How to Maximize Concurrent Training
By Marc Lewis
Simultaneously training for adaptations associated with resistance and endurance training (RT & ET), otherwise known as concurrent training (CT), is widely debated by fitness professionals and strength coaches alike. CT has been criticized due to the potential for chronic overreaching, as well as the competing adaptations associated when performing RT and ET, concurrently. However if programmed carefully, CT can produce a lean and sculpted physique, while obtaining a high level of fitness as measured by health aspects as well as athletic parameters. Therefore, the purpose of this article is to elucidate the ways in which the adaptations associated with both RT and ET can be maximized when training concurrently.
In 1980, Dr. Robert Hickson introduced the concept of “interference” when training for adaptations associated with both RT and ET simultaneously (1). Currently, it is generally accepted that you cannot fully maximize skeletal muscle hypertrophy, strength, and power, while engaging in an aggressive ET program. Nevertheless, there is a growing body of literature supporting the theory that high-intensity RT not only does not impede adaptations associated with ET, it can actually improve endurance performance (2-11). Furthermore, it has been postulated that ET may not significantly blunt adaptations associated with RT, and can accelerate a reduction in fat mass as well as improve sleep, and cardiac efficiency (12-15).
The Interference Theory
As previously mentioned, the interference theory originated from some pioneering research by Dr. Robert Hickson in 1980. Dr. Hickson investigated the training affects of a high frequency, high volume CT program, which utilized running as the ET modality and compared it to strength or endurance training alone over a ten-week period (1). Dr. Hickson found that strength increased in the CT group until approximately weeks 6-7, which was followed by a “leveling-off period” and a sharp decrease in strength the final two weeks (1). Additionally, Dr. Hickson noted no statistically significant differences in aerobic capacity between the ET only group and the CT group. Nevertheless, there were a couple of interesting outcomes associated with body composition. The CT group decreased their body fat significantly (p <0.05), and to a greater extent than either the ST only or ET only groups (1). Furthermore, the CT group increased their thigh girth 54.7 to 56.4 cm (p <0.05), which was similar to the strength only group 53.3 to 55.5 cm (p <0.01) (1). This is an indication of type I muscle fiber hypertrophy, which is commonly seen in certain endurance athletes such as cyclists or cross-country skiers.
Dr. Hickson’s results provided the foundational research concerning the inference phenomenon, while setting the platform from which many other investigations were launched. Rather than discuss every significant study conducted in the past 35 years, this article will provide you with the rationale for competing adaptations, discuss the benefits associated with RT and ET alone, as well as provide a set of practical recommendations to maximize RT and ET adaptations when training concurrently.
Inference Effects and Competing Adaptations
Two points are crystal clear from the current literature: 1) inference effects are multifactorial, and 2) there is a dose-response relationship between ET volume (i.e. frequency & duration) and its potential negative effects on RT outcomes. Interference is thought to be a combination of chronic overreaching, which can lead to overtraining, and long-term competing adaptations at the cellular level (16). In addition, the dose-response relationship that exists with increased ET volume does not appear to exist to the same extent with RT volume when examining endurance outcomes (i.e. VO2max, aerobic enzymatic activity, etc) (2-11). In fact, RT has been shown in numerous studies to improve endurance performance directly (i.e. time trial) (8, 17), as well as endurance parameters (VO2max and running/cycling economy) (2-11, 17). Furthermore, high-intensity RT (loads >85% 1RM) paired with explosive, high velocity RT has been suggested to be a superior method of RT in recreationally trained, highly trained, and elite endurance athletes (3-6, 8-9, 12, 18).
Chronic overreaching, and ultimately overtraining, is theorized to be a product of high volume, high intensity, and/or high frequency training bouts over an extended period of time (16). This theory is generally termed the “chronic hypothesis,” and is limited in its literary support. These effects are suggested to be exacerbated when the training bouts involve large muscle groups and excess exercise-induced muscle damage, as seen in repetitive eccentric contractions (i.e. running) (12, 16). ET has a natural high volume component, therefore, when combined with high volumes of RT it can be suggested that an overreaching stimulus could be created over time (12, 16). Therefore, when structuring a CT program it can be theorized that strategically programming ET around RT would be most effective for maximizing adaptations concurrently.
