A critical evaluation of the physiological adaptions of concurrent resistance training in endurance.

Essay I recently penned for my masters, enjoyed researching this.

Resistance training (RT) is the strengthening of muscles using the progressive overload principle, (gradually increasing the resistance a muscle must overcome) that results in increases in muscle contraction force. RT achieves this through a combination of increased muscle activation and muscle fibre hypertrophy (Bird, 2005). Many studies have shown it to be beneficial to endurance athletes (Beatie et al, 2014), with increases in speed and economy in runners (Jung, 2003; Wilson et al, 2012), as well as guarding against injury (Hewett, 2006; Howe, 2017). This has led many coaches to train their athletes with both RT and aerobic training (AT) concurrently.

The physiological compatibility of concurrent training (CT) with RT and AT has been the subject of great interest for decades (Hickson, 1980). This essay will look at the physiological adaptions of RT in the context of CT for endurance runners (ER). I shall be looking at the physiological adaptions brought about by RT, but also looking at if (and how) they could be affected by the concurrent AT the athletes are also undertaking. This essay will take three parts. Part one will look at the physiological adaptions to RT and how these could be of advantage/disadvantage to ER. Part two will look at the interference effect (IE), that is if and how the adaptions of RT could be interfered with by concurrent AT. Part three will conclude with suggestions on how to combine RT and AT to lessen any IE, therefore being of the most use to ER.

RT can be defined as the progressive overload of a skeletal muscle that is characterized by high muscle contraction force and anaerobic ATP resynthesis (Ahtiainen, 2019). Given time the muscle adapts to the greater levels of resistance encountered and increases its maximal force output mainly using enhanced muscle activation and muscle fibre hypertrophy (Folland, 2007). The RT program used will have different effects on the muscle depending on various factors such as volume, intensity, and frequency.

Neural adaptions to RT are essentially adaptions in coordination and learning that facilitate greater recruitment and activation of the involved motor units in a task. They can be split in to three main subcategories, motor unit recruitment, firing rate and inter-muscular coordination. Muscle fibres are controlled by motor units (Aargaard, 2003), these consist of a single motoneuron and all the muscle fibres it innervates. Motor units can be classified as either slow (Type I), fast (Type IIa) and fast fatigable (Type IIx). (Burke, 1967). Type I motor units have smaller cell bodies and develop a relatively lower force than Type II but for a longer amount of time (60-120ms). They are also fatigue resistant as they work aerobically. Type IIa and IIx motor units as stated develop higher forces and fatigue quicker (10-50ms). Type I motor units are the first to be activated according to the Heneman size principle (Heneman, 1965), the lower force producing type I fibres are recruited by the central nervous system first when a muscle is activated, Type II are then recruited when and if they are needed. If force production is gradually applied then muscles recruit all motor units between 50% and 95% of maximum force production (Grillner & Udo, 1971). Untrained individuals cannot recruit as many high threshold motor units containing type II muscle fibres as trained individuals. Research has shown that in untrained individuals only 71% of muscle tissue was activated in maximal contractions (Adams et al. 1993). It has been suggested that the early stages of strength gains in RT is mainly through neural adaptions as little morphological adaptions have taken place (Folland, 2007). The muscle unit recruitment pattern may change with long-term strength training. As the type I fibres become stronger, they will not need to call on the type II fibres until a later time. This has been shown to be beneficial to endurance athletes with improvements at sub maximal cycling after 2 hours of continuous work, suggesting a sparing effect of the type II fibres (Mujika et al, 2016).

Higher motor neuron firing rates have been shown to produce more force in a muscle. With increased firing rates the muscle fibres are activated by overlapping action potentials, which is expressed as greater contractile strength in the muscle (Aagaard, 2003). Firing rates have been shown to be increased following 14 weeks of heavy resistance training (Aargaard et al, 2002). Holtermnan et al, (2005), found a 16% increase in strength with no evidence of greater motor unit recruitment after 9 training sessions of the dorsiflexors, hinting at other factors including firing rate as the cause of strength gains. It would appear improvements in firing rates are one of the first adaptions made to increase strength, with improvements seen as early as 3 weeks (Vila-cha et al, 2012).

