The warm-up is a widely accepted practice within sport and designed to prepare an athlete for training and competition. It has also been viewed as an opportunity to apply a potentiation stimulus (20). The idea of potentiation comes from observations that preconditioning muscle through prior exercise can improve performance, a phenomenon referred to as postactivation potentiation (PAP) (20,32). Although PAP is relatively robust at the muscle level, its elicitation at a whole-body or athletic level remains equivocal. For example, power or strength improvements have been reported following different squatting or leg press protocols (5,6,15,22), whereas other reports have found no changes or decreases in these parameters using a similar approach (1,19,29).
Numerous factors appear to influence PAP arising from previous exercise. It has been suggested that sufficient intensity and duration must be applied during the potentiating stimulus to achieve reliable potentiations and that movement pattern specificity, training experience, and gender all contribute to the performance outcomes (4,6,33). The duration of potentiation also remains controversial. Classic muscle studies suggest that PAP is only present for the order of minutes (7,37), whereas Kilduff et al. (22) stated that at least 8 to 12 minutes are needed for fatigue recovery associated with the potentiating stimulus when athletic movements are performed in humans. In fact, a recent study in humans suggested that potentiation might be present for several hours following its elicitation (35). It is likely that PAP is coupled to various physiological mechanisms that express different timescales, thereby explaining the variability observed in literature.
Postactivation potentiation has been attributed primarily to the phosphorylation of myosin regulatory light chains (RLC), which make actin and myosin more sensitive to Ca2+ to enhance the contractile response (20). Steroidal hormones may provide a further mechanism to explain the skeletal muscle response to previous exercise. Experimental research has shown that testosterone or cortisol can produce rapid changes in intracellular Ca2+ when applied to skeletal muscle cells (14,30), thereby potentially contributing to skeletal muscle function. These hormones can also regulate the electrophysiological and contractile properties of skeletal muscle (10,24). Consequently, athletic performance may be coupled with the hormonal environment and any changes therein, including those induced by a potentiation stimulus.
Short high-intensity or sprint exercise promotes rapid and dynamic changes in testosterone and/or cortisol concentrations (9,16,28). Therefore, short sprints may produce beneficial changes in the hormonal milieu for potentiating performance. Indeed, a study reported an improvement in power after a short-cycle sprint that increased testosterone concentrations (28). Intense exercise has also been used to elevate testosterone and/or cortisol concentrations during individual workouts and achieve greater training adaptation (18,26). The use of leg exercise to modify arm strength also implies that the hormonal changes occurring may offer systemic benefits for other muscle groups (18). To our knowledge, no studies have examined the effects of short sprints on power and strength and in different muscle groups, along with the hormonal responses in elite athletes.
The aims of this study were to (a) determine if short-cycle sprints could potentiate power and strength (and in different muscle groups) across 2 different workouts in elite rugby players, and (b) examine the effects of the short-cycle sprints on salivary testosterone (Sal-T) and/or cortisol (Sal-C) concentrations across each workout. Given previous findings, it was hypothesized that cycle sprints would elevate salivary hormone concentrations and improve workout performance.
Experimental Approach to the Problem
A crossover design was used to assess the effects of short-cycle sprints on power, strength, and salivary hormones in elite rugby players over a 4-week period. In the first 2 weeks, participants performed an upper-body power and lower-body strength (UPLS) workout with and without a prior lower-body cycle sprint. In the second 2 weeks, a lower-body power and upper-body strength (LPUS) workout was performed with and without a prior upper-body cycle sprint. Power and strength were chosen as the primary outcome measures because both are important physical attributes for elite rugby players (12). The allocation of players to each workout group (cycle sprint and control) was randomized. Hormones were monitored using saliva, a noninvasive medium for determining the bioactive “free” hormone (17). Each workout was performed at a similar time of day (9 am ± 1 hour) to account for diurnal variation, with participants instructed to replicate their dietary intake 24 hours before assessment.
Thirty professional or semi-professional male rugby players (mean ± standard deviation: age 23.1 ± 3.3 years, mass 100.1 ± 12.8 kg, height 184.9 ± 7.6 cm, and body fat 13.9 ± 3.1%) were recruited, each with at least 2 years of strength training experience. The experimental procedures were conducted over a 4-week period during the national provincial rugby competition. During the experimental period, participants were performing intensive but low-volume training that included power and strength, sports speed, and skill conditioning and played in 2 official games. Each participant had the risks and benefits of the investigation explained to them and provided written informed consent. The Human Subject Ethics Committees of the Waikato Institute of Technology and Southern Cross University provided ethical approval.
