In sports, such as soccer and rugby union, a single match or game can increase the circulating concentrations of intracellular proteins/enzymes (2,10), which is indicative of skeletal muscle damage (2,10,38). For example, Cunniffe et al. (10) reported large increases in creatine kinase (CK) at 14 (approximately 227%) and 38 hours (approximately 45%) after an international rugby union match. In addition, Thorpe and Sunderland (39) also found approximately 84 and 238% increases in CK and myoglobin, respectively, immediately after a competitive soccer match. The induction of skeletal muscle damage is also likely to impair neuromuscular function (NMF) (14,40) with Twist et al. (40) reporting reductions in NMF (countermovement jump [CMJ] performance) and increases in CK and muscle soreness 24 and 48 hours after match in professional rugby league players. The associated muscle damage may also induce changes in the hormones testosterone and cortisol (10,39). Cunniffe et al. (10) found decreases (−43%) and increases (+40%) in testosterone and cortisol concentrations, respectively, immediately after a rugby union match. Seemingly, these hormones, in addition to markers of muscle damage and NMF, are important to monitor and to assess the physiological stress imposed during exercise, and to monitor recovery from competition and potentially training adaptation (6).
Conditioning coaches often incorporate strength (e.g., back squat, deadlift, and bench press) and power training sessions (e.g., complex/contrast training, plyometrics) during the competitive season to maintain and develop performance characteristics. However, these types of programs have been shown to induce some degree of muscle damage and reduce NMF (14,32). For instance, Gee et al. (14) reported decrements in CMJ height and peak power output (PPO) (ranging from 3–10% across participants) along with concomitant increases in CK at 2 (approximately 45%), 24 (approximately 285%), and 48 hours (approximately 45%) after a strength training session in trained rowers. Seemingly, traditional training methods, which consist of a large contribution from the stretch shortening cycle (eccentric-concentric contraction), can also induce both muscle damage and influence NMF for 24–48 hours after exercise (4,14,32). Thus, optimizing training and recovery, such that the accumulative effects of training and games do not negatively impact on subsequent competition, is crucial to athlete performance. Therefore, it is important that training methods which offer reduced recovery times are available to both coach and athlete.
Concentric-only exercise offers a potentially useful training tool, as it may negate the muscle damage, soreness, fatigue, and inflammation associated with eccentric exercise (22). One such example is the strongman-style sled pull (15). The distinguishing feature of the sled pull is the lack of stored elastic energy in the muscle (24), indicating that the force generated is mainly of a concentric nature. This method of training is effective at inducing strength gains (13), and strongman-style training (e.g., atlas stone, chain drag, farmers walk) also provides an effective stimulus for increasing testosterone concentrations to a comparable magnitude of that elicited by traditional resistance training (15).
Sled dragging exercises are routinely prescribed in team-based sports on the basis that they provide a potent stressor of multiple systems (e.g., cardiorespiratory, strength endurance, hormonal). However, there is limited information on the impact of these sessions and the subsequent recovery profiles of these systems after this type of training. Profiling these measures would provide useful information for both coach and athlete when considering the implementation of this type of training during program design. In light of the above, we sought to investigate the NMF, metabolic, muscle damage, and anabolic-catabolic hormonal responses of weight-trained males to a sled drag-pulling training session (STS). We hypothesized that the exercise session will only acutely reduce NMF, will not result in muscle tissue damage, and will raise post-exercise testosterone and cortisol concentrations when compared with baseline.
Experimental Approach to the Problem
This study profiled a sled training session (STS) to determine whether this exercise can elicit metabolic and hormonal responses in the absence of (or with limited) muscle damage and NMF. After baseline testing for lactate, CK, hormones, and CMJ performance, participants completed a weighted STS, which consisted of 5 sets of 2 × 20-m sled pulls with sled loaded with 75% of their body mass. The drag position of participants (i.e., facing the sled and moving backward) emphasized concentric muscle actions in the lower limbs. Participants were retested immediately, after 15 minutes, 1, 3, and 24 hours after STS. Countermovement jump were processed for PPO, blood samples were processed for lactate and CK, and saliva was analyzed for testosterone and cortisol.
