Recovery: Sleep, Hormones, and The Brain

In the context of training one of the most important things to do is recover. Recovery allows us to continue to perform in our training program, which has to happen in order to be successful with the long term or even short-term goal. Not to mention the health perspective that fits into this conversation, too much stress from training or other stimuli (life stressors) are not good.

There is a lot that is going on during and after a training session. In order to optimize the adaptations you are seeking an emphasis must be put on the recovery process. Recovery comes in many forms, but the most natural form is something we are designed to do, sleep.

There are many mechanisms of energy, from objective to subjective, and most of them are largely impacted by our recovery. This is not just the case in the exercise context. If you do not get enough rest or sleep you will feel drained, psychologically and physiologically.

First let’s take a look at how sleep is regulated. When looked at in its most basic purpose sleep is a reset for the central nervous system. That means it is regulated by mechanisms within this system to ensure that reset is taken advantage of. In fact, if an organism doesn’t get the appropriate amount it can die. This is seen in humans who have fatal familial insomnia [1]. A body of research also suggests that this applies to other organisms (rats, cockroaches, and flies) that have their sleep taken away [2]. Although it should be noted there is some evidence that indicates the pigeon can survive without sleep [3]. Even so, sleep (and recovery) is very important especially when physical goals are being sought out by stressing the body with a taxing training program.

Death may sound extreme but your body needs a time of lower stimuli to rest and reset. This is part of why if you don’t have insomnia and you go for a period of time without sleep it will take you forcing yourself to stay awake. Consider the last time you had a hard training session/competition or hit mid-day and felt like you could use a nap. Your body needs some time to recover and wants you to sleep. This is the nervous system trying to get some rest and preserve itself.

The nervous system is the monarch of the body and its main concern is surviving the external environment. One of its mechanisms of accomplishing this is sleep. Of special interest to athletic populations and those looking to improve performance, body composition, and even longevity is the relationship between the endocrine system and sleep. Basically, the question is, how do hormones fluctuate when sleep isn’t optimal?

The first hormone to look at in this context is going to be cortisol. Cortisol is the primary stress hormone, but the idea that cortisol is a bad hormone is not accurate. Cortisol’s biggest role is increasing fuel availability. It can get very high during exercise [4] to ensure the active tissues have enough energy to perform the work you are doing, but when you are resting this would not be a good situation. Simply put, cortisol facilitates the breakdown of fat and protein into smaller molecules that can be used for fuel. While we need cortisol to survive and it is a normal part of our physiology, to optimize the training process it is best to reduce cortisol spikes when it is not needed.

After waking there is a dramatic increase in cortisol. This is known as the cortisol awakening response and the highest point resting cortisol will reach. After the awakening response cortisol levels will slowly go down. However, when sleep is restricted and not as much rest is achieved cortisol levels will stay high for longer than someone who sleeps a full night [5]. Poor sleep quality also causes increases in elevated nighttime cortisol levels [6]. So, your sleep quality impacts the cortisol release while you are awake and while you are asleep.

The next hormone to look at is testosterone. Testosterone and cortisol live in somewhat of a balance, because cortisol is the primary catabolic steroid and testosterone is the primary anabolic steroid. Usually when one is high the other is low, but that is not always the case. With that said, sleep deprivation has a similar impact on testosterone. When waking levels of testosterone are compared between males who are sleep deprived and those who are not, the sleep deprived have lower testosterone [7] and males who are sleep deprived have a lower reactive aggression response [8]. In data that includes both males and females, in the context of sleep deprivation, before sleep deprivation all participants had higher levels of testosterone [9]. Negatively impacting testosterone dynamics may be of more concern for females than males, however any negative change in either sex is the opposite of what any person should desire in the context of training recovery, health and functionality, or longevity.

Unfortunately, there has not been a lot of research on sleep quality/quantity and the effect on female androgens. Most of the literature looks at the opposite and how the estrogens influence sleep cycle and REM sleep. That means that we have to use the male data and extrapolate for females, it is not ideal but it would make sense that increasing stress on the body via not having ideal sleep would cause a negative change in the primary female androgens (estradiol and progesterone).

The next and final set of hormones that we are going to investigate are GH and IGF-1 (growth hormone and insulin-like growth factor-1). Outside of the context of training (normal function and maintenance of body tissues) these are very important as they have roles in maintaining functional tissues of the body. But they become even more important in the context of exercise and training. The role of GH is contrary to what it sounds it is. While GH, IGF-1, and the androgens have roles in growth during and before puberty, after puberty the role of GH becomes maintaining existing structures. As our body’s age they inherently become less capable at doing their jobs. This comes in many forms, the one I want to focus on in this moment is the building and maintaining of new tissues. After a certain point GH is only there to slow down the natural loss of tissues. Take, for example, bone density, all persons begin to lose bone minerals after about mid-way through the third decade of life. Growth Hormone is one of the mechanisms the body uses to slow down the loss, it is important to consider that GH acts systemically, not just on muscle tissue. So, the question becomes, how does sleep quality impact GH dynamics?

