The placebo effect is broadly defined as any treatment or intervention aimed at precipitating positive psychological and/or physiological effects (33,39). In most cases, the resultant changes associated with the treatment are most likely a result of the belief and/or expectancy of the intervention to actuate the outcome and not the implicit results of the treatment or intervention (11). That is, the treatment is fundamentally inert but the individual's belief in the efficacy of the treatment will most likely elicit positive changes and manifest the desired physiologic and/or psychological benefit (7). Although the precise mechanism is not completely understood, the placebo effect is most likely a result stemming from interactions among motor, cognitive-verbal, and physiochemical responses, which is associated with the expectancy theory (5,33,40).
In brief, the expectancy theory states that any resultant change in performance is largely mediated to the degree that an individual who was administered a treatment (i.e., placebo) believes it to be beneficial (4,5,25,40). Interestingly, improvements in performance are most commonly associated with the analgesic effect (i.e., pain mediating) that a placebo is known to induce, as research has confirmed that the anterior cingulate cortex, an area of the brain with a high concentration of opioid receptors, is similarly activated during placebo and opioid analgesia trials (34). This suggests that a placebo may elicit the same neural response associated with decreases in pain sensitivity owing to the binding of opioid receptors. This may yield increases in performance as studies have found that pain sensation can negatively impact performance (10,15). For example, a negative correlation (R = −0.45) between pain sensation and motor unit firing rates has been shown (10), whereas others report a negative effect on time to exhaustion, when comparing an experimentally induced pain group with a no pain group, during a trial in which subjects were asked to maintain dorsiflexion at 80% of maximal voluntary contraction (MVC) until they declined to 30% of MVC (15). Collectively, this evidence suggests that administration of a placebo may allow an individual to maintain performance by mediating pain and/or fatigue.
There have been a number of studies over the past 10 years that have clearly identified and quantified the extent to which a placebo can affect an acute bout of exercise or sport performance (3). For example, Beedie et al. (4) found that performance during a 10-km cycling time trial was positively affected depending on the level of expectancy by increasing perceived doses of caffeine. Indeed, they reported a decrease of 1.4% during the time trial when individuals did not receive the expected dose. In a subsequent study, Beedie et al. (2) examined the role of a placebo effect during repeated sprint work. In that study, a placebo group was informed that the treatment was “proven” to improve repeated sprint performance, whereas another group was informed that the pill would have a detrimental effect on sprint performance, referred to as a “nocebo.” Results show that the nocebo group's mean sprint performance was negatively impacted, whereas the placebo group's mean sprint performance improved. Overall, the literature, although not overwhelming, does seem to indicate an improvement during a bout of exercise because of a placebo effect either through mediation of fatigue (i.e., time to exhaustion) or improved power output (7). The available evidence from these studies does seem to suggest that there is, indeed, a placebo effect that may occur during a variety of exercise intensities.
Although studies clearly show the effect of an acute placebo effect during a bout of human performance, there exists a need to determine the extent to which a placebo effect may carryover to a subsequent day of training when delivered to an individual in an effort to improve recovery overnight. This, however, has not been investigated. This is surprising given the importance and growing interest in recovery in sport and exercise performance with the concomitant interest in supplements intended to augment recovery. Indeed, recovery from training is gaining attention in the scientific literature and represents a growing market for nutritional and supplement companies (6,32). It is well recognized that the ability to recover within or after a session of repeated high-intensity exercise is critically important in sport, with studies showing a positive correlation between recovery and subsequent performances (19,23,26). Additionally, within sports that typically incur events on consecutive days (e.g., tournament play, etc.), it is important for athletes to be recovered and to optimize performance with perhaps only an overnight period of recovery (30). Thus, despite the volumes of studies aimed toward investigating the efficacy of recovery modalities and other nutritional supplements aimed at improving recovery, there is a lack of data investigating the impact of a potential placebo effect on recovery between sessions of exercise.
Therefore, the purpose of this study was to determine the effect that the administration of a placebo has on recovery from both perceptual and performance standpoints during and between sessions of repeated sprint work. It was hypothesized that individuals in the placebo group will demonstrate improved recovery and/or performance at parallel time points when compared with the control group.
Experimental Approach to the Problem
The experimental designs of the available literature regarding the placebo effect, although novel, fail to simulate what typical ergogenic aid consumers would experience in a real-world environment. That is, although existing studies maintain a high-degree of internal validity by implementing a single- or double-blind approach, there is perhaps an attenuation of the true expectancy effect that individuals experience in an ecologically valid setting. When an individual consumes or purchases a supplement, they generally do so expecting it to positively affect performance, thus increasing the expectancy effect. In a nonblind experimental design, subjects would expect to see improved performance because of the administration of the ergogenic aid, which would provide researchers an opportunity to gauge a more realistic understanding of the placebo effect in a sport or exercise session. Therefore, in this study, a nonblind approach is taken to improve the expectancy effect and to maximize ecological validity.