With university ethical approval and informed consent, 11 strength-trained male athletes (mass, 88.8 ± 8.0 kg; height, 181.2 ± 10.2 cm; age, 25.1 ± 3.5 years; 1 repetition maximum back squat, 180 ± 25 kg) volunteered to take part in the study. Subjects were recruited on the basis that they were healthy, injury-free, and engaged in structured weight training and conditioning programs for at least 4 years before the start of the study. Subjects were familiar with the backward sled drag training session through their own individual training programs.
Subjects arrived at the laboratory at 10:00 AM having refrained from alcohol, caffeine, and strenuous exercise in the previous 48 hours and having consumed their typical breakfasts. Subjects then performed a standardized dynamic warm-up. Once the warm-up was completed, subjects performed 3 baseline CMJs on a portable force platform (Type 92866AA; Kistler, Amherst, NY, USA). The baseline measures were collected 15 minutes after the cessation of the warm-up. The sled drag-pulling session (STS) was performed on an indoor running surface and involved subjects facing backward and dragging a sled with maximal effort over a 20-m distance, recovering for 30 seconds before repeating the 20-m drag. This was performed 5 times with 120 seconds of recovery between sets. The sled was loaded with 75% of the individual body mass. On completion of the final sled tow, subjects performed 3 CMJs before further whole blood and saliva samples were collected. Subjects then rested before further CMJs, whole blood, and saliva samples were collected at 15 minutes, 1, and 3 hours after STS. Subjects returned to the laboratory the following morning, at 24 hours after STS, for final CMJ, whole blood, and saliva samples. Subjects were not permitted to carry out any further training during the 24-hour testing period.
Plasma and Saliva Collection and Testing
Whole blood was collected via fingertip puncture using a spring-loaded disposable lancet (Safe-T-Pro Plus, Accu-Chek; Roche Diagnostics GmBH, West Sussex, Germany). First, a 5 μl sample of whole blood was taken for the immediate determination of lactate (Lactate Pro; Arkray, Kyoto, Japan). Next, a 120 μl sample was collected in a capillary tube and immediately centrifuged (Labofuge 400R; Kendro Laboratories, Langenselbold, Germany) at 3,000 rpm for 10 minutes for the extraction of plasma, which was subsequently stored at −20° C. The plasma samples were left to thaw before 6 μl was used in the analysis of CK using a semi-automated analyzer (COBAS MIRA; ABX Diagnostics, Northampton, United Kingdom). Sample testing was carried out in duplicate, and the mean coefficient of variation (CV) for CK assays was 1.6%.
At all time points, 2 ml of saliva was collected by passive drool into sterile containers (9), approximately 2 ml over a timed collection period of 2 minutes, and these samples were stored at −20° C until assay. After thawing and centrifugation (2000 rpm × 10 minutes), the saliva samples were analyzed in duplicate for testosterone and cortisol concentrations using commercial kits (Salimetrics LLC, State College, PA, USA). The minimum detection limit for the testosterone assay was 6.1 pg·ml−1 with an interassay CV of <10%. The cortisol assay had a detection limit of 0.12 ng·ml−1 with interassay CV of <7%.
Countermovement Jump Testing
For the measurement of lower-body PPO, the CMJ was completed on a portable force platform (Type 92866AA; Kistler). To isolate the lower limbs, participants stood with arms akimbo (43). After an initial stationary phase of at least 2 seconds in the upright position, for the determination of body mass, participants performed a CMJ, dipping to a self-selected depth and then exploding upward in an attempt to gain maximum height. Participants landed back on the force platform and their arms were kept akimbo throughout the movement. Countermovement jumps were performed at baseline and 8 minutes after preload stimulus.