Aside from chronic overreaching, some researchers have put forth an “acute hypothesis,” which contends that residual fatigue from the endurance component of CT compromises the ability to develop muscular tension during the RT component (16). According to this theory, the tension generated by the working musculature during RT would not be sufficient enough to maximize strength development (16). In addition, proponents of this theory have suggested that performing RT directly preceding ET can alter endurance performance due to residual fatigue (16). Therefore, the acute hypothesis focuses on the scheduling of training sessions as the main interference effect associated with CT, as opposed to simply training concurrently (16).
RT adaptations can be broadly described as increases in muscular hypertrophy, strength, and power.
Muscular Hypertrophy: Exercise-induced muscular hypertrophy is centered on the mechanistic or mammalian target of rapamycin (mTor) signaling molecule, which demonstrates increased activity post-RT (20-21). mTor exists in two complexes, but for the purposes of this article we will only focus on mTor1. Increased mTor1 activity results in an increase in protein synthesis through a cascade of intracellular transduction pathways triggered by a mechanical tension/overload stimulus (19). Furthermore, amino acids (specifically leucine) have been shown to increase protein synthesis predominantly by increasing the primary leucine transporter (LAT1), which acts to up-regulate mTor1 (22). Therefore, this would theoretically result in an increase in the cross sectional area (CSA) of the muscle fiber, which directly relates to muscular strength.
Muscular Strength: Muscular strength is a combined effect of neural activation, muscle fiber size, and connective tissue stiffness (2-11). Neural alterations elicited by RT include an increased neural drive, selective activation of motor units (MUs), increased motor unit synchronization, increased rate of force development (RFD), increased inhibition of golgi tendon organs (GTOs) (termed autogenic inhibition), and a reduced antagonist inhibition (2-11, 23). Neural alterations elicited by RT do not appear to be significantly altered by ET, although repeatedly engaging in high-intensity ET could play a role in the milieu associated with neuromuscular fatigue, and/or factor into chronic overreaching (16). Additionally, changes in motor unit recruitment could reduce patters associated with maximal voluntary contractions, which could partially explain reductions in power parameters discussed by Wilson et al (2012) (12, 16). However, these effects should only be considered significant if concurrently training a power sport athlete. Furthermore, there is no research indicating that CT has detrimental effects on connective tissue stiffness, but one could surmise that without chronic overreaching, or an energy deficit, connective tissue stiffness should not be negatively altered by CT.
Muscular Power: Muscular power (force x distance/time) is simply rate of performing work, which can be described as the product of force and velocity. Improvements in muscular power rely primarily on neural alterations, specifically increases in RFD and motor unit synchronization, as well as a reduced antagonist inhibition. A meta-analysis by Wilson et al (2012) suggested that decrements in muscular power may be more likely associated with CT than decrements in either strength or hypertrophy. However, there is a clear dose-response relationship between the volume of ET, and decrements in muscular power (12). Therefore, it can be theorized that individuals wishing to maximize muscular power should limit the volume of ET performed when concurrently training. Furthermore, it can be suggested that performing cycling or rowing for endurance exercise can preserve RT associated adaptations when compared to running (2, 10, 12, 16).
ET adaptations can be broadly described as improvements in cardiovascular, muscular, and metabolic function.
Cardiovascular: ET elicits a multitude of cardiovascular adaptations that assist in improving blood flow and delivery. These adaptations include an increase in stroke volume (SV), an increase in heart size (termed cardiac hypertrophy), an increase in cardiac output (due to an increased SV), and a decrease in sub-maximal heart rates for a given intensity. RT has been shown to have a positive impact on exercise capacity (i.e. VO2max) when concurrently training, while initiating a physiological form of cardiac hypertrophy- read more here. These cardiovascular adaptations can have positive impacts on RT training (i.e. work capacity) and recovery, as well as improve cardiac efficiency.
