Secondary Logo

Share this article on:

Effects of Load-Volume on EPOC After Acute Bouts of Resistance Training in Resistance-Trained Men

Abboud, George J.1; Greer, Beau K.2; Campbell, Sara C.3; Panton, Lynn B.4

Journal of Strength and Conditioning Research: July 2013 - Volume 27 - Issue 7 - p 1936–1941
doi: 10.1519/JSC.0b013e3182772eed
Original Research

Abboud, GJ, Greer, BK, Campbell, SC, and Panton, LB. Effects of load-volume on EPOC after acute bouts of resistance training in resistance-trained men. J Strength Cond Res 27(7): 1936–1941, 2013—Recent investigations have shown excess postexercise oxygen consumption (EPOC) to be elevated for up to 48 hours in both untrained and trained subjects after resistance training (RT). The purpose of this study was to investigate the effect of load-volume on EPOC. Eight trained men (aged 22 ± 3 years) participated in 2 randomized RT bouts separated by at least 1 week with total load-volumes of 10,000 and 20,000 kg, respectively. Intensity of RT (85% 1 repetition maximum) did not differ between trials. Exercise energy expenditure and resting metabolic rate (RMR) were measured by indirect calorimetry at 8.5 hours before, 1.5 hours before, and during RT bouts and 12, 24, 36, and 48 hours after exercise. Creatine kinase (CK) was measured before and after RT, and 12, 24, 36, and 48 hours postexercise; ratings of perceived muscle soreness were measured on a similar time course save the immediate postexercise time point. Analysis of variance with repeated measures was used to analyze dependent variables. During the 20,000 kg trial, subjects expended significantly (p < 0.01) more energy (484 ± 29 kcal) than the 10,000 kg lift (247 ± 18 kcal). After the 20,000 kg lift, 12 hours postexercise, CK (1,159 ± 729 U·L−1) was significantly elevated (p < 0.05) as compared with baseline (272 ± 280 U·L−1) and immediately postexercise (490 ± 402 U·L−1). No significant time or trial differences were found in RMR between the 10,000 and 20,000 kg trials. In conclusion, high-intensity RT with load-volumes of up to 20,000 kg using resistance-trained men does not significantly increase EPOC above baseline RMR.

1Department of Sport and Movement Science, Salem State College, Salem, Massachusetts

2Department of Physical Therapy and Human Movement Science, Sacred Heart University, Fairfield, Connecticut

3Department of Exercise Science and Sports Studies, Rutgers, The State University of New Jersey, New Brunswick, New Jersey

4Department of Nutrition, Food, and Exercise Sciences, Florida State University, Tallahassee, Florida

Address correspondence to Beau K. Greer, greerb@sacredheart.edu.

Back to Top | Article Outline

Introduction

Current evidence suggests that there is minimal benefit to resistance training (RT) for weight loss when compared with caloric restriction (5,13,20,21,28) and that weight loss associated with aerobic training is not enhanced by RT (32). Data indicate that energy expenditure during RT is relatively low even during high-intensity bouts of exercise (6,10,19). Because of the relatively minor amount of energy used compared with aerobic training, this mode of training has not been recommended as an effective method for controlling weight (18).

However, RT can increase excess postexercise oxygen consumption (EPOC) from 1 to 48 hours above resting levels (11,22,23,27,35). Excess postexercise oxygen consumption may be the result of energy-requiring processes such as the replenishment of oxygen stores in muscle and blood, replenishment of adenosine triphosphate and creatine phosphate stores, increased ventilation, increased heart rate, increased body temperature, increased triglyceride or fatty acid cycling, substrate utilization shifts from carbohydrates to fats, glycogen resynthesis, and increased sympathoadrenal activity (2–4,7,31,34). In addition, RT induces muscular protein breakdown (i.e., damage), which in turn invokes a healing response (i.e., synthesis) (9,33). The metabolic costs of protein synthesis are well documented (26); therefore, the degree of muscular damage may be a significant determinant in the EPOC response post-RT.