The broad answer to that question is that poor quality of sleep causes negative changes in GH dynamics. Growth Hormone is released by the control center of the body, and in this case the control center of the endocrine system, the hypothalamus and pituitary located in the brain. One of the most significant stimuli for GH release is sleep, and sleep deprivation is known to almost completely remove the release of GH and IGF-1 in a rat model [10]. Although in humans it appears that this is not the case.

When men are sleep deprived the sleep-related GH response is lower. However, this is compensated for by random GH release throughout waking time so that there is no significant difference between sleep deprived and normal sleep when looked at in totality [11]. It should also be noted that exercise stimulates the release of GH. This is evidenced in an investigation that found men who were put through 24 hours of sleep deprivation had a higher GH response to exercise than those who were not deprived of sleep [12]. This can be thought of as a way to ensure enough total GH is released throughout the full 24-hour period. This does not discount the other negative hormonal consequences of poor sleep quality or take into consideration the need for the full spectrum of anabolic stimuli to mediate optimal recovery.

IGF-1 is released as part of the anabolic response and is needed in normal function like all the other hormones that have been highlighted so far. IGF-1 is just one of the growth factors involved in this process but a very important one to consider when it comes to recovery. The significance of IGF-1 does not just come in the form of anabolism, data suggests that IGF-1 actually plays a role in combating inflammation [13]. With exercise being inherently inflammatory IGF-1 seems to play two important roles in recovering from exercise training. With that said we need to evaluate the relationship that sleep has on our body’s ability to produce/release this hormone. The findings on this question are similar to those on GH and the others we have looked into, sleep deprivation inhibits the release of IGF-1 [14]. While we can’t dive too deep into why this is not a good thing it should be understood that IGF-1 (along with testosterone and GH) has a significant synergistic role in anabolic pathway stimulation.

It is obvious that poor sleep quality is detrimental to hormonal dynamics and anyone who is trying to optimize training adaptations should prioritize their sleep. We are basing this proclamation simply on what we have looked at so far, but we still need to consider what sleep is doing for the monarch of the human body. Sleep is a reset for the nervous system and everything else is merely a product of that.

The cognitive benefits of sleep, alone, speak volumes of why it is of utmost importance to get enough sleep-in normal function. In that regard lets evaluate the decrements that occur when sleep is limited or taken away.

A risk factor of developing Alzheimer’s Disease is the accumulation the peptide Amyloid-β (Amyloid-Beta) as a plaque instead of being soluble in the cerebrospinal fluid. Alzheimer’s has a close relationship to poor quality sleep. Twenty-five to forty percent of adults who develop Alzheimer’s often have nighttime insomnia, sleep a lot during the day, and are agitated by sunlight. The severity of these symptoms correlates with the severity of the condition [15]. The detection of Amyloid-Beta plaque is a preclinical marker for the diagnosis of Alzheimer’s. There seems to be a feedback system where poor-quality sleep has a relationship with its accumulation and the accumulation causes poor quality of sleep. This is seen where unrestricted sleep causes a decrease in Amyloid-Beta but sleep deprivation counteracts this decrease [16] and where individuals with this preclinical measure of Alzheimer’s have poorer quality sleep compared to their normal peers [17].

While it is commonly accepted that developing this disease has other risk factors like genetics and environmental elements outside of sleep quality it is imperative that we see what poor sleep quality can lead to in the scope of pathology to give us an understanding of the other side, optimization. Amyloid-Beta is a normal cerebrospinal fluid constituent, the plaque is the abnormality. The body keeps plaque from forming by cleaning out the Amyloid-Beta that accumulates during times of wakefulness during the sleep cycle. We see this in the previously mentioned research that observed a decrease in cerebrospinal fluid Amyloid-Beta in participants with unrestricted sleep but no decrease in those that were sleep deprived in a 24hour period [16]. The cardiovascular system uses what are called lymph vessels to clean up and move any fluid that is left in the tissue spaces back into systemic circulation. It seems that there is some clean up occurring in the cerebrospinal fluid compartments in the brain during sleep.

In closing, sleep is a very important part of the recovery process and while there are other parts of that sleep impacts the two most important systems of the body, the endocrine and nervous systems. These two act to control the body; you can think of the nervous system as the short-term control system and the endocrine as the long-term control system. In this construct the nervous system mediates muscle contraction and the endocrine system mediates how the body recovers from that contraction. There are situations where this does not fit, but in any case, they work in unison to accomplish the common goal of controlling how the body can respond to stimuli. Providing enough rest and recovery in the form of sleep allows these two systems to operate optimally.

