Different sports require athletes to possess various components of functional ability (e.g., strength, muscle mass, power, and cardiovascular endurance) to excel. Unfortunately, enhancing each of these variables can take a considerable amount of time, with hypertrophic, strength, and cardiovascular gains occurring several weeks after initiation of training (10). One way that strength and conditioning professionals approach this difficulty is through using concurrent endurance and strength training. Concurrent training is operationally defined as endurance and strength training in immediate succession or with up to 24 hours of recovery separating the 2 exercise modes. Although concurrent training allows for optimization of time while attempting to train multiple components of functional ability, this method may hinder adaptations compared with training performed independently (10). It appears that concurrent training can increase strength, though not to the same extent as strength training alone (15,23,25,27,33), whereas cardiovascular adaptations are not affected by the inclusion of resistance training (5,12,17,18,25,27).
Concurrent training was first systematically studied 30 years ago by Hickson (18), who found that the combination of endurance and strength training led to diminished increases in strength compared with strength training alone, giving indication that endurance training hindered strength gains. These findings gave way to the concept of “interference” describing the effect of concurrent training (18). A number of theories have been developed regarding the mechanisms or causes of interference: specificity of training or differential adaptation (endocrine and neuromuscular responses) (12,17,18,20), cell signaling in the form of AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) (2,16,19,24,32), and the acute fatigue theory (1,5,9,15,20,31).
Determination of the interference effect sparked a new field of study; however, though more than 30 years have passed since the initial publication, the available research is equivocal and the exact mechanisms of this interference effect are largely still unknown. Of the aforementioned theories, it is of our interest to assess interference induced by acute fatigue. Sporer and Wenger (30) analyzed the effects of varying recovery periods during a concurrent training session on leg and bench press repetitions using high-intensity (3 sets of six 3-minute intervals at maximum heart rate [MHR]) and low-intensity (36 minutes at 70% maximum power associated with V[Combining Dot Above]O2max) aerobic exercise bouts. They found that at 4 and 8 hours postexercise, individuals could not replicate the same number of repetitions as in the control protocol, and to do so, 24 hours of rest was necessary (30). This finding indicates that acute responses play a role in the interference mechanism. More importantly, the accumulation of the acute physiological interference, when applied over a chronic training program, may lead to suboptimal training adaptations.
It is possible that interference occurs as a result of local fatigue induced when aerobic exercise precedes resistance exercise. This has been shown when comparing lower-body (leg press) with upper-body (bench press) strength performance after lower-body aerobic exercise (9). Bench press performance, as measured by repetitions completed, was not hindered by the preceding aerobic exercise. Although acute fatigue induced by cycle ergometry hinders leg press performance, the mechanisms of this effect are not yet known.
Acute fatigue could occur through neuromuscular mechanisms, affecting muscle activation, through electromyography (EMG), and maximal force generation. The amount of muscle mass and load used during training determine the effect and scope of performance-enhancing adaptations. Prior endurance activity could lead to suboptimal activation and force production and therefore the observed interference of performance adaptations. Although no acute responses regarding the effects of prior aerobic exercise on EMG pattern have been documented, chronic adaptations of muscle activation have been analyzed after a 22-week concurrent training program (15). It was observed that activation of the right and left vastus lateralis had a nonsignificant increase of 29 and 22% for the concurrent training group and 26 and 19%, respectively, in those completing strength training only. Although these results suggest that suppressed EMG activity does not occur with concurrent training, it must be noted that the individual concurrent training sessions were separated by 24 hours, which has shown no acute interference (30). Therefore, it is plausible that an acute bout of aerobic exercise immediately occurring before a resistance exercise session causes decreased activation of the exercised muscle group (EMG activity) and maximal force generation, which would in turn lead to performance decrements.
Gaining insight into the mechanisms that induce fatigue during concurrent training could provide practitioners information on how to program training protocols to effectively avoid or minimize these detrimental effects. It is possible that the aforementioned mechanisms of interference occur as a result of accumulated acute neuromuscular and metabolic responses, thus causing the compromised strength and hypertrophic gains, as speculated by current literature (9,11,21,22). Coincidentally, the lack of interference and fatigue associated with lower-body aerobic exercise on a subsequent upper-body resistance exercise provides a base of which to assess the differing theories of interference (local vs. systemic). Therefore, it was the intent of this investigation to compare how an acute fatiguing bout of cycle ergometry affects the metabolic and neuromuscular milieu and subsequent upper-body (bench press) or lower-body (back squat) resistance exercise performances. We hypothesized that a preceding cycle exercise would attenuate exercise performance of the lower body, with no effect on upper-body performance.
