Resistance training is a well-recognized method for improving health and fitness levels for most populations (10,12). In general, the specific nature of the improvement is determined by the configuration of the training variables (e.g., intensity, volume, rest intervals) or the resistance exercise scheme (RES) design (4,10,12). For example, RES using heavy loads, low repetitions, and a moderate-to-high number of sets are typically performed to maximize strength gains. However, moderate-to-heavy loads with moderate-to-high repetitions and multiple sets per exercise are characteristics of muscle hypertrophy training. To improve local muscular endurance, light-to-moderate loads performed with multiple sets and relatively high repetitions often are used. Thus, RES design determines the degree of stress imposed on the organism triggering nervous-, hormonal-, and muscular-specific responses that mediate long-term adaptation (4,10,12).
Several studies have demonstrated the importance of the number of sets performed (i.e., total volume) as a major stimulus regulating the testosterone and/or cortisol responses to a given RES (7,14,16). Similarly, it has been demonstrated that when different RES are equated by the volume of load lifted (3), or when the same relative or absolute load is lifted using different muscle actions (6,9), then similar hormonal responses have resulted. Accordingly, the manner in which a volume of load is lifted (i.e., scheme design) may be less important than the overall volume of load lifted across a workout as a stimulus for activating the hormonal axes that regulate testosterone and cortisol secretion. However, few studies have equated different RES by total volume to isolate the effect of the underlying design on these hormonal responses.
Muscle damage is often thought to contribute to the hypertrophy process by stimulating various compensatory mechanisms that ultimately lead to muscle protein accretion (18). Endocrine responses play a key role in this process, mediating both the breakdown of muscle protein via the catabolic hormones (e.g., cortisol) and the rebuilding muscle protein through the anabolic hormones (e.g., testosterone, growth hormone) (4,13). Various reports have indicated a causal relationship (i.e., both increasing) between the exercise-induced changes in cortisol and those of creatine kinase (CK), a common marker of muscle damage (1,2,15). Still, it remains to be seen if muscle damage is related to the total volume lifted across a RES or its underlying design and if equating by total volume would also result in similar hormonal and CK responses.
Because the hormonal environment contributes to the training outcome, a better understanding of how different configurations of training variables affect these responses will improve the prescription of resistance exercise. Therefore, the present study assessed the effect of 4 different RES of similar total volume on the temporal responses of testosterone, cortisol, and CK. These schemes were described by their 1 repetition maximum (1RM) load (50%-1RM RES, 75%-1RM RES, 90%-1RM RES, and 110%-1RM RES), based on the loading guidelines prescribed in literature (10,12). On the basis of previous research, it was hypothesized that the different RES would exhibit similarities in their hormonal responses. We also hypothesized that the cortisol responses to the different RES would parallel the magnitude of the muscle damage (i.e., CK responses).
Experimental Approach to the Problem
Resistance exercise scheme design plays a key role in activating the endocrine system, thereby mediating long-term adaptation. Muscle damage associated with resistance exercise would also seem an integral part of the adaptive process. However, few studies have equated different RES by total volume to isolate the effect of their underlying design on the hormonal responses and muscle damage markers. Thus, the present study compared 4 different bench press schemes (50%-1RM RES, 75%-1RM RES, 90%-1RM RES, 110%-1RM RES) based on the loading recommendations for improving hypertrophy, strength, and endurance (10,12). These RES were designed to ensure that total volume was equal among groups. Blood samples were collected before and after each RES to compare the responses of testosterone, cortisol, and CK. These parameters are commonly used to assess hormonal and cellular activity related to resistance exercise.
Twenty-seven male soldiers volunteered to participate in this study. The mean (± SD) age, height, and body mass of subjects were 19.9 ± 2.5 years, 177.5 ± 6.8 cm, and 72.5 ± 8.4 kg, respectively. Each subject was engaged in military physical training (running for 60 minutes and circuit training with bodyweight exercises for 30 minutes) 3 times per week for at least 1 year before this study. Subjects had previous resistance training experience including the bench press exercise for a minimum of 1 year; however, they had not been involved in resistance training since the military training program started. Subjects were informed of the purpose and risks of the study and provided informed consent. Each subject was also screened for musculoskeletal, neurological, and shoulder and elbow joint problems. This experiment was approved by the Institute of Biomedical Sciences of University of Sao Paulo Ethics Committee.