Calculating Peak Power Output
The vertical component of the ground reaction force (GRF) during performance of the CMJ was used in conjunction with the participants' body mass to determine instantaneous velocity and displacement of his center of gravity (19). Instantaneous power was determined using the following standard relationship as per the previously described methods of West et al. (43):
Data were analyzed using repeated measures analysis of variance. Where significant main effects of time were identified, changes from baseline were further explored with Bonferroni corrected pair wise comparisons. Relationships were examined using Pearson’s product moment correlation coefficient. Effect size was assessed using partial η2. Statistical analysis was performed using SPSS software (version 16; SPSS, Inc., Chicago, IL, USA), with significance set at p ≤ 0.05. Where significant differences have been identified, 95% confidence intervals (CIs) are presented for an estimation of the population mean difference. Data are presented as mean ± SD.
The PPO, relative PPO, and jump height responses are presented in Figure 1. There was a significant time effect for PPO (p < 0.001, partial η2 = 0.598), relative PPO (p < 0.001, partial η2 = 0.582), and jump height (p < 0.001, partial η2 = 0.676). After completion of the STS, PPO decreased from baseline (baseline, 4,445 ± 705 vs. 0 minute post, 3,464 ± 819 W; p = 0.001; 95% CI, −547 to −1,414 W) and remained below baseline at 15 minutes (p < 0.001; 95% CI, −260 to −496 W) and 60 minutes (p = 0.001; 95% CI, −199 to −522 W; Figure 1A). At 3 hours post-STS, PPO had recovered and was similar to baseline (p = 0.443). Both relative PPO and jump height displayed comparable time course changes to PPO (Figures 1B, C).
Metabolic and Biochemical Responses
The blood lactate and CK responses to the protocol are presented in Table 1. There was a significant time effect within the blood lactate responses to the protocol (p < 0.001, partial η2 = 0.876) but no significant changes in CK concentrations (p = 0.42). Blood lactate significantly increased from baseline immediately after STS (p < 0.001; 95% CI, 9.2–12.2 mmol·L−1; Table 1) and remained elevated at 15 minutes (p = 0.001; 95% CI, 5.1–9.5 mmol·L−1) and 60 minutes (p = 0.004; 95% CI, 1.0–3.3 mmol·L−1; Table 1). At 3 hours post-STS, blood lactate concentrations were comparable with baseline (p = 0.286; Table 1), this was also the case for concentrations at 24 hours (p = 0.12; Table 1).
The testosterone, cortisol, and T/C ratio responses are presented in Figure 2. There was a significant time effect on testosterone (p < 0.001, partial η2 = 0.468; Figure 2A) and cortisol (p = 0.001, partial η2 = 0.345; Figure 2B) but not on the T/C ratio (p = 0.34; Figure 1C). Testosterone concentrations increased from baseline and peaked at 15 minutes (baseline, 158 ± 45 vs. 15 minutes post, 217 ± 49 pg·ml−1; p < 0.001; 95% CI, 38–80 pg·ml−1; Figure 2A) before returning to baseline concentrations after 1 hour (p = 0.864; Figure 2A). At 3 hours, testosterone concentrations decreased below baseline (Figure 2A; p = 0.008; 95% CI, −16 to −62 pg·ml−1) but increased above baseline at 24 hours (Figure 1A; p = 0.04; 95% CI, 5–53 pg·ml−1). Cortisol concentrations tended to increase at 15 minutes after STS (baseline, 3.4 ± 1.8 vs. 15 minutes post, 5.2 ± 2.7 ng·ml−1; p = 0.07; 95% CI, −0.1 to −3.8 ng·ml−1) before declining after 1 hour; at 3 hours, cortisol concentrations decreased below baseline (p = 0.012; 95% CI, −0.6 to −2.8 ng·ml−1) and at 24 hours were comparable to baseline (p = 0.51; Figure 2B).
Peak blood lactate concentrations were related to peak testosterone (r = 0.53, p = 0.041) and cortisol (r = 0.55; p = 0.039) concentrations; moreover, the delta change, from baseline to peak concentrations, was also related between lactate and testosterone (r = 0.67, p = 0.026) and lactate and cortisol (r = 0.55, p = 0.042).
