Toolbox: Crank Down the Pain
Many ergogenic aids, both legal and illegal, have been touted as the magic bullet that will improve cycling performance. What about something that many of us take on a regular basis to relieve minor aches and pains after cycling? Can pain relievers dampen our perception of pain during cycling, and what does that tell us about how the body regulates exercise?
King of Pain
At its core, cycling is about pain tolerance. Every single race comes down to a critical point where you either keep up or get left behind. This single moment happens in every discipline of cycling, whether it’s a road race, crit, grand fondo, cyclocross, time trial, or track. That ability to suffer can be all that separates those who take the podium and those who end up as pack fill.
Behind all the mumbo jumbo about physiology, training, sport psychology, and tactics, the very essence of every single race comes down to whether you or your competitors are willing or able to handle the discomfort. Indeed, one way of thinking about training is that, physiological adaptations aside, it simply desensitizes you to the discomfort of hard efforts. Eventually, you just become used to it and can put up with it.
There is some scientific basis for this. When exercising in a hot environment at a constant speed, both moderately and highly fit subjects experienced the same heart rate and core temperatures over the course of exercise (5). However, the fit group consistently ranked their perceived exertion and thermal discomfort lower than the moderately fit group. Studies from my doctoral laboratory demonstrated that highly fit subjects could consistently tolerate a higher final core temperature than moderately fit subjects when exercising at a steady pace in a hot environment (4), and I demonstrated that this difference remained whether we were normally hydrated or hypohydrated, or whether we were heat acclimated or not (1).
Another way of looking at the above is that you regulate your work based on your perception of discomfort, rather than any single physical cue like lactate levels, breathing rate, or heart rate. One of the famous quotes attributed to Greg LeMond is: “It still hurts just as much, but you just go faster.” This philosophy is reflected in the “Central Governor” model (CGM) of exercise regulation put forward by Prof. Tim Noakes from U. Cape Town in South Africa. In very broad terms, the CGM proposes that the human integrates a broad range of physical cues, matches it with what they’ve previously experienced in terms of how that effort feels, then adjusts their work effort so that it is at a sustainable mental and physical level (3).
Dial the Pain-O-Meter
So if we accept the premise that our subjective tolerance to pain or discomfort plays a major role in how hard we’re willing the exercise, the obvious experiment (note to self: “why the heck didn’t I think of this first!”) would be to figure out ways to manipulate our subjective sensations, and then see whether that results in a higher self-selected workload. In simple terms, if we reduce the “pain per watt” signals coming to the brain, do we then choose to ride at a higher wattage so that the overall sensation of discomfort remains constant?
This was the essential premise of a UK study that was just published in January in the Journal of Applied Physiology by Mauger et al. (2). Their manipulation of choice is one that many of us take regularly for pain relief: acetaminophen, more commonly known by the trade name Tylenol. We generally take Tylenol or other non-steroidal anti-inflammatory drugs (NSAIDS) like ibuprofen (Advil) or acetacylic acid (ASA or aspirin) after exercising to reduce soreness. Would taking such drugs beforehand serve to reduce the sensation of effort?
Prescription for Pain
The basic study designs were straightforward:
• 13 fit young male cyclists (VO2peak ~ 65 mL/kg/min) participated. They trained ~13.4h/week and regularly competed in weekly time trials.
• Subjects ingested three tablets containing either 500 mg of acetaminophen (ACT) or else three placebo (PLA) tablets. The study was “double blinded,” such that neither the subjects nor the experimenters knew which trial was which until after the study was over. Exit interviews determined that subjects could not distinguish between the two conditions.
• After ingesting the tablets, subjects rested, stretched, or did a mild warmup on the bike. The time trials began ~1h after ingestion to allow for peak plasma concentrations of the drug.
• The primary test consisted of a 10 mile time trial test performed on their own bicycles on a CompuTrainer. Subjects saw the virtual rider, the distance cycled, and the distance remaining. They received no other feedback. Lactate was measured at 5 miles and upon completion, while perceived effort and pain was asked every kilometre.
