**2.1 Space motion sickness**

How do we humans sense our relative positions in three-dimensional space? There are three sensory systems in the human body that help us define position: the visual, somatosensory, and vestibular systems. Most of the information from the outside world is processed by the visual system, but the combination of somatosensory and vestibular systems from the inner body helps define the positional status.

The vestibular organs include the otolith organs and semicircular canals. The otolith organs, saccules (sagittal direction) and utriculi (horizontal direction), sense linear acceleration. The semicircular canals, anterior, posterior, and horizontal, detect angular velocity of the head. The vestibular organs in the inner ear detect and measure linear and angular acceleration. These responses—already a complex set of signals—are further integrated with visual and proprioceptive inputs.

Exposure to microgravity alters some of these input signals, leading to misinterpretation and inadequate responses by the brain. This may cause vertigo, nausea, vomiting, appetite loss, headache, pallor, etc. As the symptoms are like those of motion sickness, this set of symptoms is termed "space motion sickness," but unlike conventional motion sickness, antiemetic drugs cannot suppress the symptoms of space motion sickness. Approximately 60–80% of astronauts develop the symptoms within 2 or 3 days after launch. Space motion sickness is considered important because of its potential impact on the astronauts' operational performance.

Although sensory misinterpretation may play a role in space motion sickness, its exact mechanism remains unknown. There are, however, several hypotheses: (1) sensory conflict, (2) fluid shift, (3) otolith asymmetry, and (4) orientation adaptation [9, 10].

The sensory conflict hypothesis suggests that loss of tilt-related otolith upon entry into microgravity causes a conflict between actual and anticipated signals from sense organs subserving spatial orientation. Such sensory conflicts are thought to induce motion sickness in other environments.

The fluid shift hypothesis suggests that space motion sickness results from the caudad fluid shifts, which in turn result from the hydrostatic pressure gradients in the lower body to the thoracic cavity or to the cranial cavity when entering microgravity. The cephalad fluid shift leads to visible puffiness in the face and is thought to increase the intracranial pressure, the cerebrospinal fluid pressure, or the inner ear fluid pressure, altering the response properties of the vestibular receptors and inducing space motion sickness.

The otolith asymmetry hypothesis is based on the theory that a mass difference in otolith between the left and right ear is the origin of space sickness and that there is interindividual susceptibility.

The otolith adaptation theory, or otolith tilt-translation reinterpretation theory, is the theory that space motion sickness is caused during the process of the brain learning to reinterpret novel otolith quasi-static signals to represent linear acceleration in space rather than the usual interpretation of tilt relative to the vertical direction on Earth.

Until now, it was unclear which of these theories (if any) was most likely. However, evidence from Space Shuttle missions suggests that the otolith asymmetry and otolith adaptation theories are unlikely.

**15**

lower degree.

*Effects of Microgravity on Human Physiology DOI: http://dx.doi.org/10.5772/intechopen.90700*

effects of fatigue on the saccadic reaction time.

**3.1 Effects of microgravity in the cardiovascular system**

strated by changes in the magnetic resonance imaging (MRI).

2 weeks after the reduction in circulatory plasma volume [13–17].

in rotation time.

of this maladaptation.

ing" [13–17].

**3. Cardiovascular system**

pharmacotherapy. Dornhoffer [11] reported the effects of four drug countermeasures (lorazepam, meclizine, promethazine, and scopolamine) for alleviating motion sickness induced by vestibular stimulation with a rotary chair and found that scopolamine was the only countermeasure to significantly change the mean duration of rotation compared with the placebo (p < 0.008), with a > 40% increase

In the Shuttle study, administration of promethazine at 20–50 mg was recommended by intramuscular injection or suppository. In the ISS study, meclizine and dimenhydrinate with cinnarizine were hypothesized to affect the medial vestibular nucleus. Promethazine is a vestibular suppressor, but a more recent report [12] demonstrated that *d-*amphetamine counters this suppression and inhibits the

We propose that artificial gravity is also effective in preventing space motion sickness because constant gravity on the otolith is effective against all four etiologies

The changes in the cardiovascular system begin solely with the fluid shift associated with microgravity, followed by the decreased circulatory blood volume, cardiac size, and aerobic capacity, and the most prominent symptom, postflight orthostatic intolerance. These symptoms are generically known as "cardiovascular decondition-

When the spacecraft reaches low Earth orbit (LEO), body fluids move from the lower body to the thorax, which is associated with the increase in the intraocular pressure and morphological alterations in the central nervous system, demon-

As a result of fluid shift, the leg volume decreases and the face becomes puffy. The leg volume decreases by 1 L, whereas subcutaneous tissue at the forehead thickens by as much as 7% compared with in the preflight supine position. The pulmonary capillary blood volume increases by approximately 25%, and intraocular pressure can nearly double. Fluid shift increases the cardiac volume and stroke volume at the beginning of the spaceflight (first 24 to 48 hours), but over time, the heart rate, stroke volume, and cardiac output stabilize to the preflight sitting level. The arterial blood pressure slightly decreases compared with the preflight level. Compared with "space motion sickness," cardiovascular and fluid balance adaptation is gradual. The symptoms appear in 3–5 days and disappear after 1–2 weeks, causing facial edema, nasal stiffness, heavy headedness, papilledema, or jugular vein dilatation. These symptoms upon exposure to microgravity disappear at most