Muscular/Metabolic: ET initiates a variety of adaptations in active skeletal muscle, which include increased mitochondrial volume and density, increased capillary density, and improved fat and glucose oxidation. In addition, there are muscle fiber type transitions that occur as type IIx fibers become more oxidative and resemble type IIa fibers. This muscle fiber transition could theoretically reduce the power output and force per unit of area of the muscle fiber, since myosin heavy chain isoform content of type IIx – IIa – I muscle fibers differ considerably, and have been correlated with various strength indices (16). However, current literature investigating CT has reported little difference in fiber type change between the CT groups and the RT only groups (16). RT training that results in an increase in muscular hypertrophy can blunt the increased capillary density, or decrease capillary density through the increase in CSA. However, unless you are a competitive endurance athlete this should not be a concern. This result can be negated by focusing on high-intensity, low volume RT with loads >85% 1RM (2-11).
The metabolic and hormonal signals initiated during ET turn on certain signaling proteins in skeletal muscle that lead to the aforementioned adaptations. ET involves repeated muscle contractions, which repeatedly releases calcium following each muscular contraction. This calcium activates the calcium-calmodulin kinase (CaMK) family of proteins, which is CaMKII in skeletal muscle (24). Active CaMK can increase the capacity for glucose uptake through the upregulation of the glucose transporter GLUT4, as well as increase mitochondrial volume by transcriptional upregulation of peroxisome proliferator-activated receptor-y coactivator 1a (PGC-1a), which serves as the mitochondrial biogensis regulator (25). With high-intensity endurance exercise there is a decrease of ATP and glycogen, which consequently increases ADP and AMP concentrations. This activates AMPK- activated protein kinase (AMPK), which facilitates an increase in fat oxidation during exercise, while also playing a role in the long-term regulation of mitochondrial volume (19).
In addition, the decrease in glycogen activates the 38 kDa mitogen-activated protein kinase (p38), which can increase the activity of PGC-1a (26-27). Through the rise of lactate and NAD+, there is the activation of the NAD+ dependent deacetylase family of sirtuins (SIRT) (26-27). Members of the SIRT family control the metabolic influx through the tricarboxylic acid (TCA) cycle, insulin sensitivity, and PGC-1a activity (26-27). There is speculation that one or more of these metabolic signaling pathways inhibit mTorc activation and limit hypertrophy when concurrently training, however there is more research needed (19).
There are certain mechanisms by which lactate removal, and ultimately the lactate concentration at a given exercise intensity, could be improved in endurance athletes through a RT program, however it is by no means fully conclusive. Hoff et al (1999) demonstrated improved short-term performance and improved work efficiency in cross-country skiers after a concurrent RT/ET program. Hoff and her colleagues observed a training-induced increase in RFD, which would allow for a shorter propulsion phase for a given overall power (9). This shorter propulsion phase would facilitate an extended muscle relaxation phase, which would reduce the time of contraction-induced muscle occlusion, and hence increase the time of muscle perfusion given the prolonged relaxation phase. This increase time for muscle perfusion would increase the mean capillary transit time (MCTT), which could ultimately allow for an increased MCTT every stride/revolution of an endurance event (9).
Hoff and her colleagues have suggested that due to the relatively large size of free fatty acids (FFA), the increased MCTT could enable an increased diffusion of FFAs into the muscle cells (9). This increased diffusion of FFAs could be described as glycogen sparing, which has been suggested to delay muscle fatigue through a reduced production of lactate (2). Furthermore, an increased MCTT could lead to an enhanced removal of metabolites produced by the contracting skeletal muscle, which could potentially delay fatigue and improve efficiency of the contracting muscle.
- Use ET wisely, and strategically program it into your RT blocks. Intersperse HIIT and low-to-moderate intensity ET to keep ET volume at a minimum, while reaping the benefits of ET.
- Use low-to-moderate intensity ET (40-60% HRR) as a therapeutic tool to enhance recovery and improve mood state.
- Perform ET on a cycle or rower when available. This will reduce the exercise-induced muscle damage associated with running, which has a significant eccentric component. Cycling will also reduce the caloric expenditure since you are activating less musculature than with running, if you are struggling to maintain energy balance.
- Alternate between RT and ET “volume focused” weeks with ET frequency no greater than 3 days per week and duration no longer than 30 minutes.
