Hybrid training is a very relevant subject right now, with the rise of multi-sport competitions such as, CrossFit, National Fitness Games, decathlon, spartan, and athletes claiming to do hybrid training to name a handful. Can you train to get cardiovascular improvements, and stronger simultaneously? The old advice used to be train what you want the adaptation from first, but is this correct? Traditionally strength training and endurance sports do not mix, so the question arises, how can you improve your maximum strength potential and aerobic endurance concurrently? Training systems such as the CrossFit method claim to improve an athlete, or general populations aerobic, anaerobic, agility, force, and power qualities collectively! Have they found the key to concurrent training? Training for cardiovascular endurance and strength qualities collectively is characterised as concurrent training. With concurrent training there are an abundance of physiological adaptations taking place, there is a molecular process transpiring and the interference effect of the protein pathways must be considered. The molecular reaction at a cellular level may induce training stimuluses that have opposing physiological results than what you are trying to induce. Both training modalities initiate diverse protein synthesis pathways. How can these pathway work in unison to create the ultimate hybrid athlete! Let us define our terms so we can delve in.
What is aerobic endurance? Aerobic endurance is highly oxygenated continuous exercise that uses the aerobic energy system (fully oxidative), this system has been recognised to activate fully after approximately 240 seconds of continuous training (Bosquet et al., 2002). ATP-PCr and the anaerobic glycolysis systems will be used in the prior stages and during intense bouts during aerobic endurance for example in a hill climb, but an athlete will be working predominantly in the aerobic energy system or fully oxygenated. In aerobic endurance training, it is the athlete’s ability to repeatedly produce force, this force expression will happen sub maximally of Vo2 and is described as aerobic economy (Saunders et al., 2004). This would suggest that Vo2 max is a significant indicator of aerobic endurance performance, the higher the Vo2 max the greater the performance potential? Athletes with similar Vo2 max scores have different race performances so Vo2 cannot fully explain true endurance performance! (Beattie et al., 2014).
Molecularly, repeated aerobic endurance training induces an intercellular stimulus and increase PGC-1α which helps to increase the density of Type I muscle fibres (Saunders et al., 2004), the fatigue resistant muscle fibre and gathers much of its energy from the aerobic system. Type I muscle fibres have a high concentration of mitochondria and mitochondria biogenesis is induced from PGC-1α protein (Marcotte et al., 2015; McGlory & Phillips, 2015; Toigo & Boutellier, 2006); increased mitochondria levels have been demonstrated to be a key contributor to aerobic performance (Saunders et al., 2004).
What is strength training or specifically maximal strength training, (Higbie et al., 1996; Hill & Goldspink, 2003) talk about strength in relation to the force velocity curve, a high force low velocity movement would indicate a strength-based exercise, as a high velocity, low force movement would not be a strength exercise. Force expression can be explained in instances by the amount of impulse an athlete has, the longer an athlete can contract or shorten a muscle or grouping of muscles, the greater the force potential (Suarez et al., 2019). Consequently, if you are lifting a load that requires a greater contractile time, and demands greater amounts of impulse, these movements are maximal in nature. From a molecular standpoint strength training is highly reliant on the ATP-PCr and glycolytic energy systems for initial force requirements (Gastin, 2001), however the oxidative aerobic pathway can be utilised in strength training if rest periods or length of training is manipulated (Beattie et al., 2014). Strength training induces the intercellular pathway mTOR (phosphatidylinositol 3-kinase-Akt-mammalian target of rapamycin cascade) (Deldicque et al., 2005). Akt-mTOR signalling are the proteins implicated in transitional control and ribosomal protein S6 kinase (p70 S6k) exerts its effect through multiple substrate targets and regulates various cellular functions, including cell size and protein synthesis (Coffey & Hawley, 2007; Marcotte et al., 2015). Strength training can initiate an increase p70 S6k, maximal strength and type IIa cross sectional area (Deldicque et al., 2005). Type IIa and IIx muscle fibres relay on the ATP-PCr and glycolytic energy systems for energy supply.
From this brief definition of terms and an overview of the molecular signalling pathways induced from aerobic endurance and strength training, we can see aerobic endurance initiates mitochondria biogenesis within type I muscle fibres and favours the oxidative aerobic energy system. Strength training induces mTOR protein synthesis within type IIa and type IIx muscle fibres favouring the ATP-PCr and glycolytic energy systems, this sounds great as you are utilising everything, let us look closer. You are off on a five-kilometre run, your oxidative energy system is activated, and the concentration of AMP-activated protein kinase (AMPK) is increasing in the muscles. AMPK is an enzyme that regulates cellular energy homeostasis, it regulates the activation of glucose and fatty acid uptake and oxidation when cellular energy is low (Campos et al., 2002; Hardie & Sakamoto, 2006), think of this as your body’s own fuel gauge within the skeletal muscles and is activated when fuel is becoming scarce and starts the process of gathering more energy to replace the fuel already used, consider slowly feeding a fire with just enough wood to keep it burning for a long period of time. (Hardie & Sakamoto, 2006). Winder et al., (1997) and Yu et al., (2004) showed that repeated oxidative training stimulus will increase PGC-1α inducing mitochondria biogenesis and the density of type I muscle fibres, great our endurance system is improving. Then you hit the weight room, you are now working on strength development, trying to initiate mTOR protein synthesis, unfortunately AMPK inhibits the activation of this protein synthesis and endurance training increases AMPK phosphorylation (Coffey & Hawley, 2007; Neufer et al., 1996). You are in the weight room, but mitochondria biogenesis is still firing on all cylinders and your mTOR process is yet to start. This is the interference effect, and the interference process is magnified even more if you are predominantly an endurance trained individual (Wilson et al., 2012). (Coffey & Hawley, 2007) found that the overriding stimulus will create the strongest signalling pathway, if your main signalling pathway is mTOR then when you are completing endurance training mTOR will be produced and vice versa. How can you control this interference effect, there must be a way?
