Previous investigators have concluded that the excess postexercise oxygen consumption produced after aerobic exercise may be an important contributor to weight management when exercise is performed on a regular basis (1,2,14,36). Excess postexercise oxygen consumption (EPOC) is the elevation of metabolic rate (V̇O2) above preexercise levels during recovery (8). Previous studies have demonstrated elevated V̇O2 after aerobic exercise of low to high intensities and short to long durations (1–4,14,30,36,37). This increase in metabolism after exercise may have important implications concerning weight control and obesity (1,2,4,14,36,37).
Evidence suggests that high-intensity intermittent exercise (interval training) has the greatest impact on the magnitude of EPOC, with most of the effect occurring during the fast component phase of EPOC (2,4,30). The caloric cost from EPOC under these conditions contributes a substantial portion of the total exercise energy expenditure. Recently, more studies have examined EPOC responses after resistance exercise (5,13,31,32). Generally, these studies have documented the EPOC responses to heavy-resistance exercise and circuit weight training (CWT) and have compared resistance exercise EPOC responses to those responses from aerobic modes of exercise. These studies suggest that resistance exercise produces greater EPOC responses than aerobic exercise, possibly due to greater alteration of homeostasis. For example, greater heart rate, ventilatory rate, and lactate levels are produced during resistance exercise than during aerobic exercise at the same relative V̇O2 (5).
Previous resistance exercise research has established that rest interval duration between sets is a very potent factor influencing physiological responses to resistance exercise (26–29). CWT uses short rest interval durations of 15–60 s in between sets depending upon the workload of each lift (9–12,38,39). To our knowledge, no studies have documented EPOC responses to heavy-resistance exercise or CWT after manipulation of rest interval duration. These data would be important for the development of resistive exercise regimens that are used as a means of affecting caloric expenditure. Therefore, we designed a study to determine whether a CWT protocol using short, 20-s rest intervals would produce a different 1-h EPOC response than a CWT protocol using longer, 60-s rest intervals. We used 20-s and 60-s rest intervals because they closely represented the range of rest interval duration used for CWT protocols (9–12,38,39). Moreover, W. J. Kraemer et al. (26–29) have shown that decreasing rest interval length will increase physiological (hormonal and metabolic) responses to resistance training. Thus, we expected dissimilar physiological responses to the CWT protocols. We examined EPOC for 1-h after exercise since pilot data revealed that rest interval manipulation did not produce V̇O2 and other physiological differences beyond 1-h postexercise, although metabolism remained slightly elevated for both protocols. We hypothesized that a 20 s rest interval between sets of a CWT protocol would elicit a greater 1-h EPOC response than a 60-s rest interval.
The study was approved by the Southeastern Louisiana University Institutional Review Board and all subjects gave written consent to participate in the study. Each subject completed two preliminary and two experimental sessions. Each session was separated by 7 d, and the subjects were instructed not to exercise 2 d before testing.
Seven adult men participated in this study. The men had the following descriptive characteristics: mean (± SE) age 26.9 ± 1.4 yr; height 180.4 ± 2.8 cm; weight 85.4 ± 3.0 kg; body fat 16.1 ± 0.6%; fat-free mass 71.5 ± 2.2 kg; and V̇O2max 48.4 ± 1.7 mL·kg−1·min−1. The men completed a medical history questionnaire to screen for cardiovascular and metabolic disorders. All of the men reported a minimum of 6 months of experience with resistance exercise training. The men also reported no prior use of anabolic steroids or any current medications that would alter basal metabolism.