Subjects visited the laboratory on 2 separate occasions, separated by at least a week. Bench press 1RM was determined on the first day, using a standard bench, an Olympic barbell, and free weights. On the second day, subjects were randomly assigned into 1 of 4 groups to perform a bench press workout using different RES designs. The 50%-1RM RES group (n = 8) performed 4 sets of ∼20 repetitions, the 75%-1RM RES group (n = 7) 5 sets of ∼11 repetitions, the 90%-1RM RES group (n = 6) 10 sets of ∼4 repetitions, and the 110%-1RM RES group (n = 6) 8 sets of ∼4 repetitions. Each group was matched by 1RM performance for the bench press exercise (Table 1). The RES were equated by the total volume of load lifted across each workout (repetitions × sets × load in kg), with each set performed until repetition failure. The rest interval between sets was 2 minutes for all schemes. Before each workout, subjects performed a standard warm-up comprising 2 sets of 12 repetitions with a 30%-1RM load for the bench press exercise, followed by stretches for the upper body.
The lifting technique involved consecutive eccentric and concentric actions for all RES, except for the 110%-1RM RES, where individuals performed only eccentric actions. During the concentric phase of the 110%-1RM RES, the primary researcher and 2 spotters raised the loaded bar for each subject. Lifting cadence was identical for all RES (i.e., 2 seconds in the eccentric phase and 1 second in the concentric phase) and 3 second muscle actions were performed in the eccentric phase of the 110%-1RM RES. Lifting cadence was set by a metronome (Seiko SQ70, Japan). The same investigator supervised each workout to ensure correct lifting technique was used and provided verbal encouragement to maintain maximal effort. Subjects were assessed at the same time of day (between 7 and 8 am) to account for diurnal variation. Each subject was instructed to refrain from any strenuous activities for 72 hours before reporting to the laboratory.
Blood Sampling and Analyses
After a 12-hour overnight fast, blood samples (10-mL) were drawn pre-exercise (Pre) from the antecubital vein by venipuncture, with additional samples collected post-exercise (Post) at 1 and 24 hours (24h). Subjects returned to the laboratory for the 24h sample and were seated for 1 hour before each collection. The blood samples were separated into 2 vacutainers (Becton Dickinson, USA) after collection, the first containing EDTA for plasma separation and the second with EDTA for serum separation. Both samples were centrifuged at 2,500 rpm for 15 minutes, with the plasma and serum aliquots then stored at −80°C until analysis. Testosterone (total and free) and cortisol (total) concentrations were analyzed by enzyme-linked immunoassays (DSL, USA) following the manufacturer's protocols. The minimum detection limit of the total testosterone assay was <0.15 mol·L−1 with intraassay and interassay coefficients of variation (CV) of 3.6% and 9.5%, respectively. The free testosterone assay had a detection limit of <0.7 ρmol·L−1 with intraassay and interassay CVs of 4.9% and 8.5%, respectively. The detection limit of the cortisol assay was <3 mol·L−1 with intraassay and interassay CVs of 4.1% and 9.8%, respectively.
Plasma CK was measured in a single assay with a Beckman DU 640 spectrophotometer using a commercial kit (Labtest, Brazil) and the manufacturer's instructions. The normal reference range for CK concentrations using this method is 30 to 200 U·L−1. The intraassay CV for this assay was 9.4%. Blood samples for each subject were analyzed in the same assay to eliminate interassay variance.
Standard statistical methods were used for calculating means (± SD) for the hormonal variables and CK. Changes within groups and differences between groups were assessed using analysis of variance with repeated measurements and Tukey post hoc analysis. Before analysis, log-transformation was applied to each data set to normalize the distribution and reduce nonuniformity bias. The criterion level for significance was set at p ≤ 0.05.
No significant differences were detected among the 4 experimental groups in terms of mean age, height, body mass, or bench press 1RM (p > 0.05, Table 1). As observed in Figure 1, there were also no differences in the total volume of load lifted across each group (p > 0.05). The cortisol responses to the different RES are plotted in Figure 2a. In relation to pre-exercise concentrations, cortisol increased significantly by 20% at the Post sample, after the 75%-1RM RES (p < 0.05) (Figure 2b). This response was also greater than the other lifting schemes (p < 0.05) (Figure 2a). In the 90%-1RM RES, a 17% increase in cortisol was observed at the 24h sample (p = 0.05), but this response did not differ from any other scheme (p > 0.05) (Figure 2a).
