There is increasing evidence highlighting the benefits of including plyometric exercise to induce further improvements in endurance performance (31,32,36). Although the mechanism is not clearly understood, it is thought that improvements in neuromuscular function, as a result of plyometric exercise, translate into an improved exercise economy (31). However, a consequence of such a training, particularly when the individual is unaccustomed, is the immediate and prolonged appearance of symptoms associated with exercise-induced muscle damage (EIMD) (27,39,40). Therefore, to structure training, it seems pertinent that fitness professionals and exercising individuals should be aware of any acute changes in endurance performance that might follow in the days after unaccustomed plyometric exercise.
Although EIMD has been reported to impair muscle strength and power (5,6,39,40), the effects on endurance performance are still equivocal. Although maximal oxygen uptake (o2) appears to be unaltered after muscle-damaging exercise (17), EIMD appears to affect oxidative metabolism in 2 possible ways: either submaximal o2 for a given workload is unaltered (12,18,41) or, conversely, the o2 increases after muscle-damaging exercise (4,9). However, the possible influence of different modalities of muscle-damaging protocols and the intensity at which they are performed may explain the variable o2 response between studies.
Changes in lactate metabolism as a consequence of EIMD are also not consistent in the literature. Scott et al. (35) reported no change in blood lactate (Blac) response after EIMD during running corresponding to 67% o2max, deemed to be below the lactate threshold (LT). They proposed that because type I muscle fibers are predominately recruited at intensities below the LT, and are less susceptible to injury from eccentric exercise than in comparison to type II fibers (16), they are able to maintain normal recruitment patterns and metabolic function. Similarly, Twist and Eston (41) have reported no significant increase in Blac concentration during cycling at exercise intensities corresponding to 60 and 80% o2max. However, caution should be exercised when interpreting either of these studies, which both failed to account for the interindividual domains of exercise response (23).
Changes in the rating of perceived exertion (RPE) during submaximal exercise suggest that participants demonstrate an altered perceptual response after EIMD (11,41). Such responses may be associated with the increase in muscle pain after eccentric exercise, which has clearly been shown to alter the sense of effort during force matching tasks (33). Similarly, increases in RPE have also coincided with an increased ventilatory response (E) (11,18,41), which may transcend from disruption to nerve afferents located in and around the blood vessels of exercising muscle that are involved in controlling E (20). Moreover, a recent study by Davies et al. (12) proposed that a reduced time to fatigue during severe intensity cycling after EIMD might have been the result of an altered perceived exertion. However, the utility of open-loop protocols to replicate typical training scenarios is limited in that they possess low ecological validity and poor reliability (22).
Marcora and Bosio (26) have investigated the effects of EIMD on time-trial running and found that the average running speed and distance covered were significantly reduced during a 30-minute running time trial at 48 hours after EIMD. More recently, Twist and Eston (41) investigated the effects of EIMD on 5-minute time-trial cycling performance and reported that cardiovascular and metabolic responses, power output (PO), and distance covered were all significantly lower at 48 hours after plyometric muscle-damaging exercise. Although RPE remained unchanged, this implied that a participant's sense of effort was altered after EIMD. However, although this study attempted to examine the effects of EIMD during a more ecologically valid cycling performance test, the time trial adopted was relatively short and might have been dependent on the participant's ability to generate a higher peak PO and recruitment of type II muscle fibers, which have been reported to be susceptible to EIMD (16,39). This is in contrast to a longer duration time trial that would presumably adopt a different pacing strategy. Van Ingen Schenau et al. (42) indicate that variations in time-trial distance result in substantial changes in pacing strategy. Although the 1-km time-trial performance adopts a maximal “all-out” strategy, the 4-km time-trial performance elicits a short but powerful start followed by a constant or slightly decreased PO.
Therefore, we tested the hypothesis that E would increase concomitantly with perceptual responses during submaximal cycling after EIMD, whereas o2, heart rate (HR), and Blac would remain unchanged and that the effects of EIMD would impede cycling time-trial performance via altering effort perception.