Lab Results Are In
Simple study, but very interesting results:
• There was a definite tilt towards faster TTs with ACT, with 12/13 subjects performing faster TTs with ACT. Overall time was significantly faster with ACT (26:15 +/- 1:36 min) compared with PLA (26:45 +/- 2:02 min).
• Both trials featured the typical “J curve profile of an initial surge, gradual decrease over the middle, and a final big spike in power output near the end. Mean power output was higher with ACT (265 +/- 12 W) than with PLA (255 +/- 15 W). There was a slight significant trend of the ACT having less of a decline in power output during the middle portion of the TT.
• At the midpoint of the TT, blood lactate and heart rates were higher with ACT, but no difference in endpoint blood lactate and heart rates were reported.
• The interesting finding in this study was that, despite the higher power outputs, lactate, and heart rates, no differences were observed at any point in either the perceived effort or pain. This strongly supports the hypothesis that subjects “up-regulated” their self-selected effort to maintain a constant sensation of effort.
Take Three Tablets and Call Me After the TT?
First the disclaimer. My interest in this study comes from my personal research focus on how we regulate exercise, not from promoting any kind of drug use. Many think of acetaminophen and other non-prescription painkillers as generally benign. However, like any drug or medicine, there are numerous potential side effects (liver and kidney damage in the case of acetaminiphen), and there is always the potential for overdose. I do NOT advocate the use of any drug or medicine simply for performance gain!
This study raises a number of interesting scientific and ethical questions. First off, as the primary pharmacology of acetaminophen is an analgesic (dampening pain signals) rather than any effect as a stimulant, its use in this study nicely isolated pain perception without causing a stimulating effect or altered function within the muscle or metabolism. Therefore, the results appear to strongly argue that pain/discomfort regulation is a major determinant of voluntary exercise capacity.
In essence, the dampening of pain signals permitted the subjects to ride at a harder pace, up-regulating their effort (as evidenced by the higher power output and consequently the blood lactate and heart rate) so that their subjective sensations remained similar to how they felt when given the placebo. This was definitely seen in the identical perceived exertion and pain with both conditions. So in this study, LeMond was definitely right!
Up-regulating was especially seen in the middle portion of the time trial, where the ACT condition essentially slowed down less than the PLA. This is interesting from an anecdotal standpoint too, as the middle portion of the TT is often the most painful part mentally, because the initial surge of excitement is gone and the finish seems so far away.
With cycling in such a doping spotlight, the ethical considerations of using any substance is murky and shaky at best. Pain is often the body’s way of warning you of danger, so messing with it can be as dangerous as taking the batteries out of your fire alarm or turning down its volume. Especially in elite athletes who are already performing near the physiological capacity of the human system, tuning down that warning signal can make stepping over the line to catastrophic failure much more likely.
1. Cheung SS and McLellan TM. Influence of heat acclimation, aerobic fitness, and hydration effects on tolerance during uncompensable heat stress. 84: 5: 1731-1739, 1998.
2. Mauger AR, Jones AM and Williams CA. Influence of acetaminophen on performance during time trial cycling. J.Appl.Physiol. 108: 1: 98-104, 2010.
3. Noakes TD, St Clair Gibson A and Lambert EV. From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans: summary and conclusions. 39: 2: 120-4, 2005.
4. Selkirk GA and McLellan TM. Influence of aerobic fitness and body fatness on tolerance to uncompensable heat stress. 91: 5: 2055-63., 2001.
5. Tikuisis P, McLellan TM and Selkirk G. Perceptual versus physiological heat strain during exercise-heat stress. 34: 9: 1454-61, 2002.
Stephen Cheung is a Canada Research Chair at Brock University, and has published over 50 scientific articles and book chapters dealing with the effects of thermal and hypoxic stress on human physiology and performance. He has just published the book Advanced Environmental Exercise Physiology dealing with environments ranging from heat and cold through to hydration, altitude training, air pollution, and chronobiology. Stephen’s currently writing “Cutting Edge Cycling,” a book on the science of cycling, and can be reached for comments at [email protected] .