Ten healthy, asymptomatic men (age = 22.2 ± 2.4, height = 1.8 ± 0.01 m, body mass = 81.2 ± 7.4 kg, body fat (%) = 8.1 ± 2.4) volunteered to participate in the study. The age range for the subjects was 19–28. To be included in this study, subjects must have reported performing sprint training or competition in an intermittent-type sport (e.g., basketball, football, tennis, soccer) at least 2 days per week. Before testing, subjects were instructed to refrain from drinking alcohol 24 hours and caffeine 4 hours before beginning physical activity. Subjects were also instructed to abstain from intense physical activities 48 hours before testing. Before each testing session, subjects were queried regarding adherence to the guidelines set for dietary intake and physical activity. No subjects were excluded from testing for having failed to adhere to these guidelines. This study was approved by the local human subject review board, and written informed consent was obtained before testing the subjects.
All subjects were provided a brochure upon arrival to the laboratory noting that the purpose of the study is to determine the impact an FDA-approved substance has on performance during multiple sessions of repeated sprint work. The brochure contained an overview of previous research regarding the substance that they will be given. However, the results provided to the subjects detailed results from studies investigating the placebo effect and exercise performance (e.g., 2,9,25,36). The brochure only included an overview of the positive findings from these studies; no author names were included in the brochure to ensure that subjects would not be able to search for the studies, relying only on the credibility of the researchers as authority figures, thus ensuring expectancy.
After the subjects read the informational brochure, they completed a medical history questionnaire. An inquiry was added to the medical history questionnaire to screen for people with a low expectancy of effectiveness of an ergogenic aid. The subjects must not have had a negative bias as to the effectiveness of ergogenic aids because this may decrease the expectancy of the ergogenic aid to work and result in no placebo response. This was used as a criterion of exclusion to ensure that no subject had a preconceived bias against ergogenic aids.
Upon arrival, subjects were assessed for height (cm) and body mass (kg), using a stadiometer and beam scale (Detecto Scale Company, Webb City, MO, USA). Body fat percentage estimations were also performed using the 3-site method (men: chest, abdomen, and thigh; women: tricep, iliac, and thigh; (35)) by skinfold calipers (Lange, Cambridge, MD, USA). Subjects then performed 1 running-based anaerobic sprint test (RAST) (8), on a Curve nonmotorized treadmill (Woodway USA, Inc., Waukesha, WI, USA). In brief, the RAST consists of six 35-meter sprints performed maximally, with 10 seconds of rest between each sprint. After the RAST, subjects were encouraged to ask any questions or express any concerns they may have about the procedures during this session.
After at least 24 hours after the familiarization trial, subjects reported to the laboratory. Upon arrival, they were given 10 minutes to ingest 600 ml of the placebo beverage (25). The placebo beverage consisted of distilled water and a commercially available, noncaloric “water enhancer” used to flavor the water. The 2 sweeteners used, sucralose and acesulfame potassium, have been shown to be nonnutritive and have no significant effect on blood insulin levels (28). The first dose of 600 ml was prepared in front of the subjects. Researchers extracted 1 ml of the “water enhancer” from a beaker and extracted it into an Erlenmeyer flask containing approximately 600 ml of distilled water chilled to 10° C. The other doses of 150 ml were prepared beforehand, with the same concentration as the first dose. Subjects were informed that the beverage they were consuming upon arrival and the additional doses of 150 ml that they would be consuming during the sprinting trials were the same beverage and that they should expect the same ergogenic benefits listed in the expectancy brochure.
Immediately after ingestion of the placebo, subjects performed a standardized warm-up in agreement with procedures developed by Vetter (43). After the warm-up, each subject performed 3 RAST protocols. The investigators gave the subject a 5-second countdown in which they were prompted to start walking on the belt. At the conclusion of the 5-second countdown, individuals were given a verbal cue to initiate their sprint. Verbal encouragement was provided to the subjects in a similar manner throughout the series of RASTs. Immediately after the completion of the 35-m sprint, subjects were given a verbal cue to straddle the treadmill belt again for their 10-second recovery period. Once 6 sprints had been completed (i.e., 1 complete RAST), the subjects were given a 7-minute passive recovery period. The recovery period of 7 minutes was chosen to allow optimal phosphocreatine repletion (17). During the recovery period, each subject was asked to ingest 150 ml of the placebo beverage, in accordance with McClung and Collins (25), and was permitted to drink water ad libitum.