The total and free testosterone responses to each scheme are presented in Figures 3 and 4, respectively. Total testosterone responded only to the 50%-1RM scheme, decreasing significantly by 18% at the 24h sample (p < 0.05), but no intergroup differences were found in the post-exercise period (p > 0.05). As seen in Figure 4, no temporal changes in free testosterone were observed following any RES (p > 0.05). In addition, no differences in free testosterone were found between the RES at any time post-exercise (p > 0.05).
The CK responses to the different workouts are presented in Figure 5. The 75% 1RM RES produced a significant change in CK concentrations, from the pre-exercise sample, increasing by 200% at the 24h sample (p < 0.05). No temporal changes in CK were identified among the other lifting schemes post-exercise (p > 0.05).
The present study was conducted to assess the effect of 4 different RES of similar total volume on the responses of testosterone, cortisol, and CK. In general, there were no changes in the testosterone and cortisol responses to any RES, nor were there any differences among the different RES. The only exception was the 75%-1RM RES, producing an elevated cortisol profile at the Post sample. The CK responses paralleled those of cortisol, increasing only after the 75%-1RM RES at the 24 h sample.
Cortisol showed little responsiveness to the different RES and a likely function of the absolute volume of load lifted across each workout because total volume is an important factor regulating the cortisol responses to resistance exercise (3,7,14,16). A recent study compared 2 low-volume schemes (strength, power) and a high-volume scheme (hypertrophy) involving squats (3). As expected, the hormonal responses were greater in the hypertrophy scheme, but no differences were found between the equal-volume strength and power schemes. Subsequently, it was suggested that if different RES were equated by total volume, then similar hormone responses may be expected (3). Such a notion is partly confirmed by the current results. The lack of hormonal change might also be explained by the relatively small amount of muscle mass activated during the bench press exercise. Nonetheless, the 75%-1RM RES did produce an elevated cortisol response 1 hour after exercise, which was also greater than the other RES. This finding is not uncommon, with hypertrophy schemes generally producing large cortisol responses and more so than maximal strength and power schemes (3,8,16,20). Hypertrophy schemes are synonymous with a high volume of load lifted across a single workout (i.e., multiple repetitions, sets, and exercises per muscle group), thereby stimulating the hypothalamic-pituitary-adrenal axis to secrete cortisol and its hormonal precursors. It would seem from the present results that hypertrophy schemes might also produce greater cortisol responses than other RES of equal total volume.
As a stress hormone, the cortisol response to the 75%-1RM RES might be explained by a greater level of training strain imposed by this scheme design. As mentioned previously, the configuration of hypertrophy schemes (i.e., high volume of load lifted across a single workout) also induces a greater level of mechanical overload that is possibly related to muscle damage. In fact, resistance exercise is a potent stimulus for provoking muscle damage, as indicated by post-exercise (up to 4 days) increases in CK (1,2,15). This myotrauma stimulates the release of growth factors that influence satellite cells in a cascade of regenerative events that ultimately lead to protein accretion and myofiber hypertrophy (18). The muscle remodeling process is also affected by the acute secretion of hormones following a bout of resistance exercise (4,13). Although the catabolic (and antianabolic) actions of cortisol would intuitively inhibit the recovery process, these actions appear necessary for maximizing protein metabolism by potentially increasing the pool of amino acids for protein synthesis and increasing protein turnover rate (4). Taken together, it appears that the 75%-1RM RES design initiates a variety of hormonal and cellular changes important to muscle hypertrophy. It also appears that these changes are less dependent on the volume of load lifted compared with other RES designs.
The similar responses observed for cortisol and CK following the 75%-1RM RES are corroborated by other research (1,2,15). Collectively, the data presented herein suggest that the cortisol responses to resistance exercise are, in some capacity, related to subsequent muscle damage. Whether the similarities in the cortisol and CK responses are causative or causal remains to be seen. Although the 4 RES were equated by total volume, the temporal change in these variables might be explained by the specific kinematics and kinetics of the 75%-1RM RES. Previous research examined the mechanical (e.g., force and power output, time under tension, work performed, impulse) responses to 3 loading conditions of equal volume (90% 1RM × 2 repetitions, 60% 1RM × 3 repetitions, 30% 1RM × 6 repetitions), using ballistic squats (5). Despite the equalization of total volume, the mechanical responses to each condition varied considerably. Of interest, most mechanical variables were superior in the lightest condition, except for the impulse (force × time) produced, which increased with the heavier conditions (5). If the kinematics and kinetics of upper- and lower-body exercises exhibited similar patterns, then the impulse produced during the bench press workouts might be 1 factor differentiating between the RES and, as a consequence, the cortisol and CK responses. The higher work-to-rest ratio (training density) of the 75%-1RM RES, as compared to 90%-1RM and 110%-1RM RES, offers another mechanism to explain present results because the rest periods used were identical.
