In the attempt to understand my sleep and fatigue problems, I have been reviewing the available scientific literature. Years ago, when I engaged in aerobic running, it was understood that fatigue was a consequence of the build up of lactic acid in the muscle and the depletion of muscle glycogen. This resulted in the sense of fatigue.
Contemporary science appears to distinguish between this form of muscle fatigue and what is known as “central fatigue,” fatigue which originates within the brain rather than within the muscle. The neurobiological effects of physical exercise are described in this Wikipedia entry.
Current research on central fatigue suggests an interaction between neurotransmitters having impact on fatigue:
However, it is important to note that brain function is not determined by a single neurotransmitter system and the interaction between brain serotonin and dopamine during prolonged exercise has also been explored as having a regulative role in the development of fatigue.
Matsui, T., Soya, S., Okamoto, M., Ichitani, Y., Kawanaka, K., and Soya, H. (2011). Brain glycogen decreases during prolonged exercise. J. Physiol. 589, 3383–3393. doi: 10.1113/jphysiol.2010.203570
It has been established that muscle increases its glycogen content in response to a training stimulus, and it appears that this also occurs within the brain. More recently this was confirmed with the observation that basal glycogen levels in the cortex and hippocampus increase with 4 weeks of exercise training (Matsui et al., 2012).
Walk Therapy – Phase One – Strolling
Walk therapy has been undertaken in different phases and each phase as been of improved benefit. The first phase (August to November 2012, most of 2013) concerns walk therapy conducted at Dr H’s behest in the period immediately following diagnosis of mTBI. This took the form of regular prolonged walks (2 to 3 hours duration) but there was no means of obtaining performance feedback. This activity would best be described as “strolling,” with questionable aerobic benefit. There was no noted impact on cognitive performance. I did experience regular severe headaches while walking. I have not had similar headaches since this first period.
Walk Therapy – Phase Two – Smartphone Moderated Speed Walking
The second phase (June to December 2014) concerns walk therapy conducted after I obtained a smart phone and an app that records distance, pace, and calories burned. With this feedback I immediately upped my performance goals and commenced what might best be described as speed walking, attempting to beat my prior record on a known circuit. I also commenced to eat “brain friendly” food items prior to walking in the belief this might assist in promoting neurogenesis. During this phase I did notice changes in cognitive behaviour. I felt that I was more focused and targeted, there was an improvement in mood and self esteem. I also found that I began to surface some degree of anger in regard to my treatment by the medical establishment in Québec. I did not experience headaches.
Walk Therapy – Phase Three – Endurance Walking and High Aerobic Demand
This third phase commenced in April 2015. I first needed to rebuild muscle tone following the winter fallow period. After building a base of slow, long distance endurance walks, I increased the aerobic effect by including hill climbs of approximately 60 feet up a rugged cliff face. Even though I had established a solid fitness baseline, the first hill climb left me breathless and in need of three or four minutes of stationary recovery. Six months later I am able to make multiple repetitions of the same climb with no noticeable ill effect, and no need for a stationary recovery period.
I have also noted a concurrent improvement in cognitive functioning. There has been a significant improvement in mood. Events that previously served as depressive triggers were now handled with aplomb. I appear better able to engage in conceptual thought and believe there has been a general overall improvement in cognitive health.
My present chief concern is fatigue and sleep disruption. During the Work Experiment I experienced an intraday decline in performance while also noting a gradual performance decline over the five day period of the experiment. These declines occurred despite adequate sleep and nutrition.
. . . but it is interesting from an applied perspective that brain glycogen may accumulate very slowly with sleep, perhaps taking up to 9 h to restore to baseline levels after a period of sleep deprivation. Brain glycogen may not be the only concern following sleep deprivation as recently it has been observed that sleep plays an important role in cleansing the brain of neurotoxic waste
I have two hypotheses to explain these effects.
Hypothesis Number One – Glycogen Store Depletion
The first hypothesis concerns the decline in performance over the period of the experiment. I was sleeping almost 9 hours a night. This should have been sufficient sleep to restore brain glycogen. The day following the end of the experiment I experienced the need to sleep for an additional six hours during the day (I normally find it very difficult to sleep during the day). I believe that some aspect of my injury impairs my capacity to perform normal replenishment of brain glycogen supplies. Even though I was getting sufficient sleep for a “normal person” to make full recovery, my injury inhibited the ability of my brain to bring brain glycogen back to baseline levels. Over the course of the Work Experiment I continued to deplete glycogen stores to the point that each day I experienced the earlier onset of fatigue symptoms and an increased degree of cognitive impairment.
Hypothesis Number Two – Increased Glycogen Usage Rate
The second hypothesis concerns intraday performance. There was a noted decline in performance over the course of a single shift. This was true of each day. My hunch is that the damaged brain seeks to compensate for cognitive impairment by burning glycogen at an increased rate. A task that a normal person might be able to execute over an eight hour period before experiencing fatigue can only be executed by me over a four hour period before I begin to experience both fatigue and increased cognitive impairment. My belief is that I am consuming brain glycogen at an increased rate in an attempt to compensate for some impairment in brain function. This increased “burn rate” results in my only being able to complete a half day 4 hour shift as opposed to a normal full day 8 hour shift. The increased “burn rate” also results in earlier fatigue onset and increased cognitive dysfunction.
—————————————
Update – Hypothesis Number Three – Energy Theory
Reviewing the foregoing, I realize I have made an unstated assumption. The literature on brain injury appears to focus on physical damage to brain matter, or the tearing and separation of brain cells. Some current research examines microscopic (< 10 µ) damage. I am basing my hypothesis not on physical damage but on an inability of the brain to properly distribute the energetic stores required for proper brain function. This is believed to be due to an electro-chemical change in a single protein. But the reader needs to be aware that I have an energy industry background and therefore interpret most significant events in terms of their energy component.