Intermuscular co-ordination refers to the co-ordination of different muscles to achieve a task. Any co-activation of antagonist muscles will reduce force but will also (by reciprocal inhibition) impair the full activation of the agonists. Carolan and Cafarelli (1992), found deactivation in antagonist muscles following 2 weeks of strength training.

These neural adaptions have been cited as improving power in the muscle and to rapidly produce force after a sustained period of high-intensity exercise (Nummela et al, 2006). This will allow a stronger sprint finish and can be the difference in reaching the podium in middle- and long-distance running (Beattie et al, 2017). This improvement in rate of force development (RFD) has also been cited as improving running economy (RE) (Paavolainen et al, 1999; Nummela et al, 2006; Yamamoto et al, 2008). RE is the metabolic cost to cover a given distance at a constant velocity (Shaw et al, 2014). By increasing RFD and the maximum force output, the force required during each stride to produce a certain running velocity could theoretically decrease (Beattie et al, 2017).

To elicit these neural adaptions endurance runners should be looking to train with high loads (Cormie et al, 2011). It has been shown training with 80% to 90% of 1 repetition maximum (RM) gave greater neural adaptions than 30% to 50% 1RM , despite more volume being performed at 30% to 50% 1RM (Jenkins et al, 2017; Looney et al, 2016).

One of the most noticeable adaptions to RT is muscle hypertrophy (MH). Athletes new to RT will have very limited MH with strength gains mainly coming from neural adaptions (Folland, 2007). Within a couple of months of training, hypertrophy begins to become noticeable (Mulligan et al, 1996). MH induced by RT occurs with increased protein content of muscle fibres (Luthi et al, 1986). Most of the skeletal muscle fibre cytoplasm is made up of myofibrils, the most abundant proteins being myosin and actin filaments (Macdougal et al, 1980). Hypertrophy is thought to be brought about by satellite cells that activate when a mechanical stimulus is imposed on skeletal muscle (Hawke & Garry, 2001). Satellite cells donate extra nuclei to muscle fibres, increasing the capacity to biosynthesize new proteins, and co-express myogenic regulatory factors aiding in, regeneration, muscle repair and growth (Moss & Leblond, 1970).

Three main theories have been put forward explaining the initiation of MH after RT. Mechanical tension: the time muscles work under tension, can also be thought of as the volume of work under tension. Muscle damage: the damage caused to muscle fibres after RT. Metabolic stress; the accumulation of metabolites produced (Evans 2002; Hornberger & Chien 2006; Rutherford & Jones 1987; Vandenburgh 1987). These set off a chain of events leading to the biosynthesis of new fibres within a myofibril, as well as an increase of new myofibrils within a muscle fibre, and ultimately an enlargement of the muscle. (Toigo & Boutellier, 2006).

MH due to RT is made possible by several molecular signalling pathways that shift muscle protein balance to favour synthesis over degradation. The three primary pathways have been identified as the Akt/mammalian target of rapamycin pathway (mTOR1). The mitogen-activated protein kinase pathway (MAPK), and the calcium-dependent pathway (Ca2+) (Schoenfeld, 2010). The mTOR1 pathway is thought to have the greatest effect and is activated via contractile activity and essential amino acid provision after RT (Bodine et al, 2001). Specific to MH, MAPK has been shown to link cellular stress with adaptions in muscle cells, stimulating growth (Roux & Blenis, 2004). Ca2+ dependent pathways are involved in muscle hypertrophy. Calcineurin (Cn), is critical in the Ca2+ signalling cascade. Cn has been linked to hypertrophy of all fibre types, and its inhibition has been shown to prevent muscle growth even after high loads of RT (Dunn et al, 2000).

