There has been growing interest within the physique and elite training community of the role of circadian rhythms and periodicity in such key areas as sleep, rest and recovery, the stress response system, feeding behavior, and also in conceptualizations of psychoneuroendocrinological models of adaptation and regulation during drastic body recomposition efforts. This article, a fourth in my developmental regulatory series, will attempt to outline the basic properties of the timing mechanisms within the hypothalamus and the periphery, and to link what we know about the properties of this timing system with observed training phenomena and symptomatology. In addition, it will attempt to articulate how to better design and integrate training and nutritional programs (e.g., ‘cut’ programs and ‘bulk’ programs) around them. This article should be considered a modestly detailed overview of the timing system and its implications. Much more detail is provided in the citations as well as a plethora of related academic literature on the topic.
The main timing system for circadian rhythms is located in the suprachiasmatic nucleus (SCN) of the hypothalamus. This nucleus is located superior to the optic chiasm, hence [supra] chiasmatic. Within this nucleus are a range of neurons with different histochemical and functional properties, some of which are co-localized with each other. A primary group of neurons however, are photosensitive via direct retinal projections. These photosensitive neurons have widespread connections to other areas of the hypothalamus, which have been implicated in other bodily mechanisms, most notably (for considerations discussed here) eating, stress-system functioning, and reproductive behaviors. Of these projections, the majority project to the subparaventricular zone (SPZ) and the dorsomedial nucleus (DMN) of the hypothalamus (Saper et al., 2005).
Neurons within both the SPZ and the DMN are necessary for subsequently orchestrating the circadian rhythms of body temperature, sleep, waking, feeding, and corticosteroid production (Saper et al., 2005). SCN neurons can both make direct synaptic connections with neurosecretory neurons or SCN neuronal signals may set the phase of ‘clock genes’ that regulate circadian function at the level of the neurosecretory cell (Kriegsfeld & Silver, 2006). These same SCN signals may also act in an endocrine fashion enabling the establishment of circadian timing in peripheral organs. Circadian proteins include CLOCK and BMAL1 which drive the transcription of the Per (period) and Cry genes (Per1-3, Cry1-2). Tim (Timeless) is an additional related clock gene.
Of the hypothalamic nuclei mentioned above, recent studies have shown that the DMN and the subparaventricular zone are the nuclei most responsible for organizing the circadian rhythms that are arguably most impacted by elite training and/or body recomposition efforts (e.g., hunger/appetite, sleep, stress system regulation). Saper et al., (2005) sum up the role of the DMN in the following manner:
Training and nutrition for the elite athlete, as well as other variables within their lifestyle (e.g., supplementation usage) tend to be highly controlled variables by the individual (personal observations). They are typically temporally coordinated and this temporal coordination subsequently affects both the establishment and maintenance of circadian patterns that are non-normative or not necessarily in-train with photic input (i.e., the light cycle). Feeding schedules and time of training are examples highly individual variables and as such, facilitate different circadian profiles for different individuals. It can be argued that a key goal for the elite athlete is to maximize the establishment and most importantly the consistency of these circadian patterns so that they may be considered adaptive by the individual in his or her state of evolutionary adaptiveness (i.e., the particular training phase and environment in which one is engaged).
As an illustration of the above, I have personally shifted my largest meal to the pre-bedtime hour after long-bouts of sleepless nights due to prolonged cutting (dieting) at low digit body-fat levels so as to avoid the nighttime hunger and associated vigilant behaviors which often lead to less than desired appetitive behavior (e.g., bingeing). My own observations suggest that my endocrine/metabolic-energetic system has adapted well to this shift, with reduced night struggles and improved sleep quality as well as subsequent delays in food anticipatory activity (FAA) during the day during times of prolonged dieting. This might suggest (albeit somewhat evangelically) that an approach such as this is able to downregulate the expression of the Per2 gene, which has been shown to be a critical driver of food anticipatory activity in mice (Feillet et al., 2006). Breakfast is unknown in my nutritional scheme, which is oriented to the consistent preservation of the lean state. By eating a pre-bed meal of 1260 calories (on a daily average intake of approximately 2318), I am able to replenish my system before the normative circadian pulses of anabolic hormone secretion during sleep. Further, I speculate that due to my optimal insulin sensitivity (particularly at lowered adipostatic states) that by waking time, my own metabolic milieu is primed for optimal adipose partitioning at the expense of skeletal muscle as well as an amphibolic physiological milieu.
Other circadian patterns, particularly that of the HPA axis, are important to consider for the elite athlete who needs to be aware of the catabolic, over-trained condition. While there are individual patterns in the functioning of the HPA axis, it is generally agreed that there is a morning peak in the final common outcome (i.e., cortisol release) with subsequent decline throughout the day. However, given various stressors this ‘normative’ HPA circadian pattern can and has been shown to become disrupted. A stressor that may advance the diurnal pattern of cortisol secretion is intense training including a resistance or endurance component or a hybrid of the two. This most probably is at least one explanation for the intense night sweating and other cortisol-mediated effects that are commonly experienced by elite athletes training at extremely lean adipostatic states.
A recent observation of mine with respect to the above, is that there is a threshold of HIIT-based cardio activity that one can do before he or she will advance the diurnal cortisol rhythm. Such phase advancing of the HPA axis, I have observed, appears to be associated with such negative sequela as sleep difficulty, anxiousness, fatigue, and increased appetite sensitivity (i.e., the degree to which appetite can be cognitively restrained). By modifying the cardio component of my evening training to be more aerobic-based one by nature, my sleep and ability to diet successfully to extremely lean states with minimal physiological and psychological maladaptation has greatly improved.
This article argues that knowledge of circadian rhythms is an important consideration with respect to optimal training times, eating schedules, recovery protocols, and more advanced considerations such as the role of supplementation and drug interactions on various metabolic parameters. However, it is prudent for each individual to consider their ‘control’ circadian state with respect to their current environment and how modifications such as the ‘phase-shifting’ procedure(s) describe herein will work for them. However, notwithstanding, I will offer that consideration of both a large pre-bed meal and reduction of HIIT-based cardio during the later stages of dieting are both wise considerations to avoid circadian involved disruption of optimal endocrine functioning. This would also apply to the novice dieter or physique competitor who is unaware of the stress that awaits them at their later stages of (contest) preparation.
The practice of ‘night-training’ is called into question by the available evidence. However, the key question is whether the body adapts to this new circadian pattern. The evidence suggests that the capability to re-regulate around new timing patterns is in fact possible. This would make evolutionary sense. However, it must be considered whether the environmental variables are in place to maximize this phase shift (e.g., appropriate recovery, mental discipline, cognitive ability and functioning). This leads us back to the idea of reprogramming of set-points and adaptation-regulation. If a circadian pattern can be adaptively re-regulated, albeit with much greater ease than the adipostat, then more advanced recomposition possibilities may well be within reach.
1. Feillet, C. A., Ripperger, J. A., Magnone, M. C., Dulloo, A., Albrecht, U., & Challet, E. (2006). Lack of food anticipation in per2 mutant mice. Current Biology, 16,2016-2022.
2. Gooley, J. J., Schomer, A., & Saper, C. B. (2006). The dorsomedial nucleus is critical for the expression of food-entrainable circadian rhythms. Nature Neuroscience, 9, 398-407.
3. Kriegsfeld, L. J., & Silver, R. (2006). The regulation of neuroendocrine functioning: Timing is everything. Hormones and Behavior, 49, 557-574.
4. Saper, C. B., Lu, J., Chous, T. C., & Gooley, J. (2005). The hypothalamic integrator for circadian rhythms. Trends in Neuroscience, 28, 152-157.