In general, total and free testosterone showed little change following the different RES, which we attribute to the absolute volume of load lifted. Once again, total load volume plays an important role in regulating testosterone secretion following a given RES (7,16) and the testosterone responses to different RES (3,8,11,16). Collectively, these observations confirm the importance of considering total volume to stimulate the hypothalamic-pituitary-gonadal axis and the secretion of testosterone and its precursors. Post-exercise increases in testosterone are thought to contribute to the rebuilding of muscle protein by increasing protein synthesis, reducing protein degradation, and stimulating the release of other anabolic factors (e.g., growth hormone, insulin growthlike factors) (4,13). The amount of muscle activated in this study is another consideration because most experimental designs have involved a greater number of exercises and/or lower-body exercises that stimulate larger muscle mass (3,7,8,11). Regardless, the hormonal responses to the 75%-1RM RES, in conjunction with other research findings, suggest that the volume of load prescribed in hypertrophy schemes is important for increasing the circulating levels of testosterone and cortisol and that the specific design of these schemes may also accentuate the cortisol response through greater training strain.
In agreement with the findings of this study, similar testosterone responses have been observed following workouts using the same relative or absolute loads but performed using different muscle contractions (eccentric vs. concentric) (6,9), or when lifting the same volume of load across different scheme designs (power vs. strength) (3). These results again support the belief that if different RES were equated by volume, then similar hormonal changes may be expected. We do acknowledge some of the limitations of this study, such as the small number of subjects in each group and the lack of control data for making baseline comparisons. The design of this study (i.e., parallel groups) presents other problems because individuals are known to vary in the direction, magnitude, and timing of the hormonal responses to an exercise stimulus (17,19). Addressing these issues would contribute to our understanding regarding the hormonal contribution to the adaptive processes, particularly if combined with the kinematic and kinetic profiling of resistance exercise to determine those mechanical factors underlying the activation patterns of the endocrine system and muscle damage.
In conclusion, the lack of hormonal change may be attributed to the relatively low volume of load lifted and/or the small muscle mass activated by the bench press schemes. The only exception was the 75%-1RM RES, producing both elevated cortisol and CK responses, thereby suggesting a greater amount of training strain for the same volume of load.
The results of the present study confirm previous recommendations regarding the prescription of total volume (repetitions × sets × load) as one of the major determinants of the endocrine responses to resistance exercise. However, even when total volume was matched among the 4 different RES, the hypertrophy scheme (75%-1RM RES) still imposed a greater amount of training strain, leading to an increase in both cortisol and CK. Therefore, resistance exercise workouts could be prescribed on 2 different levels to activate the hormonal and cellular systems and achieve long-term adaptation. First, the organization of the training variables based on total load volume lifted and, second, the organization of these variables according to the amount of training strain produced within a given volume of load.
Our sincere thanks are extended to Andres Constantino, Dr. Eivor Martins Junior, Alex S. Yamashita, and the Brazilian Army officers Paulo Roberto Cardoso, Roberto Gueiros da Silva, Marcio Luís Soares Bezerra, and the study subjects. We also would like to address a special thank you for Dr. Luis Fernando Bicudo Pereira Costa Rosa (in memoriam). This study was supported by FAPESP (n°06/54683-8) and Colégio Marista Arquidiocesano de São Paulo-ABEC.
1. Baty, JJ, Hwang, H, Ding, Z, Bernard, JR, Wang, B, Kwon, B, and Ivy, JL. The effect of a carbohydrate and protein supplement on resistance exercise performance, hormonal response, and muscle damage. J Strength Cond Res
21: 321-329, 2007.