In the first session, all of the subjects were tested to determine V̇O2max (17) and body composition. Each subject completed a modified Astrand treadmill protocol to exhaustion (35) on a motorized treadmill that was interfaced with a 12-lead EKG. An automated metabolic analysis system (Rayfield Equipment Ltd., Waitsfield, VT, or Consentius Technologies, Sandy, UT) was used to determine V̇O2max in session 1 and V̇O2 in subsequent sessions. During the study, the metabolic system was updated from Rayfield to Consentius software; however, the same O2 and CO2 analyzers (Ametek S-3A/1 and CD·3A) were used with both systems. Before each metabolic measurement, the gas analyzers were calibrated with gases of known composition. We configured both systems to measure the O2 consumption every 30 s and both systems measured the O2, CO2, and flow signals continuously within the 30 s time period. Five of the subjects completed all testing with the Rayfield system; two subjects completed all tests with the Consentius system. We compared the two systems simultaneously by treadmill testing 10 subjects at a steady workload and determined that the systems produced very similar results. There was a mean difference of 5%, which is comparable to the limits of variation obtained by repeated studies (19) and an intraclass correlation of R = 0.9926. Before the V̇O2max test, body composition was determined using a four site skin-fold measurement (18).
In the second session we determined 75% of a 20-repetition maximum (20-RM) load for eight exercises: 1) leg press, 2) bench press, 3) leg extension, 4) lat-pull, 5) leg curl, 6) seated row, 7) triceps extension, and 8) biceps curl. All of the exercises were performed on standard resistance equipment (Master Trainer 1 and BK 602 Super Jungle, Body Master, Rayne, LA; Gladiator/SR-5 Station, Universal Gym Equipment, Fresno, CA). The load that was used in the present study, 75% of a 20-RM (41.4% of 1-RM), allowed all subjects to complete the same amount of work for both protocols (20 RI and 60 RI) and also represented a load commonly used for circuit weight training. Circuit weight training is performed typically at a resistance of 40–60% 1-RM (6). To determine a 20-RM for each exercise, the subjects attempted to lift 20 repetitions at 40% of the estimated 1-RM attained through a resistance exercise questionnaire. Ten pounds were added to each exercise (40% of 1-RM + 10 lbs) until the subjects were not able to complete 20 repetitions. At this point, the greatest completed exercise load was considered to be the 20-RM. Subjects were allowed to rest 5–10 min between successive attempts and the exercise stations were alternated between upper and lower body movements to prevent muscle fatigue. For each exercise, the distance the weight was displaced was determined with metal meter sticks and pointers mounted to the resistive exercise equipment in an effort to maintain consistency of work per repetition in subsequent sessions.
Session 3 and 4.
In sessions 3 and 4, the subjects completed one of two randomly assigned CWT protocols; each protocol was completed at 75% of a 20-RM load for all exercises. The only difference between the two protocols was that one protocol used 20-s rest intervals (20 RI) and the other used 60-s rest intervals (60 RI). Subjects reported to the laboratory for sessions 3 and 4 at 0630 h. Each subject completed both protocols. Meals were not standardized before sessions 3 and 4; however, subjects were instructed not to eat after 8:00 p.m. the night before. Thus, all subjects began each session in an overnight fasted condition to avoid any alteration in resting metabolism due to dietary thermogenesis. Resting V̇O2, heart rate, and blood pressure were recorded during the final 15 min of a 30-min preexercise session with the subject in a supine position. Both CWT protocols began at the leg press station and were completed after two circuits equaling 16 stations. The stations were completed in the same order as session 2. All repetitions were performed at a pace of one repetition for every 1.5 s set by a metronome. After the completion of the 20th repetition, the subjects moved to the next station and were instructed to rest for either 20 or 60 s. All subjects completed 20 repetitions at each station for both protocols. Oxygen consumption was measured continuously in 30 s intervals throughout the preexercise resting period, CWT exercise, and 1-h recovery. The metabolic analysis system was mounted on a movable cart that could be easily maneuvered with the subjects as they changed exercise stations.
Total volume of work (J) completed during exercise was calculated by multiplying the resistance load by the stack displacement and the number of repetitions per set. Magnitude of 1-h EPOC was calculated by the equation: [Total Gross Recovery V̇O2 − (V̇O2 rest·min of recovery)]. Net and gross caloric expenditure (kcal) during exercise and recovery were calculated by multiplying the oxygen consumption values by the caloric equivalents 5.05 kcal·L−1 and 5.00 kcal·L−1, respectively. Caloric equivalents have been used previously to estimate energy expenditure (EE) from resistance exercise (13,32) because resistance exercise greatly affects blood pH and the bicarbonate buffering pool during exercise and recovery, rendering the use of respiratory exchange ratios inaccurate. Thus, we did not use respiratory exchange ratio (RER) values to compute EE in the present study; however, we have reported resting preexercise RER values and exercise RER values to compare metabolic conditions before and during exercise for both protocols.