After each sprint, rating of perceived exertion (RPE) was provided within a 10-second period between each sprint, using the Adult OMNI Scale of Perceived Exertion for running (42). Raw treadmill belt speed data (peak power [watts], mean power [watts], peak speed [km·h−1], and mean speed [km·h−1]) from the nonmotorized treadmill were recorded by a transducer in the nonmotorized treadmill platform and monitored “real time” on a personal computer containing the manufacturer's computer software (World Wide Software Solutions Firmware version 1.32). Immediately after (within 1 minute) each RAST bout, blood lactate concentration was assessed through samples by means of a fingerstick and capillary puncture and analyzed by an enzymatic portable blood lactate analyzer (Lactate Plus; Nova Biomedical Corp., Waltham, WA, USA).
Ten seconds into the recovery period between RASTs, subjects were presented with and asked to make a horizontal mark on a visual analog scale to assess pain (VASPAIN) (38). The VASPAIN is a 100-mm horizontal line with descriptions of “no pain at all” and “almost unbearable pain” on either end of the scale. With 10 seconds remaining in the recovery period, subjects were asked to rate their perceived recovery status (PRS) using a modified Perceived Recovery Status Scale developed by Laurent et al. (23). The PRS scale is a 0–10 scale used to determine an individual's PRS with a score of 0 representing very poor recovery and a score of 10 representing very well recovered. Approximately 15–20 minutes after the total exercise session, subjects provided a global rating of perceived effort scale using the Session RPE (SRPE) scale (12). After the final recovery bout and assessment of SRPE, subjects were provided a subsequent 150 ml of the placebo beverage that was promoted to augment overnight recovery. Subjects were asked to consume the beverage before leaving the laboratory to ensure that the beverage was consumed. Finally, subjects were reminded to abstain from any physical activity until the trial was completed the next day and to replicate their diet from the current day. The subjects then reported 24 hours later to complete the same RAST protocol to observe the placebo effect in recovery not only within a session but also between consecutive days of sprint work (see Figure 1 for a schematic illustration of the protocol for a single condition).
The control trial followed the same protocol as the placebo trial. However, in this session, individuals in the control group were not given a placebo but instead were given 600 ml of water, and 150 ml of water during the recovery period between RASTs. Trials were counterbalanced to ensure that a learning effect did not impact the measurements that were being recorded. All testing took place at approximately the same time of the day.
After all subjects had completed both control and experimental conditions, a debriefing letter was sent to all by traditional mail. This letter followed the guidelines of the American Psychological Association. A questionnaire was sent to the subjects along with the debriefing letter. The questionnaire asked subjects whether they felt like they were being deceived as to the true nature of the experiment at any time during the experiment. It was revealed that 80% of the respondents did not feel that they were being deceived at any time during the experiment.
A 2 (condition) × 3 (RAST) repeated-measures analysis of variance (ANOVA) was performed to determine main effects for mean power, peak power, pain, and RPE for day 1 and day 2 of testing. When appropriate, post hoc measures including paired t-tests with a Bonferroni correction applied to the alpha level were used to determine any significant differences between condition or RASTs if a main effect was observed. Cohen's d effect sizes for post hoc measures were also calculated when applicable. Session RPE was analyzed using a paired t-test. An a priori power analysis indicated that a minimum of 10 subjects were needed to yield a power of 0.80 for detecting a moderate effect size with significance set at α = 0.05. Statistical significance was determined a priori at α ≤ 0.05. All data was analyzed using SPSS version 20.0 (SPSS, Inc., Chicago, IL, USA).
The peak power achieved in all RASTs for control and placebo conditions during the 2 sessions are displayed in Figure 2A. No significant interaction effect of condition × RAST (p = 0.55) or main effect of condition during day 1 testing (p = 0.21) was found. There was a significant main effect of RAST (p < 0.01). Post hoc measures show that peak power significantly decreased from RAST1 to RAST2 (p < 0.01; d = 0.45), and also from RAST2 to RAST3 (p = 0.001; d = 0.50). Subjects also produced a significantly lower peak power in RAST3 than in RAST1 (p < 0.01; d = 0.95). All differences ranged from moderate to large with respect to effect size (d = 0.45–0.95).
There was a significant interaction between condition and RAST (p = 0.006). A significant main effect of condition on peak power (p = 0.01) and RAST on peak power (p < 0.01) on day 2 were also observed. Bonferroni follow-ups revealed that peak power was not significantly different in RAST1 (p = 0.13; d = 0.16) or RAST2 (p = 0.23; d = 0.13), with congruently small effect sizes. Subjects in the placebo condition produced a significantly higher peak power in RAST3 (p < 0.01; d = 0.41). Peak power also significantly decreased when comparing each consecutive RAST completed (e.g., RAST1 to RAST2). Peak power for RAST1 was significantly higher when compared with RAST2 (p = 0.002; d = 0.28), and RAST3 (p < 0.01; d = 0.63). Subjects produced significantly higher peak power in RAST3 than in RAST2 (p = 0.003; d = 0.50). All differences ranged from small to moderate, in terms of effect size.