MH has some important implications for ER. MH can occur either by adding sarcomeres in series or in parallel (Schoenfeld, 2010). Sarcomeres added in parallel will produce more force while sarcomeres added in series will increase muscle shortening velocity (Lieber & Ward, 2011). It has been shown that low load high velocity movements such as plyometrics will lead to sarcomeres being added in series where high load/force training will add sarcomeres in parallel (Stone et al, 2007). If as stated earlier it will be more beneficial to increase a runner’s RFD, then runners should be looking to maximise the force they can produce. This will be achieved through higher load RT. Once runners force capacity is improved then plyometrics and explosive movements will teach the runner to access this force in a short time frame. A periodised training approach would best solve this problem. MH will add weight to an ER in the form of muscle. Runners should not be looking to put on more muscle as the added weight will have consequences to their performance regardless of if it is muscle or fat (Maciejczyk et al, 2014, Maciejczyk et al, 2015). The type of RT deployed will influence how much MH takes place. Low-load high volume resistance programs have been found to stimulate muscle protein synthesis more than high-load low volume resistance programs. (Burd et al, 2010).

Muscle fibre type transitions with RT have been observed (Schiaffino et al, 2007). These tend to be type II fibres, with the main outcome being a shift from a more glycolytic fibre (type IIx) to a more oxidative fibre (type IIa). This has been suggested to be better for endurance athletes as the type IIa fibres have greater oxidative and fatigue resistance qualities (Rønnestad & Mujika, 2014). Fibre type transitions were not related to the relative intensity used for training, so most types of RT will be beneficial in this respect (Fry, 2004).

Connective tissue hypertrophies after RT (Kongsgaard et al, 2007). The renewal of tissue is slower than that of muscle and so adaptions will take longer to show (Magnusson et al, 2008). One adaption that does not seem to be related to hypertrophy is tendon stiffness. Tendons will increase their stiffness before hypertrophy occurs, due to adaptations in internal structures of the tendon mainly in the cross-link composition between collagen molecules (Kubo et al, 2002). Tendon stiffness increases the utilization of elastic energy in the stretch shortening cycle. This allows for increases in RFD during fast muscle actions (Kubo et al, 2007). This is of great importance to distance runners who use the SSC in the Achilles tendon on every foot strike, any increase in RFD will allow for faster running and greater RE.

Literature shows that RT is beneficial for ER with gains in RE seen (Yamamoto et al, 2008). Implementing RT into training schedules has proven difficult due to the IE of concurrent RT with AT (Fyfe, 2014). The IE can be broken down into two categories. The acute IE whereby one form of training fatigues the athlete to perform worse in the other form (Doma & Deakin, 2014), and the chronic IE, whereby the two forms of training interfere with each via the resulting adaptions to training (Wilson et al, 2012).

Acute IE from RT on AT has been broken down into 4 mechanisms, these can be thought of collectively as ‘residual fatigue’ (Doma et al, 2017). 1. Impaired neural recruitment patterns, muscle force generating capabilities can be impaired for up to 72 hrs following RT (Doma & Deakin, 2013). 2. Reduced movement efficiency due to alteration in kinematics during endurance exercise and increased energy expenditure. Some studies have shown reductions in lower limb joint range of motions during running following RT (Dutto & Braun, 2004;Paschaliset al, 2007), it should be noted that these are not permanent changes. 3. Increased muscle soreness, delayed muscle soreness (DOMS) can alter gait patterns as discussed. DOMS will be worse in untrained individuals but will subside to an extent when athletes are familiar with the exercise (Smith & Lucille, 1992). 4. Reduced muscle glycogen, muscle glycogen levels can remain depleted for up to 6 hours after training (Pascoe et al, 1993) Levels can be raised faster depending on post-exercise nutritional intake and activity levels following the session (Knuiman et al, 2015). Glycogen depletion has been shown to be detrimental to running performance (Green, 1990). The implications of residual fatigue for runners can impair subsequent running performance. For instance, if a runner is training to a rate of perceived exertion (RPE), then any fatigue from RT will increase his RPE. A pace that feels 7/8 RPE might be 5/6 RPE without the fatigue from RT. This could negate the purpose of the running session. Various studies have shown decreased time to exhaustion scores on various forms of AT 24-72 hrs after RT training (Burt & Twist, 2011; Doma & Deakin, 2013; Doncaster & Twist, 2012). This can be seen in Figure 1. That is not to say RT should not be used by runners. RT has been shown to be beneficial to runners especially for RE. Residual fatigue is a short term (<72 hrs) occurrence and should be planned for in an athletic programme, to not impact on AT.