Participants sat quietly for 10 minutes before a standard warm-up was performed, comprising aerobic exercise, light resistance exercise, and stretching (Figure 1). After the warm-up, participants were randomly assigned to either a cycle sprint or no cycle sprint group, with the crossover session performed within 3 to 5 days, but at least 2 days after, a game to minimize the effects of rugby competition (13). The lower-body cycle sprint was performed on a standard cycle (Lifecycle 9500HR; Life Fitness, Auckland New Zealand), set on the manual mode at the highest resistance (level 20). Seat height was adjusted for each individual and participants remained seated. The upper-body cycle sprint was performed on a standard grinder (Pro circuit; Fitness Works, Auckland, New Zealand). Participants stood a comfortable distance behind the machine with their feet shoulder-width apart. Both exercises were performed at maximal intensity for 40 seconds with strong encouragement given. This protocol was based on previous experiments (9,16,28) and adapted for use in a practical setting. It was important to use an exercise that was tolerable within the workout setting, so as not to adversely affect the ability of players to train, and to use equipment that was available. The control group rested during the sprints, after which both groups rested for a further 2 minutes before commencing their workouts.
Each workout comprised 2 power exercises with similar movement patterns followed by a strength exercise (Figure 1). The UPLS exercises were push-ups (2 sets × 10 repetitions, body-weight load), bench throws (BT; 2 sets × 4 repetitions, 50-kg load), and a box squat (BS; 4 sets × 2-10 repetitions, increasing loads). The LPUS exercises were vertical jumps (2 sets × 10 repetitions, body-weight load), squat jumps (SJ; 2 sets × 4 repetitions, 70-kg load), and a bench press (BP; 4 sets × 2-10 repetitions, increasing loads). The order of exercises was designed to facilitate muscle recovery after the sprint exercises, with 2 minutes of rest also separating each set. For both workouts, the power (2-10 minutes) and strength (12-20 minutes) exercises were performed on the same timescale after the initial cycle sprint. The lifting techniques used are described elsewhere (8,11,22). Briefly, the power exercises were performed on a Smith machine (Fitness Works) using controlled eccentric and ballistic concentric movements, with participants attempting to project themselves and/or the load with each lift. The strength exercises were performed using an Olympic barbell, a squat rack, and bench (Fitness Works) and involved controlled eccentric and explosive concentric movements using a traditional (i.e., nonprojection) technique.
Power and Strength Assessment
Concentric mean power (MP) and peak power (PP) were calculated for the BT and SJ exercises using a data collection and analysis system (Gymaware; Kinetic Performance Technology, ACT, Australia), which consists of a linear encoder attached to the bar via a retractable cord (11). Four repetitions were performed per set to ensure maximal power was maintained (11), with the best trial used for analysis. Squat jump power was calculated from the combined mass of the load and participant (i.e., system power), with BT power derived from the load only (22). The reliability of these power measures tested in our laboratory was high (intraclass correlation coefficients, r = 0.94-0.98; coefficients of variation [CV], 2.0-2.4%). For safety reasons, the BS and BP exercises were performed with increasing loads until a 2 to 4 repetition maximum (RM) lift was achieved in the last set, after which the 1RM lift was estimated (25). The assessment of strength in this manner is highly reliable with respective coefficients of variation of 1.5 and 2.3% (8).
Saliva samples were collected before the warm-up (Time 1) and immediately after the BT (Time 2), BS (Time 3), SJ (Time 2), and BP (Time 3) exercises (Figure 1). Sugar-free gum was used to increase saliva flow, with samples collected in sterile containers and stored at −80°C. Saliva was assayed for testosterone and cortisol using radioimmunoassay kits (Diagnostic System Laboratories, Webster, Texas, U.S.A.) and modified methods (17,27). Testosterone assay sensitivity was 3.5 pmol·L−1 with intraassay and interassay CVs of <7.0 and <8.0%, respectively. Cortisol assay sensitivity was 0.14 nmol/L−1 with respective intraassay and interassay CVs of <9.9% and <8.7%. Samples for each subject were analyzed in the same assay to eliminate interassay variance.
The performance responses to the cycle sprint and control workouts were compared using paired t-tests. A 2-way (group × time) analysis of variance with repeated measures was used to evaluate group, time, and group × time interactions for the hormonal variables. A repeated-measures analysis of covariance was used when significant group differences in hormone concentrations were observed at Time 1. Fisher's t-test was used as the post hoc procedure. Relationships between the relative differences in hormone concentrations and performance (cycle sprint vs. control workouts) were assessed using Pearson correlation coefficients (r). The hormone data were log transformed before analysis to normalize the distribution and reduce nonuniformity bias. The significance level was set at p ≤ 0.05.