This study examined the metabolic, hormonal, biochemical, and NMF responses for 24 hours after a backward sled drag training session (STS). The STS provided a metabolic and hormonal stimulus, with subsequent rises in lactate, testosterone, and cortisol concentrations. Furthermore, the STS did not induce any significant change in CK, suggesting that there was no significant muscle damage, and although NMF was reduced for up to 1 hour after exercise, CMJ performance recovered to baseline levels after 3 and 24 hours of recovery, thus, indicating full recovery of NMF. The use of predominantly concentric contractions in the lower limbs is a likely explanation behind these physiological responses.
Countermovement jump performance was reduced for 1 hour, before returning to baseline at 3 and 24 hours post-STS, which is consistent with our initial hypothesis. The reduction in NMF immediately after the STS was likely because of the observed metabolic changes. In addition to the potential for depleted muscle phosphocreatine in the immediate post-exercise period to contribute to reducing PPO, acid-base disruption also likely played a role. Increases in blood lactate (approximately sixfold in this study) and inorganic phosphates can impair muscle contractility in the lower-body musculature (30,37). For example, H+ accumulation is associated with an inhibition of cross-bridge binding (31), and increases in inorganic phosphates can reduce the number of active cross bridges and reduce the myofibrillar sensitivity to Ca2+ (37). Because blood lactate was elevated at 1 hour post-STS (Table 1), it is reasonable to suggest that disruptions to acid-base homeostasis played a role in the reduction in PPO immediate post-exercise. Speculatively, the STS may have also produced some degree of peripheral fatigue resulting in reduced excitation-contraction coupling, as demonstrated previously for at least approximately 60 minutes after intense concentric exercise (27,28).
The approximately sixfold increase in blood lactate concentrations immediately after the STS (Table 1) indicates that a large metabolic (and primarily anaerobic) stress was placed on the subjects during exercise testing. However, CK concentrations did not change significantly over the 24-hour testing period, which supports (although there are other markers such as myoglobin that we did not measure) our initial hypothesis of little to no muscle damage occurring from this type of training. The eccentric phase of the stretch shortening cycle is considered a key component behind exercise-induced skeletal muscle damage (4), where a combination of high forces (during muscle lengthening) and lower muscle fiber recruitment subsequently places greater mechanical stress on the contractile proteins (4). Thus, it seems that the STS provided an effective metabolic stimulus, but the mechanical stressors imposed were insufficient to induce skeletal muscle damage; likely because of greater emphasis on concentric muscle contractions.
Salivary testosterone concentrations increased by approximately 38% at 15 minutes post-STS, and this post-exercise rise has been demonstrated in prior research examining resistance (26) and strongman training (15). In the study by Ghigiarelli et al. (15), a strongman protocol (3 × 20-m chain drag, farmers walk, keg carry, tire flips, and 3 sets of 10 of atlas stone lifts) promoted a approximately 70% increase in salivary testosterone concentrations immediately and 30 minutes after exercise. The acute testosterone response is influenced by the muscle mass involved (17,42) and the intensity and volume of the exercise (34). Large muscle mass exercises are potent metabolic stressors, and the metabolic component to the session is an important stimulus for testosterone secretion (26), with a high glycolytic contribution seemingly important (26). This was confirmed by the correlation between the delta measures of testosterone and lactate, which also supports the notion that testosterone increases are likely because of lactate accumulation (29) and possibly, but not measured in our study, adrenergic stimulation (23). Testosterone is suggested to have a protective effect against proteolytic pathways and a sparing effect on glycogen stores (16); therefore, the drop in testosterone (up to 3 hours post-STS) may be to limit these protective effects and allow an increase in energy supply from these cellular substrates (12). However, it is also possible that the decline in testosterone concentrations could be part of normal diurnal changes, with research showing that salivary testosterone concentrations decline from morning to late evening, regardless of the inclusion of heavy resistance exercise (25). However, this does not explain our finding that basal testosterone was elevated at 24 hours after training. The increase in testosterone at 24 hours could represent a rebound effect to aid recovery from the STS (10,12), and this could have further implications for subsequent physical performance (7–9) (e.g., motivation to train, training performance (6)) and competition outcomes (9) and cognitive function (1,6,33). Moreover, elevated testosterone concentrations are associated with a reduction in fear (41) and increased aggression (18); these psychological changes are potentially advantageous for athletes during recovery and preparing for competition.