2. Boone, JB, Lambert, CP, Flynn, MG, Michaud, TJ, Rodriguez-Zayas, JA, and Andres, FF. Resistance exercise effects on plasma cortisol, testosterone and creatine kinase activity in anabolic-androgenic steroid users. Int J Sports Med
11: 293-297, 1990.
3. Crewther, B, Cronin, J, Keogh, J, and Cook, C. The salivary testosterone and cortisol response to three loading schemes. J Strength Cond Res
22: 250-255, 2008.
4. Crewther, B, Keogh, J, Cronin, J, and Cook, C. Possible stimuli for strength and power adaptation: acute hormonal responses. Sports Med
36: 215-238, 2006.
5. Cronin, J and Crewther, B. Training volume and strength and power development. J. Sci. Med. Sport
7: 144-155, 2004.
6. Durand, RJ, Castracane, VD, Hollander, DB, Tryniecki, JL, Bamman, MM, O'Neal, S, Herbert, EP, and Kraemer, RR. Hormonal responses from concentric and eccentric muscle contractions. Med Sci Sports Exerc
35: 937-943, 2003.
7. Gotshalk, LA, Loebel, CC, Nindl, BC, Putukian, M, Sebastianelli, WJ, Newton, RU, Hakkinen, K, and Kraemer, WJ. Hormonal responses of multiset versus single-set heavy-resistance exercise protocols. Can J Appl Physiol
22: 244-255, 1997.
8. Hakkinen, K and Pakarinen, A. Acute hormonal responses to two different fatiguing heavy-resistance protocols in male athletes. J Appl Physiol
74: 882-887, 1993.
9. Kraemer, RR, Hollander, DB, Reeves, GV, Francois, M, Ramadan, ZG, Meeker, B, Tryniecki, JL, Hebert, EP, and Castracane, VD. Similar hormonal responses to concentric and eccentric muscle actions using relative loading. Eur J Appl Physiol
96: 551-557, 2006.
10. Kraemer, WJ, Adams, K, Cafarelli, E, Dudley, G, Dooly, C, Feigenbaum, MS, Fleck, SJ, Franklin, B, Fry, AC, Hoffman, J, Newton, RU, Potteiger, J, Stone, M, Ratamess, NA, and Triplett-McBride, T. Progression models in resistance training for healthy adults. Med Sci Sports Exerc
34: 364-380, 2002.
11. Kraemer, WJ, Gordon, SE, Fleck, SJ, Marchitelli, LJ, Mello, R, Dziados, JE, Friedl, K, Herman, E, Maresh, CM, and Fry, AC. Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females. Int J Sports Med
12: 228-235, 1991.
12. Kraemer, WJ and Ratamess, NA. Fundamentals of resistance training: Progression and exercise prescription. Med Sci Sports Exerc
36: 674-688, 2004.
13. Kraemer, WJ and Ratamess, NA. Hormonal responses and adaptations to resistance exercise and training. Sports Med
35: 339-361, 2005.
14. Mulligan, SE, Fleck, SJ, Gordon, SE, Koziris, LP, and Triplett-McBride, NT. Influence of resistance exercise volume on serum growth hormone and cortisol concentrations in women. J Strength Cond Res
10: 256-262, 1996.
15. Paulsen, G, Benestad, HB, Strom-Gunderson, I, Morkrid, L, Lappegard, KT, and Raastad, T. Delayed leukocytosis and cytokine response to high-force eccentric exercise. Med Sci Sports Exerc
37: 1877-1883, 2005.
16. Smilios, I, Pilianidis, T, Karamouzis, M, and Tokmakidis, SP. Hormonal responses after various resistance exercise protocols. Med Sci Sports Exerc
35: 644-654, 2003.
17. Tsopanakis, A, Stalikas, A, Sgouraki, E, and Tsopanakis, C. Stress adaptation in athletes: Relation of lipoprotein levels to hormonal response. Pharmacol Biochem Behav
48: 377-382, 1994.
18. Vierck, J, O'Reilly, B, Hossner, K, Antonio, J, Byrne, K, Bucci, L, and Dodson, M. Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int
24: 263-272, 2000.
19. Viru, A, Karelson, K, and Smirnova, T. Stability and variability in hormonal responses to prolonged exercise. Int J Sports Med
13: 230-235, 1992.
20. Zafeiridis, A, Smilios, I, Considine, RV, and Tokmakidis SP. Serum leptin responses after acute resistance exercise protocols. J Appl Physiol
94: 591-597, 2003.