Travelling to Compete: How to Shift Your Circadian Clocks And Lift at Your Best When Travelling Across Time Zones
By: Thomas Kaminski
With the IPF World Classic Powerlifting Championships approaching, I thought it would be useful to write an article explaining how the human circadian systems work and how athletes can adjust their body clocks to the new time zone so that they can lift at their best. Ensuring that your body clock is adjusted for the time of the competition is essential for performing optimally. This is because athletic performance can vary greatly depending on your internal circadian time (Teo et al., 2011; Dijk, 1992). Contrary to the opinions of some, your muscles will not work optimally by simply setting an early alarm and just giving them some time to ‘wake up’ before the competition. The fact is, if they are at a point in their circadian cycle where they are not meant to be working, then they simply cannot work at their maximum capacity. To illustrate this point, when you have jet lag induced insomnia the reason you can’t sleep is because your circadian system is telling your brain that it is not time to sleep, and just as trying harder to sleep cannot fix this problem, trying to get your muscles working when they aren’t supposed to be isn’t going to work either! For this reason, it is extremely important to adjust your circadian clock so that your body is ready for the competition.
In this article, I give a brief overview of some of the relevant human circadian systems and how both light and melatonin can be manipulated to help to adjust your circadian clock. After this, I discuss travelling to a time zone that is behind yours, as well as provide a protocol for travelling to a time zone that is ahead of your own.
Introduction to human circadian rhythms:
A circadian rhythm is defined as an internally generated rhythm that lasts about a day and persists in the absence of environmental stimuli. Most of our bodies systems are regulated in a circadian manner, including sleep, cognitive performance, and metabolism (Beersma et al., 2007; Mishima, 2016; Dijk, 1992). The human circadian rhythm is roughly 24.4 hours long, despite us living on a planet whose days are 24 hours in length (Burgess and Eastman, 2008). Therefore, when isolated from the environment, such as in a bunker, we display a sleep-wake cycle that lasts longer than a day and quickly become out of phase with the outside environment. This additional 0.4 hours, provides us with flexibility in our circadian cycle that enables us to adjust more easily to changes in the environmental light cycle. However, this also means that our circadian rhythm must be advanced every day to maintain synchrony with the 24-hour day (Wever, 1979; R.L. Sack et al., 2000). The stimuli that cause the advance or delay of the circadian rhythms are called zeitgebers (German for time givers). The most powerful zeitgeber is light, specifically high-intensity blue light, as seen in the sunlight photo-spectrum (Dai et al., 2017). When you wake up in the morning the exposure to light causes a specialised part of your brain called the suprachiasmatic nuclei (SCN or colloquially referred to as the master clock) to shift the timing of your circadian rhythm and bring you into synch with the environment (Gooley et al., 2001; Chen et al., 2012). Essentially, the sunlight in the morning tells your body, ‘wake up, it’s daytime’ and starts preparing all the systems you need working for that day ahead of schedule. Similarly, at night-time, if you are exposed to light when it should be dark, the light delays your circadian phase as your SCN thinks it is still day time and you shouldn’t be preparing for sleep. However, your body can only advance or delay your circadian phase so much in one day. This is why it takes multiple days to accommodate to new time zones when travelling aboard.
When we are travelling abroad to compete we can use these zeitgebers to manipulate our circadian phase and shift our body clock to be ready to compete at our best in the new time zone. The primary method of doing this is through manipulating light exposure, but I also recommend the adjunct use of supplemental melatonin to aid in this process (T.M. Burke et al., 2013). Because I cannot give a protocol for every possible situation, first I am going to give a basic overview of light and melatonin’s functions as zeitgebers, so that you can understand the science and utilise this information for your specific circumstance.
Light as a zeitgeber and the light phase response curve:
As previously mentioned, light input at different times of the day, or more specifically times relative to your circadian phase, can shift your circadian clock in different directions and to varying degrees. This has been investigated and from the research, something called a light phase response curve has been created, as shown below. The term ‘phase response’, simply means how much does the stimulus shift your clock and in what direction does the shift occur.