Experimental Approach to the Problem
To investigate whether EIMD affects cycling endurance performance, participants initially performed an incremental test to exhaustion to determine o2peak and the PO corresponding to the ventilatory threshold (VT). This was then followed by a habituation session, where participants were familiarized with perceived muscle soreness, isokinetic muscle function, and cycling time-trial procedures. After a minimum of 24 hours, participants completed baseline measurements, which consisted of perceived muscle soreness, peak isokinetic strength of the knee extensors, and a preloaded time trial consisting of 5 minutes at a submaximal workload corresponding to the participant's VT followed by a 15-minute self-paced time trial. Participants were then randomly allocated to a muscle damage (n = 7 men, 1 woman) or control (n = 8 men, 1 woman) group. After 30 minutes of rest, the muscle damage group completed a bout of plyometric exercise to induce symptoms of EIMD. All participants then returned at 48 hours, where previous research (e.g., ) has reported muscle soreness to peak, to complete the measures of muscle strength, soreness and cycling performance.
Seventeen recreationally active university student participants (male: n = 15; female: n = 2), were recruited to the study. All participants trained a minimum of twice per week, incorporated some element of endurance training as part of their weekly routine, and had experience of cycle ergometery. In addition, participants had not undertaken any regular form of resistance or plyometric training of the lower limbs in the 6 months before this investigation. A Faculty Ethics Committee approved all procedures before commencement of the study. All participants provided written informed consent before taking part and were asked to refrain from any strenuous exercise 24 hours before each visit, maintain a normal balanced diet, and avoid using any analgesic agents. Individual testing at each time point was carried out at the same time of the day (±1 hour) to avoid any effects of diurnal variation. Participant characteristics are shown in Table 1.
Assessment of Peak Oxygen Uptake and Power Output Corresponding to Ventilatory Threshold
Participants performed a ramp protocol to exhaustion using an electronically braked cycle ergometer (Lode Excalibur Sport, Lode Medical Technology, Groningen, The Netherlands). All tests were performed under similar environmental conditions (23.4 ± 1.3°C, 43.3 ± 5.1% relative humidity, 758.5 ± 8.0 mm Hg). After a 5-minute warm-up at 25 W, the test commenced at an initial workload of 50 W and increased by 25 W.min−1. Participants were instructed to maintain a pedal cadence between 60 and 80 rpm, and the test was terminated when the participant could no longer maintain the required cadence. Expired gases were collected continuously during the test using an online metabolic system (Cosmed Quark b2, Cosmed S.r.l., Rome, Italy), which was calibrated before each test with a 3-L syringe (Cosmed C00600-01-11, Cosmed S.r.l.) and a span gas mixture of 14.98% O2 and 5.06% CO2. o2peak was accepted as the highest o2 recorded over 20 seconds. The VT was defined using the ventilatory equivalent method (7) from which the corresponding PO was calculated.
Perceived Muscle Soreness
Participants were asked to indicate perceived muscle soreness in the knee extensors using a 0-10 visual analog scale. The scale consisted of written cues from left (no soreness) to right (muscles too sore to move), which corresponded to a number (0-10 unseen by the participant) on the reverse side. Although squatting to an approximate 90° angle, with hands on hips and heels planted on the floor, participants indicated their level of soreness on the scale. The corresponding numerical value on the reverse side was then accepted as the perceived soreness value. This procedure has been used successfully in previous studies (e.g., [26,41]).
Peak Isokinetic Knee Extensor Torque Measurement
Isokinetic strength was measured using an isokinetic dynamometer (Biodex 3, Biodex Medical Systems, Shirley, NY, USA) at a velocity of 60°.s−1. Each participant performed a standardized warm-up of 3-minute cycling at 50 W. Participants were positioned in an upright position with the knee and hip of the test limb fixed at 90°. The ankle was fastened to the input arm of the dynamometer aligned with the lateral femoral epicondyle ensuring that only motion around the knee joint was possible. The upper body and opposite limb were secured to avoid any extraneous movement. The total range of movement was manually determined by the investigator, and the mass of the limb was recorded by the dynamometer to enable gravitational correction of peak torque values. After habituation trials, participants performed 5 maximal efforts at 60°·s−1 from which the highest value was recorded.
