top of page

Critical analysis of the physiological adaptations of maximal strength training on endurance running

Critical evaluation of the physiological adaptations from maximal strength training on endurance runners:

Maximal strength training and endurance running are two subjects that do not traditionally mix. There has been a body of research looking into the effects of strength training on endurance running. The aim of this paper is to critically pull together different bodies of research, analyse how the research has been performed and whether it is applicable. Analysing different sports and training methods to see if there is more specific information to establish an overriding message and if a key piece of information is being missed that could help guide future research. Socially and traditionally endurance athletes and in particular runners steer clear of any form of maximal strength training, the question is, should they? Is there a physiological benefit for them to perform maximal strength training and how should this training be accommodated for? Endurance athletes are notorious for increasing the volume of training to an already heavily loaded training schedule, if there is an added element of strength training should it be in addition to their current training schedule or should they reduce the volume of endurance work to incorporate maximal strength training in their training schedule?

Firstly, there needs to be a definition of what endurance is, endurance is highly aerobic and sits predominately in the aerobic energy system, although it will utilise the aerobic pathways of the ATP-PCr and the anaerobic glycolysis systems at stages. For the aerobic system to start working fully, Davis., et al., (2000) showed that an athlete must be working for a duration longer than 240 seconds. Aerobic economy is critical in endurance sports and being able to repeatedly express force at a submaximal power and submaximal V02 is critical for success in endurance performance (Saunders et al., 2004). However, in the systematic review of strength training on performance in endurance they stated that “Elite endurance athletes with similar V02 max levels can have differing abilities during a race and therefore maximum oxygen uptake cannot fully explain true racing ability” (Beattie et al., 2014). The economy of endurance running is multi-factorial and is measured by the metabolic expenditure or cost at a given velocity or power output (Fletcher., et al., 2010). The power demands of endurance, endurance specific power, is highly reliant on the neuromuscular system for the body to rapidly and repeatedly produce force following a sustained period of exercise (Paavolainen., et al., 1999), taking into consideration the metabolic effect this will place the body into a highly glycolytic and oxidative energy demand.

Secondly, defining maximal strength, the simplest way to quantify this is to look to the force velocity curve (Hill., 1938) and Gordon., et al., (1966) discussed that the curvature relationship related to maximum power output of skeletal muscle, the slower a muscle shortens the more force or power the skeletal muscles are having to produce per se. Therefore, exercises or loads that sit towards the top of the force velocity curve can be considered to be maximal in nature. Looking into the metabolic pathways of maximal strength training there is going to be a high demand on the ATP-PCr and glycolytic systems for initial force requirements. It has been suggested that, depending on the length of the training session and the rest periods implemented between sets that, a strength training session could become reliant on the aerobic system (Beattie et al., 2014). Therefore, maximal strength training can be classified as being high force or power related and places a high demand on the ATP-PCr and glycolytic energy pathway system. In all concurrent training models, there is an interference effect that will have to be considered. Looking into molecular physiology there should be clear information into the intercellular signalling, and whether concurrent maximal strength training and endurance training compromise the cellular adaptations desired.

