Running economy (RE) is one of 3 (along with V̇o2 max and lactate threshold) primary contributors to aerobic performance (3,5,12) and is defined as the steady-state V̇o2 for a given velocity (27). Assuming steady-state aerobic conditions, an individual with superior RE can run faster at a given submaximal V̇o2 compared with an individual with an identical V̇o2 peak (12); differences in RE often explain the performance variance in athletes with comparable aerobic capacities (27).
Numerous studies have shown that chronic resistance training (RT) or plyometric exercise improves RE in runners without negatively affecting aerobic capacity or body mass (21,25,30,35,38,40). However, studies directly examining the acute effects of RT on RE show conflicting results. Doma and Deakin (14) (2014) report no difference in RE 6 hours after strength training, but a decrease in time to exhaustion running performance after high-intensity (6 repetition maximum [RM]) workloads. The same authors have also reported that the cost of running at 70 and 90% of ventilatory threshold (VT) was significantly greater the day after strength training was performed before endurance training (13), but not vice versa. Alternatively, Scott et al. (36) showed no alterations in RE 24–30 hours after a bout of lower-body RT. In a highly aerobically trained group of runners, RE was impaired at 1 and 8 hours after RT but not at 24 hours (31). Conversely, Burt et al. (8) report 4–5% impairment in RE 24–48 hours after an initial bout of squatting-induced muscle damage, although the effect was nonexistent after a subsequent bout of squatting. In a review, Assumpção et al. (3) concluded that strength exercises are likely to impair RE only at higher (≥90% V̇o2 max) exercise intensities.
A smaller body of evidence exists to support the effect of plyometric training alone on RE. Saunders et al. (35) report an improvement in RE at a velocity of 18 km·h−1 after 9 weeks of plyometric training in highly trained runners, although no significant differences were found at slower velocities. Six weeks of plyometric training has also been shown to improve RE in a moderately trained subject pool (40). Likewise, 9 weeks of low-load, explosive strength training improved RE in highly trained subjects, but because this protocol included sprint work, it is difficult to ascertain whether the degree to which plyometric work was a contributing factor (30).
Numerous hypotheses exist as to why muscle damage per se affects RE and have been described elsewhere (2). However, rationales for why plyometric or RT may cause an immediate (i.e., before the development of secondary, immune-mediated damage) decrease in RE are less clear. Resistance training causes an increase in glycogen usage and lactate production (16) with a consequent rise in hydrogen ion concentrations. Hydrogen ions dissociate calcium from troponin and interfere with muscle contractions which may result in a reduction of force production (1,17). Hydrogen ions can also inhibit oxyhemoglobin formation which may result in poor oxygen delivery to working muscles and a greater oxygen demand (39). In addition, heavy-load RT causes neuromuscular fatigue and a reduction in force production (18). This reduction in force production results in reduced muscle stiffness and impairment of RE (34).
The purpose of this study was to determine the acute effects of a single, lower-body plyometrics and RT (PRT) session on RE in male collegiate distance runners. This investigation is unique in the use of a highly aerobically trained subject pool, the addition of plyometrics to a RT protocol to increase external validity of results, and measuring RE immediately after the PRT protocol. It was hypothesized that the PRT protocol would cause impairment in RE lasting at least 24 hours.
Experimental Approach to the Problem
The purpose of this study was to determine the acute (≤24 hours) effects of a single PRT session on RE in highly trained distance runners. On 2 separate occasions, subjects performed a RE test followed by either a PRT workout or rest of equal duration. A high-intensity (85% 1RM), moderate-volume (6 exercises, 3 sets of 5 repetitions each) training protocol was developed to mimic similar programs used by collegiate cross-country teams and those previously used in the scientific literature (25,38). Subsequent RE tests took place immediately after the intervention and 24 hours later. Subjects repeated the protocol 6 days after the last RE test with the opposing intervention; a crossover design was used as it better controls for reported individual daily variances in RE (6).
Before testing commenced, all procedures were approved by the lead author's university Institutional Review Board, and all subjects provided signed informed consent. Nine members of local collegiate cross-country teams volunteered for the study. Subject size was calculated a priori by a power analysis using an effect size (0.43) determined during pilot testing. An additional subject was recruited to account for potential attrition.
Subjects (mean age = 21 ± 1 year, range = 18–22) were required to have engaged in RT at least once in the last 3 months to ensure uniformity regarding the repeated bout effect (8,11) and could not be taking any dietary supplements other than multivitamins or minerals. All subjects were running at least 6 days per week with a range of 50–100 miles per week. Subject characteristics can be seen in Table 1.
The study design is represented in Figure 1. On first reporting to the laboratory, subject height, weight, and body fat percentage by skinfold technique using Lange Skinfold Calipers (Beta technology, Santa Cruz, CA, USA) were measured; the 3-site Jackson-Pollock skinfold equation (20) was used to estimate body fat percentage. Participants then underwent a 1RM test in accordance with National Strength and Conditioning Association guidelines (28) for the following 3 exercises: barbell squats, Romanian deadlifts, and barbell lunges. Subjects completed the eccentric phases of the lifts in 3 seconds while completing the concentric phase as quickly as possible. Acceptable squat depth was considered to be when the hip and knee joints were equidistant from the floor. The eccentric portion of Romanian deadlifts was executed until subjects could no longer maintain a slightly lordotic curve in the lumbar region. Lunges were considered complete when the front knee reached 90° of flexion and the back knee had barely touched the floor. A 5RM lateral lunge was performed using resistance bands with the goal of fatiguing subjects at 5 lateral steps of a standard distance (3 feet).
