chronic exposure to an HA
environment may have a similar neural mechanism to cognitive aging, or
chronic exposure to HA may accelerate brain aging, but this inference
needs more evidence to be confirmed.
After returning to sea level, the
body makes adjustments to adapt to the sea level, and all the
physiological parameters (SpO2, VC, HR, SBP and DBP) recover to
baseline. Compared with HA, SBP decreased one week after returning to
sea level, even though it had not been significantly altered by HA
adaptation. These findings imply that the autonomic nervous system
outcomes induced by HA exposure are reversible within one week after
returning to low altitudes. P1 and N170 latency also returned to
baseline less than one week after descending to lowlands, suggesting
that the change in the perceptual process was also reversible after
returning to sea level. However, hypoxia was found to have a longer
lasting effect on brain activity than on blood, which might be because
the brain consumes the most oxygen and is more sensitive to hypoxia
. Cortical activation recovery
under the HA deadaptation process always took more than one week in
previous studies . A neuroimaging
study showed that entering the HA or returning to sea level in one week
were both associated with a sustained greater level of excitement in the
posterior parietal cortex and occipital cortex, which are the foundation
of the perceptual processes . A
longitudinal EEG study also conforms to this view; increased beta power
was found after one month of HA exposure (3,800 m), and reoxygenation
occurred seven days after returning to sea level, which revealed a
sustained higher level of cortical excitation within the visual cortex
during HA deadaptation, which may be explained by the rise in
capillaries induced by chronic hypoxia
. The latency recovered to
baseline sooner in our study, which indicates that the change in
cortical activation may not be the direct cause of the change in
latency. The change in latency may be modulated by a more basic
physiological process, which may also regulate the activation of the
cortex. The subtle changes in
perceptual organization observed here may be a result of synergistic
interactions between physiological deadaptation and the aftereffect of
hypoxia on neurons . The
physiological mechanism of latency changes and its relationship with
cortical activation need to be further studied.
During the deadaptation process, compared with HA, the incomplete P1
amplitude decreased one week after returning to sea level, while the
complete P1 amplitude decreased after one month. As the P1 amplitude was
associated with attention arousal
, the decrease in the P1
amplitude may reflect lower arousal to the low-level visual features
during the HA deadaptation process. An MRI study was conducted on
participants who carried out the same task following the same schedule
and found that after one week of
reoxygenation exposure, cell
activity was inhibited in the visual cortex . This implied that the
low-level face perception process was inhibited for sojourners who went
through the deadaptation process because of the shortage of sufficient
arousal. Although this initial visual processing of faces under both the
incomplete condition and complete condition in the deadaptation process
showed no difference compared to the baseline at sea level, the
low-level face perception process of incomplete faces and complete faces
was different after HA deadaptation. This may be because compared with
the complete face, the processing of incomplete faces involves not only
parietal lobe activity but also frontal lobe activity to compensate for
incomplete visual information . After returning to sea level, this
compensation mechanism of incomplete faces soon disappeared, so the P1
amplitude decreased in one week. For complete faces, attention arousal
decreased gradually, leading to progressively smaller P1 amplitudes.
Seven days after descending to the lowlands, the N170 amplitude remained
larger in the right hemisphere, but it was no longer detectable after
one month, indicating that it takes more than one week but less than one
month for configural face-encoding processing to recover to baseline.
This face processing configuration stage is also reversible, although
slower than autonomic nervous system recovery. Previous studies found
physiological retention (arterial blood gases and hemoglobin) of
adaptation after returning to sea level after seven days. During hypoxia
in rats for three weeks, microvessels in the brain significantly
increased, and remained elevated after reoxygenation . Therefore, the
found N170 retention might be relevant to physiological responses that
we had not measure or molecular and cellular responses in the brain .
Only a tentative interpretation is possibly based on the present data,
and further studies should be conducted to elaborate the neural
mechanisms.
Both P1 and N170 tend to exhibit a larger amplitude in the right
hemisphere than in the left hemisphere , and this dominance of face
perception in the right hemisphere did not change under HA exposure. Our
results also revealed that the complete face still evoked larger P1 and
N170 amplitudes than the incomplete face in the HA exposure condition.
Moreover, P1 latency for incomplete faces is shorter than that for
complete faces, while N170 latency is longer in incomplete faces than in
complete faces . This pattern represents the basic law of face
perception organization processing, which was not altered by HA
adaptation or deadaptation.
Notably, there are several limitations regarding the current study.
First, it lacks a sea level control cohort. Moreover, we did not collect
ERP data when participants arrived at HA immediately because hair
washing is not recommended within three days of arrival at HA to prevent
cold. Further study could assess the acute effects of HA exposure on
perceptual process and compare it with chronic HA exposure condition.
One more limitation is that we examined healthy, young, and prepared
university students during an incremental ascent. Before entering HA,
they had regular exercise training and took nutrition products in
advance to prevent any possible sickness. As such, some generalization
to a broader population may be limited.
Following the limitations
outlined above, it would be advisable to replicate our findings in
different altitude exposure circumstances (e.g., different HA durations,
different altitudes, and different rates of ascent). Another useful
addition to the design would be to elucidate the impact of HA adaptation
and HA deadaptation on other cognitive function types. Finally, future
studies could broaden existing research by investigating the specific
relationships between physiological parameters (such as cerebrovascular
and cardiovascular parameters) and cognitive alterations, especially how
physiological and biochemical activities regulate neuronal activities.