The cardiovascular changes in actual spaceflight differ from those in stimulations such as head-down bedrest or dry immersion. First, the volume of fluid shift is much larger than the orthostatic change from the supine to upright positions. The fluid volume loss during simulated microgravity (e.g., head-down bedrest or dry immersion) is less than 50% of that observed in actual spaceflight. Second, the central venous pressure measured during spaceflight does not increase as much as in head-down bedrest. Third, the diuresis caused during simulated microgravity is to a

Then what is the cause of reduced blood volume after adaptation to microgravity? Diedrich et al. [18] explained the reduced blood volume in space as (1)

#### **2.2 Countermeasures for space motion sickness**

In the Shuttle program and in the case of the International Space Station (ISS), the most commonly used countermeasure for space motion sickness is

### *Effects of Microgravity on Human Physiology DOI: http://dx.doi.org/10.5772/intechopen.90700*

*Beyond LEO - Human Health Issues for Deep Space Exploration*

How do we humans sense our relative positions in three-dimensional space? There are three sensory systems in the human body that help us define position: the visual, somatosensory, and vestibular systems. Most of the information from the outside world is processed by the visual system, but the combination of somatosensory and vestibular systems from the inner body helps define the positional status. The vestibular organs include the otolith organs and semicircular canals. The otolith organs, saccules (sagittal direction) and utriculi (horizontal direction), sense linear acceleration. The semicircular canals, anterior, posterior, and horizontal, detect angular velocity of the head. The vestibular organs in the inner ear detect and measure linear and angular acceleration. These responses—already a complex set of signals—are further integrated with visual and proprioceptive inputs.

Exposure to microgravity alters some of these input signals, leading to misinterpretation and inadequate responses by the brain. This may cause vertigo, nausea, vomiting, appetite loss, headache, pallor, etc. As the symptoms are like those of motion sickness, this set of symptoms is termed "space motion sickness," but unlike conventional motion sickness, antiemetic drugs cannot suppress the symptoms of space motion sickness. Approximately 60–80% of astronauts develop the symptoms within 2 or 3 days after launch. Space motion sickness is considered important because of its potential impact on the astronauts' operational performance.

Although sensory misinterpretation may play a role in space motion sickness, its

The sensory conflict hypothesis suggests that loss of tilt-related otolith upon entry into microgravity causes a conflict between actual and anticipated signals from sense organs subserving spatial orientation. Such sensory conflicts are thought

The fluid shift hypothesis suggests that space motion sickness results from the caudad fluid shifts, which in turn result from the hydrostatic pressure gradients in the lower body to the thoracic cavity or to the cranial cavity when entering microgravity. The cephalad fluid shift leads to visible puffiness in the face and is thought to increase the intracranial pressure, the cerebrospinal fluid pressure, or the inner ear fluid pressure, altering the response properties of the vestibular receptors and

The otolith asymmetry hypothesis is based on the theory that a mass difference in otolith between the left and right ear is the origin of space sickness and that there

The otolith adaptation theory, or otolith tilt-translation reinterpretation theory, is the theory that space motion sickness is caused during the process of the brain learning to reinterpret novel otolith quasi-static signals to represent linear acceleration in space rather than the usual interpretation of tilt relative to the vertical direction on Earth. Until now, it was unclear which of these theories (if any) was most likely. However, evidence from Space Shuttle missions suggests that the otolith asymmetry

In the Shuttle program and in the case of the International Space Station (ISS), the most commonly used countermeasure for space motion sickness is

exact mechanism remains unknown. There are, however, several hypotheses: (1) sensory conflict, (2) fluid shift, (3) otolith asymmetry, and (4) orientation

to induce motion sickness in other environments.

inducing space motion sickness.

is interindividual susceptibility.

and otolith adaptation theories are unlikely.

**2.2 Countermeasures for space motion sickness**

**2. Neurovestibular system**

**2.1 Space motion sickness**

adaptation [9, 10].

**14**

pharmacotherapy. Dornhoffer [11] reported the effects of four drug countermeasures (lorazepam, meclizine, promethazine, and scopolamine) for alleviating motion sickness induced by vestibular stimulation with a rotary chair and found that scopolamine was the only countermeasure to significantly change the mean duration of rotation compared with the placebo (p < 0.008), with a > 40% increase in rotation time.

In the Shuttle study, administration of promethazine at 20–50 mg was recommended by intramuscular injection or suppository. In the ISS study, meclizine and dimenhydrinate with cinnarizine were hypothesized to affect the medial vestibular nucleus. Promethazine is a vestibular suppressor, but a more recent report [12] demonstrated that *d-*amphetamine counters this suppression and inhibits the effects of fatigue on the saccadic reaction time.

We propose that artificial gravity is also effective in preventing space motion sickness because constant gravity on the otolith is effective against all four etiologies of this maladaptation.