Wilcoxon matched pairs t-tests were used for the following: 1) to confirm that preexercise V̇O2, heart rate, and blood pressure did not differ between the two protocols; 2) to assess whether the two protocols produced different responses for net V̇O2 (L), net EE (kcal), average V̇O2 (mL·min−1), average EE (kcal·min−1), and average RER during exercise; and 3) to determine whether the two protocols produced different responses for 1-h EPOC (L), 1-h EPOC EE (kcal), and total gross (exercise + recovery) EE (kcal). Post hoc power analyses were conducted for a sample size of seven, comparing group differences using dependent t-tests (P < 0.05). Power to detect effect size differences of 0.95 or greater was 0.70. If the value of 0.80 was used as the lower limit of large effect sizes, the power of these analyses was 0.60 (21).
To determine whether V̇O2 during exercise was greater during the 20 RI protocol than the 60 RI protocol, V̇O2 values at six time points during exercise were analyzed using a 2 × 6 (trial × time point) repeated-measures ANOVA. V̇O2 was measured in 30-s time intervals. Due to the difference in rest interval duration, V̇O2 measurements taken immediately after the exercise set occurred for both protocols after six exercise sets: 1, 4, 7, 10, 13, and 16. To examine the recovery V̇O2 responses from 0 to 60 min postexercise in 5-min intervals, a 2 × 13 (trial x time point) repeated-measures ANOVA was conducted.
Wilcoxon t-tests revealed no significant differences for resting V̇O2, heart rate, RER, or resting systolic and diastolic blood pressures (SBP, DBP) between the 20 RI and 60 RI CWT groups (Table 1). Individual values for resting V̇O2, heart rate, SBP, and DBP were all between the 50th and 100th percentile scores for their age (35).
The mean (± SEM) total volume of external work for each protocol was the same, 3.62·105 ± 1.91·104 J. During both CWT protocols, subjects exercised for 8 min, but due to the different rest intervals, the 20 RI CWT protocol was of shorter duration than the 60 RI protocol, 13 min compared with 23 min, respectively. The average exercise V̇O2 from continuous 1-min intervals (Table 2) was greater during the 20 RI protocol due to the shorter rest intervals. The net exercise V̇O2 for the 60 RI protocol was significantly higher than the 20 RI protocol due to the longer rest intervals. RER was not significantly different between the 20 RI and 60 RI CWT protocols and remained above 1.0 for all subjects during both protocols.
Figure 1 represents the mean V̇O2 values measured immediately after the 20th repetition of sets 1, 4, 7, 10, 13, and 16 during the two CWT protocols. The repeated-measures ANOVA analyzing these data yielded a significant main effect for trial [F (1,12) = 6.48, P < 0.05] and time [F (5,60) = 9.44, P < 0.0001]. The significant trial main effect indicated that across these six time points, V̇O2 during exercise was significantly higher during the 20 RI protocol than the 60 RI protocol (Fig. 1). Although the trial × time interaction did not reach significance, we thought it important to verify V̇O2 differences between protocols at specific time points. Therefore, the postset V̇O2 values of the 20 RI and 60 RI trials at each time point were compared using t-tests. The results indicated significant differences at time points 4, 7, 10, 13, and 16.
One-hour EPOC was significantly greater after the 20 RI CWT protocol than after the 60 RI CWT protocol (Table 3). The net recovery EE for the 20 RI CWT protocol was also significantly greater than that of the 60 RI CWT protocol (Table 3).
V̇O2 at each 5-min time point after CWT is shown in Figure 2. V̇O2 remained significantly elevated above resting baseline levels for all participants 1-h post exercise. A repeated-measures ANOVA revealed no main effect for group [F (1,12) = 3.03, P = 0.1073]. Mean 1-h recovery V̇O2 responses were 0.53 ± 0.04 L·min−1 and 0.488 ± 0.032 L·min−1 for the 20 RI and 60 RI conditions, respectively. However, there was a significant time effect [F (12,144) = 492.73, P = 0.0001) and interaction [F (12,144) = 8.739, P = 0.0047). These two significant values reflect the Geisser-Greenhouse adjustment. t-tests investigating the significant interaction indicated that V̇O2 was significantly higher at time 0 and 5 min for the 20 RI protocol.