An incremental treadmill running test to volitional exhaustion was used to determine V̇o2 peak. This test, previously used in elite runners (26), entails subjects approximating their 3K race pace for treadmill speed and a progressive increase in grade every 2 minutes. All metabolic testing was conducted using ParvoMedics TrueOne Metabolic Cart (Parvomedics, Sandy, UT, USA) and a Woodway Desmo treadmill (Woodway USA, Inc., Waukesha, WI, USA). Subjects did not engage in RT for 72 hours before testing and did not run or consume caffeine or alcohol 24 hours before testing. These restrictions were also imposed before all subsequent testing procedures. Subjects fasted for 4 hours before testing and were required to wear the same footwear for all testing procedures.
All subjects performed a continuous 12 minutes RE test immediately followed by a PRT protocol or a resting period (CON). The RE test involved 6 minutes of running at a pace corresponding to 60% V̇o2 peak and, without a rest period, 6 additional minutes at 80% V̇o2 peak. Only metabolic data from the last 2 minutes of each stage were analyzed to minimize the chance of using nonsteady-state V̇o2 measurements. Steady-state conditions were further verified by ensuring less than a 10% change in V̇o2 occurred per minute within the collection period (33). These paces were chosen both to mimic common training intensities for the subject pool and low enough workloads to ensure that steady-state conditions would be met within 4 minutes. It was a general assumption that an intensity of 80% V̇o2 peak would be below lactate threshold for the highly trained subject pool (4). Because of recent criticisms of solely using relative V̇o2 as the determinant of RE (37), energy expenditure (EE) was calculated for each exercise intensity using the respiratory exchange ratio (RER) (22).
The PRT protocol consisted of 3 sets of 5 repetitions of barbell squats, Romanian deadlifts, and barbell lunges at 85% 1RM with a 2-minute rest between sets; lateral lunges were completed using resistance bands and step distance that corresponded to the 5RM. In addition, subjects performed 3 sets of 5 repetitions of box jumps and depth jumps with the same 2-minute rest interval. The same apparatus (45 cm vertical height) was used for both jumps.
Immediately after PRT or resting period, subjects completed another RE test, identical in methodology to the previous one. An additional (third) RE test took place 24 hours later. All subjects were recommended to eat the same meals at the same time intervals between the second and third RE tests, although dietary intake data were not available for analysis. Six days after the post-24 hours RE test, the groups crossed over and performed the alternate protocol.
All data were tested for normal distribution by a Shapiro-Wilk test. Metabolic data were analyzed parametrically using a repeated-measures analysis of variance (ANOVA), whereas post hoc analysis was performed by Fisher's least significant difference test. Order effects were also examined. Effect sizes were calculated as partial eta squared () since repeated measures were used. Significance was set a priori at p ≤ 0.05, and all data analysis was performed using SPSS V23.0 (IBM, Armonk, NY, USA).
Eight subjects completed all testing procedures; one subject withdrew from the study because of an injury unrelated to this investigation. With the withdrawal of 1 subject, the order of treatment was equal among subjects with 4 subjects initially undergoing the PRT protocol and 4 initially assigned to the CON protocol. No order effects were present (p > 0.05).
Data for the 60 and 80% V̇o2 peak RE trials are presented in Tables 2 and 3, respectively. At the 60% V̇o2 peak intensity, ANOVA revealed a significant (p ≤ 0.05) elevation in V̇o2 ( = 0.47) and EE ( = 0.52) immediately after PRT as compared to the CON condition. No significant within or between-trial differences were found for V̇o2 ( = 0.18; = 0.24, respectively) or EE ( = 0.06; = 0.30, respectively) at 80% V̇o2 peak, although a nonsignificant trend was present for between-trial EE (p = 0.08) immediately after PRT.
No significant differences were found for RER during the 60% V̇o2 peak trial. At 80% V̇o2 peak, RER was significantly (p ≤ 0.05) reduced 24 hours after PRT as compared to the CON trial ( = −0.44). There was a nonsignificant (p = 0.06) within-trial trend for RER between the immediately post-CON and 24 hours post-CON time points ( = 0.33).
The primary finding of this study was that a high-intensity, lower-body PRT protocol significantly reduced RE at a moderate exercise (60% V̇o2 peak) intensity in highly trained runners; however, the attenuation lasted less than 24 hours and was not statistically significant at a higher running intensity (80% V̇o2 peak). The reliability of baseline EE measures at both 60 and 80% V̇o2 peak (R2 = 0.81 and R2 = 0.66, respectively) suggests successful testing sessions and compares favorably with previous investigations (37).