Cortisol concentrations increased by approximately 54% at 15 minutes post-STS before declining below baseline at 3 hours (Figure 2B). Cortisol is considered one of the primary stress hormones and has been shown to increase after resistance training (5). Moreover, the rise in cortisol is suggested to reflect the metabolic demand placed on the body (26), with post-exercise changes in lactate and cortisol shown to be related (35); this was also evident in our data (r = 0.55). The decline in cortisol to concentrations below baseline at 3 hours is potentially to mediate recovery from the STS. Cortisol reduces skeletal tissue glucose uptake (36), potentially hindering glycogen replenishment, and may suppress testosterone synthesis (6,11), reducing muscle anabolism. Overall, increases in lactate, testosterone, and cortisol after STS are indicative of a positive training stressor. The implications for the lack of change in the T/C ratio is difficult to discern, as its use as a marker of an acute change in skeletal muscle anabolism-catabolism is questionable (26), and it has also been demonstrated not to change after exercise despite large changes in both testosterone and cortisol (39).
Many athletes are required to perform multiple training sessions each day or may have narrow time frames for training between competing. With this in mind, it is essential that training time is maximized and any recovery period required after these sessions is limited (i.e., hours rather than days). Maximal backward sled dragging provides a sufficient enough stimulus to place stress on multiple systems associated with athletic performance (e.g., strength endurance, metabolic, and hormonal), yet does not induce muscle damage and only acutely decreases NMF. With NMF function restored after 3 hours, sled dragging offers coaches a training tool, which requires limited recovery time and is of a potent enough stress to promote favorable changes in basal testosterone concentrations. Albeit there is potential for this training to induce some degree of muscle glycogen depletion, it is important to consider that as muscle damage was likely negated, there would be no hindrance to glycogen resynthesis because of reduced glucose uptake across the damaged sarcolemma (3); therefore, optimal nutritional strategies in the 3 hour post-STS period, where NMF is decreased, would maximize recovery.
A limitation in our data is the lack of a control group to confirm that the changes in the measured hormonal markers are because of the backward sled drag session, rather than natural diurnal variation. Furthermore, as CK often peaks approximately 48 hours after damaging exercise, we cannot rule out that markers of muscle damage may have increased outside our period of measurement. However, there are some data demonstrating that CK can peak at 24 hours after intense exercise (20,21). The lack of a control group and more prolonged measurement window should not detract from our finding that the backward sled drag provides a large metabolic stress, as indicated by lactate changes, which will only acutely reduce NMF.
In conclusion, we have demonstrated that a training session involving backward sled dragging imposes a large metabolic stress in strength-trained men, inducing rises in lactate, testosterone, and cortisol concentrations. However, this type of training did not induce muscle damage (as measured by CK levels) over a 24-hour period and only acutely impaired NMF.
Our data support the use of concentric-only training as a means to elicit favorable physiological responses in strength-trained athletes. It appears that STS can stress multiple systems associated with athletic performance, whereas only acutely reducing NMF and likely without any accompanying muscle damage. Keeping in mind the potential for traditional training methods to induce muscle damage and reduce NMF for approximately 48 hours (4,14). The recovery of NMF within 3 hours of a STS potentially allows athletes to conduct another training session at this time. Moreover, a training session performed 24 hours later could make use of an elevated testosterone profile. In competitive situations likely to induce muscle damage, this type of exercise could also be used as a supplementary training or recovery method. Thus, STS could be used to support more traditional concentric-eccentric training methods on several levels.
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