- Any high-intensity ET should be performed early in the day, if engaging in RT and ET on the same day. After the morning ET, there should be a recovery period of at least 3 hours to allow AMPK and SIRT1 activity to return to baseline.
- RT should be performed in a fed-state, while being supported by a leucine-rich protein source immediately following RT. If performing RT and ET on the same day, it is suggested that a protein-rich source be consumed immediately before bedtime as well.
- If performing ET and RT on the same day, you must fully refuel between the morning high-intensity ET session and the afternoon RT session. This will ensure that muscle glycogen levels are restored, while not activating AMPK or SIRT1 activity.
- Low intensity, non-depleting ET can be performed before RT, which can provide an improvement in the ET response as well as improve the strength response during RT. However, the key is that the ET must be low intensity and non-depleting.
- Program your ET volume around your RT volume. In other words, if you are having a high volume RT week, you should lower your ET volume to compensate for that excess muscle damage and metabolic stress.
- Focus on maintaining energy balance! When concurrently training, you need to strive to replace the calories that you are burning. If you train in a caloric deficit, this will undoubtedly compromise your gains in muscular strength and hypertrophy.
CT can improve endurance performance through improving work efficiency and increasing anaerobic capacity. There is no literature indicating that CT is detrimental to any performance outcome associated with ET. In contrast, the literature indicates that there is a sharp dose-response relationship with ET frequency and duration (i.e. volume) on RT associated outcomes such as muscular strength, power, and hypertrophy. Therefore, strategically implementing ET based on the current scientific literature will assist in developing an optimal program for maximizing benefits associated with RT and ET, respectively. In addition, there are benefits from low, moderate, and high intensity ET that are maximized by performing ET at a variety of intensity levels. Therefore, interspersing low-to-moderate intensity ET with high intensity ET is crucial, as well as utilizing the current literature to program these strategically.
About the Author
Marc Lewis M.S.(c), CSCS, ACSM-CPT is a graduate teaching/research assistant in the Department of Exercise Science at the University of South Carolina and the Director of Sports Performance for Winston Salem Personal Training.
Personal Training: www.winstonsalempersonaltraining.com
- Hickson RC. Interference of strength development by simultaneously training for strength and endurance. European Journal of Applied Physiology. 45: 255-263, 1980.
- Aagaard P and Anderson J. Effects of strength training on endurance capacity in top-level endurance athletes. Scandinavian Journal of Medicine & Science in Sports. 20(2): 39-47, 2010.
- Hoff J, Gran A, and Helgerud J. Maximal strength training improves aerobic endurance performance. Scandinavian Journal of Medicine & Science in Sports. 12: 288-295, 2002.
- Millet GP, Jaouen B, Borrani F, and Candau R. Effects of concurrent endurance and strength training on running economy and VO2 kinetics. Medicine & Science in Sports & Exericse. 34(8): 1351-1359, 2002.
- Mikkola J, Rusko H, Nummela A, Pollari T, and Hakkinen K. Concurrent endurance and explosive type strength training improves neuromuscular and anaerobic characteristics in young distance runners. International Journal of Sports Medicine. 28: 602-611, 2007.
- Lanao-Esteve J, Rhea MR, Fleck SJ, and Lucia A. Running-specific, periodized strength training attenuates loss of stride length during intense endurance running. Journal of Strength and Conditioning Research. 22(4): 1176-1183, 2008.
- Mikkola J, Vesterinen V, Taipale R, Capostagno B, Hakkinen K & Nummela A. Effect of resistance training regimens on treadmill running and neuromuscular performance in recreational endurance runners. Journal of Sport Sciences. 29(13): 1359-1371, 2011.
- Paavolainen L, Hakkinen K, Hamalainen I, Nummela A & Rusko H. Explosive strength training improves 5-km running time by improving running economy and muscle power. Journal of Applied Physiology. 86: 1527-1533, 1999.
- Hoff J, Helgerud J & Wisloff U. Maximal strength training improves work economy in trained female cross-country skiers. Medicine & Science in Sports & Exercise. 31: 870-877, 1999.