Thorton and Potteiger (29) report that high-intensity RT (85% 1 repetition maximum [1RM]) produces greater EPOC volume than lower intensity (45% 1RM) when equated for load-volume. However, in an alternative study, Thorton et al. (30) state that intensity did not influence EPOC in overweight African American women. As opposed to investigating the influence of intensity, the purpose of this study was to compare the effects of load-volume on EPOC after 2 bouts of RT. In previous investigations the absolute loads used during RT bouts were not held constant (5,12,13), except in one case in which rest periods were varied (16). In addition, none of the investigations used high-intensity protocols (≥85% 1RM) with high resistance-trained recreational lifters (5,12,13,27,29,30).

Back to Top | Article Outline

Methods

Experimental Approach to the Problem

Two RT bouts of equal intensity but different load-volumes were performed. Resting metabolic rate (RMR) was assessed both before (PM baseline and AM baseline to account for circadian shifts) and at 12, 24, 36, and 48 hours postexercise. Rating of perceived muscle soreness (RPMS) and creatine kinase (CK) levels, both indirect indicators of muscle damage, were also measured to determine if any differences in EPOC were because of greater muscular damage.

Back to Top | Article Outline

Subjects

Eight healthy men between the ages of 19 and 29 years volunteered for the experiment. Sample size estimation was based on an effect size of 1.1 from a previous study concerning acute effects of RT on EPOC (11). Subjects had at least 12 months of RT experience with no more than 2 weeks rest at a time, less than a total of 4 weeks off within the last 6 months, or 9 weeks off within the last 12 months. Subjects reported no previous or current use of illegal performance enhancing substances. This study was approved by the Florida State University Institutional Review Board, and all subjects signed a consent form informing them of the aims, procedures, and risks of the study. Subject characteristics are presented in Table 1.

Table 1

Table 1

Back to Top | Article Outline

Procedures

The general study design can be viewed in Figure 1. Four to seven days before the initiation of the first trial, subjects arrived at the laboratory for height/weight measurements (Seca Model 707; Columbia, MD, USA), body composition assessment via 3-site skinfold (Beta Technology, Inc., Santa Cruz, CA, USA), to undergo protocol familiarization for all exercises, and for 1RM testing. Subjects self-reported their approximate 8RM for each exercise. This weight was applied to a prediction table (1) to determine the first weight attempted for their 1RM. The load attempted was approximately 10 lbs lighter than predicted; 10 lb increments were used in most cases until a weight was attempted that the subject could not successfully lift. Three minutes of rest were provided between each lift, and limb placements were recorded to be used for better control during future experimental trials. Verbal encouragement was used for all lifts, and the last successful lift was recorded as the 1RM (Table 1).

Figure 1

Figure 1

Subjects were given a food diary log to record their diet 3 days before and 48 hours after the first exercise trial. Subjects were instructed to replicate this diet before and after the second experimental trial. Subjects refrained from RT for 72 hours before and from high-intensity aerobic exercise 48 hours before each trial as this represents adequate time for muscular recovery in trained subjects (9).

On the evening before the first trial, subjects reported to the laboratory at approximately 2000 hours (military time) after a 4-hour fast. Subjects underwent a 30-minute period of supine rest after which V[Combining Dot Above]O2 was collected to determine RMR and respiratory exchange ratio (RER) during a 30-minute period. A ParvoMedics' TrueMax 2400 metabolic cart (ParvoMedics, Sandy, UT, USA) was used to collect all metabolic data.

After the baseline evening RMR was taken, subjects slept overnight in the laboratory. Resting metabolic rate was once again determined the following morning before the exercise protocol at 0600 hours. Blood was drawn after the morning baseline RMR measurement to determine CK levels (8). After the blood draw and 30 minutes before exercise, subjects were fed a Balance Bar Gold containing 22 g of carbohydrates, 15 g of protein, and 7 g of fat. Trial order was randomized, and RPMS for 4 muscle groups were collected immediately before RT using a visual analog scale (25). During the exercise trials, indirect calorimetry was used to determine energy expenditure. Blood was also collected immediately postexercise. Subjects returned to the laboratory for the next 2 evenings at 2000 hours to have blood drawn and for RMR and RPMS measurements, and then stayed overnight for morning measurements. Subjects repeated these procedures with the alternate load-volume no earlier than 7 days after the initial exercise trial.

