You've probably had a night where you were exhausted at 9 PM, kept working or scrolling instead of going to bed, and by 11 you suddenly weren't tired anymore. Or the opposite: dead tired after a long flight, lying in a hotel bed at what your body insists is the middle of the afternoon, wide awake despite genuine exhaustion. Both of those experiences make no sense if you think sleepiness is just a matter of "how long have I been awake." It isn't. Two separate systems in your brain are running at the same time, often pulling in opposite directions, and understanding how they interact explains more about your sleep than almost anything else.
Two Processes, Not One
The framework sleep researchers actually use for this is called the two-process model, first proposed by Alexander Borbély in 1982 and still the working model in sleep medicine today (Borbély AA, Human Neurobiology, 1982 — PMID: 7185792). It names two separate, interacting systems.
Process S is your homeostatic sleep pressure. Every hour you're awake, a molecule called adenosine accumulates in your brain, particularly in a region called the basal forebrain, and it acts like a slow-building brake, gradually inhibiting the neurons that keep you alert. This isn't a metaphor. Researchers have measured it directly: adenosine levels rise progressively across a period of prolonged wakefulness and decline during recovery sleep (Porkka-Heiskanen T et al., Science, 1997 — PMID: 9157887). The longer you've been awake, the more adenosine you've built up, and the sleepier you get. This is also exactly what caffeine interrupts, by blocking the receptors that let your brain detect that adenosine, which is a different topic covered elsewhere on this blog.
Process C is your circadian alerting signal, generated by your central clock, the suprachiasmatic nucleus (SCN), sitting in your hypothalamus and synchronized primarily by light hitting your eyes. Left alone, Process S alone would mean you get steadily, linearly sleepier from the moment you wake up until the moment you sleep. That's not what actually happens, because Process C is simultaneously producing a wake-promoting signal that counteracts it, and that signal doesn't stay flat across the day. It builds through the afternoon and peaks in the early evening, before beginning to fall in the hours before your usual bedtime.
Why You Get a Second Wind at 8 PM
Put the two processes on the same timeline and the second wind stops being mysterious. By early evening, your adenosine-driven sleep pressure is high, you've been awake for 12-plus hours. But your circadian alerting signal is near its own daily peak at the exact same time, actively working against that sleep pressure. The two nearly cancel out, and you get a stretch of the evening where you feel more alert than you'd expect given how long you've been up. Then, as your circadian system transitions toward biological night, its wake-promoting signal drops off, usually faster than your sleep pressure does, and the balance tips hard toward sleep, often within an hour or two. That's the "I was wide awake at 9, and suddenly exhausted by 10:30" experience, and it's not a mood swing. It's the brake finally releasing while the accumulated pressure is still there.
The Same Framework Explains Jet Lag and "Tired But Wired"
This is also why you can be simultaneously exhausted and unable to sleep. If you've been awake 18 hours, Process S is enormous. But if your circadian clock still believes it's daytime, because you haven't shifted time zones or because your evening light exposure has delayed it, Process C is still generating a strong wake signal. Both can be true at once: profound sleep pressure and a circadian system actively working against sleep. That combination is what jet lag and shift work actually are at the mechanistic level, and it's also, less dramatically, what happens to anyone who keeps bright light on late into the evening: the light delays the circadian half of the equation while the homeostatic half keeps climbing regardless.
A related, separate hormonal signal worth naming here is cortisol. Your cortisol rhythm is also under SCN control, rising sharply in the first 30 to 60 minutes after waking, a distinct, well-studied phenomenon called the cortisol awakening response, and one that persists on its own circadian schedule even independent of when you actually got up (Bowles NP et al., Frontiers in Neuroscience, 2022, PMCID: PMC9669756). Cortisol isn't the same thing as Process C, but it's one of the downstream outputs of the same central clock, which is part of why chronic circadian misalignment, shift work being the clearest example, tends to disrupt more than just when you feel sleepy.
Why This Framework Is Actually Useful, Not Just Interesting
Once you separate these two systems, "I can't sleep" stops being one problem and becomes a diagnostic question. Is this a Process C problem, meaning your circadian timing itself is misaligned with when you're trying to sleep, which points toward morning light and consistent wake times as the fix? Or is this a Process S problem, meaning you genuinely haven't built up enough sleep pressure, often from oversleeping, napping too late, or too little daytime activity? Or is something else entirely overriding both systems, most commonly stress-driven physiological arousal, which doesn't show up cleanly in either process and needs its own approach? Most people, and most generic sleep advice, treat all of this as one undifferentiated problem called "bad sleep." It isn't one problem. It's usually one of these three, and they don't respond to the same fix.
What to Actually Do With This
Morning light exposure, ideally outdoors, within the first hour of waking is the single highest-leverage lever on Process C, because it's the strongest signal your SCN receives to anchor your circadian clock to the correct time. Consistent wake time, more than consistent bedtime, keeps that anchor stable, since your clock entrains more reliably to a fixed wake time than a fixed sleep time. Reducing bright light, especially blue-wavelength light, in the hour or two before bed protects the natural evening decline in your circadian wake signal instead of artificially propping it back up right when you need it to fall. None of this requires supplements or a prescription. It requires understanding which of the two systems you're actually working with.
If your sleep has felt inconsistent in ways that don't have an obvious explanation, understanding which signal is actually misaligned, rather than treating "poor sleep" as one generic problem, is usually the fastest way to a real fix.
Do you tend to get a second wind in the evening, or run out of steam early? That alone is a clue about which system dominates for you.
A free consultation is a good place to start that conversation, no commitment required, just a chance to look at the full picture together. To request one, email drwilcox@precisionhormoneconsulting.com.
— Darrell Wilcox, MD | @wellnessdoc_4everyoung on Instagram
References
Borbély AA. A two process model of sleep regulation. Human Neurobiology. 1982;1(3):195-204 — PMID: 7185792.
Porkka-Heiskanen T, Strecker RE, Thakkar M, Bjørkum AA, Greene RW, McCarley RW. Adenosine: a mediator of the sleep-inducing effects of prolonged wakefulness. Science. 1997;276(5316):1265-1268 — PMID: 9157887.
Bowles NP, Thosar SS, Butler MP, et al. The circadian system modulates the cortisol awakening response in humans. Frontiers in Neuroscience. 2022;16:995452 (PMID not independently confirmed this session; PMCID: PMC9669756).
This content is for educational purposes only and does not constitute medical advice. Circadian rhythm disruption can stem from many causes, and persistent sleep difficulty deserves individualized evaluation. Individual results vary, and no outcome is guaranteed. Dr. Wilcox is licensed to practice in Texas and Arizona.