Endurance training elicits an increase in mitochondrial levels and an increase in respiratory rate within trained muscle fibres (Holloszy., 1967). Increases in the respiratory rate leads to a slower utilisation of muscle glycogen and blood glucose, more resilience to fat oxidation and less lactate production during submaximal exercise (Holloszy., et al., 1984). Goodman., et al., (2004) found, after a six-day endurance training intervention, plasma volume, V02max and stroke volume all increased and maximal heart rate decreased. They concluded that this short intervention increased left ventricular filling and stroke volume. This information, coupled with the plasma volume increase, can suggest that cardiac function is quick to adapt and will increase cardiac function for endurance exercise. The aerobic pathway and the delivery of 02 can be termed V02 kinetics. V02 is a standardised measurement of performance within endurance. Research from Paavolainen., et al., (1999) highlights a need for more thorough assessments for elite athletes and suggests velocity and power test during maximal V02 uptake and maximal anaerobic running velocity (vMART) tests for elite level competitors. The reasoning for changing the testing procedure for elite endurance athletes is due to competitors with similar V02max outputs having differing results on race day. They believe that the ability to produce more power at higher Vo2max outputs is where the athletic advantage comes from. Vo2max is believed to be skeletal muscle and location specific and therefore needs to be trained specifically for the sport you are competing in. There is a limiting factor in the V02 kinetics of skeletal muscle, the major delaying factor involved in 02 delivery is the ability of the muscle fibre to receive 02 (Grassi., 2006). A possible rate limiting factor of Vo2 kinetics is the activation of pyruvate dehydrogenase and availability of acetyl group within mitochondrial cells. Holloszy., et al., (1984) termed the phrase “mitochondrial biogenesis” which is an increase in mitochondria and oxidative enzyme levels. Type I muscle fibres have the highest concentration of mitochondria and use the oxidative system as an energy source, whereas Type IIa and IIx generate ATP through glycolysis which make them more susceptible to fatigue. Lin., et al., (2002) found that adult skeletal muscle has a certain level of plasticity within the distribution of muscle fibre types and can be adapted through mechanical stress. Repeated bouts of endurance training will increase the levels of PGC-1α which then drive a muscle fibre type conversion in skeletal muscles normally rich in type II muscle fibres. This activates the start of the process for mitochondria biogenesis and the oxidative metabolism. For an endurance athlete or coach, the ability to transfer muscle fibre types to the more fatigue resistant type I muscle fibres is a desirable training outcome. To elicit a training response at a molecular level it requires repeated training stimuluses to increase the accumulation of specific protein pathways, the pathway induced will depend heavily on the stimulus that is applied (Hansen., et al., 2005). A desirable adaptation to endurance training is the increase in mitochondria and oxidative enzymes. Mitochondria protein levels can be increased by 50%-100% within a 6-week endurance training intervention (Zierath., et al., 2004) but the protein turnover will be short, around 5-7 days and therefore will require repeated bouts of training stimulus to maintain heightened mitochondrial levels. Inducing mitochondria biogenesis requires the activation of PGC-1α and is mediated in the second phase by the increase of PGC-1α protein (Wright., et al., 2007). AMP also plays a vital role in the increased concentration of mitochondria. When endurance-based training, stimulus is applied the concentration of AMP in the muscle is increased, heightened levels of AMP activate the enzyme process of AMP-activated protein kinase (AMPK). AMPK is a metabolic gauge within the skeletal muscle system and becomes activated when energy levels are becoming depleted, it inhibits the ATP-consuming pathway and activates the pathways involved with carbohydrate and fatty acid catabolism to restore ATP levels to normal (Hardie., et al., 2006). AMPK promotes fatty acid oxidization by inhibiting acetyl-CoA carboxylase and activation of malonyl-CoA. This removes the inhibition of acyl-CoA carboxylase (Rasmussen., et al., 1997; Yu., et al., 2003). Repeated mechanical stimulus in endurance running will increase PGC-1α which is associated with increasing the density of Type I muscle fibres. Type I muscle fibres are more fatigue resistant and gather their energy from the oxidative system, Type I muscle fibres have a high concentration of mitochondria and mitochondria biogenesis is activated from PGC-1α protein pathways, how will this process be affected by concurrent training?