Back to Top | Article Outline

Creatine Kinase Analysis

Before RT, and immediately after, 12 , 24 , 36 , and 48 hours postexercise, subjects had approximately 25 ml of blood drawn from an antecubital vein using sterile venipuncture techniques. The blood was collected in EDTA-coated tubes and centrifuged for 10 minutes. Two clear non-hemolyzed serum samples were separated and stored at −80° C. Creatine kinase was determined by manual assay (Pointe Scientific, Inc., Detroit, MI, USA) (17).

Back to Top | Article Outline

Resistance Protocols

Each RT bout consisted of 4 exercises performed on a non-counterbalanced Smith Machine so that range of motion could be controlled for easily. A bench press, squat, bent-over row, and Romanian deadlift were used. One trial required lifting a total load-volume of 10,000 kg and the other a total load-volume of 20,000 kg. During pilot testing, the regression coefficients for RMR 24 hours after 10,000 and 20,000 kg trials were β = 0.977 (95% confidence interval [CI]: −1.984 to 4.194) and β = 0.971 (95% CI: −2.886 to 5.578), respectively.

The loads were divided between the 4 exercises as follows: 35% to squats, 30% to bench press, 20% to bent-over rows, and 15% to Romanian deadlift. For each set, subjects lifted approximately 85% of their 1RM for 6–8 repetitions. If 6 repetitions could not be completed at any point, the load was reduced by 10% for the subsequent set.

During each lifting session, 3 testers were present; one to monitor the metabolic cart, one to ensure proper range of motion, and one to monitor proper lifting form. Subjects were instructed to perform the concentric portion of each lift with maximal speed and ensure a controlled eccentric descent, although a specific time interval was not dictated. The tester monitoring lifting form, present during every lifting session, monitored the lifting speed to aid speed consistency without the use of a metronome. A set was stopped if subjects broke form and the repetition would not be counted. The subjects continued to perform sets until the load-volume for each respective trial was reached. Two-minute rest periods were given between sets.

Studies using load-volumes ranging from 3,000 to 6,000 kg do not report significant elevations in EPOC beyond 90 minutes (24,34). Greater load-volumes of approximately 11,000 kg and higher have been shown to increase RMR for up to 48 hours postexercise (11,35). The lower load-volume chosen for this study was similar to those used in the protocol by Dolezal et al. for one muscle group (11). The higher load-volume was similar to those used by both Gillette et al. (14) and Melby et al. (22); however, these studies used a lower intensity.

Back to Top | Article Outline

Statistical Analyses

The study followed a 2 × 6 and 2 × 5 within-subjects design with repeated measures in regards to CK and RPMS, respectively. A 2 × 3 design was used for metabolic measurements (nighttime baseline measure, after 12 hours, and after 36 hours), and a separate 2 × 3 design was used for alternate time points (morning baseline, after 24 hours, after 48 hours). Within-group differences were also examined. Repeated-measures analysis of variance was used to analyze the variance of experimental treatments. A Tukey HSD post hoc test was used to identify significant differences between mean values. Pearson product-moment correlations were used examine the relationship between CK and RMR. Significance for all tests was set at p < 0.05. Statistical analysis was performed using SPSS for Windows version 15.0 and 16.0 (SPSS, Inc., Chicago, IL, USA).

Back to Top | Article Outline

Results

All 8 subjects who initially volunteered completed the study. Data for the 2 exercise bouts are presented in Table 2. The exercise duration was significantly longer (p ≤ 0.01) for the 20,000 kg protocol (90.3 ± 16.1 minutes) compared with the 10,000 kg protocol (43.6 ± 7.9 minutes). Energy expended in kilocalories for each protocol was also significantly different (p < 0.01). Mean oxygen consumption was significantly greater (p ≤ 0.01) during both the 10,000 and 20,000 kg trials when compared with their respective morning baselines. Mean V[Combining Dot Above]O2 and RER did not differ both the between trials.