Figure 1.

Mechanisms of acute fatigue brought about by resistance training.

Chronic interference. Levels of satellite cells have been shown to be blunted in CT as opposed to RT (Babcock et al, 2012). This will lower levels of hypertrophy of muscle fibres as they are instrumental in donating nuclei for protein synthesis. The mTORC1 signalling pathway has been cited as a site of chronic interference (Wilson et al, 2012; Fyfe et al, 2014). Many theorise that because RT and AT use different molecular signalling pathways to bring about different adaptations then these pathways can interfere with each other (Hawley, 2009; Wilson et al, 2012). It seems AT interferes with strength gains from RT much more than RT interferes with AT (Hickson, 1980). Many studies have shown no decrease of VO2max after concurrent RT and AT training (Hickson, 1980; Paavolainen et al, 1999; Yamamoto et al, 2008). AMPK is a sensor of cellular energy status and is activated when ATP levels become low in cells, it is activated after AT. Research has shown that AMPK activation can inhibit mTORC1 activity therefor reducing MH in rodents (Bolster et al, 2002). This theory has been termed the AMPK switch (Ruderman et al, 2003). The AMPK phosphorylates tuberous sclerosis complex−2, switches off the mTORC1-signaling cascade. Figure 2 shows how the combined factors of acute and chronic interference can theoretically lower hypertrophy in muscle fibres.

Figure 2.

Concurrent training interference on muscle hypertrophy.

More recently researchers have begun to question this hypothesis in humans, a meta-analysis by Wilson et al, (2012) found that CT increases strength and muscle mass and was not statistically different to RT alone. In a subset of analyses, different modes of endurance training were associated with different degrees of interference, with running but not cycling impairing increases in lower body strength and muscle mass. It has been proposed this could be down to the high impact and eccentric loading of the muscles during running (Wilson et al, 2012). The amount of interference was found to be linked with the volume and intensity of AT. AT performed at high volume, intensity and duration inhibited RT adaptions. This could have consequences for high level athletes, but recreational athletes (3-6 training sessions a week) should be spared the IE (Coffey & Hawley, 2017).

Another cause for interference of the mTOR1 pathway has been theorised to be levels of the tumour suppressor protein p53 (Budanov & Karin, 2008). P53 is released following endurance exercise, but also through cellular stressors such as calorie deficit and ageing. The protein Leucine activates the mTOR1 pathway by binding to sestrin, which is an mTOR1 pathway suppressor. P53 is an up regulator of sestrin, so when p53 levels are high so are sestrin levels (Tachtsis et al, 2016). This has been theorised to be the cause for muscle wastage outside of exercise science, in ageing individuals and bed bound patients (De Bandt, 2016). Coaches and athletes should pay attention to calorie levels and other stressors that will also raise levels of p53 thus impairing the mTOR1 pathway.

One of the strongest effects of the IE is on power (Wilson et al, 2014). CT results in larger hypertrophy of Type I fibres and limiting growth of Type II fibres (Aagaard et al, 2011). The muscle would therefore have a greater proportion of slow twitch type I fibres than a muscle trained in RT alone. Some studies have also shown alterations in activation patterns reducing power after CT (Eklund et al, 2015). CT has been shown to increase power in ER (Trowell et al, 2020), but not as much as could be expected with RT alone (Hickson, 1980).