|Figure 1: Light Phase Response Curve|
|Figure 1 has been altered and adapted from Burgess et al., 2002. Figure 1 shows a light phase response curve. On the x-axis is phase shift (relative magnitude in time), on the y-axis is time measured as both clock time and time relative to usual sleep onset. The black block denotes normal sleeping time, with the onset of sleep at the start of the block at 23:00 clock time and 0 hours from usual sleep onset time. The total length of sleep is 8 hours.|
Phase response graphs have the magnitude of the phase shift on the x-axis, and chronological time on the y-axis, measured as either clock time or time relative to a circadian phase marker. As you can see, light from 10 pm to 4 am delays your circadian phase, with the maximal effect occurring at 4 am. Whereas light from 5 am to 10 am advances the cycle, with peak effect being seen at 5 am. The quick-witted may have noticed that due to the fact circadian rhythms are internally generated, clock times may not be an accurate method for determining what the timing of a stimulus should be. This is why in the literature typically the timing of zeitgeber input is recorded as the time relative to either dim light melatonin onset, peak plasma melatonin concentration or body temperature minimum. Because we will also be needing to manipulate the timing of zeitgebers relative to our own circadian phase, we will be using sleep onset as our circadian phase marker. Relative to sleep onset, light exposure delays the circadian phase between 2 hours prior and 4 hours after sleep onset, whereas it advances the clock between 5-11 hours after onset of sleep. Peak responses occur at 4 hours and 5 hours after onset of sleep respectively. Sleep onset is a less accurate marker but it should be accurate enough for most individuals. Due to the fact that the time of sleep onset is fairly variable, it will be useful for athletes to attempt to build consistency in their sleep timing prior to the intervention.
Other than the timing of the light exposure, the type of light input is also important to generate a phase shift. The particular photoreceptors primarily responsible for signalling to the SCN are receptive to blue light of 480nm wavelength (Thapan et al., 2001). This wavelength of light is found at high intensities in sunlight and is also emitted by electronic devices, such as mobile phones, computer monitors, etc. However, most importantly the light input must be at a high intensity, as lower light intensities produce much smaller responses (Dai et al., 2017; Hilaire et al., 2012; Khalsa et al., 2003). Therefore, if you want to induce a phase shift, you must subject yourself to high-intensity light, preferably sunlight. But in the absence of available sunlight, turning all the lights on in your house will make do. A counterpoint to this is that if you want to prevent a phase shift from occurring which contradicts the direction you want to shift your circadian rhythm, you must avoid light input during those opposing times. If you simply cannot remove light input at those times you could use glasses with an orange tint in the lenses, which will block blue light and decrease the amplitude of the undesirable phase shift. In a similar vein, you can install apps onto your mobile phones and laptops that reduce the amount of blue light emitted by the screen.
Melatonin as a zeitgeber and the melatonin response curve:
Melatonin is a hormone secreted by the pineal gland, despite commonly being described as such, melatonin is not a sleep hormone, although it does promote sleep in humans. Instead, melatonin is a night hormone. It is secreted in a circadian fashion and its secretion is rapidly suppressed by light exposure (Thapan et al. 2001). Due to this, in essence, melatonin tells your body that is it night time. Melatonin can act as a zeitgeber, although the magnitude of its effect is less than that of light. Its secretion occurs in the late evening but only when light levels are low enough to not cause its suppression. Melatonin can help synchronise your circadian rhythm with the environment, by its secretion either being or not being suppressed in the morning or evening by the presence of sufficient levels of environmental light. In the absence of light in the evening, melatonin will cause a small phase advancing effect upon its secretion, which starts roughly 2 hours prior to sleep onset. Similarly, if there is no light in the morning melatonin will not be suppressed and will continue to elicit a delaying effect on your circadian clock until its secretion has ceased (Lewy., 2003).
|Figure 2: Melatonin Phase Response Curve|
|Figure 2 has been altered and adapted from Burgess et al., 2002. Figure 2 shows a melatonin phase response curve. On the x-axis is phase shift (relative magnitude in time), on the y-axis is time measured as both clock time and time relative to usual sleep onset. The grey block denotes normal sleeping time, with the onset of sleep at the start of the block at 23:00 clock time and 0 hours from usual sleep onset time. The total length of sleep is 8 hours.|
As seen in the melatonin phase-response curve, between 10 hours prior and 2 hours after sleep onset, melatonin causes a phase advancing effect, and from 2-12 hours after sleep onset, it causes a phase delaying effect. Peak effects occur at 5-6 hours before and 5 hours after sleep onset respectively. Due to melatonin’s ability to induce a phase advance during the hours prior to sleep onset, melatonin supplementation can be a useful aid when travelling to a time zone that is ahead of an athlete’s current location. Melatonin is easily attainable from supplement stores in the USA and online in other countries. There seem to be no reported toxic effects from its intermittent use at moderate doses and unlike almost all other hormones there does not seem to be any negative feedback loop by which exogenous supplementation results in the suppression of endogenous sources (A.J. Lewy, 2003). As I understand, melatonin supplementation is not restricted by WADA, as last checked on 31/05/2017 (http://www.globaldro.com/UK/search/input?pls=true). A specific protocol will be described later, but it may be important to note that some studies on blind free-running individuals have shown that 10mg supplementation of melatonin did not result in entrainment of all subjects, whereas 0.5mg has (Hack et al., 2003; Lewy, 2003; Burgess et al., 2010; Sack et al., 2000). Entrainment means the alignment of the subject’s circadian rhythms to the regularly timed doses of the melatonin. This is likely due to the 10mg dose resulting in the extended elevation of the concentration of plasma melatonin. It is conceivable that this resulted in the hormone being present in both delaying and advancing periods of the melatonin response curve. Whereas it seems that a 0.5mg dose does not persist in the blood for as long, and thereby caused a shorter lived but non-contradictory phase-shifting stimuli. Due to these contradictions in the literature, I recommend using 0.5mg of melatonin for most athletes and up to 1mg of melatonin for larger athletes, as these doses have reliably resulted in entrainment. This potential dose-dependent effect of melatonin supplementation is also important to note for those using it as a sleeping aid, as a larger dose of melatonin immediately prior to sleep may result in a large phase delaying effect between 2-12 hours after sleep onset. This would likely result in being more tired the next morning, despite having had a good night sleep. It seems with melatonin small well-timed doses are the best.