Preloaded Time Trial
The submaximal exercise protocol required the participants to cycle at a workload corresponding to their previously determined VT for 5 minutes. This intensity was selected to account for interindividual differences that occur during submaximal domains of exercise (23). o2, E, HR, and RPE were recorded in the final 60 seconds of the submaximal workload. Blood lactate concentration was measured from a capillary sample of blood taken from the fingertip at rest and at the end of fixed-intensity protocol. Each sample was analyzed immediately (Lactate Pro, Arkray, Kyoto, Japan).
After the 5-minute submaximal workload, participants went immediately into a 15-minute time trial, with the aim to cover as much distance as possible. The ergometer was programmed to switch into linear mode, where the following formula was applied in accordance with the manufacturer's instructions: W = L × (rpm)2 (where W = workload, L = linear factor, rpm = pedal revolutions per min). In the linear mode the ergometer acts as a mechanically braked ergometer enabling increases in work rate with increasing pedal cadence (22). The highest PO (W) value during the time trial was recorded as the peak PO, whereas the average value was taken as the mean PO. The distance covered (kilometers) during the 15 minutes was also recorded. The HR and RPE were measured every 3 minutes, whereas o2 was measured continuously throughout the time trial and later averaged over (a) the 15-minute time trial, (b) each 3-minute period. Blood lactate concentration using a fingertip capillary sample was recorded at the end of the time trial and 10-minute post exercise.
Participants in the treatment group performed 10 sets of 10 maximal vertical jumps, interspersed by 1-minute recovery between each set. Before the commencement of the exercise, a maximal vertical countermovement jump was performed, and the corresponding height was recorded using an infrared timing system (Optojump, Microgate S.r.l., Bolzano, Italy). Participants were asked to maintain this target height for each jump and ensure that an approximate knee angle of 90° was achieved on landing. Previous research has shown this protocol to be successful in inducing symptoms of muscle damage to the knee extensors (e.g., [27,39]).
Independent t-tests were performed on all baseline measures between the muscle damage and control groups to ensure no significant differences existed. Separate 2-way (time  × group ) Analysis of variance (ANOVA) with repeated measures on time were calculated to assess changes to each performance variable in both submaximal and time-trial protocols. Changes in distance covered, PO, and o2 at 3-minute stages during the time trial were analyzed using separate 3-way (time  × group  × stage ) repeated-measures ANOVA. Assumptions of sphericity were assessed using Mauchly's test of sphericity, with any violations adjusted by use of the Greenhouse-Geisser correction. Paired t-tests with Bonferroni adjustment were used to follow up any significant results. Where appropriate, values are reported as mean ± SD, and in all cases, the alpha level was initially set at p ≤ 0.05.
Independent t-tests on the physiological characteristics indicated that no significant differences existed between the muscle damage and control groups (p > 0.05, Table 1). This indicates that the recruitment and random allocation procedures were successful in forming 2 groups of similar performance level.
Perceived Muscle Soreness
The muscle-damaging protocol was effective in inducing significant increases in perceived muscle soreness in the muscle damage group (p < 0.05), with values increasing from 1.7 ± 1.5 at baseline to 6.3 ± 2.2 at 48 hours. Values remained unchanged in the control group (0.8 ± 1.1, 0.9 ± 1.2 at baseline and 48 hours, respectively).
Peak Isokinetic Knee Extensor Torque
Peak isokinetic torque measurements from baseline (198.1 ± 40.8 N·m) demonstrated a significant loss of knee extensor strength in the muscle damage group at 48 hours (179.2 ± 39.9 N·m) after eccentric exercise (p < 0.05). Values remained unchanged in the control group (227.97 ± 49.5 and 225.3 ± 52.8 N·m at baseline and 48 hours, respectively).
Submaximal Exercise Responses to Exercise-Induced Muscle Damage
There was no significant interaction of time by group on HR (p > 0.05), Blac (p > 0.05), E/o2 (p > 0.05), or E/co2 (p > 0.05) in submaximal cycling at 48 hours. However, there was a significant interaction of time by group on o2 (p < 0.05) and E (p < 0.05). Furthermore, a significant interaction of time by group for RPE (p < 0.05) indicated that the muscle damage group perceived submaximal exercise to be harder after EIMD (Table 2).