The literature shows interference effects for both RT and AT when trained concurrently. Coaches and runners should be more concerned about interference to their AT than RT. In fact, most of the interference from RT to AT is short term and can be classed as residual fatigue. Good programming and allowing for proper recovery before hard aerobic sessions should be of great importance to coaches and athletes. Many running sessions are performed at a low intensity, allowing for recovery days to be programmed without disrupting run volume. MH is largely an unwanted by product of RT in ER and any interference from AT to MH should not cause alarm. RFD from neural adaptions to RT has been shown to improve RE and at an elite level could be the difference between gold or silver. This combined with injury prevention due to strengthening connective tissue is a strong argument to include RT in ER training schedules.


Aagaard, P. (2003). Training induced changes in neural function. Exercise and sport science, 31, 61-67.

Aagaard, P., Andersen, J. L., Bennekou, M., Larsson, B., Olesen, J. L., Crameri, R., Magnusson, S. P., & Kjaer, M. (2011). Effects of resistance training on endurance capacity and muscle fiber composition in young top-level cyclists. Scandinavian journal of medicine & science in sports, 21(6), e298–e307.

Aagaard, P., Simonsen, E. B., Andersen, J. L., Magnusson, P., & Dyhre-Poulsen, P. (2002). Neural adaptation to resistance training: Changes in evoked V-wave and H-reflex responses. Journal of Applied Physiology, 92(6), 2309-2318.

Adams, G. R., Harris, R. T., Woodard, D., & Dudley, G. A. (1993). Mapping of electrical muscle stimulation using MRI. Journal of applied physiology (Bethesda, Md. 1985), 74(2), 532–537.

Ahtiainen, J, P. (2019). Physiological and Molecular Adaptations to Strength Training. Concurrent Aerobic and Strength Training, 51-73.

Babcock, L., Escano, M., D'Lugos, A., Todd, K., Murach, K., & Luden, N. (2012). Concurrent aerobic exercise interferes with the satellite cell response to acute resistance exercise. American journal of physiology. Regulatory, integrative and comparative physiology, 302(12), R1458–R1465.

Beattie, K., Kenny, I. C., Lyons, M., & Carson, B. P. (2014). The effect of strength training on performance in endurance athletes. Sports medicine (Auckland, N.Z.), 44(6), 845–865.Beattie, K., Carson, B. P. , Lyons, M. , Rossiter, A. & Kenny, I. C. (2017). The Effect of Strength Training on Performance Indicators in Distance Runners. Journal of Strength and Conditioning Research, 31(1), 9–23.

Bird, S. P., Tarpenning, K. M., & Marino, F. E. (2005). Designing resistance training programmes to enhance muscular fitness: a review of the acute programme variables. Sports medicine (Auckland, N.Z.), 35(10), 841–851.

Bodine, S. C., Stitt, T. N., Gonzalez, M., Kline, W. O., Stover, G. L., Bauerlein, R., Zlotchenko, E., Scrimgeour, A., Lawrence, J. C., Glass, D. J., & Yancopoulos, G. D. (2001). Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nature cell biology, 3(11), 1014–1019.

Bolster, D. R., Crozier, S. J., Kimball, S. R., & Jefferson, L. S. (2002). AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin (mTOR) signalling. The Journal of biological chemistry, 277(27), 23977–23980.

Budanov, A. V., & Karin, M. (2008). p53 target genes sestrin1 and sestrin2 connect genotoxic stress and mTOR signaling. Cell, 134(3), 451–460.

Burd, N. A., West, D. W., Staples, A. W., Atherton, P. J., Baker, J. M., Moore, D. R., Holwerda, A. M., Parise, G., Rennie, M. J., Baker, S. K., & Phillips, S. M. (2010). Low-load high volume resistance exercise stimulates muscle protein synthesis more than high-load low volume resistance exercise in young men. PloS one, 5(8), e12033.

Burke, R.E. (1967). Motor unit types of cat triceps surae muscle. J Physiol. 193(1), 141–60.

Burt, D. G., & Twist, C. (2011). The effects of exercise-induced muscle damage on cycling time-trial performance. Journal of strength and conditioning research, 25(8), 2185–2192.

Carolan, B., & Cafarelli, E. (1992). Adaptations in coactivation after isometric resistance training. Journal of applied physiology (Bethesda, Md. : 1985), 73(3), 911–917.