Maximal strength training stimulates myofibrillar proteins responsible for hypertrophy and culminating in increases in maximal strength (Fry., 2004; Tesch., 1988). Maximal strength training has the ability to improve force, power, and velocity in athletes (Zatsiorsky., 1995). Neuromuscular adaptations, motor unit recruitment, intra and intermuscular coordination, cross sectional area and neural inhibitions have all been associated with a structured strength training routine. Neurological adaptations are found primarily within the coordination of a task in the activation and co-activation of appropriate agonist, synergist and stabiliser muscles and minimal antagonist activation (Folland., et al., 2007). Neurological adaptations help to facilitate recruitment and firing sequences of muscles in a coordinated fashion to produce the desired movement or athletic outcome. Having the correct firing sequence and the correct force and power output in a desired sequence can have profound effects on athletic performance without compromising other attributes. Running requires ankle, knee and hip flexion and extension to produce force against the ground in a coordinated triple extension firing pattern. Closed chain multiple joint exercises, including all compound lifts, Olympic lifts and derivatives thereof have been shown to improve neuromuscular coordination and have a strong dynamic correspondence to improving running performance and economy of running. It is possible to create minimal improvements with open chain exercises, but the neurological pathways aren’t as strong, and coordination of multiple joints is lost. A lot of the literature on neurological adaptations to strength training for endurance athletes, derive from relatively short-term interventions and are normally conducted on untrained or inexperienced athletes within strength training (Kraemer., et al., (2004). Like with endurance training, maximal strength training relays on specific stimulus’s repeated to accumulate heightened levels of specific proteins. Muscle protein anabolism requires the rate of protein synthesis to be greater than the rate of protein breakdown to elicit a positive response, hence why hypertrophy is a relatively slow process (Hawley., 2009) Acute bouts of maximal strength training can increase the rate of protein turnover in skeletal muscles. Chesley., et al., (1992) demonstrated that a single bout of resistance training increased protein synthesis by ~50% four hours post exercise and ~115% twenty-four hours post exercise. Strength training induces the intercellular pathway for phosphatidylinositol 3-kinase-Akt-mammalian target of rapamycin cascade (mTOR). To create cell growth the mTOR integrates signals of the energetics of the cell and environmental stimuli to control protein synthesis and protein breakdown (Deldicque., et al., 2005). Akt-mTOR signalling are the proteins implicated in transitional control, ribosomal protein S6 kinase (p70 S6k) and eIF4E-binding protein (4E-BP1). S6k exerts its effect through multiple substrate targets and has been implicated in orchestrating the regulation of numerous cellular functions, including cell size and protein synthesis (Coffey., et al., 2007). A 14-week resistance training study found increases in p70 S6k, in the same study they found that they strongly correlated with fat free mass, maximal strength and type IIa cross sectional area. Hypertrophy of skeletal muscles has a strong correlation to the force producing capacities of the muscle. For many sports this is a desirable outcome and, in order to promote maximal cellular growth, amino acids are required to fully activate the protein signalling within the muscles (Deldicque., et al., 2005).

Concurrent training of endurance running and maximal strength training can be complimentary if applied in the correct ratio and at appropriate stages in an athlete’s training cycle and with suitable exercise selection. A major benefit for an endurance athlete is the ability to rapidly absorb and create force, if the potential power or force of an athlete is increased the force/power output can be at a lower percentile value than their maximum potential force and power output. As previously seen if an athlete can utilise a lower percentage of their potential force/ power output their running economy will increase and become more economical at submaximal outputs (Paavolainen., et al., 2000). Increases in muscle-extracellular matrix and tendon unit will help to improve ground contact time, increase elastic energy storage, and reduce the energy cost or expenditure of the athletes (Arampatzis., et al., 2006; Fletcher., et al., 2010.). Highly trained individuals tend to have the capacity to increase muscle coactivation, leg stiffness and more efficient eccentric to concentric activation of muscle, which leads to a much more efficient usage of stored elastic energy and increasing to running economy of the athlete (Paavollainen., et al., 1999; Heise., et al., 2008). The main adaptations for endurance athletes from strength training have been observed within the neuromuscular system and are centred around skill acquisition by increasing maximum muscle activation through motor unit synchronization, muscle recruitment, and increased neural activation (Enoka., 1988; Jones., et al., 1989). In well trained endurance athletes, specific training drills such as tempo or interval sessions have been found to be less beneficial at improving neuromuscular function and coordination. However, the improvements documented on neuromuscular function in endurance athletes were found after a short intervention of a basic resistance training programme with relatively inexperienced strength trained endurance athletes. Paavolainen., et al., (1999); Spurrs., et al (2003) and RØnnestad., et al., (2011) found that strength training can significantly improve 3km and 5km time trial performance in runners and improvements were also found in 5 minute and 45-minute time trial performance in cycling. Maximal strength training was found to improve the neuromuscular pathways and coordination of the athletes which led to an improvement in running economy. Economy is expressed as the given velocity or power output at a submaximal V02 (Saunders., et al., 2004). Millet., et al., (2002) found significant improvements in running economy after a strength training intervention, but the improvements in running economy were found to be velocity specific. Therefore, an athlete would not see a general improvement amongst a variety of velocities and would only see improvement in their given discipline. For example, they would not improve at shorter running events but would see improvement in their current discipline. Simultaneous training of endurance and strength have difficulty eliciting positive responses in both. Hickson., (1980) observed that endurance training cannot exceed double the kilocalorie expenditure of strength training without it affecting the 1 repetition maximum of the athlete, and it is advised that concurrent training should remain below four days per week so muscle growth from strength training can occur naturally. To generate a suitable transfer to training, appropriate considerations should be taken into account, force and joint positioning needs to be considered in the exercise selection of the programme (Cormie., et al., 2011). Joint kinematics, force production, direction of force, muscle recruitment, neuromuscular adaptation, strength improvement and endurance indicators of improvement can all show potential advances in performance. It was noted that endurance trained athletes with high force capabilities may need to follow a more explosive or reactive strength training programme to see significant improvements in neuromuscular function and force capabilities.