Experimental Approach to the Problem
This study was designed to compare the acute metabolic and neuromuscular responses to an acute bout of (a) aerobic endurance exercise preceding upper-body strength exercise, (b) upper-body strength exercise, (c) aerobic endurance exercise preceding lower-body strength exercise, and (d) lower-body strength exercise. The approach of this design loosely follows that of de Souza et al. (9), in that both studies observed the acute effects of concurrent training on subsequent upper-body and lower-body resistance exercise. However, we used a longer aerobic exercise protocol, separated upper-body and lower-body resistance exercise sessions by 1 week, incorporated the back squat instead of leg press, and required different intensity and sets of resistance exercise while also analyzing metabolic and neuromuscular variables associated with acute fatigue. Therefore, based on the limited knowledge of the acute effects of interference, we hypothesized that aerobic exercise would result in a reduction of repetitions performed during the back squat but not bench press when compared with a control of no aerobic exercise. Finally, we expected preceding aerobic exercise to cause an immediate increase in blood lactate, and a decrease in EMG, maximal voluntary contraction (MVC), and EMG:force for the back squat but not bench press.
Fifteen men (aged 21–40 years) were recruited to participate. Of the 15 men recruited, 9 were determined resistance-trained after 1RM testing. The classification of “resistance trained” was defined by the ability to back squat 1.5 times body weight and bench press 1.2 times body weight and also having participated in a structured exercise training program for no less than 2.5 hours per week over the 6 months before testing. Guidelines such as these allow for a standardization of training status and also helped to minimize the repeated-bout effect of training. Subject descriptive characteristics are presented in Table 1. Before participation, each subject was informed of all procedures, potential risks, and benefits associated with the study both verbally and in written form in accordance with the procedures approved by the university review board for human subjects research. Subjects completed a health history and physical activity assessment, and a detailed description of the procedures, before inclusion within the investigation. Upon inclusion, subjects were asked to continue their normal daily routine, including prescribed medications, diet, sleep, and prior physical activity throughout the duration of the study, but were required to refrain from consuming any nutritional supplements before exercise testing and to abstain from exercise in the 48-hour period before each exercise session.
The initial laboratory visit occurred 1 week before the first experimental session in the morning after 1 hour of fasting (water was allowed ad libitum). For all following sessions, subjects tested at the same time of day as their initial laboratory visit. During the subjects' initial visit, height and body weight were measured using conventional equipments. After anthropometric measurements, subjects underwent a 1RM test for both the back squat and the bench press (3). Upon successful determination of inclusion, subjects reported back to the laboratory 72 hours after the initial visit and underwent a graded exercise test (GXT) using a cycle ergometer (Monark 828E; Monark, Vansbro, Sweden) to determine MHR for use during the aerobic exercise prescription.
Strength testing began with a general warm-up of 5 minutes on a cycle ergometer. Before each separate lift (bench press and back squat), subjects performed a warm-up set of 8–10 repetitions with a lightweight. The weight was then progressively increased for the subsequent trials until no more than 1 repetition could be completed, according to the guidelines for testing 1RM set forth by the National Strength and Conditioning Association (3). An acceptable lift for the bench press involved a controlled descent in which the bar briefly touched the chest before concentric contraction. Once the arms were fully lowered, a verbal press command was given and the bar pressed upward until achievement of full extension. For a complete lift to be awarded, both feet maintained contact with the floor at all times with the buttocks, shoulders, and head in contact with the bench. For the back squat, subjects unracked the weight and walked back, standing with the knee joint fully extended no more than 1 m away from the squat rack. The lifter then, under control, descended until 90° at the knee or lower, at which a verbal “up” command was given. Once fully standing, the bar was racked and a successful lift counted. All testing sessions were supervised by a Certified Strength and Conditioning Specialist.