Coffey, V. G., & Hawley, J. A. (2017). Concurrent exercise training: do opposites distract? The Journal of physiology, 595(9), 2883–2896.

Cormie, P., McGuigan, M. R., & Newton, R. U. (2011). Developing maximal neuromuscular power: Part 1--biological basis of maximal power production. Sports medicine (Auckland, N.Z.), 41(1), 17–38.

De Bandt J. P. (2016). Leucine and Mammalian Target of Rapamycin-Dependent Activation of Muscle Protein Synthesis in Aging. The Journal of nutrition, 146(12), 2616S–2624S.

Doma, K., & Deakin, G. B. (2013). The effects of strength training and endurance training order on running economy and performance. Applied physiology, nutrition, and metabolism, 38(6), 651–656.

Doma, K., Deakin, G. B., & Bentley, D. J. (2017). Implications of Impaired Endurance Performance following Single Bouts of Resistance Training: An Alternate Concurrent Training Perspective. Sports medicine (Auckland, N.Z.), 47(11), 2187–2200.

Dunn, S. E., Chin, E. R., & Michel, R. N. (2000). Matching of calcineurin activity to upstream effectors is critical for skeletal muscle fiber growth. The Journal of cell biology, 151(3), 663–672.

Dutto, D. J., & Braun, W. A. (2004). DOMS-associated changes in ankle and knee joint dynamics during running. Medicine and Science in Sports and Exercise, 36(4), 560-566.

Eklund, D., Pulverenti, T., Bankers, S., Avela, J., Newton, R., Schumann, M., & Häkkinen, K. (2015). Neuromuscular adaptations to different modes of combined strength and endurance training. International journal of sports medicine, 36(2), 120–129.

Evans W. J. (2002). Effects of exercise on senescent muscle. Clinical orthopaedics and related research, (403 Suppl), S211–S220.

Folland, J. P., & Williams, A. G. (2007). The adaptations to strength training: morphological and neurological contributions to increased strength. Sports medicine (Auckland, N.Z.), 37(2), 145–168.

Fry A. C. (2004). The role of resistance exercise intensity on muscle fibre adaptations. Sports medicine (Auckland, N.Z.), 34(10), 663–679.

Fyfe, J. J., Bishop, D. J., & Stepto, N. K. (2014). Interference between concurrent resistance and endurance exercise: Molecular bases and the role of individual training variables. Sports Medicine (Auckland), 44(6), 743-762.

Green H. J. (1991). How important is endogenous muscle glycogen to fatigue in prolonged exercise? Canadian journal of physiology and pharmacology, 69(2), 290–297.

Grillner, S., & Udo, M. (1971). Recruitment in the tonic stretch reflex. Acta physiologica Scandinavica, 81(4), 571–573.

Hawke, T. J., & Garry, D. J. (2001). Myogenic satellite cells: physiology to molecular biology. Journal of applied physiology (Bethesda, Md. 1985), 91(2), 534–551.

Hawley J. A. (2009). Molecular responses to strength and endurance training: are they incompatible? Applied physiology, nutrition, and metabolism, 34(3), 355–361.

Henneman, E., Somjen, G., & Carpenter, D. O. (1965). Functional significance of cell size in spinal motoneurons. Journal of neurophysiology, 28, 560–580.

Hewett, T. E., Ford, K. R., & Myer, G. D. (2006). Anterior cruciate ligament injuries in female athletes: Part 2, a meta-analysis of neuromuscular interventions aimed at injury prevention. The American journal of sports medicine, 34(3), 490–498.

Hickson R. C. (1980). Interference of strength development by simultaneously training for strength and endurance. European journal of applied physiology and occupational physiology, 45(2-3), 255–263.

Holtermann, A., Roeleveld, K., Vereijken, B., & Ettema, G. (2005). Changes in agonist EMG activation level during MVC cannot explain early strength improvement. European journal of applied physiology, 94(5-6), 593–601.