Effect sizes were lower than those expected based on pilot data specific to the protocol, and consequently, a type-II error may have occurred in regards to RE measured immediately after PRT at 80% V̇o2 peak. We observed proportionally greater variance in RE at 80% V̇o2 peak as compared to the 60% segment, making statistical significance more difficult to achieve. However, this greater variability at higher running intensities does not seem to be a universal finding (13,14,31). When examining the similarity of RE results between conditions at the 24-hour posttreatment time point, it is clear that no other type-II errors took place at any other time point.
Although this was not a mechanism-based investigation, it is assumed that RE was decreased immediately after PRT because of induced skeletal muscle damage and decreases in muscle stiffness. Multiple investigations have identified both force production and muscle stiffness as primary constituents of RE (1,21,29,34). High-load RT results in a decrease of neural activation in exercised muscle (18) and a loss in maximal force production (41). Likewise, high-volume plyometric training inhibits force and rate of force production, both functional markers of muscle damage (15). Although it may have been ideal to include separate trials of plyometrics alone and RT alone to better distinguish their individual effects on RE, this was deemed logistically unrealistic for our highly trained subject pool because of the required rest (i.e., no running) periods.
Results related to the time course of RE impairment are consistent with those reported by Palmer and Sleivert (31) who used a subject pool with a similar aerobic capacity and a RT protocol with similar intensity and volume, albeit lacking in plyometric exercise and more upper body focused. That particular investigation found attenuations in RE at 1 and 8 hours after RT, but not at 24 hours (31). Generally, evidence is equivocal as to whether RT affects RE within 48 hours (8,13,14,31,36); however, available evidence suggests that performing aerobic training before RT is necessary to avoid acutely unfavorable outcomes in RE (13) or chronically unfavorable outcomes in running performance (10) when both training modes are completed on the same day. To our knowledge, no investigation reports a time course of RE impairment following a workout consisting solely of plyometric exercise. However, results from Drinkwater et al. (15) suggest that any impairment of RE stemming from force or rate of force production impairment will last <2 hours after exercise which is consistent with the results from this study.
Doma and Deakin (13) (2013) reported a decrease in RE at 70 and 90% of VT the day after a RT and aerobically-oriented endurance workout. Even though it is population dependent, 70 and 90% of VT are marginally comparable intensities to 60 and 80% V̇o2 peak. Their subject pool was more diverse regarding frequency of aerobic training than the pool for this study, but the reported V̇o2 max of 62.6 ± 6.0 ml·kg−1·min−1 was very similar. Consequently, minor differences in routine RT practices of subjects may account for some of the discrepant results between the investigations. Subjects in this study must have engaged in RT at least once in the 3-month period before testing; conversely, subjects for Doma and Deakin were restricted from lower-body RT for 2 months before testing. While this may seem potentially trivial, Burt et al. provides evidence that even low-intensity RT provides a repeated bout effect in regards to RE (9). The repeated bout effect refers to muscles' decreased susceptibility to damage following an initial injury or stress. The RT-induced repeated bout effect in relation to future attenuations in muscle damage lasts for up to 6 months (11); consequently, our subject pool may have been less susceptible to the muscle damaging effects of the PRT protocol even though subjects in the Doma and Deakin study would have acquired some degree of protection when undergoing baseline strength testing.
As RT may require a significant amount of glycogen use (23), the decrease in RER observed 24 hours after the PRT protocol was potentially due to reduced glycogen stores that would cause a shift away from glycolytic metabolism (19,32) while running. This phenomenon was not present immediately after exercise as lactate formed during the PRT protocol may have provided a readily available, carbohydrate-based source of aerobic energy (7) during the RE trial, ultimately raising RER to a comparable level of the CON trial. Although lactate was not measured, evidence suggests that blood lactate concentrations were likely increased as a result of the PRT protocol (16). The observed decrease in RER was only present in the 80% V̇o2 peak trial; this is not surprising as higher degrees of carbohydrate use by function of exercise intensity would be more susceptible to alterations.
Strength and conditioning professionals should appreciate that RE is just one component of running performance which rarely has been measured directly in relation to acute response to plyometrics or RT. It should be noted that Marcora and Bosio report a 4% decrease in 30-minute time trial running performance without alterations in RE after 100 jump landings from a 35-cm bench (24). However, Burt et al. (9) (2015) displayed that the repeated bout effect in response to muscle damaging exercise (weighted squats) aids in the preservation of a 3-km running time trial performance.
In conclusion, RE returned to baseline levels within 24 hours after a high-intensity, lower-body PRT protocol in a highly trained subject pool. Future studies may benefit from investigating the timing effects of plyometric training on RE without the influence of RT and including performance testing in addition to standard metabolic tests while employing PRT protocols that mimic typical collegiate or professional runner workouts.
Despite significant research evidence to the contrary, there remains concern in the running community that high-intensity resistance- or power-oriented training may harm endurance performance. Results from this study should further alleviate concerns as the acute, deleterious effects of PRT are short-lived among a highly aerobically trained population. However, strength and conditioning coaches should be mindful that aerobic performance depends on multiple physiological factors beyond RE and employ caution when prescribing high-intensity power- or strength-oriented training within 48 hours of competition.
The authors have no conflicts of interest to report.
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