A GXT was conducted to determine MHR and maximal aerobic power output expressed in watts using a cycle ergometer (Monark 828E; Monark). After strength testing, participants were instructed not to perform any strenuous physical tasks during the 48-hour period before the GXT. After warming up at 50 W for 5 minutes, subjects were given a brief period to recover, after which the test began. Initial workload was set at 30 W and progressively increased by 30 W every minute (4,26). At the culmination of each minute, MHR was recorded using a heart rate monitor (Polar Electro, Lake Success, NY, USA) and rate of perceived exertion (RPE) using the Borg scale of exertion (range of 6–20, with 7 denoting very, very light [rest] and increasing linearly so that 19 signifies very, very hard with 20 representing complete exhaustion) (6). The test was terminated when the participant could no longer continue because of fatigue (revolutions per minute drop below 50) and the RPE was rated as ≥19. Maximum heart rate obtained during testing was used to calculate the steady-state exercise workload. Participants were allowed to actively cool-down (e.g., slow-speed cycling) for several minutes until the heart rate fell below 120 b·min−1 or stabilized.
Experimental Testing Sessions
Subjects underwent each of the following exercise sessions in a randomized order with 1 week separating each session: (a) lower-body aerobic and upper-body resistance exercise (bench press, AE + BP); (b) upper-body resistance exercise (bench press, BP); (c) lower-body aerobic and lower-body resistance exercise (back squat, AE + BS); and (d) lower-body resistance exercise (back squat, BS).
All exercise protocols required subjects to first complete a 5-minute warm-up via cycle ergometry. For the aerobic endurance protocols, 45 minutes of cycle ergometry at 75% MHR achieved by the GXT completed during baseline testing were completed before all resistance exercise. Based on literature, the average time for aerobic conditioning protocols during combined aerobic and strength training is between 30 and 60 minutes at an average of 75% MHR, thereby the average exercise interval was set forth at 45 minutes (5,8,12,15,17,18,25,27,33).
All resistance exercise protocols were preceded by either a back squat or a bench press isometric MVC, during which EMG data were also collected. Upon completion of the MVC, subjects performed either an upper-body or lower-body resistance exercise session. Both upper-body and lower-body protocols used a load of 80% of 1RM for 6 sets to voluntary failure. A 2-minute rest was given between each set. Determination of volume load during resistance exercise was completed by summing the total number of repetitions completed in each of the 6 sets multiplied by load in kilograms.
Blood Collection and Analysis
Blood samples for analysis of whole-blood lactate were collected via finger stick and immediately analyzed using a Lactate Plus portable lactate analyzer (Nova Biomedical, Waltham, MA, USA). Collection of lactate occurred before exercise initiation for each of the 4 sessions and immediately after cessation of aerobic exercise for a maximum total of 2 analyses per session.
Maximal Voluntary Contraction Testing
Isometric back squat was performed in a modified squat rack, where subjects stood on a force plate (Rough Deck, Rice Lake, WI, USA) with a standardized knee angle of 120° and braced against a fixed bar. Subjects were instructed upon an auditory cue to push as hard and as fast as possible for 3–5 seconds (termination of the contraction occurred when force had reached a plateau). A total of 3 contractions were completed, with 1 minute separating each. Data were sampled at 1,000 Hz using a 12-bit analog to digital board and filtered at 30 Hz using a fourth-order low-pass Butterworth filter with Datapac 5 software (Run Technologies, Mission Viejo, CA, USA). Measure of maximum force was accessed via the mean force achieved for a 1,000-millisecond period commencing at the beginning of the plateau period (force no longer increasing).
Isometric bench press was performed in the same rack as the back squat with the addition of a standard bench. The fixed bar was set for 90° of elbow flexion with the forearm perpendicular to the floor, and the bar in line with the midsternum. As in the back squat, subjects were instructed to push against the bench as hard and fast as possible upon an auditory cue until a verbal stop command after 3–5 seconds (when force had reached a plateau). A total of 3 contractions were completed, with 1 minute separating each. Data were sampled and analyzed in the same manner as in the back squat.