The BS 1RM in the UPLS cycle sprint workout was greater (2.6 ± 1.2%) than the control workout, but there were no workout differences in BT PP or BT MP (Table 1). The LPUS cycle sprint workout also produced a greater BP 1RM (2.8 ± 1.0%) than the control workout and no differences in SJ PP or SJ MP between these workouts.
UPLS Hormonal Responses
No differences in Sal-T concentrations were found between the UPLS cycle sprint and control workouts at Time 1, but the control workout did exhibit higher Sal-C concentrations and a lower Sal-T/C ratio at this time point (Figure 2). A significant main group effect (p = 0.036) was identified for Sal-T, with higher concentrations demonstrated in the cycle sprint (vs. control) workout. A group × time interaction (p = 0.01) was also identified for Sal-T, thereby reflecting the divergent changes in Sal-T concentrations at Time 2 and Time 3. A significant time effect (p < 0.001) was noted for Sal-C concentrations and the Sal-T/C ratio, after adjustments were made for the workout differences at Time 1. The concentrations of Sal-C at Time 2 and Time 3 were both significantly lower than Time 1, with the Sal-T/C ratio higher at Time 3 than at Time 1. No other group, time, and group × time interactions were identified for the UPLS hormones.
LPUS Hormonal Responses
No differences in Sal-T and/or Sal-C concentrations were found between the LPUS cycle sprint and control workouts at Time 1 (Figure 3). A significant main time effect (p < 0.001) was identified for both Sal-C and the Sal-T/C ratio. The concentrations of Sal-C at Time 2 and Time 3 were both found to be significantly lower than Time 1, with the Sal-C values at Time 3 also lower than that seen at Time 2. Likewise, the Sal-T/C ratio was significantly elevated at Time 2 and Time 3, compared with Time 1, with the Sal-T/C ratio at Time 3 also greater than that observed at Time 2. There were no other group, time, and group × time interactions for the LPUS hormonal variables.
Significant correlations were identified between the relative LPUS workout differences in Sal-C concentrations at Time 1 (r = 0.42, Figure 4A) and Sal-T concentrations at Time 2 (r = −0.59, Figure 4B) and BP 1RM. Significant correlations were also found between the relative LPUS workout differences in the Sal-T/C ratio at Time 1 (r = −0.49, Figure 5A) and Time 2 (r = −0.66, Figure 5B) and BP 1RM. No significant correlations were identified between the LPUS hormonal and power variables, nor between any of the UPLS hormonal and performance variables.
To our knowledge, this is the first study to examine short-cycle sprints as a potentiating stimulus for power and strength and a possible hormonal mechanism in elite rugby players. The cycle sprints improved BS and BP 1RM strength, but BT and SJ power were unaffected by the sprints. In terms of the accompanying hormonal profiles, the lower-body cycle sprint elevated Sal-T concentrations for the BS exercise. The upper-body cycle sprint had no hormonal effect, but relationships were identified between the workout differences (%) in hormonal concentrations and BP performance.
The cycle sprints produced similar improvements in BS (2.6%) and BP (2.8%) 1RM strength to support previous studies where high-intensity exercise has been found effective in potentiating muscle performance in trained populations (5,6,15,22,28,33,35). The type and level of training history may also be important. Chiu et al, (6) reported an increase in SJ power in explosive strength-trained subjects following multiple sets of heavy squats, but no performance changes were found in recreationally trained subjects. Rixon, Lamont, and Bemben (33) also reported greater countermovement jump (CMJ) height in experienced strength trainers after a single set of heavy squats, compared with inexperienced lifters. It has been suggested that strength-trained athletes possess a greater percentage of type II fibers that respond more readily to PAP (6). Strength training may also increase the probability of a potentiation response by developing the type II fibers and allowing more of the high-threshold motor units to be recruited (33). As a result, the weight-training background of the study population is likely to be a contributing factor to the strength gains in this study.
Bench throw and SJ power were unaffected by the cycle sprint exercises, which could be explained by the treatment protocol in which different muscle groups were exercised and assessed. Power changes in the exercised muscle groups are still much larger (6% on average) (5,6,15,22,28,33) than the strength gains we saw herein. Indeed, most studies assessing strength have failed to see any performance change (1,4,15,16). The lack of strength changes is consistent with the phosphorylation of the myosin RLC because high-frequency tetanic contractions typically occur where Ca2+ levels are close to or at saturation (32). Under these conditions, increased sensitivity would have minimal effect during maximal contractions. The strength gains in this study could be related to the fatiguing nature of the sprint exercises because fatigue and potentiation can coexist (32). Fatigue can condition the contractile environment to produce greater twitch force for a given change in RLC phosphorylation and/or a potentiated twitch response at lower phosphorylation levels (32). Fatiguing exercise may also recruit a greater number of muscle fibers to maintain force output, especially those fibers (type II) that play a greater role in both PAP and maximal strength. Thus, exercise that induces a high level of muscle fatigue may be necessary for potentiating strength, as others have found (31).