Results revealed no significant interaction effect of condition × RAST (p = 0.75) or main effect of condition during day 1 (p = 0.51). There was, however, a significant main effect of RAST (p = 0.005; Figure 2B). Post hoc measures show that mean power was significantly lower when comparing RAST1 with RAST2 (p < 0.01; d = 0.54), and RAST1 to RAST3 (p < 0.01; d = 0.74). No significant differences were observed from RAST2 to RAST3 (p = 0.46; d = 0.14). Significant differences (p ≤ 0.05) were found to have correspondingly large effect sizes when compared with the moderate effect sizes calculated for differences that did not reach significance (p > 0.05).
Analyses revealed a significant interaction between condition × RAST (p < 0.01), a significant main effect of condition (p = 0.04), and a significant main effect RAST (p = 0.04) on day 2. Bonferroni follow-ups revealed that placebo and control groups were not significantly different during RAST1 (p = 0.22; d = 0.19) or RAST2 (p = 0.26; d = 0.11), with congruently small effect sizes. However, subjects in the placebo condition produced significantly higher mean power in the third RAST (p = 0.002; d = 0.36). Within subjects, RAST1 was significantly higher when compared with RAST2 (p = 0.011; d = 0.30), and RAST3 (p = 0.02; d = 0.47). No significant differences were observed between RAST2 and RAST3 (p = 0.38; d = 0.32). All differences ranged from small to moderate with respect to effect size.
Perceived Recovery Status
The PRS reported for control and placebo conditions during experimental sessions is displayed in Figure 3. Results revealed no significant interaction for condition × RAST (p = 0.50) and no main effect of condition on PRS during day 1 (p = 0.54). There was a significant main effect of RAST (p < 0.01). Post hoc measures show significantly higher PRS values, indicating a greater perception of recovery before RAST1 compared with RAST2 (p < 0.01; d = 2.48), and RAST2 with RAST3 (p < 0.01; d = 0.98). The PRS was significantly higher before RAST1 than RAST3 (p < 0.01; d = 3.41). All differences in PRS are considered large with respect to effect size.
Results revealed no significant interaction of condition × RAST (p = 0.08) and no significant main effect for condition (p = 0.75) on day 2. There was a significant main effect of RAST (p < 0.01). Post hoc analysis revealed that PRS significantly decreased from RAST1 to RAST2 (p < 0.01; d = 0.99) and from RAST2 to RAST3 (p < 0.01; d = 1.44). PRS was significantly higher before RAST1 than RAST3 (p < 0.01; d = 1.85). Significant differences (p ≤ 0.05) were found to have correspondingly large effect sizes.
Rating of Perceived Exertion
No interaction effect of condition × RAST was observed (p = 0.43). Results also revealed no significant main effect for condition (p = 0.47) during day 1. However, a significant main effect was found for RAST (p < 0.01) during day 1. Post hoc measures show RPE was significantly lower in RAST1 vs. RAST2 (p < 0.01; d = 0.80) but not RAST2 to RAST3 (p = 0.07; d = 0.94). Subjects also reported significantly higher RPE in RAST3 than RAST1 (p < 0.01; d = 1.39; Figure 4). All differences were found to be large in regard to effect size.
Analyses revealed no interaction effect of condition × RAST (p = 0.07) and no main effect of condition on RPE during day 2 (p = 0.24). However, there was a significant main effect of RAST (p < 0.01). Post hoc analyses revealed that RPE was significantly lower in RAST1 vs. RAST2 (p < 0.01; d = 0.70) and from RAST2 to RAST3 (p = 0.02; d = 0.69). Subjects also reported significantly higher RPE in RAST3 than RAST1 (p < 0.01; d = 1.33). Comparisons of all significant differences (p ≤ 0.05) were coupled with correspondingly large effect sizes.
Figure 5 shows perceived pain reported directly after each respective RAST for control and placebo conditions during day 1 and day 2. A repeated-measures ANOVA revealed that a significant interaction effect of condition × RAST on perceived pain was observed (p = 0.01) with follow-ups showing control having greater reported pain than placebo (p < 0.01). However, there was no significant overall main effect of condition during day 1 (p = 0.23). There was a significant main effect of RAST on pain (p < 0.01). Post hoc analysis showed that perceived pain significantly increased from RAST1 to RAST2 (p < 0.01; d = 0.70), and from RAST2 to RAST3 (p < 0.01; d = 0.71). Subjects also experienced significantly more perceived pain in RAST1 than RAST3 (p < 0.01; d = 1.63), with congruently large effect sizes.