Preparation of the skin for EMG was conducted before the general warm-up in all sessions. This included marking of electrode placement via permanent marker, shaving of body hair, and abrasion with sandpaper. After completion of this initial preparation, the 5-minute cycle ergometry warm-up was performed. After finishing the warm-up or aerobic exercise protocol, a 5-minute period was taken, which allowed for final preparation of bodily surfaces for EMG, including alcohol swab cleansing and electrode placement. Electrodes were placed on the vastus lateralis, vastus medialis, and gluteus maximus of the upper right leg (back squat) and the right pectoralis major, anterior deltoid, and lateral head of the triceps (bench press). A ground electrode was placed on the patella of the right leg for both squat and bench press EMG. All electrodes were placed in accordance with the European Recommendations for Surface Electromyography, 2nd edition (Roessingh Research and Development, 1999). Once the electrodes had been placed, subjects were instructed on the MVC protocol as described previously. EMG data were collected at 1 kHz, with the root mean square and electrical activity per unit of force (EMG:force) calculated during the 1,000-millisecond plateau period similar to MVC.
Repetitions per set and lactate were compared using a group (AE + BP, BP, AE + BS, BS) × time (pre/post) repeated measures analysis of variance (ANOVA). EMG, force, and EMG:force were measured using dependent t-tests with a no aerobic exercise versus aerobic exercise model. All analyses were performed using SPSS statistical software (SPSS, Inc., Chicago, IL, USA). Statistical significance was set at p ≤ 0.05. When the underlying assumption of sphericity associated with repeated measures ANOVA was not met, the Greenhouse-Geisser adjustment was used as the determinant of statistical significance. When significance was observed, Tukey's honestly significant difference post hoc tests were performed. Data are presented as mean ± SD, with effect sizes for dependent t-tests presented as ω2, with 0.2–0.4 representing small, 0.5–0.7 representing medium, and 0.8–1.0 representing large differences (31).
Descriptive characteristics of the subjects can be viewed in Table 1. Individual repetitions per set for bench press and back squat are presented in Figures 1 and 2, respectively. Individual repetitions per set were not significantly different between bench press protocols (p > 0.05). Aerobic exercise preceding back squat exercise (AE + BS) resulted in fewer repetitions during the first set as compared with the BS bout (10.00 ± 3.54 vs. 12.56 ± 4.50; p = 0.000). No differences were noted in each of the subsequent sets (p > 0.05). However, total repetitions for the first 3 sets (Figure 3) were significantly higher in BS (27.11 ± 10.56) than in AE + BS (23.11 ± 9.19; p = 0.014, ω2 = 0.33), with no differences between either bench press protocol (p = 0.665).
Lactate was significantly higher than baseline after cycle ergometry (2.49 ± 1.57 vs. 1.49 ± 0.54; p = 0.05). Root mean square EMG (Figure 4) for the lateral triceps was higher in BP as compared with AE + BP (p = 0.011, ω2 = 0.36), whereas MVC (Figure 6) was significantly greater in BP compared with AE + BP (p = 0.044, ω2 = 0.21). Root mean square EMG (Figure 5) and MVC (Figure 6) were not different regardless of the inclusion of aerobic exercise for either back squat protocol (p > 0.05). Analysis of EMG:force revealed a significantly higher value for BP as compared with AE + BP (p = 0.023, ω2 = 0.28). Similarly, BS exhibited a significantly greater EMG:force than AE + BS (p = 0.048, ω2 = 0.20).
We hypothesized that potential differences in the acute metabolic and neuromuscular responses between a no-aerobic-exercise condition and a moderate-intensity-aerobic-exercise condition performed before resistance exercise would impact physical performance in subsequent resistance exercise. Our main finding is that moderate-intensity aerobic exercise at 75% MHR for 45 minutes resulted in a significant decrease in back squat repetitions during set 1 (AE + BS < BS) and cumulatively after the third set, with no significant differences within subsequent sets of the back squat. No differences were noted for single-set or cumulative repetitions between bench press protocols (with and without prior aerobic exercise). We also noted a significant increase in blood lactate after aerobic exercise. Muscle activity during MVC was significantly lower after aerobic exercise in the lateral triceps, with no other differences between muscle groups for either bench press or back squat protocol. This decline in muscle activity for the lateral triceps did result in a slight decline in maximum force production in the bench press. No difference in maximum force generation was noted between back squat protocols. Finally, the ratio of maximum force generation to muscle activity was significantly greater without preceding aerobic exercise for both bench press and back squat.