Table 2

Table 2

No significant differences in RMR were observed across time or between conditions. Data from metabolic measurements made in the AM and PM can be seen in Tables 3 and 4, respectively. The only significant changes (p < 0.05) were observed was between the 24- and 48-hour RER. As expected, PM baseline RMR trended higher as compared with the AM measurement but was not significantly different (p > 0.05). Data regarding indirect indicators of muscle damage are presented in Table 5, with the only significant difference (p < 0.05) in the 20,000 kg trial between 24 hours CK and before and after exercise measurements.

Table 3

Table 3

Table 4

Table 4

Table 5

Table 5

Back to Top | Article Outline

Discussion

The primary finding of this study was that high-intensity RT with load-volumes of 10,000 and 20,000 kg do not significantly affect RMR in highly trained recreational male lifters. The study is unique with regard to the training experience of the subjects, evidenced by training duration history and high 1RM measurements, and the lifting intensity, which was held constant between trials.

As subjects in this study were well adapted to RT, the training stimulus needed to elicit increases in EPOC arguably needed to be much higher compared with that used in previous research (11,22,23,27,35). Two studies using intensities of 70% 1RM report significant increases in RMR. Melby et al. (22) had subjects perform 6 sets of 10 different exercises for a total of 60 sets. The repetition range for this protocol was 8–12 repetitions per set. This amounts to approximately 600 repetitions performed during the course of the exercise bout. The range of load-volume lifted by these subjects was 15,000–38,000 kg. Gillette et al. (14) used a similar protocol having subjects complete 5 sets of 10 different exercises for a total of 50 sets. The repetition range was also 8–12 meaning approximately 500 repetitions were performed. The mean load-volume lifted by these subjects was approximately 25,000 kg. The load-volume difference between these studies and the higher load-volume in this study (20,000 kg) is relatively minor compared with the difference in effect size regarding EPOC. However, the subjects in this study completed their trials with a drastically lower number of repetitions, a mean of 199. If subjects in this study performed a similar number of repetitions the load-volume would have been close to 50,000 kg. Perhaps, this would have been the threshold to induce a significant EPOC response. In other words, perhaps repetition volume is also significant in addition to load-volume or intensity in elevating RMR postexercise. Hackney et al. (15) support this contention because RMR was elevated up to 72 hours postexercise in trained individuals with a lower load-volume than this study but a higher repetition volume, although this was observed when the eccentric component of the lift was emphasized. Both Dolezal et al. (11) and Hackney et al. (15) focused on longer eccentric contractions, which may have caused greater protein degradation (9), and therefore higher EPOC levels were needed for skeletal muscle protein repair. The independent effects of repetition volume, as opposed to load-volume, and contraction type should be further investigated.

Hackney et al. (15) report that higher EPOC is observed in untrained subjects as compared with trained (15). This is not surprising as many acute energetically costly responses to RT, particularly the sympathoadrenal response (34), are downregulated as individuals become better adapted. In addition, untrained individuals experience a far greater degree of muscular damage in response to RT (9). As protein synthesis required for repair is energetically expensive, it is logical that untrained subjects will show greater and longer alterations in EPOC post-RT. Judging by training history, strength levels, and CK responses, subjects in this study had most likely reached a higher level of adaptation than the ones in previous studies and therefore were less sensitive to the metabolic effects of recovery from RT.

Back to Top | Article Outline

Practical Applications

Although most practitioners understand that aerobically oriented exercise can provide a greater caloric expenditure during exercise, RT is often promoted as an effective modality for weight loss because of its potential increases in RMR for hours or days postexercise. However, as an individual becomes better adapted to RT, the increase in EPOC is so minor that it may not be practically important. Although RT is an important component in any weight loss program to attenuate the loss of fat-free mass and therefore better preserve RMR, it is unlikely that the total energetic cost (during and after exercise) of a typical duration workout will be adequate for significant weight reduction in highly trained recreational lifters without caloric restriction and/or additional aerobic or high-intensity interval training.

