The chemical adenosine is released by brain cells when those cells are active. Adenosine then binds to more and more...
GMAT Critical Reasoning : (CR) Questions
The chemical adenosine is released by brain cells when those cells are active. Adenosine then binds to more and more sites on cells in certain areas of the brain, as the total amount released gradually increases during wakefulness. During sleep, the number of sites to which adenosine is bound decreases. Some researchers have hypothesized that it is the cumulative binding of adenosine to a large number of sites that causes the onset of sleep.
Which of the following, if true, provides the most support for the researchers' hypothesis?
Passage Analysis:
| Text from Passage | Analysis |
| The chemical adenosine is released by brain cells when those cells are active. |
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| Adenosine then binds to more and more sites on cells in certain areas of the brain, as the total amount released gradually increases during wakefulness. |
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| During sleep, the number of sites to which adenosine is bound decreases. |
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| Some researchers have hypothesized that it is the cumulative binding of adenosine to a large number of sites that causes the onset of sleep. |
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Argument Flow:
The passage starts by explaining what adenosine is and when it's released, then shows how it accumulates during wakefulness and decreases during sleep. Finally, it presents a hypothesis that this accumulation pattern is what actually causes sleep to begin.
Main Conclusion:
Researchers believe that the buildup of adenosine binding to brain cell sites is what triggers the start of sleep.
Logical Structure:
The evidence about adenosine's release, accumulation, and clearance patterns supports the hypothesis that adenosine buildup causes sleep onset. The timing relationship (buildup during wake, decrease during sleep) suggests a cause-and-effect connection.
Prethinking:
Question type:
Strengthen - We need to find evidence that makes the researchers' hypothesis more believable. The hypothesis is that when adenosine builds up and binds to enough brain cell sites, it triggers sleep.
Precision of Claims
The key claims involve quantity (how much adenosine binds), timing (when sleep occurs), and causation (adenosine buildup causing sleep onset). We need to be precise about the relationship between adenosine accumulation and sleep initiation.
Strategy
To strengthen this hypothesis, we need evidence that supports the causal relationship between adenosine buildup and sleep onset. We should look for scenarios that show:
- When adenosine binding increases, sleep is more likely to occur
- When adenosine binding is prevented or reduced, sleep is delayed or doesn't happen
- There's a clear threshold effect where reaching a certain level of adenosine binding consistently triggers sleep
This choice tells us that even after long sleep periods when adenosine concentration is lowest, many brain cells still have adenosine bound to them. This doesn't strengthen the hypothesis because it suggests that high levels of bound adenosine don't necessarily correlate with sleep onset. If anything, this creates confusion about the relationship between adenosine binding levels and sleep timing.
This perfectly strengthens the hypothesis through what we call 'reverse causation' evidence. The researchers claim that adenosine buildup causes sleep. Caffeine interferes with adenosine binding AND keeps people awake. This creates a clear logical chain: when we prevent the proposed cause (adenosine binding), we prevent the proposed effect (sleep onset). This directly supports the causal relationship the researchers hypothesized.
This tells us adenosine has other functions throughout the body beyond brain binding. This information is irrelevant to whether adenosine binding in the brain specifically causes sleep onset. It neither strengthens nor weakens the sleep-related hypothesis.
This mentions that inactive brain areas still release some adenosine. This doesn't help establish whether adenosine buildup triggers sleep. The hypothesis focuses on cumulative binding reaching a threshold, not on whether all brain areas contribute equally to adenosine release.
This describes how stress can keep people awake even when adenosine binding levels are high. This actually weakens the hypothesis because it shows that high adenosine binding doesn't always lead to sleep onset. If other factors can override adenosine's sleep-inducing effects, then adenosine binding may not be the primary cause of sleep initiation.