Combined V̇O2 and energy expenditure of exercise and recovery.
Because the total gross V̇O2 and EE for exercise alone was higher for the 60 RI than the 20 RI protocol, whereas the total gross V̇O2 and EE for recovery alone was higher in the 20 RI than the 60 RI protocol, we compared the total combined exercise and recovery EE of both protocols. The 60 RI gross total EE (exercise + recovery) was 277.23 ± 11.36 kcal, which was greater than the 242.21 ± 8.13 kcal produced by the 20 RI protocol. This difference was due to longer exercise rest intervals during the 60 RI protocol.
In the present study we found that short rest intervals (20 s, 20 RI) between sets of a typical CWT protocol elicited a greater 1-h recovery EPOC and subsequent EE than a CWT protocol with longer rest intervals (60 s, 60 RI). The mean 1-h recovery EPOC 10.3 L and 7.4 L represented an average elevation in V̇O2 above rest of 39.4% and 30.6%, respectively. In addition, the estimated 1-h recovery EE after the 20 RI and 60 RI CWT protocols represented approximately 21.2% and 13.4% of the total gross EE (exercise + recovery) for the two CWT sessions.
The EPOC produced by both the 20 RI and 60 RI trials can be attributed to a number of physiological mechanisms including: 1) elevated body temperature (Q10 effect), 2) elevated hormone levels, 3) replenishment of ATP and PC stores, 4) replacement of O2 in circulation and in muscle, 5) elevated ventilatory rate, 6) elevated heart activity, 7) oxidation of lactate, 8) glycogen resynthesis, and 9) sodium-potassium pump activity (2,8,33). Although all of the factors above could have affected the EPOC of the two CWT protocols in the present study, two factors have been attributed to the finding that weight training exercise produces greater EPOC than aerobic exercise (5). One is the large hormonal responses that can alter metabolism, specifically catecholamines, cortisol, and growth hormone (GH) (7,22–27). The other is tissue damage and accompanying stimulus for hypertrophy of tissue. Catecholamines have been shown to rise in response to resistive exercise, although training does not appear to alter these responses (15,25). Additionally, cortisol has been shown to rise in response to greater repetitions and lighter resistance (10 RM) versus fewer repetitions heavier resistance (5 RM); moreover, increasing the rest interval from 1 min to 3 min reduced the cortisol response (28). Finally, these same acute program variables (repetition, resistance, and rest interval duration) during heavy-resistance exercise have been shown to have much the same effect on GH (27,28) as cortisol, and we have previously shown that even low-volume resistive exercise with moderate rest periods (10 RM, 2-min rest intervals) produces substantial increases in GH (22,23).
It has been shown that the magnitude of a measured response to resistance exercise is dependent upon the intensity or stress of the resistance exercise which is determined by the interaction between volume of work, resistance load, set duration, and rest interval duration (26–29). In the present study the volume of work, resistance load, and set duration were held constant for both CWT protocols, whereas rest interval duration was manipulated. The majority of the difference in the EPOC responses to the two protocols was observed during the initial 5 min of the 1-h recovery period (times 0 and 5 during recovery were significantly different, see Fig. 2), indicating that shorter rest intervals in CWT result in greater rapid component EPOC. A greater V̇O2 after set 16 for the 20 RI compared with the 60 RI protocol is consistent with previous studies in which the magnitude of the rapid component V̇O2 after cycling exercise (within first 5 min) was related to exercise intensity (16). This would be expected because the depletion of creatine phosphate and ATP during the initial phase of submaximal exercise is also determined by exercise intensity (16,20).