Results revealed no interaction effect for condition × RAST (p = 0.72). Although no main effect was revealed for condition on perceived pain, it was approaching significance (p = 0.07) during day 2. There was a main effect of RAST on perceived pain (p < 0.01). Post hoc analysis showed that perceived pain significantly increased from RAST1 to RAST2 (p < 0.01; d = 1.03), and from RAST2 to RAST3 (p < 0.01; d = 0.83). Subjects also experienced significantly more perceived pain in RAST1 than they did in RAST3 (p < 0.01; d = 1.87). All differences were found to have large effect sizes.
There was no interaction effect for condition × RAST (p = 0.25). Also, no main effect of condition was observed during day 1 (p = 0.70); however, there was a significant main effect of RAST on blood lactate (p < 0.01; Figure 6). Post hoc analysis showed that blood lactate significantly increased from RAST1 to RAST2 (p < 0.01; d = 1.56), but not from RAST2 to RAST3 (p = 0.169; d = 0.72). Blood lactate concentrations were also found to be significantly higher in RAST3 than in RAST1 (p < 0.01; d = 2.19). All differences were found to have large effect size.
Results revealed no interaction effect for condition × RAST (p = 0.69). No main effect of condition on blood lactate on day 2 was observed (p = 0.24); however, there was a significant main effect of RAST on blood lactate (p < 0.01) during day 2. Post hoc analyses show that blood lactate increased significantly from RAST1 to RAST2 (p < 0.01; d = 2.09), and from RAST2 to RAST3 (p = 0.01; d = 0.49). Blood lactate concentrations were also found to be significantly higher in RAST3 than in RAST1 (p < 0.01; d = 2.98). All differences ranged from moderate to large with respect to effect size.
Session Rating of Perceived Exertion
A paired t-test revealed that SRPE did not significantly differ between control and placebo conditions during the day 1 (8.1 ± 0.99 vs. 8.0 ± 0.94; p = 0.82; d = 0.10) or the day 2 session (8.1 ± 1.1 vs. 7.3 ± 1.3; p = 0.14; d = 0.68). Although not significantly different (p > 0.05), values between conditions were found to have moderate effect size on day 2 compared with only a small effect size during day 1.
The purpose of this study was to determine the potential effect the administration of a placebo may have on recovery on consecutive sessions of repeated sprint work. Although some studies have investigated the impact a placebo may have during a single session, this is the first study that aimed to examine the influence administration of a placebo may have on recovery both within and between sessions. Moreover, previous work has used a single-blind, double-blind, or Latin square approach to investigate the placebo effect, whereas this study used a counterbalanced, nonblind approach. This was done to best replicate the potential presence of a placebo effect as it would exist in a day-to-day training situation. That is, most individuals will have purchased or consumed a product with the intention of it to be beneficial, thus increasing the expectancy effect. The most salient finding from this study reveals that administration of a placebo tended to yield improved performance, in terms of power output, after 24 hours of recovery. The subjects in the placebo condition demonstrated significantly higher peak and mean power when compared with the control condition during latter portions of the repeated sprint protocol.
Statistical analyses revealed that the placebo condition produced significantly greater peak and mean power outputs in RAST3 during the day 2 session (Figures 2A, B). These differences were observed independent of any significant changes in perceptual or metabolic response. This finding confirms previous work noting significantly improved performance in high-intensity work with similar RPE and blood lactate responses upon administration of a placebo (37). It seems that the administration of a placebo was able to attenuate loss of power output during the later stages of a repeated sprint protocol leading to overall improved performance. Previous research has shown that most individuals accustomed to sprint-type training demonstrate the ability to reproduce optimal repeated sprint performance with similar perceptual and metabolic measures after only 24 hours of recovery (22). This notion is confirmed as subjects were able to reproduce similar performance during a repeated sprint session. Interestingly, though, administration of a placebo seems to produce attenuation of the decline in mean and peak power, especially during latter portions of the trials, during consecutive days of repeated sprint work. During these latter portions it is most likely when an individual, under normal circumstances, may experience a loss of optimal performance due to the negative consequence of high-intensity work (i.e., pH disruption, metabolic by-product accumulation, etc.) (14). It seems, though, that the placebo effect may have mitigated this loss of power output, which would have elicited the improved sprint performance during the final RAST of the session.