At 48 hours after EIMD, participants in the muscle damage group covered less distance at each time point and subsequently less distance overall (p < 0.05), whereas the control group remained unchanged. Consequently, the o2 response was lower (p < 0.05) at all time points, and PO was lower at 3, 6, and 9 minutes during the time trial (p < 0.05) in the muscle damage group 48 hours after EIMD (Figures 1 and 2, respectively). However, peak PO (p > 0.05) was unchanged in both groups at 48 hours from baseline. Peak HR was significantly lower for the muscle damage group than the baseline value at 48 hours (p < 0.05), whereas time by group interactions indicated trends to suggest that mean HR (p = 0.07) and postexercise Blac (p = 0.07) were lower in the muscle damage group after EIMD. There was no significant interaction of time by group (p > 0.05) for mean RPE, suggesting that the perceptual response remained unchanged by EIMD during the time trial. All data are shown in Table 3.
Increases in perceived muscle soreness and a reduction in isokinetic peak torque at 48 hours indicate that the plyometric exercise was effective in inducing symptoms of EIMD. These observations are consistent with those of previous studies adopting plyometrics to induce EIMD (27,40) and are also comparable to different modalities of exercise used to elicit muscle damage (11).
In contrast to previous research (12,18,41), this study observed an increase in o2 during submaximal cycling after plyometric exercise. Studies that have previously reported an increase in o2 after EIMD have used treadmill running and are probably attributed to alterations in gait kinematics (4,9). Therefore, the findings observed here were not expected given that cycling kinematics was presumably unchanged. However, it can be concluded that after EIMD, the injured muscle required more o2 to perform the same task undertaken in a rested state. The possible mechanisms attributed to the rise in o2 could be because of an increased reliance on slow-twitch muscle fibers after selective damage to fast-twitch fibers after EIMD (16). Slow-twitch fibers are known to possess a greater oxidative capacity, and their enhanced recruitment to compensate for damaged fast-twitch fibers may have increased o2 during submaximal cycling (1). Furthermore, the increase in o2 could have been to facilitate the observed rise in E, in that the lungs evoked an added metabolic cost with increased ventilation (3,28).
In agreement with previous studies, the increase in E during submaximal exercise observed in this study cannot be explained by a nonlinear rise in ventilation to cope with excess CO2 as a result of increased acidosis, as Blac response after EIMD remained unchanged (12,41). Furthermore, E/co2 was also unchanged, indicating that E was not increased to excrete accumulating CO2 during submaximal exercise (2). The rise in E observed herein might be attributed to changes in neural factors after muscle-damaging exercise (20), whereby stimulated group III and IV muscle afferents, located in the blood vessels of the exercising muscles, provoke the altered ventilatory response during submaximal exercise.
In line with previous research (26,35,41), there was a significant increase in RPE during the submaximal workload after EIMD. Marcora (25) recently challenged the view that effort perception during exercise was dependent on feedback from the skeletal muscles, heart, and lungs, postulating that the increase in RPE in this study may have been centrally governed from the brain. However, it is known that E is an important sensory cue for effort perception particularly during exercise perceived to be difficult (19,21). Activation of mechanoreceptors in the chest wall, lungs, and airways may have increased breathing rate, influencing the participant in perceiving the exercise to be harder after EIMD (18,19). Furthermore, the significant reduction in pedaling cadence at 48 hours, combined with a concomitant increase in muscle soreness, might have resulted in the increased perception of effort. Indeed, Deschenes et al. (14) have reported a higher RPE at slower pedaling cadences for the same metabolic cost.
This is the first study to investigate the effects of EIMD during 15-minute time-trial cycling. Time-trial performance at 48 hours after EIMD resulted in a 6% decrease in distance covered and is consistent with previous studies, which have reported a 4% reduction in the distance covered during a 5-minute cycling time trial (41) and a 30-minute running time trial (26). Although these findings are unlikely to be extrapolated to highly trained cyclists, it would appear that muscle-damaging exercise impairs endurance performance in a group of recreationally active participants. Moreover, the findings observed herein have practical significance for individuals embarking on concurrent training regimes that incorporate novel resistance training modalities (i.e., plyometrics) to enhance endurance performance.