Back to Top | Article Outline

References

1. Baechle T, Earle R. Essentials of Strength and Conditioning. Champaign, IL: Human Kinetics, 2000.
2. Bahr R. Excess postexercise oxygen consumption—magnitude, mechanisms and practical implications. Acta Physiol Scand Suppl 605: 1–70, 1992.
3. Bahr R, Hansson P, Sejersted OM. Triglyceride/fatty acid cycling is increased after exercise. Metabolism 39: 993–999, 1990.
4. Bahr R, Sejersted OM. Effect of intensity of exercise on excess postexercise O2 consumption. Metabolism 40: 836–841, 1991.
5. Ballor DL, Katch VL, Becque MD, Marks CR. Resistance weight training during caloric restriction enhances lean body weight maintenance. Am J Clin Nutr 47: 19–25, 1988.
6. Binzen CA, Swan PD, Manore MM. Postexercise oxygen consumption and substrate use after resistance exercise in women. Med Sci Sports Exerc 33: 932–938, 2001.
7. Borsheim E, Bahr R, Hostmark AT, Knardahl S. Effect of beta-adrenoceptor blockade on postexercise oxygen consumption and triglyceride/fatty acid cycling. Metabolism 47: 439–448, 1998.
8. Brancaccio P, Lippi G, Maffulli N. Biochemical markers of muscular damage. Clin Chem Lab Med 48: 757–767, 2010.
9. Clarkson PM, Hubal MJ. Exercise-induced muscle damage in humans. Am J Phys Med Rehabil 81: S52–S69, 2002.
10. Deschenes MR, Kraemer WJ. Performance and physiologic adaptations to resistance training. Am J Phys Med Rehabil 81: S3–S16, 2002.
11. Dolezal BA, Potteiger JA, Jacobsen DJ, Benedict SH. Muscle damage and resting metabolic rate after acute resistance exercise with an eccentric overload. Med Sci Sports Exerc 32: 1202–1207, 2000.
12. Elliot D, Goldberg L, Kuehl K. Effect of resistance training on excess post-exercise oxygen consumption. J Strength Cond Res 6: 77–81, 1992.
13. Geliebter A, Maher MM, Gerace L, Gutin B, Heymsfield SB, Hashim SA. Effects of strength or aerobic training on body composition, resting metabolic rate, and peak oxygen consumption in obese dieting subjects. Am J Clin Nutr 66: 557–563, 1997.
14. Gillette CA, Bullough RC, Melby CL. Postexercise energy expenditure in response to acute aerobic or resistive exercise. Int J Sport Nutr 4: 347–360, 1994.
15. Hackney KJ, Engels HJ, Gretebeck RJ. Resting energy expenditure and delayed-onset muscle soreness after full-body resistance training with an eccentric concentration. J Strength Cond Res 22: 1602–1609, 2008.
16. Haltom RW, Kraemer RR, Sloan RA, Hebert EP, Frank K, Tryniecki JL. Circuit weight training and its effects on excess postexercise oxygen consumption. Med Sci Sports Exerc 31: 1613–1618, 1999.
17. Horder M, Magid E, Pitkanen E, Harkonen M, Stromme JH, Theodorsen L, Gerhardt W, Waldenstrom J. Recommended method for the determination of creatine kinase in blood modified by the inclusion of EDTA. The Committee on Enzymes of the Scandinavian Society for Clinical Chemistry and Clinical Physiology (SCE). Scand J Clin Lab Invest 39: 1–5, 1979.
18. Jakicic JM, Clark K, Coleman E, Donnelly JE, Foreyt J, Melanson E, Volek J, Volpe SL; American College of Sports Medicine position stand. Appropriate intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 33: 2145–2156, 2001.
19. Kraemer WJ, Ratamess NA, French DN. Resistance training for health and performance. Curr Sports Med Rep 1: 165–171, 2002.