A unique approach used to identify the placebo effect in this study was to assess perceived pain during the bout. Surprisingly, this is not a measure that has been investigated in placebo research during repeated sprint training despite indications in the literature of the beneficial role of placebo analgesia. Although no significant differences were found, the observed measure of pain in this study may still lend explanation to the observed differences in mean and peak power during the day 2 session between condition. As shown in Figure 5, pain increased significantly throughout each RAST during day 1 and day 2 sessions for both the control and placebo conditions. The concomitant increase in pain as work increased was expected and is in agreement with other research investigating the relation of pain to exercise performance (1,10). However, no significant difference in perceived pain was observed between the control and placebo conditions at any equivalent time point (e.g., RAST1 day 1 of the placebo condition compared with RAST1 day 1 of the control condition). Of note is that perceived pain between conditions was lower in the placebo condition, albeit not significantly different, in RAST3 during the day 2 session despite the placebo condition producing significantly higher peak and mean power outputs.
It seems plausible that the current findings indicate that placebo analgesia may have occurred during RAST3. Research has indicated that perception of pain from active muscles increases as power output increases, and it may be that the analgesic effect of the placebo modulated the nociceptive signal (18). This, in turn, may have resulted in subjects in the placebo condition reporting statistically equivalent levels of perceived pain despite higher peak power outputs. Likewise, increases in mean power output may have been due to a decreased afferent signal to the areas of the brain involved in pain processing (e.g., rACC, thalamus, and PAG) (24). As seen in Figure 6, subjects consistently produced similarly high concentrations of blood lactate at parallel time points between conditions. Given the similarity in blood lactate levels, it seems that subjects exerted the same amount of effort in both conditions during RAST3 of the day 2 session. Moreover, it seems plausible that these data may indicate an increased motor unit recruitment strategy that could have facilitated increases in peak and mean power. It may be then, as previous literature suggests, that the significantly lower power produced in the control condition may have been a result of downregulation of motor unit recruitment rather than a decrease effort (27). Further research is needed to examine whether administration of a placebo facilitates motor unit recruitment (e.g., recruitment strategies and/or alterations in muscular recruitment).
It was expected to see RPE rise throughout the bouts (Figure 4) as a number of studies have shown that RPE increases as the total amount of work increases (22,36). The levels of perceived exertion reported by the subjects were similar despite the placebo condition producing significantly higher mean and peak power. It has been suggested that perceptual strain is a mechanism used subconsciously to regulate performance in an effort to titrate recruitment strategies to both optimize performance and prevent muscle damage (31). In addition, it has been reasoned that overall muscular strain and pain serve as important afferent sensations mediating RPE (16). More recently, Twist and Eston (41) found that muscle damage impairs performance, increases RPE, and decreases the amount of work able to be completed. It may be that the administration of a placebo can modulate the sensation of pain because of the inhibition of nociceptive signals at the level of the spinal cord (29), which, in turn, may trigger an upregulation in performance or, at the very least, the attenuation of a decline in performance as seen in this study. It seems plausible that the decreased nociceptive signal to the central nervous system, perhaps due to placebo analgesia, may have allowed for consistent upregulation of performance through increased motor unit recruitment to muscles that would otherwise have been inhibited because of the noxious environment created by metabolite accumulation (e.g., high blood lactate). It seems that a reduced sensation of pain may have precipitated an upregulation in performance to allow for greater maintenance of peak and mean power output in the placebo condition despite similar RPEs reported across both conditions. Although there are multiple theories that exist attempting to explain the regulation of perception and performance with respect to fatigue and recovery, it is important to note that, in most cases, they are not to be viewed as mutually exclusive, rather, integrative in nature (21).
Results from this study showed that SRPE (i.e., global difficulty) was not significantly different across conditions despite the placebo condition producing significantly higher peak and mean power outputs during the day 2 session. This would be expected given the lack of overall differences in acute RPEs observed during the session. It seems that an ergogenic effect of placebo administration extends beyond the actual session as overall perceived difficulty of the session was not significantly different between conditions while total work performed was greater. That is, despite significantly higher peak and mean power outputs, subjects in the placebo conditions did not feel that the session was any more difficult than when power outputs were reduced.
A unique approach to identify changes in recovery was used in this study as many of the resultant effects of placebo administration may be a consequence of changes in perception. Thus, the Perceived Recovery Status Scale was used to identify any perceived changes in recovery. The PRS was originally designed to monitor recovery on a day-to-day basis to ensure that overtraining did not occur or to detect underrecovery (23); however, a modified version of this scale was used to assess changes in PRS relative to expected performance not only between bouts but within a session as well. Results from the study show that PRS values did not vary significantly between RASTs or condition but did trend toward significant interaction (p = 0.08). As shown in Figure 3, PRS values between conditions diverged somewhat with the placebo group reporting higher PRS values, which may be evidence of a partial placebo response. To that end, it seems the administration of a placebo does not cause a disassociation between subjective recovery and physiological recovery. Moreover, it seems beneficial that the administration of a placebo, although ergogenic with respect to power production, will not produce a PRS to be incongruent with physiological recovery. At least within the context of this investigation, an individual will still be able to determine as to whether they are adequately recovered to perform optimally rather than continue training when insufficiently recovered. This, indeed, seems to be an important finding as underrecovery has been identified as one cause of overtraining that can lead to decreases in performance (20).