Hornberger, T. A., & Chien, S. (2006). Mechanical stimuli and nutrients regulate rapamycin-sensitive signaling through distinct mechanisms in skeletal muscle. Journal of cellular biochemistry, 97(6), 1207–1216.

Howe, L. P., Waldron, M., & Read, P. (2017). A systems-based approach to injury prevention for the strength and conditioning coach. Strength and Conditioning Journal, 39(6), 60-69.

Jenkins Nathaniel D. M., Miramonti Amelia A., Hill Ethan C., Smith Cory M., Cochrane-Snyman Kristen C., Housh Terry J., Cramer Joel T. (2017) Greater Neural Adaptations following High- vs. Low-Load Resistance Training, Frontiers in Physiology, 8, 331.

Jung A. P. (2003). The impact of resistance training on distance running performance. Sports medicine (Auckland, N.Z.), 33(7), 539–552.

Kongsgaard, M., Reitelseder, S., Pedersen, T. G., Holm, L., Aagaard, P., Kjaer, M., & Magnusson, S. P. (2007). Region specific patellar tendon hypertrophy in humans following resistance training. Acta physiologica (Oxford, England), 191(2), 111–121.

Kubo, K., Kanehisa, H., & Fukunaga, T. (2002). Effects of resistance and stretching training programmes on the viscoelastic properties of human tendon structures in vivo. The Journal of physiology, 538(Pt 1), 219–226.

Kubo, K., Morimoto, M., Komuro, T., Yata, H., Tsunoda, N., Kanehisa, H., & Fukunaga, T. (2007). Effects of plyometric and weight training on muscle-tendon complex and jump performance. Medicine and science in sports and exercise, 39(10), 1801–1810.

Lieber, R. L., & Ward, S. R. (2011). Skeletal muscle design to meet functional demands. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 366(1570), 1466–1476.holterma

Looney, D. P., Kraemer, W. J., Joseph, M. F., Comstock, B. A., Denegar, C. R., Flanagan, S. D., Newton, R. U., Szivak, T. K., DuPont, W. H., Hooper, D. R., Häkkinen, K., & Maresh, C. M. (2016). Electromyographical and Perceptual Responses to Different Resistance Intensities in a Squat Protocol: Does Performing Sets to Failure With Light Loads Produce the Same Activity? Journal of strength and conditioning research, 30(3), 792–799.

Lüthi, J. M., Howald, H., Claassen, H., Rösler, K., Vock, P., & Hoppeler, H. (1986). Structural changes in skeletal muscle tissue with heavy-resistance exercise. International journal of sports medicine, 7(3), 123–127.

MacDougall, J. D., Elder, G. C., Sale, D. G., Moroz, J. R., & Sutton, J. R. (1980). Effects of strength training and immobilization on human muscle fibres. European journal of applied physiology and occupational physiology, 43(1), 25–34.

Maciejczyk, M., Wiecek, M., Szymura, J., Szygula, Z., & Cempla, J. (2015) Physiological response during running in athletes with similar body mass but different body composition, Science & Sports, 30(4), 204-212.

Maciejczyk, M., Więcek, M., Szymura, J., Szyguła, Z., Wiecha, S., & Cempla, J. (2014). The influence of increased body fat or lean body mass on aerobic performance. PloS One, 9(4), e95797-e95797.

Magnusson, S. P., Narici, M. V., Maganaris, C. N., & Kjaer, M. (2008). Human tendon behaviour and adaptation, in vivo. The Journal of physiology, 586(1), 71–81.

Moss, F. P., & Leblond, C. P. (1970). Nature of dividing nuclei in skeletal muscle of growing rats. The Journal of cell biology, 44(2), 459–462.

Mujika, I., Rønnestad, B. R., & Martin, D. T. (2016). Effects of Increased Muscle Strength and Muscle Mass on Endurance-Cycling Performance. International journal of sports physiology and performance, 11(3), 283–289.