To conclude, appropriate strength training systems helps to improve neuromuscular capacity whereas endurance training targets both the aerobic and anaerobic energy systems. Intercellular signalling may become compromised with concurrent training when compared to single mode training. Long slow distance endurance training sessions may have an interference effect on optimal neurological adaptations to strength training stimulus (Hawley., 2009). Endurance training does have localised adaptations in skeletal muscle, increased mitochondria, and capillary density aid in the transportation of oxygen to aid in the production of energy which, in prolonged endurance events, will delay the onset of muscle fatigue (Joyner., et al., 2008). The activation of AMPK in the process from endurance training will inhibit the mTOR signal from strength training and inhibit the protein signalling pathway. Maximal strength training and endurance sports have their limitations, mechanical signals generated during contractions and adapting these signals into molecular events that promote adaptation require primary and secondary messengers to activate or supress signalling pathways to induce gene expression or protein synthesis (Coffey., et al., 2007; Williams., et al., 1996). Each discipline ignites a signalling pathway and creates a protein synthesis or gene response in accordance with the stimulus that is being placed upon the system. Resistance training increases the phosphorylation of Akt-mTOR signalling cascade along with p70 S6k but has little to no effect on AMPK PGC-1 pathway. Endurance exercise increases AMPK phosphorylation and PGC-1 protein levels (Atherton., et al., 2005). Specific signalling pathways can explain the adaptations to the stimuluses applied and a notion of an AMPK-Akt master switch has been hypothesised but there is no research to substantiate this claim. Coffey., et al., (2006) performed a study on explicitly trained endurance athletes and explicitly trained strength athletes, when both sets of athletes were exposed to different stimuluses the outcome was surprising. Strength trained athletes increased AMPK after cycling whereas the endurance athletes did not see an increase, strangely endurance trained athletes saw a rise in AMPK after resistance training. Endurance athletes also say an increase in p70 S6k phosphorylation after resistance training whereas the strength trained group saw no increase. S6 protein was elevated immediately post resistance training for the endurance group whereas the strength trained group saw no alteration in levels. Increased levels of AMPK post cycling for the strength trained group and post resistance training for the endurance trained group indicates that the overloading stimulus will create a stronger signalling pathway rather than the mode of training currently undertaken. This research would indicate that in concurrent training there would be a large interference effect in place and therefore would delay the response and reduce the capacity for simultaneous acquisition of hypertrophy or mitochondria training responses.


Arampatzis, A., De Monte, G., Karamanidis, K., Morey-Klapsing, G., Stafilidis, S., & Bruggemann, G. (2006). Influence of the muscle-tendon unit’s mechanical and morphological properties on running economy. Journal of Experimental Biology. 209(17), 3345-3357.