In conclusion, findings from this study support the hypothesis that administration of a placebo can precipitate a positive influence on recovery with respect to repeated sprint performance. Specifically, despite similar perceptual and metabolic responses through most of the sessions, there were significant differences found between conditions in the final RAST after 24 hours of recovery. These findings suggest that the possible impact of the placebo on performance may be mediated by intensity and exercise-induced perturbations of homeostasis. It does seem, at least within this mode of exercise, that the manifestation of the placebo effect is seen not initially but as exercise continues. Future work investigating the effect of a placebo during this type of exercise paradigm over longer periods of time is certainly worthy of merit and warranted. In addition, the role of personality and its influence on the manifestation of a placebo effect has been noted in the literature (13) and, although this study did not address this phenomenon, it is worthy of mention and future research efforts.
Although significant differences between conditions were only identified at a single time point, there exist important practical implications from this study. It seems that during sport or exercise sessions that consist of high(er) intensities, the place placebo effect may provide benefit in maintaining power output without any negative consequences to levels of perceived exertion or recovery during or after the session, which may aid in compliance during subsequent training bouts. Importantly, the ability of a placebo to facilitate a greater recovery of raw power without causing a disassociation between PRS may have important practical implications. That is, a placebo will facilitate optimal performance that could allow for overload through a reduction in the downregulation of performance while still allowing athletes to detect inadequate recovery.
1. Astorino TA, Terzi MN, Roberson DW, Burnett TR. Effect of caffeine intake on pain
perception during high-intensity exercise. Int J Sport Nutr Exerc Metab 21: 29–30, 2011.
2. Beedie CJ, Coleman DA, Foad AJ. Positive and negative placebo effects resulting from the deceptive administration of an ergogenic aid. Int J Sport Nutr Exerc Metab 17: 259–269, 2007.
3. Beedie CJ, Foad AJ. The placebo effect in sports performance. Sports Med 39: 313–329, 2009.
4. Beedie CJ, Stuart EM, Coleman DA, Foad AJ. Placebo effects of caffeine on cycling performance. Med Sci Sports Exerc 38: 2159–2164, 2006.
5. Benedetti F. Placebo analgesia. Neurol Sci 27: s100–s102, 2006.
6. Bishop P, Jones E, Woods A. Recovery
from training: A brief review. J Strength Cond Res 22: 1015–1024, 2008.
7. Clark VR, Hopkins WG, Hawley JA, Burke LM. Placebo effect of carbohydrate feeding during a 4KM cycling time trial. Med Sci Sports Exerc 32: 1642–1647, 2000.
8. Draper N, Whyte G. Here's a new running based test of anaerobic performance for which you need only a stopwatch and a calculator. Peak Perform 97: 3–5, 1997.
9. Duncan MJ, Lyons M, Hankey J. Placebo effects of caffeine on short term resistance exercise to failure. Int J Sports Physiol Perform 4: 244–253, 2009.
10. Farina D, Arendt-Nielsen L, Merletti R, Graven-Nielsen T. Effect of experimental muscle pain
on motor unit firing rate and conduction velocity. J Neurophysiol 91: 1250–1259, 2004.
11. Foad AJ, Beedie CJ, Coleman DA. Pharmacological and psychological effects of caffeine ingestion in 40-km cycling performance. Med Sci Sports Exerc 40: 158–165, 2008.
12. Foster C, Florhaug JA, Franklin J, Gottschall L, Hrovatin LA, Parker S, Doleshal P, Dodge C. A new approach to monitoring exercise training. J Strength Cond Res 15: 109–115, 2001.
13. Geers AL, Helfer SG, Kosbab K, Weiland PE, Landry SJ. Reconsidering the role of personality in placebo effects: Dispositional optimism, situational expectations and the placebo response. J Psychosom Res 58: 121–127, 2005.
14. Glaister M. Multiple sprint work. Sports Med 35: 757–777, 2005.
15. Graven-Nielsen T, Svensson P, Arendt-Nielsen L. Effects of experimental muscle pain
on muscle activity and co-ordination during static and dynamic motor function. Electroencephalogr Clin Neurophysiol 105: 156–164, 1997.
16. Hampson DB, Gibson ASC, Lambert MI, Noakes TD. The influence of sensory cues on the perception of exertion during exercise and central regulation of exercise performance. Sports Med 31: 935–952, 2001.
17. Harris RC, Edwards RH, Hultman E, Nordesjö LO, Nylind B, Sahlin K. The time course of phosphorylcreatine resynthesis during recovery
of the quadriceps muscle in man. Pflug Arch Eur J Phy 367: 137–142, 1976.