There was no significant change in peak PO during the time trial at 48 hours after EIMD. Previous research has reported the inability of damaged muscle to generate peak power during shorter duration time-trial performance (41), and suggests that differing pacing strategies are adopted depending on the duration of the time trial. Therefore, because performance during a short time trial requires a high PO and an “all-out” constant maximal strategy (42), EIMD is perhaps more likely to influence peak power in shorter rather than in longer time trials. Moreover, although peak power does not appear to be affected, it is noticeable that the reduction in PO at each 3-minute interval was only significantly lower for the first 9 minutes of the time trial. This suggests that the main alterations in pacing strategy as a result of EIMD were at the outset of the time trial where the highest PO values would be expected (42).
The significant decrease in distance covered, o2 and PO during the time trial at 48 hours observed in this study implies that participants adopted a slower pacing strategy in the presence of EIMD. However, although these variables were reduced, effort perception remained unchanged during the time trial after muscle-damaging exercise. This finding was also confirmed in a recent study by Twist and Eston (41) and informs that participants in a damaged state perceived a higher level of effort for a lower exercise intensity and physiological and metabolic cost. Interestingly, the treatment group demonstrated a significantly lower E consistent with a lower o2 response, which implies that an amplified ventilatory response was not responsible for driving the altered RPE response. Therefore, this suggests that if an altered sense of effort was responsible for the impaired time-trial performance, this was cued from alternative stimuli.
It is postulated that changes in performance after muscle-damaging exercise might be attributed to an altered sense of effort as opposed to damage to skeletal muscle. Miles et al. (29) reported that RPE, recorded during contractions to an eccentric exercised arm, remained unchanged from predamage values, despite significantly lower forces in the arm after EIMD. Furthermore, several studies have reported that following fatiguing exercise, individuals are capable of quantitatively scaling their effort in an attempt to internally regulate exercise intensity in the face of disturbed homeostasis (10,15). Indeed, if an altered sense of effort is the case after EIMD, our findings support those of Joseph et al. (24) who proposed that during closed-loop exercise, individuals are able to regulate their PO based upon feedback from the periphery. In our study, it may be that the central nervous system could have reduced the neural drive to the peripheral muscles during the time trial after muscle damage to protect against further injury (37). Despite the conscious efforts by the muscle damage group to cover as much distance as possible, as witnessed by the similar increasing levels of effort perception from baseline during the time trial at 48 hours, the observed decrease in PO might not solely be attributed to damage to the muscle fibers but also to motor unit reserve, whereby some fibers were “spared” during the time trial after muscle damage as part of a protective mechanism by the subconscious brain to prevent further injury (37).
It is also possible that the inflammatory response after EIMD reduced participants exercise tolerance (13). Cytokines, such as interleukin (IL)-1, are primary mediators behind the muscle's inflammatory response to EIMD (38). Once evident in the muscle, it is speculated that IL-1 can enter circulation whereby it has the potential to affect distant organs such as the brain (8). Interestingly, studies have found that evidence of increased IL-1 in the brain causes symptoms of fatigue (30,34). Indeed, Carmichael et al. (8) attributed decrements in endurance performance after EIMD in mice to elevated concentrations of IL-1 in the cortex and cerebellum regions of the brain. Moreover, this mechanism has also been postulated to explain impaired time-trial performance in male runners (26). Although this study can only assume the inflammatory response accompanied the observed muscle damage after plyometric exercise, an elevated cytokine response might have instigated central nervous system fatigue and a reduction in time-trial performance.
Notwithstanding that the findings of this study are limited to relatively short-term (i.e., 15 minutes) endurance exercise and recreationally active participants, this study indicates that EIMD impairs endurance performance that is more indicative of how humans exercise in a real-world scenario. Although the authors proposed that EIMD might have a different impact when the exercise bout was longer and relied less on an ‘all-out’ pacing strategy, these findings suggest that a reduction in the distance covered during a 15-minute time trial appears to be as a result of an altered sense of effort coupled with a reduced work capacity. Where individuals using cycling exercise as part of their training opt to incorporate unfamiliar plyometric exercise concurrently, they should be aware of the potential for muscle damage and its subsequent impact on short-term endurance performance.
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