The fatigue present at initiation of the first set, noted by the decrease in back squat repetitions, was similar to that noted by Sporer and Wenger (30) and Leveritt and Abernethy (21), who also observed significant differences during the first set of lower-body resistance exercise after aerobic exercise. Conversely, de Souza et al. (9) found no differences in the ability to complete repetitions after an aerobic exercise protocol. However, it is possible that these differences are a result of the type and intensity of the exercise used. Our investigation implemented 6 sets to failure at 80% 1RM squats compared with 4 sets to failure at 75% 1RM leg press (30) and 1 set to failure at 80% 1RM leg press (9). Leveritt and Abernethy (21) also incorporated 80% 1RM squats and noted similar significant differences in repetitions to failure, with the differences between the 2 protocols decreasing with the completion of each subsequent set. In other words, the groups that completed aerobic exercise first were more fatigued at the first set, resulting in fewer repetitions; however, as both groups continued to complete the subsequent sets, the differences in fatigue became less pronounced. Nonetheless, differences were still present between back squat protocols after the completion of the third set, resulting in the completion of fewer repetitions for the total session when aerobic endurance exercise preceded the back squat. However, because our goal was to assess the mechanisms of acute fatigue immediately after moderate-intensity aerobic exercise, these differences allow quantitative evidence to support that we did elicit fatigue to a certain degree. To the authors' knowledge, no direct evidence exists on the cumulative effects of a small decrease in repetitions from a day-to-day basis. However, based on the review of Schoenfeld (28), this resulting lower training stress might lead to the inability to reach an overreaching state and therefore hinder performance improvement. Thus, our findings support those of previous research in that lower-body aerobic exercise induces fatigue to an extent that causes a decline in the ability to perform repetitions to failure.
We found that before resistance exercise, blood lactate was significantly higher than baseline after completion of cycle ergometry. For the back squat, it seems possible that this slight elevation in lactate before resistance exercise resulted in decreased repetitions at the first set. This could occur because intramuscular lactic acid alters the ability of the muscle to contract, whereas blood lactate could also signify decreased muscle glycogen (7). Lactic acid has been noted to potentially interfere with the contractile ability of the muscle by hindering calcium release from the sarcoplasmic reticulum and also impairing actin and myosin cross-bridge activity, resulting in decreased force production, but only in extreme cases of acidosis (7). However, despite the aforementioned possibility, because the absolute differences in blood lactate before resistance exercise were so small and the overall lactate response was also minimal, it seems that the repetition decrease noted at set 1 of the back squat is caused by another factor other than an increase in acidosis of the leg muscles as noted by whole-blood lactate. Further support for this claim lies in our observation that the lactate response to cycle ergometry was the same for the bench press and did not result in a significant difference in repetitions at any set. However, the reason for decreased repetitions could be a local effect of metabolic stress or fatigue within the legs but not the upper body. Elevated lactate after cycle ergometry most likely reflects metabolic stress of the lower-body musculature involved in the lower-body endurance exercise.
It has been noted using a similar intensity and duration of cycle ergometry protocol that glycogen was depleted first in the type I fibers and then proceeding to type II (14). Therefore, it is possible that in our investigation, glycogen content may have been reduced during aerobic exercise to an extent that may have impaired back squat performance. Without direct measurement of glycogen, this observation is purely speculative and in need of future investigation.
It was also observed that muscle activity (through EMG) and maximal force generation (MVC) were significantly different between conditions for the bench press but not the back squat. Bench press EMG was significantly lower in the lateral triceps after cycle ergometry, which was followed by a statistically significant, but small, decrease in force. The reason for this decline is unclear, but based on the investigator's observation, it is feasible that the lateral triceps was somewhat fatigued because it was used for support as the subjects were leaning on the handlebar during the 45-minute cycle exercise. However, we cannot completely eliminate central fatigue as a mechanism of acute interference because of the fact that the activation of the lateral triceps muscle decreased after aerobic exercise. This alternative explanation is less likely because the activation of the primary muscles involved in the bench press exercise (pectoralis major and anterior deltoid) was not altered. Nevertheless, the small change in muscle activity and isometric force as a result of the preceding cycle exercise did not affect dynamic bench press performance. For the back squat, EMG:force was significantly different between conditions; however, the EMG activity was not significantly different between the 3 analyzed muscles. It is well known that during prolonged contraction and relaxation, muscle activity will decrease, usually resulting in a decrease in force production (13,29). Although the resultant total forces were not different between protocols, it seems that other muscles involved in the back squat contributed to a greater extent after aerobic exercise to produce the same force as seen without cycle ergometry. Our observations show conflicting results for bench press and back squat; that is, for the bench press, muscle activity was lower for the lateral triceps resulting in a lower maximum force, but did not culminate in fewer completed repetitions. Conversely, neither back squat maximum force nor muscle activity was different between groups, but fewer repetitions were completed at the first set and accumulated third set. This suggests that the interference effect could occur as a result of acute neuromuscular fatigue, but more detail is needed in future research.