Travelling to a time zone behind yours:
When travelling to a time zone behind your current location, achieving entrainment to the new light cycle will typically be less difficult than travelling forwards in time. This is because you get a head start due to the 24.4-hour period length of the human circadian rhythm. Further, when travelling backwards in time, it is typically not required to fully adjust your circadian rhythm. This is because even with an unadjusted rhythm it is likely that the competition will be at a time in your circadian cycle where your body is fully ‘awake’ and ready to compete. To explain this, I will use an example of an athlete travelling from London to Florida to compete.
Example: Athlete travelling from London to Florida (-5 hours); weigh-in 8 am and lift off at 10 am local time.
The athlete flies from London to Florida, whose time zone is five hours behind, and arrives two nights prior to the competition. They arrive at 5 pm local time (10 pm London time), get to the hotel eat and go to sleep at 8 pm local time (1 am). During the travel to the hotel and at dinner the athlete will be getting exposed to light resulting in a phase delaying effect. After a long flight, the athlete will likely have an extended sleep lasting 9 hours and wake up 5 am local time (9 am). When waking up before the sun has risen it is important to limit light exposure as this will result in a phase advancing effect which is not desirable when travelling backwards in time. When light exposure is limited upon waking, endogenous melatonin will not be suppressed and will work to delay their circadian phase. Due to the combined phase delaying effect of light in the evening and endogenous melatonin in the morning, it is likely the athlete will have phase advanced roughly 1 hour. The day before the competition the athlete will rest and go to bed typically 1-2 hours after they would have in London, at roughly 10 pm local time. After an 8-hour sleep, they wake up at 6 am and have 4 hours to get ready before the competition. From this we can assume about a 2-hour phase delay in their circadian clock, meaning that competing at 10 am local time would be the equivalent of competing at 1 pm London or circadian time. I don’t think anyone would feel that competing at a time equivalent to 1 pm is not desirable.
The above example shows that without any intervention an athlete would easily be competing at an optimal capacity when travelling to a time zone that is 5-hours behind. Even at an 8-hour difference, this would equate to competing at 4 pm circadian time. Therefore, when travelling backwards 5-8 hours the primary concern is to limit light exposure in the morning until the sun has risen. However, things become a bit more difficult when you are travelling somewhere with more than 8-hour difference. If your work schedule allows, you could attempt to partially pre-shift your circadian rhythm prior to travelling. This would be done by increasing light exposure at night during your normal sleep onset time and pushing sleep back no more than an hour a day. In the morning, you would want to limit exposure to light to prevent any phase advancing effect. Although, when the time difference is greater than 8-hours I would recommend arriving three days prior to the competition and attempt to shift your circadian clock 1-2 hours prior to travelling.
Travelling to a time zone ahead of yours.
Not only is adjusting to a time zone ahead of your own much more difficult than adjusting to a time zone behind, but further competing unadjusted will very likely have a profound negative effect on your performance. Even competing 2 hours ahead of your circadian time could mean that you would be lifting at a time when normally you would still be asleep and when your ability to perform is greatly diminished. It has been said that American lifters do not perform as well abroad as they do when they are competing on their home turf. This should be of no surprise as American lifters travelling to Europe to compete will be subject to at least a +5-hour difference between time zones. With this larger time difference, it will be difficult for athletes to fully adjust to the new time zone and therefore the competition will often be at a time when their body is still ‘asleep’. Due to this, it is vital when travelling to a time zone ahead of yours that you do everything that you possibly can to fully adjust to the local time.