In the presence of a taxing training session or program these systems are put under a lot of pressure which makes the need for sleep higher priority. The accumulation of fatigue is something that has to be factored in. We can think about fatigue coming in physical and cognitive forms. Challenging training seems to throw both of these at you at once. As you train day after day the stimuli stress the body and the physical and cognitive fatigue add up. Feeling tired is a normal occurrence for anyone but when pushing the limit feeling tired requires more attention. This is the sign that the body wants and needs rest. It is common for training individuals to ignore these perceptions and chalk it up to not having consumed enough caffeine. But, it is that ever important biofeedback your body is proving and its way of telling you to sleep or at minimum to back of the intensity so it has time to adapt.

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Sleep is a behavior like anything we as humans do, it is optimized when we treat is as such. The following are some recommendations for creating more optimal sleep:

1. Do not consume pre-workout or anything with stimulants after 2PM.

2. Set your phone so that you are not exposed to blue light 1 hour before you want to go to bed and shut your black out curtains at this time (this means TV, laptop, etc.).

3. Set an alarm on your phone that alerts you to begin your nightly routine (30 to 60 minutes before you want to go to bed).

4. Plan to go to sleep the same time each night.

5. Reduce your alcohol consumption (alcohol has a negative effect on sleep-wake cycle [18]).

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References

1. Montagna, P. And Lugareis, E. (2002). "Agrypnia Excitata: a generalized overactivity syndrome and a concept in the neurophysiology of sleep." Clin Neurophysiol 113(4): 552-60.

2. Cirelli, Chiara, and Tononi, Giulio. "Is Sleep Essential?" PLoS Biology. 6.8 (2008): E216.

3. Newman, S.M., et al. (2008). “Sleep deprivation in the pigeon using the Disk-Over-Water method.” Physiol Behav 93(1-2): 50-8

4. Popovic, B. et al. (2019). Acute Response to Endurance Exercise Stress: Focus on Catabolic/anabolic Interplay Between Cortisol, Testosterone, and Sex Hormone Binding Globulin in Professional Athletes. Journal of medical biochemistry, 38(1), 6–12.

5. Guyon, A., et al. (2014). “Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men”. The Journal of clinical endocrinology and metabolism, 99(8), 2861–2868.

6. Schüssler, P., et al. (2006). “Nocturnal ghrelin, ACTH, GH and cortisol secretion after sleep deprivation in humans”. Psychoneuroendocrinology, 31(8), 915-923.

7. Wittert, G. (2014). “The relationship between sleep disorders and testosterone”. Current Opinion in Endocrinology & Diabetes and Obesity, 21(3), 239–243.

8. Cote, K.A., et al. (2013). “Sleep deprivation lowers reactive aggression and testosterone in men”. Biol Psychol, 92(2):249-56.

9. Baumgartner, A., et al. (1990). Neuroendocrinological investigations during sleep deprivation in depression I. Early morning levels of thyrotropin, TH, cortisol, prolactin, LH, FSH, estradiol, and testosterone. Biological Psychiatry, 28(7), 556–568.

10. Everson C. A., Crowley W. R. (2004). Reductions in circulating anabolic hormones induced by sustained sleep deprivation rats. Am. J. Physiol. Endocrinol. Metab.; 286:1060-1070.

11. Brandenberger, G., & Weibel, L. (2004). The 24-h growth hormone rhythm in men: sleep and circadian influences questioned. Journal of Sleep Research, 13(3), 251–255.

12. Ritsche, K., Nindl, B. C., & Wideman, L. (2014). Exercise-Induced growth hormone during acute sleep deprivation. Physiological reports, 2(10), e12166.

13. Lee W. J. (2011). IGF-I Exerts an Anti-inflammatory Effect on Skeletal Muscle Cells through Down-regulation of TLR4 Signaling. Immune network, 11(4), 223–226.

14. Chennaoui M., et al. (2014). Effect of acute sleep deprivation and recovery on Insulin-like Growth Factor-I responses and inflammatory gene expression in healthy men. Eur. Cytokine Netw, 25(3): 52-7.

15. Morgan, M., et al. (2005). Sleep disturbance in mild to moderate Alzheimer’s disease. Sleep Medicine, 6(4), 347–352.

16. Ooms, S., et al. (2014). Effect of 1 Night of Total Sleep Deprivation on Cerebrospinal Fluid β-Amyloid 42 in Healthy Middle-Aged Men. JAMA Neurology, 71(8), 971.

17. Ju, Y.-E. S., et al. (2013). Sleep Quality and Preclinical Alzheimer Disease. JAMA Neurology, 70(5), 587.

18. Thakkar, M. M., Sharma, R., & Sahota, P. (2015). Alcohol disrupts sleep homeostasis. Alcohol, 49(4), 299–310.