In conclusion, a moderate-intensity aerobic exercise session resulted in a significant decrease in repetitions for the back squat but not the bench press, lending further support that interference induced by same-day concurrent training is local to the working muscles. Increased blood lactate associated with this design is likely not large enough to elicit a state of acidosis that would impair the contractile ability of the muscle. Force-generating capacity and muscle activity showed that a decrease in maximal force does not necessarily result in fewer repetitions in the bench press, whereas the opposite is true for the back squat. These findings indicate that the interference effect as attributed to acute fatigue induced by a moderate-intensity aerobic exercise session occurs as a result of a local metabolic stress, causing a decrease in repetitions for the back squat but not the bench press. However, we cannot completely eliminate central fatigue as a mechanism of acute interference because of the fact that bench press maximum isometric force and the activation of the lateral triceps muscle decreased after aerobic exercise. Our investigation has brought forth some insight as to the mechanisms of acute fatigue and their influences on concurrent training. To our knowledge, this is the first investigation to analyze acute neuromuscular responses to a concurrent training session. However, more research is needed to determine how metabolic stress causes fatigue and analyze the responses of both AMPK and mTOR, because of the conflicting nature of the adaptations of which these molecules are associated (2,16,19,24,33). Finally, methods to bypass the interference effect will allow for optimization of training time without concomitant hindrances in performance adaptations.
In designing a concurrent aerobic endurance and resistance training program, strength and conditioning coaches should be careful to select an exercise that, within an individual session, does not cause athletes to become excessively fatigued, thereby potentially hindering performance of a subsequent exercise in the workout. Applying this principle could include avoiding lower-body aerobic training before lower-body resistance exercise, changing the order of exercises, and separating aerobic and resistance exercise sessions by at least 24 hours.
The authors thank Dr. Richard Bloomer for his time on the first author's thesis committee, and Paul N. Whitehead and Courtney L. Collins for their help with data collection.
1. Abernethy PJ. Influence of acute endurance activity on isokinetic strength. J Strength Cond Res 7: 141–146, 1993.
2. Baar K. Training for endurance and strength: Lessons from cell signaling. Med Sci Sports Exerc 38: 1939–1944, 2006.
3. Baechle TR, Earle RW. Essentials of Strength Training and Conditioning. Champaign, IL: Human Kinetics, 2008.
4. Bassett DR Jr, Duey WJ, Walker AJ, Torok DJ, Howley ET, Tanaka H. Exaggerated blood pressure response to exercise: Importance of resting blood pressure. Clin Physiol 18: 457–462, 1998.
5. Bell GJ, Syrotuik D, Martin TP, Burnham R, Quinney HA. Effect of concurrent strength and endurance training on skeletal muscle properties and hormone concentrations in humans. Eur J Appl Physiol 81: 418–427, 2000.
6. Borg GA. Perceived exertion: A note on "history" and methods. Med Sci Sports 5: 90–93, 1973.
7. Cairns SP. Lactic acid and exercise performance: Culprit or friend? Sports Med 36: 279–291, 2006.
8. Davis WJ, Wood DT, Andrews RG, Elkind LM, Davis WB. Concurrent training enhances athletes’ strength, muscle endurance, and other measures. J Strength Cond Res 22: 1487–1502, 2008.
9. de Souza EO, Tricoli V, Franchini E, Paulo AC, Regazzini M, Ugrinowitsch C. Acute effect of two aerobic exercise
modes on maximum strength and strength endurance. J Strength Cond Res 21: 1286–1290, 2007.
10. Deschenes MR, Kraemer WJ. Performance and physiologic adaptations to resistance training
. Am J Phys Med Rehabil 81: S3–S16, 2002.
11. Docherty D, Sporer B. A proposed model for examining the interference phenomenon between concurrent aerobic and strength training. Sports Med 30: 385–394, 2000.