Athertion, P., Babraj, J., Smith, K., Cingh, J., Rennie, M., & Wackerhage, H. (2005). Selective activation of AMPK-PGC-1alpha or PKB-TSC2-mTOR signalling can explain specific adaptive responses to endurance or resistance training-like electrical muscle stimulation. FASEB Journal. 19, 786-798.

Beattie, K., Kenny, L., Lyons, M., & Carson, B. (2014). The Effect of Strength Training on Performance in Endurance Athletes. Journal of Sports Medicine. 44, 845-865.

Chesley, A., MacDougall, J., Tarnopolsky, M., Atkinson, S., & Smith, K. (1992). Changes in human muscle protein synthesis after resistance exercise. Journal of Applied Physiology. 73, 1383-1388.

Coffey, V., & Hawley, J. (2007). The molecular basis of training adaptation. Journal of Sports Medicine. 37, 737-763.

Coffey, V., Zhong, Z., Shield, A., Canny, B., Chibalin, A., Zierath, J., & Hawley, J. (2006). Early signalling responses to divergent exercise stimuli in skeletal muscle from well trained humans. FASEB Journal. 20, 190-192.

Cormie, P., McGuigan, M., & Newton, R. (2011). Developing maximal neuromuscular power. Part 2: Training considerations for improving maximal power production. Journal of Sports Medicine. 41(2), 125-146.

Davis, R., Phillips, R., Rosco, J., & Roscoe, D. (2000). Physical education and the study of sport. (4th ed.). Mosby.

Deldicque, L., Theisen, D., & Francaux, M. (2005). Regulation of Mtor by amino acids and resistance exercise in skeletal muscle. European Journal of Applied Physiology. 94, 1-10.

Enoka, R. (1988). Muscle strength and its development. Journal of Sports Medicine. 6(3), 146-168.

Fletcher, J., Esau, S., & MacIntosh, B. (2010). Changes in tendon stiffness and running economy in highly trained distance runners. European Journal of Applied Physiology. 110, 1037-1046.

Folland, J., & Williams, A. (2007). The Adaptation to Strength Training: Morphological and Neurological Contributions to Increased Strength. Journal of Sports Medicine. 37(2), 145-168.

Fry, A. (2004). The role of resistance exercise intensity on muscle fibre adaptations. Journal of Sports Medicine. 34, 663-679.

Goodman, J., Liu, P., & Green, H. (2004). Left ventricular adaptations following short-term endurance training. Journal of Applied Physiology. 98, 454-460.

Gordon, A., Huxley, A., & Julian, F. (1966). The variation in isometric tension with sarcomere length in vertebrate muscle fibres. Journal of physiology. 184, 170-192.

Grassi, B. (2006). Oxygen uptake kinetics: Why are they so slow? And what do they tell us? Journal of Physiology and Pharmacology. 57(10), 53-65.

Hansen, A., Fischer, C., Plomgaard, P., Andersen, J., Saltin, B., & Pedersen, B. (2005). Skeletal muscle adaptation: Training twice every second day vs training once daily. Journal of applied physiology. 98, 93-99.

Hardie, D., & Sakamoto, K. (2006). AMPK: A key sensor of fuel and energy status in skeletal muscle. Physiology (Bethesda). 21, 48-60.

Hawley, J. (2009). Molecular responses to strength and endurance training: Are they incompatible? Journal of Applied Physiology, Nutrition and Metabolism. 34, 355-361.

Heise, G., Shinohara, M., & Binks, L. (2008). Biarticular leg muscles and links to running economy. International Journal of Sports Medicine. 29(8), 688-691.

Hickson, R. (1980). Interference of strength development by simultaneously training for strength and endurance. European Journal of Applied Physiology and Occupational Physiology. 45, 255-263.

Hill, A. 1938. The heat of shortening and the dynamic constants of muscle. Proceedings of the Royal Society of London. Biological Sciences. 126, 136-195.

