Muscle Pain as a Regulator of Cycling Intensity

Effect of Caffeine Ingestion

Alexander R. Gonglach; Carl J. Ade; Michael G. Bemben; Rebecca D. Larson; Christopher D. Black


Med Sci Sports Exerc. 2016;48(2):287-296. 

In This Article


Caffeine's ergogenic effect on exercise performance, although well documented, remains mechanistically unresolved (for review, see.[16,18] Caffeine has also been shown to reduce muscle pain during moderate (~60% of V̇O2peak) fixed-intensity exercise,[7,24,25,27] and based on these findings, hypoalgesia has been suggested as a mechanism by which caffeine may be ergogenic. Interestingly, during high-to-severe intensity (≥80% of V̇O2peak), fixed-time[7,22] or fixed-distance[2,3] exercise, caffeine has not been shown to reduce muscle pain but does allow greater work to be performed for a given amount of muscle pain. These findings are consistent with the idea[23] perceptions of muscle pain may play in the regulation of intensity during exercise. Given the lack of data on the integration of pain as a method for regulating exercise intensity, the purpose of this study was to examine the effects of caffeine ingestion on exercise performance when participants were specifically instructed to regulate their work rate to maintain a fixed level of either "moderate" or "strong" muscle pain. Our primary findings were as follows: 1) participants reliably covered a similar distance when regulating intensity based on pain ratings, 2) caffeine ingestion improved work performed when exercise intensity was regulated to produce "moderate" levels of muscle pain, and 3) caffeine ingestion had no effect on work performed when exercise intensity was regulated to produce a "strong" level of muscle pain.

Reliability of Pain-based Regulation of Exercise Intensity

To the authors' knowledge, this is the first study to examine the reliability of work performed when participants were asked to regulate exercise intensity based on muscle pain. Our findings of high reliability expand upon research from O'Connor et al. (2001) that demonstrated young, healthy women could sustain a pain rating of "3" in the quadriceps during 20 min of cycling.[26] To produce and maintain a consistent level of pain, the participants in the present study [and in O'Connor et al.[26]], manipulated their power output to produce the required amount of nociceptive input to be perceived as a rating of "moderate" (a score of "3" on a 0–10 scale).[10] Type III and IV nociceptors are stimulated by changes in pressure, heat, and noxious biochemicals, all of which occur during exercise.[6] The findings that participants were able to perform a similar amount of work with similar physiological responses (V̇O2, HR, and RER) across the three testing days provided evidence indicating our pain-based exercise protocol was valid for use in examining the relationship between muscle pain and work performed during exercise.

Effects of Caffeine Ingestion on Regulation of Exercise Intensity

The present study used a novel exercise protocol whereby participants were specifically instructed to regulate their work rate based on perceptions of muscle pain. This was done to account for the methodological limitations of previous studies, which used fixed-time and fixed-distance time trials, which were unable to delineate the role, if any; reductions in muscle pain may have played in caffeine's ergogenic effects on performance. Our findings that caffeine leads to a small (7%: Cohen's d = 0.17 SD) improvement in distance covered during 15 min of pain-based cycling, when pain was moderate, is consistent with previous studies using fixed-time and fixed-distance cycling exercise[2,3,7,16]—suggesting perceptions of muscle pain during exercise likely represent information that is integrated as part of the regulation of intensity during exercise. Mauger[23] suggested "exercise-induced pain" among other physiological and psychological factors provides constant feedback (via type III and IV afferents) about the body's physiological and psychobiological state, allowing for changes in work rate that may aid in optimal exercise performance. The moderate pain intensity (i.e., a rating of 3 of 10) was prescribed based on previous findings[7,24,25,27] that the largest hypoalgesic effects of caffeine seem to occur when pain intensity ratings fall in this range. The fact the primary effect of caffeine on work and distance covered occurred during the final 5 to 6 min of the exercise bout is particularly interesting. It is unclear exactly why this occurred. The finding may suggest that it either takes time (8–10 min) for sufficient adenosine levels to accumulate in and around their nociceptors for caffeine to exert its hypoalgesic effect or that it takes time for other noxious inputs (pressure, biochemical such as hydrogen ions, etc.) to accrue and require a reduction in work rate to limit their contribution to overall pain perception.