The finding that the lower-body cycle sprint produced elevated Sal-T concentrations is corroborated by other research (9,16,28). Therefore, the cycle sprint produced a hormonal environment that would seem favorable for the BS exercise. As supporting evidence, an improvement in leg power was noted in the second of two 10-second sprints, separated by a 15-minute recovery period, and this was accompanied by a 9 to 13% increase in testosterone after the first sprint (28). Similar hormonal concentration trends were demonstrated after a series of short cycling sprints performed on 2 separate days (16). Despite these changes, the subsequent assessment of isokinetic strength and CMJ performance were no different from a control session on either day. As part explanation, the longer (>60 minutes) recovery periods used in this study allowed the measured hormones to return to pre-exercise values or below prior to assessment (16). Therefore, an optimal assessment period might exist after the performance of cycle sprint exercise to maximize the performance benefits arising from changes in the hormonal milieu. Such a notion warrants further investigation.
The upper-body cycle sprint had no hormonal effect, probably because of the smaller muscle mass activated, different total workload, or related metabolic (e.g., lactate) factors. The relationships between the workout differences (%) in hormone concentrations and BP performance do, however, confirm a dynamic coupling between hormones and performance during high-intensity exercise (3,21,36). Thus, the relative hormonal changes that occurred on an individual level may have contributed to the overall improvement in BP 1RM. In contrast to studies assessing the lower limbs (3,36), we found BP performance related to a more catabolic (i.e., greater Sal-C and/or lower Sal-T) response pattern between workouts. The different muscle groups assessed could explain these findings. Training history could also be important, as indicated by the relationships for body builders (positive) and sprinters (negative) when comparing the changes in testosterone concentrations and performance during half squat movements (2), especially because both groups performed a typical workout for their sport.
The hormonal mechanisms mediating the potentiation of muscle performance are still unclear but may include intracellular Ca2+ release (14,30) and modifications in the electrophysiological (e.g., end-plate potential) and contractile (e.g., twitch force) properties of muscle (10,24). Animal research indicates that the type II muscle fibers are more sensitive to the effects of these hormones (24,34), as does research involving humans (2). Consequently, the strength gains observed herein may be explained by the absolute or relative hormonal changes associated with the cycle sprint exercises, in combination with enhanced recruitment of those muscle fibers that respond more readily to these steroid hormones. It is important to recognize that the tissue response is not only dependent on hormone concentrations, but also on the number and sensitivity of steroid receptors at target tissue (23). We further acknowledge the possible contribution of other hormonal factors (e.g., catecholamines, growth hormone, insulinlike growth factors) not measured in this study, especially when a potentiating stimulus is applied.
Some of the limitations of the present study are recognized. First, the order of the power and strength exercises and the lack of crossover are major protocol deficiencies that could not be addressed within the practical aspects of this athletic group. Second, most research has used resistance exercise as the potentiating stimulus, making comparisons to existing literature difficult. Third, the hormonal findings were based on a small number of samples collected across each workout. Because different training practices also elicit different hormonal and neuromuscular adaptation, these results may only be applicable to the study population. However, the study encompassed the response of, and practical limitations inherent in, elite athletic populations.
In conclusion, the performance of short-cycle sprints before a power and strength workout subsequently improved the BP and BS 1RM strength of elite rugby players. These improvements may be explained, to some extent, by the accompanying changes in absolute or relative hormone concentrations. These novel findings support the hypothesis that potentiating performance with previous exercise involves, in part, a hormonal mechanism. Power output was unaffected by the sprint exercises in the current format.
The current findings have practical implications for athletes. For example, short-cycle sprints could be used as a warm-up exercise to modify the hormonal environment and/or workout performance. To improve performance (e.g. strength), one must ensure that the sprint exercise activates the same muscles to be trained and that sufficient recovery is provided between exercises. It may also be possible to use short-cycle sprints as a training exercise to enhance or maintain strength during later exercises or to assist with the recovery processors by modifying the hormonal milieu post-workout. Because the cycle sprints did not adversely affect power output, this type of intervention could still be trialled when similar training movements (and muscle groups) are likely to be performed within the same workout.
This study was supported by funding from The Horticulture and Food Research Institute of New Zealand Limited and the Ngati Whakaue Education Endowment Trust.
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