No studies exist that have examined the effects of rest interval duration on EPOC responses to CWT. We are aware of one study that has examined postexercise V̇O2 responses of treadmill exercise and compared those with responses from a resistive exercise protocol considered to be CWT. Burleson et al. (5) have recently reported the V̇O2 responses after a 27-min bout of CWT to be 0.41 L·min−1, 0.32 L·min−1, and 0.33 L·min−1 at 30, 60, and 90 min postexercise, respectively. A 30-min postexercise V̇O2 of 19.0 L (includes resting V̇O2) was reported. The CWT protocol used by Burleson et al. (5) resembled the 60 RI CWT protocol used in the present study in number of circuits (two), exercise stations (eight), rest interval durations (60 s), but employed a greater resistance load (60% of 1-RM compared with 41% of 1-RM in present study) and longer work interval durations (45 s compared with 30 s in present study). Moreover, resting metabolic rate of their subjects was higher than that in the present study (0.30 L·min−1 vs 0.28 L·min−1). All of these differences probably accounted for a greater postexercise V̇O2 reported in their study than in the present study.
Gillette et al. (13) demonstrated that postexercise oxygen consumption was 6.8% higher than controls for 5 h after 50 sets of 8–12 repetitions at 70% of 1-RM with 2-min rest intervals. The protocol in this previous study would not be considered a CWT protocol due to the 2-min rest intervals and higher workload. However, the 5-h EPOC after resistance exercise in their study was 12.6 L, which was comparable to the 10.3 L 1-h EPOC produced from the 20 RI CWT protocol in the present study, suggesting that CWT with short rest intervals may produce a greater EPOC than heavy resistive exercise. This may be explained by higher metabolic rates during CWT exercise compared with heavy-resistance exercise. In support of this contention, Pichon et al. (34) have reported the average EE for a typical heavy-resistance exercise protocol to be less than the average energy expenditure for CWT exercise.
Although we did not have a control session without exercise, we did incorporate a 30-min resting session before each CWT protocol. With this design, we were able to verify that 1) resting conditions before exercise were similar for both trials and 2) compare the exercise/recovery responses to the resting trial on the day of the experimental trial, controlling for diurnal variation.
The total EE (exercise + recovery EE) was significantly different between the two circuit weight training protocols. The EPOC EE was higher in the 20 RI protocol, but the contribution of the longer rest intervals in the 60 RI protocol produced higher exercise 60 RI EE. If we compare the frequency required to lose 1 lb of fat for the 20 RI and 60 RI exercise + 1-h recovery, it would require approximately 14 sessions for the 20 RI protocol (14.45 sessions × 242. 21 kcal/session = 3500 kcal) and approximately 13 sessions for the 60 RI protocol (12.625 sessions × 277.23 kcal/session = 3500 kcal). These data have important practical applications for resistive exercise prescription. The data suggest that individuals may use a more tolerable exercise intensity with longer rest intervals between sets (60 s) for a CWT protocol and burn slightly more total calories (exercise + recovery) than would be burned with the same CWT protocol using 20-s rest intervals. Conversely, individuals who can tolerate a higher intensity (20-s rest intervals) can burn slightly fewer calories (exercise + recovery) in approximately half the exercise time (13 min) because 1-h EPOC is significantly increased after exercise.
As men who use a 60 RI CWT protocol become more trained, it may be appropriate for them to reduce the rest interval length, allowing them to receive a higher training stimulus to increase fitness level. This will reduce the amount of time required to exercise. Of course, the resistance load should be increased as the subjects adapt to the CWT protocol to maintain the %20-RM. The effect of weeks or months of CWT on exercise and recovery V̇O2 is unknown.
In conclusion, this is the first study to determine that shortening the rest interval duration of CWT will increase 1-h EPOC during recovery and thus affect the caloric cost from resistive exercise. However, when total caloric costs from both exercise and recovery are examined, the effect of a 60-s rest interval yields slightly higher total caloric cost from CWT. Results indicate that both energy cost of the exercise session and recovery period should be taken into account when calculating total caloric cost of a resistive exercise bout. Future research should be conducted to establish the energy cost of CWT (exercise + recovery EPOC) when volume of work, resistance load, and set durations are manipulated. In addition, duration of EPOC after CWT exercise protocols needs to be examined. Finally, results of the study suggest that research is needed to determine how long-term (weeks and months) CWT affects metabolic responses to CWT in normal and obese populations.