Holloszy, J. (1967). Biochemical adaptations in muscle. Effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity in skeletal muscle. Journal of Biological Chemistry. 242, 2278-2282.

Holloszy, J., & Coyle, E. (1984). Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. Journal of Applied Physiology. 56, 831-838.

Jones, D., Rutherford, O., & Parker, D. (1989). Physiological changes in skeletal muscle as a result of strength training. Quarterly Journal of Experimental Physiology and cognate Medical Sciences. 74, 233-256.

Joyner, M., & Coyle, E. (2008). Endurance exercise performance: The physiology of champions. Journal of Physiology. 586(1), 35-44.

Kraemer, W., & Ratamess, N. (2004). Fundamentals of resistance training: Progression and exercise prescription. Journal of Medicine & Science in Sport & Exercise. 36(4), 674-688.

Lin, J., Wu, H., Tarr, P., Zhang, C., Wu, Z., Boss, O., Michael, L., Puigserver, P., Isotani, E., Olson, E., Lowell, B., Bassel-duby, R., & Spiegelman, B. (2002). Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres. Nature. 418, 797-801.

Millet, G., Jaouen, B., Borrani, F., & Candau, R. (2002). Effects of concurrent endurance and strength training on running economy and V02 kinetics. Medicine and Science in Sport and Exercise. 34(8), 1351-1359.

Paavolainen, L., Hakkinen, K., Hamalainen, I., Nummela, A., & Rusko, H. (1999). Explosive strength training improves 5km running time by improving running economy and muscle power. Journal of Applied Physiology. 86, 1527-1533.

Paavolainen, L., Nummla, A., & Rusko, H. (1999). Neuromuscular characteristics and muscle power as determinants of 5km running performance. Medicine & Science in sport & exercise. 31, 124-130.

Paavolainen, L., Nummla, A., & Rusko, H. (2000). Muscle power factors and V02max as determinates of horizontal and uphill running performance. Scandinavian Journal of Medicine and Science in Sports. 10, 286-291.

Rasmussen, B., & Winder, W. (1997). Effect of exercise intensity on skeletal muscle malonyl-CoA and Acetyl-CoA Carboxylase. Journal of Applied Physiology. 83, 1104-1109.

RØnnestad, B., Hansen, E., & Raastad, T. (2011). Strength training improves 5 min all out performance following 185 min of cycling. Scandinavian Journal of Medicine and Science in Sports. 21(2), 250-259.

Saunders, P., Pyne, D., Telford, R., & Hawley, J. (2004). Factors Affecting Running Economy in Trained Distance Runners. Journal of Sports Medicine. 34(7), 465-485.

Spurrs, R., Murphy, A., & Watsford, M. (2003). The effect of plyometric training on distance running performance. European Journal of Applied Physiology. 89, 1-7.

Tesch, P. (1988). Skeletal muscle adaptations consequent to long term heavy resistance exercise. Journal of Medicine & Science in Sport & Exercise. 20, 132-134.

Williams, R., & Neufer, P. (1996). Handbook of Physiology. Section 12. Exercise: Regulation and Integration of Multiple Systems. Oxford University Press.

Wright, D., Geiger, P., Han, D., Jones, T., & Holloszy, J. (2007). Calcium induces increases in peroxisome proliferator-activated receptor ϒ coactivator-1α and mitochondrial biogenesis by a pathway leading to P38 mitogen-activated protein kinase activation. Journal of biological chemistry. 282, 18793-18799.

Yu, M., Stepto, N., Chibalin, A., Fryer, L., Carling, D., Krook, A., Hawley, J., & Zierath, J. (2003). Metabolic and mitogenic signal transduction in human skeletal muscle after intense cycling exercise. Journal of physiology. 546, 327-335.

Zatsiorsky, V. (1995). Science and practice of strength training. Human Kinetics.

Zierath, J., & Hawley, J., (2004). Skeletal muscle fibre type: influence on contractile and metabolic properties. Plos Biology. 2(10), e348.

103 views0 comments
bottom of page