When shifting your circadian clock forwards, it is roughly accepted that you can adjust about an hour a day under normal circumstances. However, it may be possible to achieve more than this if you fully exploit all possible zeitgebers to maximise their combined effect. I have developed a simple protocol to follow when travelling to a time zone ahead of your own. This protocol has been broken into three phases as described below. In addition, I have provided an actogram (figure 3) that gives a visual representation of the changes in zeitgeber timings as well as the expected phase shifting that will occur throughout the protocol that is represented by the time of sleep onset (blue) and active phase (grey). A full example schedule of timings has been given in figure 4.
The standardisation phase:
As mentioned previously, we will be using time of sleep onset as a circadian marker from which we will be timing the zeitgeber administration. Therefore, it is important that prior to starting the protocol you develop a good and regular sleeping routine by limiting light exposure at night and exposing yourself to light in the morning in synchrony with the environmental light cycle. Ideally, you should have a constant sleep onset of no later than 11 pm and consistently be getting 7-8 hours of sleep. Some individuals who already have stable sleep routines can skip this phase. Generally, it shouldn’t take more than a week to develop stable sleeping habits.
It seems unlikely that one will be able to adjust more than 3 hours prior to travelling whilst still maintaining their normal daily responsibilities. Therefore, I recommend attempting to adjust 3 hours over a minimum of 4-5 days before travelling. However, the more time the better. This is because it will be unlikely that the athlete will be able to eliminate the presence of zeitgebers at contradictory times and therefore the magnitude of the phase shift will be reduced.
4-5 days before travelling, light exposure in the evening 4 hours prior to sleep onset should be limited as much as possible. An alarm should be set to wake up 7-8 hours after the time of your expected sleep onset. Upon waking the athlete should maximise exposure to light sources by turning on as many lights as possible (obviously don’t stare at any intense light source, this will damage your eyes). Melatonin will be used daily at a dose of 0.5mg, or 1mg for larger athletes, and will be taken 6 hours prior to the expected time of sleep onset. All these timings should be adjusted backwards 30-45 minutes each day.
Arrival and pre-competition phase:
At this point, the athlete has arrived at the location of the competition. The protocol for this phase will be similar to that of the pre-adjustment phase, except all timings will now advance 1 hour each day. Although, it is recommended that athletes preferentially expose themselves to natural light in the mornings upon waking, as this will likely have a more powerful phase shifting effect than artificial light. I recommend arriving ideally one day per hour time difference before the competition, minus the hours that the athlete has already adjusted. For example, if you have adjusted 3 hours prior to flying and the time difference is 8 hours, I would recommend ideally arriving 5 days prior to the competition to allow sufficient time to adjust. However, often it is not the case that arriving this early is feasible, in this situation no changes to the protocol should be made other that attempting to pre-adjust as much as possible.
|Figure 3: An actogram showing the phase shifting that would be expected to be seen in from an individual using the adjustment protocol for a +6-hour time difference.|
|The yellow (light) and black (darkness) blocks describe the environmental light conditions. The first line displays the baseline environmental light conditions. The lines labels PA 1-6 (pre-adaption day #) detail the environmental light conditions for each of those days. The line labelled arrival shows the environmental light conditions at the location of the competition. Each line under those that display environmental light conditions show the expected active periods (grey), the hour of sleep onset (blue) and the timing of melatonin administration (red).
|Figure 4: Example of adjustment protocol for a +6-hour time difference.|
|Current Sleep time: 23:00
Time difference: +6 hours
Weigh in: 7 am
Lift off: 9 am
|Pre-adjustment phase||Wake up||Lights off||Melatonin|
|Day 6 (Travel)||4:00||20:00||14:00|
|Arrival: Day 1||9:00||01:00||19:00|
|Arrival: Day 2||8:00||00:00||18:00|
|Arrival: Day 3||7:00||23:00||17:00|
Due to the fact that the athlete must ensure that they wake up early to maximise the phase shifting potential of light exposure, it is possible that total sleep length will be shortened. To minimise the effect of this, athletes can make up the missed hours of sleep between 12-7 hours before sleep onset. This is acceptable because sleep is regulated by both circadian and homeostatic systems (Wurts and Edgar, 2000). Therefore, making up missed hours of sleep during the day will not interfere with our ability to shift the circadian clocks, yet still allow the homeostatic sleep system’s demands to be satisfied.