20. Kraemer WJ, Volek JS, Clark KL, Gordon SE, Incledon T, Puhl SM, Triplett-McBride NT, McBride JM, Putukian M, Sebastianelli WJ. Physiological adaptations to a weight-loss dietary regimen and exercise programs in women. J Appl Physiol 83: 270–279, 1997.
21. Kraemer WJ, Volek JS, Clark KL, Gordon SE, Puhl SM, Koziris LP, McBride JM, Triplett-McBride NT, Putukian M, Newton RU, Häkkinen K, Bush JA, Sebastianelli WJ. Influence of exercise training on physiological and performance changes with weight loss in men. Med Sci Sports Exerc 31: 1320–1329, 1999.
22. Melby C, Scholl C, Edwards G, Bullough R. Effect of acute resistance exercise on postexercise energy expenditure and resting metabolic rate. J Appl Physiol 75: 1847–1853, 1993.
23. Melby CL, Tincknell T, Schmidt WD. Energy expenditure following a bout of non-steady state resistance exercise. J Sports Med Phys Fitness 32: 128–135, 1992.
24. Murphy E, Schwarzkof R. Effects of standard set and circuit weight training on excess post-exercise oxygen consumption. J Strength Cond Res 6: 88–91, 1992.
25. Price DD, McGrath PA, Rafii A, Buckingham B. The validation of visual analogue scales as ratio scale measures for chronic and experimental pain. Pain 17: 45–56, 1983.
26. Reeds PJ, Wahle KW, Haggarty P. Energy costs of protein and fatty acid synthesis. Proc Nutr Soc 41: 155–159, 1982.
27. Schuenke MD, Mikat RP, McBride JM. Effect of an acute period of resistance exercise on excess post-exercise oxygen consumption: Implications for body mass management. Eur J Appl Physiol 86: 411–417, 2002.
28. Sweeney ME, Hill JO, Heller PA, Baney R, DiGirolamo M. Severe vs moderate energy restriction with and without exercise in the treatment of obesity: Efficiency of weight loss. Am J Clin Nutr 57: 127–134, 1993.
29. Thornton MK, Potteiger JA. Effects of resistance exercise bouts of different intensities but equal work on EPOC. Med Sci Sports Exerc 34: 715–722, 2002.
30. Thornton MK, Rossi SJ, McMillan JL. Comparison of two different resistance training intensities on excess post-exercise oxygen consumption in African American women who are overweight. J Strength Cond Res 25: 489–496, 2011.
31. Viru A. Postexercise recovery period: Carbohydrate and protein metabolism. Scand J Med Sci Sports 6: 2–14, 1996.
32. Wadden TA, Vogt RA, Andersen RE, Bartlett SJ, Foster GD, Kuehnel RH, Wilk J, Weinstock R, Buckenmeyer P, Berkowitz RI, Steen SN. Exercise in the treatment of obesity: Effects of four interventions on body composition, resting energy expenditure, appetite, and mood. J Consult Clin Psychol 65: 269–277, 1997.
33. Walker DK, Dickinson JM, Timmerman KL, Drummond MJ, Reidy PT, Fry CS, Gundermann DM, Rasmussen BB. Exercise, amino acids, and aging in the control of human muscle protein synthesis. Med Sci Sports Exerc 43: 2249–2258, 2011.
34. Webber J, Macdonald IA. Metabolic actions of catecholamines in man. Baillieres Clin Endocrinol Metab 7: 393–413, 1993.
35. Williamson DL, Kirwan JP. A single bout of concentric resistance exercise increases basal metabolic rate 48 hours after exercise in healthy 59-77-year-old men. J Gerontol A Biol Sci Med Sci 52: M352–M355, 1997.
Keywords:

weight loss; intensity; weight training

Copyright © 2013 by the National Strength & Conditioning Association.