12. Dudley GA, Djamil R. Incompatibility of endurance- and strength-training modes of exercise. J Appl Physiol 59: 1446–1451, 1985.
13. Enoka RM, Stuart DG. Neurobiology of muscle fatigue. J Appl Physiol 72: 1631–1648, 1992.
14. Gollnick PD, Armstrong RB, Saltin B, Saubert CW IV, Sembrowich WL, Shepherd RE. Effect of training on enzyme activity and fiber composition of human skeletal muscle. J Appl Physiol 34: 107–111, 1973.
15. Hakkinen K, Alen M, Kraemer WJ, Gorostiaga E, Izquierdo M, Rusko H, Mikkola J, Hakkinen A, Valkeinen H, Kaarakainen E, Romu S, Erola V, Ahtiainen J, Paavolainen L. Neuromuscular adaptations during concurrent strength and endurance training versus strength training. Eur J Appl Physiol 89: 42–52, 2003.
16. Hawley JA. Molecular responses to strength and endurance training: Are they incompatible? Appl Physiol Nutr Metab 34: 355–361, 2009.
17. Hennessy L, Watson A. The interference effects of training for strength and endurance simultaneously. J Strength Cond Res 8: 12, 1994.
18. Hickson RC. Interference of strength development by simultaneously training for strength and endurance. Eur J Appl Physiol Occup Physiol 45: 255–263, 1980.
19. Kimball SR. Interaction between the AMP-activated protein kinase and mTOR signaling pathways. Med Sci Sports Exerc 38: 1958–1964, 2006.
20. Kraemer WJ, Patton JF, Gordon SE, Harman EA, Deschenes MR, Reynolds K, Newton RU, Triplett NT, Dziados JE. Compatibility of high-intensity strength and endurance training on hormonal and skeletal muscle adaptations. J Appl Physiol 78: 976–989, 1995.
21. Leveritt M, Abernethy J. Acute effects of high-intensity endurance exercise on subsequent resistance activity. J Strength Cond Res 13: 47–51, 1999.
22. Leveritt M, MacLaughlin H, Abernethy PJ. Changes in leg strength 8 and 32 h after endurance exercise. J Sports Sci 18: 865–871, 2000.
23. Millet GP, Jaouen B, Borrani F, Candau R. Effects of concurrent endurance and strength training on running economy and VO(2) kinetics. Med Sci Sports Exerc 34: 1351–1359, 2002.
24. Nader GA. Concurrent strength and endurance training: From molecules to man. Med Sci Sports Exerc 38: 1965–1970, 2006.
25. Nelson AG, Arnall DA, Loy SF, Silvester LJ, Conlee RK. Consequences of combining strength and endurance training regimens. Phys Ther 70: 287–294, 1990.
26. Patton JF, Vogel JA, Mello RP. Evaluation of a maximal predictive cycle ergometer test of aerobic power. Eur J Appl Physiol Occup Physiol 49: 131–140, 1982.
27. Santtila M, Keijo H, Laura K, Heikki K. Changes in cardiovascular performance during an 8-week military basic training period combined with added endurance or strength training. Mil Med 173: 1173–1179, 2008.
28. Schoenfeld BJ. The mechanisms of muscle hypertrophy and their application to resistance training
. J Strength Cond Res 24: 2857–2872, 2010.
29. Sjogaard G, Kiens B, Jorgensen K, Saltin B. Intramuscular pressure, EMG and blood flow during low-level prolonged static contraction in man. Acta Physiol Scand 128: 475–484, 1986.
30. Sporer BC, Wenger HA. Effects of aerobic exercise
on strength performance following various periods of recovery. J Strength Cond Res 17: 638–644, 2003.
31. Vincent WJ. The t test. In: Statistics in Kinesiology. Champaign, IL: Human Kinetics, 2005. pp. 125–141.
32. Winder WW, Taylor EB, Thomson DM. Role of AMP-activated protein kinase in the molecular adaptation to endurance exercise. Med Sci Sports Exerc 38: 1945–1949, 2006.
33. Wood RH, Reyes R, Welsch MA, Favaloro-Sabatier J, Sabatier M, Matthew Lee C, Johnson LG, Hooper PF. Concurrent cardiovascular and resistance training
in healthy older adults. Med Sci Sports Exerc 33: 1751–1758, 2001.