18. Jameson C, Ring C. Contributions of local and central sensations to the perception of exertion during cycling: Effects of work rate and cadence. J Sports Sci 18: 291–298, 2000.
19. Jones EJ, Bishop PA, Richardson MT, Smith JF. Stability of a practical measure of recovery
from resistance training. J Strength Cond Res 20: 756–759, 2006.
20. Kreher JB, Schwartz JB. Overtraining syndrome: A practical guide. Sports Health 4: 128–138, 2012.
21. Laurent CM, Green JM. Multiple models can concurrently explain fatigue
during human performance. Int J Exerc Sci 2: 280–293, 2009.
22. Laurent CM, Green JM, Bishop PA, Sjokvist J, Richardson MT, Schumacker RE, Curtner-Smith M. Stability of RPE
increase during repeated intermittent sprints. J Exerc Sci Fit 8: 1–10, 2010.
23. Laurent CM, Green JM, Bishop PA, Sjökvist J, Schumacker RE, Richardson MT, Curtner-Smith M. A practical approach to monitoring recovery
: Development of a perceived recovery
status scale. J Strength Cond Res 25: 620–628, 2011.
24. Loyd DR, Murphy AZ. The role of the periaqueductal gray in the modulation of pain
in males and females: Are the anatomy and physiology really that different? Neural Plast 1–12, 2009.
25. McClung M, Collins D. “Because I know it will!”: Placebo effects of an ergogenic aid on athletic performance. J Sport Exerc Psy 29: 382–394, 2007.
26. McLester JR, Bishop PA, Smith J, Wyers L. A series of studies—A practical protocol for testing muscular endurance recovery
. J Strength Cond Res 17: 259, 2003.
27. Mendez-Villanueva A, Hamer P, Bishop D. Fatigue
in repeated-sprint exercise is related to muscle power factors and reduced neuromuscular activity. Eur J Appl Physiol 103: 411–419, 2008.
28. Mezitis NH, Maggio CA, Koch P, Quddoos A, Allison DB, Pi-Sunyer FX. Glycemic effect of a single high oral dose of the novel sweetener sucralose in patients with diabetes. Diabetes Care 19: 1004–1005, 1996.
29. Millan MJ. Descending control of pain
. Prog Neurobiol 66: 355–474, 2002.
30. Montgomery PG, Pyne DB, Hopkins WG, Dorman JC, Cook K, Minahan CL. The effect of recovery
strategies on physical performance and cumulative fatigue
in competitive basketball. J Sport Sci 26: 1135–1145, 2008.
31. Noakes TD. Time to move beyond a brainless exercise physiology: The evidence for complex regulation of human exercise performance. Appl Physiol Nutr Metab 36: 23–35, 2011.
32. Nutrition Business Journal. Sports nutrition and weight-loss report. Health Med Week 2671: 13, 2012.
33. Peck C, Coleman G. Implications of placebo theory for clinical research and practice in pain
management. Theor Med 12: 247–270, 1991.
34. Petrovic P, Kalso E, Petersson KM, Ingvar M. Placebo and opioid analgesia: Imaging a shared neuronal network. Science 295: 1737–1740, 2002.
35. Pollack ML, Schmidt DH, Jackson AS. Measurement of cardio-respiratory fitness and body composition in the clinical setting. Compr Ther 6: 12, 1980.
36. Pollo A, Carlino E, Benedetti F. The top-down influence of ergogenic placebos on muscle work and fatigue
. Euro J Neurosci 28: 379–388, 2008.
37. Porcari J, Foster C. Mind over body. The American Council on Exercise (ACE) Fitness Matters. 12–13, 2006.
38. Scott J, Huskisson EC. Graphic representation of pain
2: 175–184, 1976.
39. Shapiro AK, Morris LA. The placebo effect in medical and psychological therapies. In: Handbook of Psychotherapy and Behavior Change. Garfield S.L., Bergin A.E., eds. New York, NY: Wiley, 1978. pp. 369–410.
40. Stewart-Williams S, Podd J. The placebo effect: Dissolving the expectancy versus conditioning debate. Psychol Bull 130: 324–340, 2004.
41. Twist C, Eston RG. The effect of exercise-induced muscle damage on perceived exertion and cycling endurance performance. Eur J Appl Physiol 105: 559–567, 2009.
42. Utter AC, Robertson RJ, Green JM, Suminski RR, McAnulty SR, Nieman DC. Validation of the Adult OMNI Scale of perceived exertion for walking/running exercise. Med Sci Sports Exerc 36: 1776–1780, 2004.
43. Vetter RE. Effects of six warm-up protocols on sprint and jump performance. J Strength Cond Res 21: 819–823, 2007.