Previous studies have found no hypoalgesic effects of caffeine during "endurance"[2,3,7,22] and "resistance" (i.e., weight training)[4,21] exercise when pain ratings approached or exceeded "strong" levels (≥4.5 on a 0–10 scale[10] despite consistent improvements in performance. Additionally, moderate pain levels may be too low to be ecologically valid for the pain experienced during athletic competitions. Consequently, participants who improved their performance at a moderate pain level were retested at a pain level of "5." At this higher level of pain, caffeine did not improve distance covered or work performed during the 10-min cycling trial. These findings seem to confirm previous findings from our lab[7] that during heavy-to-severe intensity exercise, the high levels of nociceptive inputs contributing to muscle pain may be too great for caffeine's adenosine antagonizing effect alone to be hypoalgesic—rather than any effect being masked by regulating exercise intensity based on perceptions of muscle pain. This assertion is strengthened by the fact all participants in the follow-up were caffeine "responders" and had covered a greater distance when asked to regulate their work rate at a "moderate" level of pain.

In relation to the mechanism(s) by which caffeine is ergogenic, the results of the present studies suggest multiple mechanisms may be at play and that the mechanism may be dependent on the intensity of the exercise bout. Caffeine is clearly hypoalgesic during moderate intensity exercise,[7,24,25,27] indicating this hypoalgesia likely contributes to an improved work rate for a given amount of muscle pain. The lack of hypoalgesia during more painful, higher intensity exercise,[2,3,7,22] combined with our findings of a lack of an improvement in work rate for a given amount of pain, suggests the consistently improved performance observed during higher intensity endurance exercise[2,3,7,16] likely results from a mechanism other than hypoalgesia. Changes in fat metabolism[11] and increases in muscular strength and endurance[32] are alternative mechanisms that have been proposed to underlie caffeine's ergogenic effects on endurance performance. More recent studies[19] and the fact caffeine improves performance during relatively short-term (10- to 15-min trials) exercise has cast doubt on whether alterations in fat metabolism, leading to sparing of muscle glycogen, impact performance. Considerably more evidence (see[[32]] for review) supports caffeine-derived improvements in strength. A recent study[7] from our lab found that caffeine reduced sensations of muscle pain during 30 min of moderate intensity (and moderate pain) exercise but that this effect was lost when participants followed the 30-min bout with a 10-min all-out performance time trial. Strength and motor-unit recruitment were improved after caffeine ingestion, and concomitant improvements in the 10-min time trial were also found.[7] Another potential mechanism is caffeine's interactions in the central nervous system (CNS). Reductions in dopamine (DA) levels and concomitant increases in serotonin (5-HT) in the CNS have been associated with fatigue.[12] Increased adenosine levels have been shown to reduce DA levels in the CNS, and caffeine has been shown to blunt this decrease via antagosim of central adenosine receptors.[28] Davis et al.[13] demonstrated that direct application of caffeine in the CNS increased run time to exhaustion and rescued the observed decrease in run time when an adenosine receptor A1 and A2 agonist 5'-N-ethylcarboxamidoadenosine was applied.

It is plausible that multiple mechanisms (e.g., improvements in strength, reductions in pain and changes in DA level in the CNS) may underlie caffeine's ergogenic effect during moderate intensity exercise, but during higher intensity exercise, improvements in strength may be the predominant ergogenic mechanism. Interestingly, the magnitude of improvements in distance covered after caffeine ingestion during moderate intensity exercise, approximately 7%, is nearly twice the magnitude seen across studies using high-intensity fixed-time or fixed-distance performance trials.[16] Although strength was not measured in the present study, our finding of a larger magnitude of improvement is consistent with the idea of multiple mechanisms working during moderate—but not high—intensity exercise.

Several experimental considerations warrant discussion. It is important to note this study tested a small group of moderately trained, caffeine naive participants. It is unclear how these results might generalize to highly trained endurance athletes who are more familiar with regulating their work rates during cycling. Chronic ingestion of caffeine does not seem to alter its hypoalgesic effect,[17] but further study of this area is needed. Only nine participants were included in testing at the strong pain level. A very small (d = 0.09 SD) improvement in distance covered was observed, and it is unclear if additional participants were tested if this effect might have reached statistical significance.

In conclusion, the present study found that individuals can reliably regulate their work rate during cycling at a constant "moderate" level of muscle pain over three testing sessions. Compared with placebo, ingestion of caffeine improved work rate and distance covered during cycling at a "moderate" level of muscle pain, but no differences were found when cycling at "strong" levels of muscle pain. These findings seem to indicate that the nociceptive inputs required to produce "strong" muscle pain may be too great for antagonism of adenosine receptors alone to induce hypoalgesia.