Mulligan, S. E., Fleck, S. J., Gordon, S. E., Koziris, L. P., Triplett-McBride, N. T., & Kraemer, W. J. (1996). Influence of resistance exercise volume on serum growth hormone and cortisol concentrations in women. Journal of Strength and Conditioning Research, 10(4), 256.

Nummela, A., Keränen, T., & Mikkelsson, L. O. (2007). Factors related to top running speed and economy. International journal of sports medicine, 28(8), 655–661.

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

Pascoe, D. D., Costill, D. L., Fink, W. J., Robergs, R. A., & Zachwieja, J. J. (1993). Glycogen resynthesis in skeletal muscle following resistive exercise. Medicine and science in sports and exercise, 25(3), 349–354.

Rønnestad, B. R., & Mujika, I. (2014). Optimizing strength training for running and cycling endurance performance: A review. Scandinavian journal of medicine & science in sports, 24(4), 603–612.

Roux, P. P., & Blenis, J. (2004). ERK and p38 MAPK-activated protein kinases: a family of protein kinases with diverse biological functions. Microbiology and molecular biology reviews:MMBR, 68(2), 320–344.

Ruderman, N.B., Park, H., Kaushik, V.K., Dean, D., Constant, S., Prentki, M. & Saha, A.K. (2003). AMPK as a metabolic switch in rat muscle, liver and adipose tissue after exercise. Acta Physiologica Scandinavica, 178, 435-442.

Schiaffino, S., Sandri, M., & Murgia, M. (2007). Activity-dependent signalling pathways controlling muscle diversity and plasticity. Physiology (Bethesda, Md.), 22, 269–278.

Schoenfeld B. J. (2010). The mechanisms of muscle hypertrophy and their application to resistance training. Journal of strength and conditioning research, 24(10), 2857–2872.

Shaw, A. J., Ingham, S. A., & Folland, J. P. (2014). The valid measurement of running economy in runners. Medicine and science in sports and exercise, 46(10), 1968–1973.

Smith, L. L. (1992). Causes of delayed onset muscle soreness and the impact on athletic performance: A review. Journal of Strength and Conditioning Research, 6(3), 135-141.

Stone, M. H., Stone, M. & Sands, W. A. (2007). Principles and Practice of Resistance Training, Champaign, IL, Human Kinetics.

Tachtsis, B., Smiles, W. J., Lane, S. C., Hawley, J. A., & Camera, D. M. (2016). Acute Endurance Exercise Induces Nuclear p53 Abundance in Human Skeletal Muscle. Frontiers in physiology, 7, 144.

Toigo, M., & Boutellier, U. (2006). New fundamental resistance exercise determinants of molecular and cellular muscle adaptations. European journal of applied physiology, 97(6), 643–663.

Trowell, D., Vicenzino, B., Saunders, N., Fox, A., & Bonacci, J. (2020). Effect of Strength Training on Biomechanical and Neuromuscular Variables in Distance Runners: A Systematic Review and Meta-Analysis. Sports medicine (Auckland, N.Z.), 50(1), 133–150.

Vandenburgh, HH. Motion into mass: How does tension stimulate muscle growth? Med Sci Sport Exerc 19(5 Suppl.): S142–S149, 1987.

Vila-Chã, C., Falla, D., Correia, M. V., & Farina, D. (2012). Changes in H reflex and V wave following short-term endurance and strength training. Journal of applied physiology (Bethesda, Md. : 1985), 112(1), 54–63.

Wilson, J. M., Marin, P. J., Rhea, M. R., Wilson, S. M., Loenneke, J. P., & Anderson, J. C. (2012). Concurrent training: a meta-analysis examining interference of aerobic and resistance exercises. Journal of strength and conditioning research, 26(8), 2293–2307.

Yamamoto, L. M., Lopez, R. M., Klau, J. F., Casa, D. J., Kraemer, W. J., & Maresh, C. M. (2008). The effects of resistance training on endurance distance running performance among highly trained runners: a systematic review. Journal of strength and conditioning research, 22(6), 2036–2044.

14 views0 comments

Recent Posts

See All

© 2019 by STRENGTH2ENDURE. Proudly created with