The authors thank the subjects who volunteered to participate in this study. Their enthusiasm and cooperation to enhance the knowledge and understanding of the benefits of circuit weight training was an inspiration.
1. Bahr, R., I. Ingnes, O. Vaage, O. Sejersted, and E. Newsholme. Effect of duration of exercise on excess post-exercise O2
consumption. J. Appl. Physiol. 62:485–490, 1987.
2. Bahr, R., O. Gronnerod, and O. Sejersted. Effect of supra-maximal exercise on excess post-exercise O2
consumption. Med. Sci. Sports Exerc. 24:66–71, 1992.
3. Brehm, B., and B. Gutin. Recovery energy expenditure for steady state exercise in runners and nonexercisers. Med. Sci. Sports Exerc. 18:205–210, 1986.
4. Brockman, L., K. Berg, and R. Latin. Oxygen uptake during recovery from intense intermittent running and prolonged walking. J. Sports Med. Phys. Fitness 33:330–336, 1993.
5. Burleson, M. A., H. S. O’Bryant, M. H. Stone, M. A. Collins, and T. T. McBride. Effect of weight training exercise and treadmill exercise on elevated post-exercise oxygen consumption. Med. Sci. Sports Exerc. 30:518–522, 1998.
6. Fleck, S. J., and W. J. Kraemer. Designing Resistance Training Programs, 2nd Ed. Champaign, IL: Human Kinetics, 1997, p. 96.
7. Fry, A. C., W. J. Kraemer, F. Van-Borselen, et al. Catecholamine responses to short-term high-intensity resistance exercise overtraining. J. Appl. Physiol. 77:941–946, 1994.
8. Gaesser, G. A., and G. A. Brooks. Metabolic bases of excess post-exercise oxygen consumption: a review. Med. Sci. Sports Exerc. 16:29–43, 1984.
9. Gettman, L., J. Ayers, M. Pollock, and A. Jackson. The effect of circuit weight training on strength, cardiorespiratory function, and body composition of adult men. Med. Sci. Sports 10:171–176, 1978.
10. Gettman, L., J. Ayers, M. Pollock, L. Durstine, and W. Grantham. Physiologic effects on adult men of circuit strength training and jogging. Arch. Phys. Med. Rehabil. 60:115–120, 1979.
11. Gettman, L., L. Culter, and T. Strathman. Physiologic changes after 20 weeks of isotonic vs. isokinetic circuit training. J. Sports Med. 20:265–274, 1980.
12. Gettman, L., P. Ward, and R. A. Hagan. Comparison of combined running and weight training with circuit weight training. Med. Sci. Sports Exerc. 14:229–234, 1982.
13. Gillette, C. A., R. C. Bullough, and C. L. Melby. Postexercise energy expenditure in response to acute aerobic or resistive exercise. Int. J. Sports Nutr. 4:347–360, 1994.
14. Gore, C., and R. Whithers. Effect of exercise intensity and duration on post-exercise metabolism. J. Appl. Physiol. 68:2362–2368, 1990.
15. Guezennec, Y., L. Leger, F. Lhoste, M. Aymond, and P. C. Pesquies. Hormone and metabolic response to weight lifting training sessions. Int. J. Sports Med. 7:100–105, 1986.
16. Hagberg, J. M., J. P. Mullin, and F. J. Nagle. Effect of work intensity and duration on recovery O2
. J. Appl. Physiol. 48:540–544, 1980.
17. Howley, E. T., D. R. Bassett, and H. G. Welch. Criteria for maximal oxygen uptake: review and commentary. Med. Sci. Sports Exerc. 27:1292–1301, 1995.
18. Jackson, A. S., and M. L. Pollock. Generalized equations for predicting body density of men. Br. J. Nutr. 40:497–504, 1978.
19. Jones, N. Clinical Exercise Testing, 4th Ed. Philadelphia: W. B. Saunders, 1997, pp. 164–165.
20. Karlsson, J., and B. Saltin. Lactate, ATP, and Cp in working muscles during exhaustive exercise in man. J. Appl. Physiol. 29:598–602, 1970.