- Aagaard P, Bennekou M, Larsson B, Anderson J, Olesen J, Crameri R, Magnusson P & Kjaer M. Resistance training leads to altered muscle fiber type composition and enhanced long-term cycling performance in elite competitive cyclists. Medicine & Science in Sports & Exercise. 39(supp. 5): S448-S449, 2007.
- Mikkola J, Vesterinen V, Taipale R, Capostagno B, Hakkinen K & Nummela A. Effect of resistance training regimens on treadmill running and neuromuscular performance in recreational endurance runners. Journal of Sports Sciences. 29(13): 1359-1371, 2011.
- Wilson JM, Marin PJ, Rhea MR, Wilson SM, Loenneke JP & Anderson JC. Concurrent Training: A meta analysis examining interference of aerobic and resistance exercise. Journal of Strength and Conditioning Research. 2012.
- Davis WJ, Wood DT, Andrews RG, Elkind LM & Davis WB. Concurrent training enhances athletes’ strength, muscle endurance, and other measures. Journal of Strength and Conditioning Research. 22(5): 1487-1502, 2008.
- DiLorenzo TM, Bargman EP, Stucky-Ropp RS, Brassington GS, Frensch PA & LaFontaine T. Long-term effects of aerobic exercise on psychological outcomes. Preventive Medicine. 28: 75-85, 1999.
- King AC, Oman RF, Brassington GS, Bliwise DL & Haskell WL. Moderate-intensity exercise and self-rated quality of sleep in older adults. Journal of the American Medical Association. 277: 32-37, 1997.
- Leveritt M, Abernathy PJ, Barry BK & Logan PA. Concurrent strength and endurance training: A review. Sports Medicine. 28(6): 413-427, 1999.
- Damasceno MV, Lima-Silva AE, Pasqua LA, Tricoli V, Duarte M, Bishop DJ & Bertuzzi R. Effects of resistance training on neuromuscular characteristics and pacing during 10-km running time trial. European Journal of Applied Physiology. 2015.
- Taipale RS, Mikkola J, Salo T, Hokka L, Vesterinen V, Kraemer WJ, Nummela A & Hakkinen K. Mixed maximal and explosive strength training in recreational endurance runners. Journal of Strength and Conditioning Research. 28(3): 689-699, 2014.
- Baar K. Using molecular biology to maximize concurrent training. Sports Medicine. 44(suppl 2): S117-S125, 2014.
- Baar K & Esser K. Phosphorylation of p70(S6k) correlates with increased skeletal muscle mass following resistance exercise. American Journal of Physiology- Cell Physiology. 276: C120-127, 1999.
- MacKenzie MG, Hamilton DL, Murray JT, Taylor PM & Baar K. mVps34 is activated following high-resistance contractions. Journal of Applied Physiology. 587: 253-260, 2009.
- Philp A, Hamilton DL & Baar K. Signals mediating skeletal muscle remodeling by resistance exercise: PI3-kinase independent activation of mTORC1. Journal of Applied Physiology. 110: 561-568, 2011.
- Behm DG. Neuromuscular implications and applications of resistance training. Journal of Strength and Conditioning Research. 9(4): 264-274, 1995.
- Rose AJ, Kiens B & Richter EA. Ca2+ calmodulin-dependent protein kinase expression and signaling in skeletal muscle during exercise. Journal of Applied Physiology. 574: 889-903, 2006.
- Akimoto T, Pohnert SC, Li P & et al. Exercise stimulates PGC-1alpha transcription in skeletal muscle through activation of the p38 MAPK pathway. Journal of Biological Chemistry. 280: 19587-19593, 2005.
- Schenk S, McCurdy CE, Philp A, Chen MZ, Holliday MJ, Bandyopadhyay GK, Osburn O, Baar K & Olefsky JM. Sirt1 enhances skeletal muscle insulin sensitivity in mice during caloric restriction. Journal of Clinical Investigation. 121: 4281-4288, 2011.
- Rodgers JT, Lerin C, Haas W, Gygi SP, Spiegelman BM & Puigserver P. Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1. Nature. 434: 113-118, 2005.