The human body does not have one circadian clock but in fact, all studied organs have their own circadian clocks and are referred to as peripheral circadian oscillators. Under normal circumstances, all these clocks are synchronised to the SCN. However, some of them can be influenced by other zeitgebers too. Further, it has been observed that not all circadian oscillators phase shift at the same rates. The main zeitgebers that act directly on the key peripheral oscillators, such as the liver, skeletal muscle and the GI tract, are physical activity and food intake (Damiola et al., 2000). Therefore, it would be advisable to maintain both physical activity and food intake in line with the shifts that we will be imposing using light and melatonin. This is so that every possible zeitgeber is working in unison to shift the SCN and the peripheral oscillators maximally.
I hope that this article can help some athletes to perform at their best in this upcoming IPF Worlds and future competitions. Good luck with your future competitions and thank you for reading.
H.J. Burgess et al. (2002). ‘Bright light, dark and melatonin can promote circadian adaption in night shift workers.’ Sleep Medicine, 6(5): 407-420.
H.J. Burgess and C.I. Eastman (2008). ‘Human Tau in an Ultradian Light-Dark Cycle’. J Biol Rhythms, August; 23(4): 374-376.
T.M. Burke et al. (2013). ‘Combination of Light and Melatonin Time Cues for Phase Advancing the Human Circadian Clock’. SLEEP, 36(11): 1617-1624.
C. Cailotto, et al. (2009). ‘Effects of Nocturnal Light on (Clock) Gene Expression in Peripheral Organs: A Role for the Autonomic Innervation of the Liver’. PLoS ONE, May: 4(5): e5650.
S.-K. Chen et al. (2012). ‘Photoentrainment and pupillary light reflex are mediated by distinct population of ipRGCs’. Nature, 476(7358): 92-95.
Q. Dai et al. (2017). ‘Effect of quantity and intensity of pulsed light on human non-visual physiological responses’. Journal of Physiological Anthropology, 36(22).
F. Damiola et al. (2000). ‘Restricted feeding uncouples circadian oscillators in peripheral tissues from the central pacemaker in the suprachiasmatic nucleus’. Genes & Development, 14: 2950-2961.
Derk-Jan Dirk, J.F. Duffy and C.A. Czeisler (1992). ‘Circadian and sleep/wake dependent aspects of subjective alertness and cognitive performance’. J. Sleep Res.: 1: 112-117.
J.J. Gooley et al. (2001). ‘Melanopsin in cells of origin of the retinohypothalamic tract’. Nature Neuroscience, 4: 1165.
L.M. Hack et al. (2003). ‘The effects of low-dose 0.5mg melatonin on the free-running circadian rhythms of blind subjects.’ Journal of Biological Rhythms, 18(5): 420-429.
C. Hamdi and S. Nizar (2012). ‘The Effect of Training at a Specific Time of Day: A Review’. Journal of Strength and Conditioning Research, 26(7): 1984-2005.
Y. Lee and E.-K. Kim, (2013). ‘AMP-activated protein kinase as a key molecular link between metabolism and clockwork’. Experimental & Molecular Medicine, 45: e33.
A.J. Lewy (2003). ‘Clinical application of melatonin in circadian disorders’. Dialogues: Clinical Neuroscience, 5: 399-413.
K. Mishima (2016). ‘Circadian Regulation of Sleep’. Springer: 103-115.
M. Münch and V. Bromundt et al. (2012). ‘Light and chronobiology: implications for health and disease’. Dialogues-CNS, 14(4): 448-453.
Pandi-Perumal et al. (2007). ‘Dim light melatonin onset (DLMO): A tool for the analysis of circadian phase in human sleep and chronobiological disorders’. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 31: 1-11.
R.L. Sack et al. (2000). ‘Entrainment of free-running circadian rhythms by melatonin supplementation in blind people’. The New England Journal of Medicine, 343(15): 1070-1077.
W. Teo et al. (2011). ‘Circadian rhythms in exercise performance: Implications for hormonal and muscular adaptation’. Journal of Sport Science and Medicine, 10: 600-606.
K. Thapan et al. (2001). ‘An action spectrum for melatonin suppression evidence for a novel no-rod, non-cone photoreceptor system in humans’. The Journal of Physiology, 535(1): 261-267.
Y. Touitou et al. (2017). ‘Association between light at night, melatonin secretion, sleep deprivation, and the internal clock: Health impacts and mechanisms of circadian disruption’. Life Sciences, 173: 94-106.
S.W. Wurts and D.M. Edgar (2000). ‘Circadian and Homeostatic Control of Rapid Eye Movement (REM) Sleep: Promotion of REM Tendency by the Suprachiasmatic Nucleus’. The Journal of Neuroscience, 20(11): 4300-4310.