21. Kraemer, H. C. How Many Subjects? Statistical Power Analysis in Research. Newbury Park, CA: Sage Publications, 1987.
22. Kraemer, R. R., R. J. Heleniak, J. L. Tryniecki, G. R. Kraemer, N. J. Okazaki, and V. D. Castracane. Follicular and luteal phase hormonal responses to low-volume resistive exercise. Med. Sci. Sports Exerc. 27:809–817, 1995.
23. Kraemer, R. R., J. L. Kilgore, G. R. Kraemer, and V. D. Castracane. Growth hormone, IGF-I, and testosterone responses to resistive exercise. Med. Sci. Sports Exerc. 24:1346–1352, 1992.
24. Kraemer, W. J. Endocrine responses to resistance exercise. Med. Sci. Sports Exerc. 20:S152–S157, 1988.
25. Kraemer, W. J., A. C. Fry, B. J. Warren, et al. Acute hormonal responses in elite junior weightlifters. Int. J. Sports Med. 13:103–109, 1992.
26. Kraemer, W. J., L. Marchitelli, S. Gordon, et al. Hormonal and growth factor responses to heavy resistance exercise protocols. J. Appl. Physiol. 69:1442–1450, 1990.
27. Kraemer, W. J., S. Gordon, S. Fleck, et al. Endogenous anabolic hormonal and growth factor responses to heavy resistive exercise in males and females. Int. J. Sports Med. 12:228–235, 1991.
28. Kraemer, W. J., J. Dziados, L. Marchitelli, et al. Effects different heavy resistance exercise protocols on plasma beta endorphin concentrations. J. Appl. Physiol. 74:450–459, 1993.
29. Kraemer, W. J., S. Fleck, J. Dziados, et al. Changes in hormonal concentrations after different heavy resistance exercise protocols in women. J. Appl. Physiol. 75:594–604, 1993.
30. Laforgia, J., R. T. Withers, N. J. Shipp, and C. J. Gore. Comparison of energy expenditure elevations after submaximal and supramaximal running. J. Appl. Physiol. 82:661–666, 1997.
31. Melby, C. L., T. Tincknell, and W. D. Schmidt. Energy expenditure following a bout of non-steady state resistance exercise. J. Sports Med. Phys. Fitness 32:128–135, 1992.
32. Melby, C. L., C. Scholl, G. Edwards, and R. Bullough. Effect of acute resistance exercise on postexercise energy expenditure and resting metabolic rate. J. Appl. Physiol. 75:1847–1853, 1993.
33. Ogaki, T., A. Saito, S. Kanaya, and T. Fujino. Plasma sulpho-conjugated catecholamine dynamics up to 8 h after 60-min exercise at 50% and 60% maximal oxygen uptakes. Eur. J. Appl. Physiol. 72:6–11, 1995.
34. Pichon, C. E., G. R. Hunter, M. Morris, R. L. Bond, and J. Metz. Blood pressure and heart rate response and metabolic cost of circuit versus traditional weight training. J. Strength Condit. Res. 10:153–156, 1996.
35. Pollock, M. L., and J. H. Wilmore. Exercise in Health and Disease: Evaluation and Prescription for Prevention and Rehabilitation
, 2nd Ed. Philadelphia, W. B. Saunders, 1990.
36. Quinn, T., N. Vroman, and R. Kertzer. Post exercise oxygen consumption in trained females: effect of exercise duration. Med. Sci. Sports Exerc. 26:908–913, 1994.
37. Sedlock, D., J. Fissinger, and C. Melby. Effect of exercise intensity and duration on post exercise energy expenditure. Med. Sci. Sports Exerc. 21:662–666, 1989.
38. Wilmore, J. H., R. B. Parr, P. Ward, et al. Energy cost of circuit weight training. Med. Sci. Sports. 10:75–78, 1978.
39. Wilmore, J. H., R. B. Parr, R. N. Girandola, et al. Physiological alterations consequent to circuit weight training. Med. Sci. Sports. 10:79–84, 1978.