When training to progress in multiple modalities an overlooked factor can be the volume of training overall, overtraining or overreaching especially in opposing discipline can create conflicting adaptations and molecular responses causing an interference effect (Wilson et al., 2012). This correlation of overtraining or overreaching causing an interference effect was first noticed in the pioneering work from Hickson, (1980) who observed that if an athlete exceeded four days of concurrent training, their strength qualities started to diminish, specifically their one repetition maximum started to decrease. This outcome was especially true if the athlete exceeded double the number of kilocalories expended performing oxidative aerobic endurance training in relation to strength training. He went onto advise that when concurrent training, athletes should monitor the amount of energy spent on each discipline to help minimise the interference effect of concurrent training and aid with muscular development naturally. (Wilson et al., 2012) found that endurance training was detrimental to strength, power, and hypertrophy, but to a specific body part! Endurance running >30 minutes created significantly greater detriments to strength than other modalities, some of these detriments could be associated to the increase volume of training and under recovering, again going into the realm of overtraining and overreaching. Interestingly strength training didn’t affect Vo2 (Häkkinen et al., 1987, p. 2). High velocity endurance training has been seen to minimise the interference effect from concurrent training (Duchateau & Baudry, 2010; Dudley, 1985; Häkkinen et al., 2003) when restricted to <20 minutes. With the interference effect effecting the body parts being trained. Careful selection of appropriate training modalities can be used to utilise training efficiency and minimise overtraining and overreaching. In conclusion if an athlete is trying to reduce the interference effect of concurrent training the research seems to suggest that you should favour high velocity endurance training for a duration of <20 minutes coupled with strength training, appropriate exercise selection and not exceeding four days a week of concurrent training. If you are training to improve Vo2 there are less considerations. In all concurrent training models, there is an interference effect that will need consideration. This is a very wide and open subject, far too big for the scope of this article, but I hope this article has given you an insight into the considerations when concurrent training.
Reference
Beattie, K., Kenny, I. C., Lyons, M., & Carson, B. P. (2014). The Effect of Strength Training on Performance in Endurance Athletes. https://doi.org/10.1007/s40279-014-0157-y
Bosquet, L., L??ger, L., & Legros, P. (2002). Methods to Determine Aerobic Endurance: Sports Medicine, 32(11), 675–700. https://doi.org/10.2165/00007256-200232110-00002
Campos, G., Luecke, T., Wendeln, H., Toma, K., Hagerman, F., Murray, T., Ragg, K., Ratamess, N., Kraemer, W., & Staron, R. (2002). Muscular adaptations in response to three different resistance-training regimens: Specificity of repetition maximum training zones. European Journal of Applied Physiology, 88(1–2), 50–60. https://doi.org/10.1007/s00421-002-0681-6
Coffey, V. G., & Hawley, J. A. (2007). The Molecular Bases of Training Adaptation. Sports Medicine, 37(9), 737–763. https://doi.org/10.2165/00007256-200737090-00001
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), 1–10. https://doi.org/10.1007/s00421-004-1255-6
Duchateau, J., & Baudry, S. (2010). Training Adaptation of the Neuromuscular System. In Neuromuscular Aspects of Sport Performance (pp. 216–253). John Wiley & Sons, Ltd. https://doi.org/10.1002/9781444324822.ch13
Dudley, G. A. (1985). Incompatibility of endurance- and strength-training modes of exercise | Journal of Applied Physiology. https://journals.physiology.org/doi/abs/10.1152/jappl.1985.59.5.1446
Gastin, P. B. (2001). Energy System Interaction and Relative Contribution During Maximal Exercise.
Häkkinen, K., Alen, M., Kraemer, W. J., Gorostiaga, E., Izquierdo, M., Rusko, H., Mikkola, J., Häkkinen, A., Valkeinen, H., Kaarakainen, E., Romu, S., Erola, V., Ahtiainen, J., & Paavolainen, L. (2003). Neuromuscular adaptations during concurrent strength and endurance training versus strength training. European Journal of Applied Physiology, 89(1), 42–52. https://doi.org/10.1007/s00421-002-0751-9
Häkkinen, K., Pakarinen, A., Alén, M., Kauhanen, H., & Komi, P. V. (1987). Relationships Between Training Volume, Physical Performance Capacity, and Serum Hormone Concentrations During Prolonged Training in Elite Weight Lifters. International Journal of Sports Medicine, 08(S 1), S61–S65. https://doi.org/10.1055/s-2008-1025705
Hardie, D. G., & Sakamoto, K. (2006). AMPK: A Key Sensor of Fuel and Energy Status in Skeletal Muscle. Physiology, 21(1), 48–60. https://doi.org/10.1152/physiol.00044.2005
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), 255–263. https://doi.org/10.1007/BF00421333
Higbie, E. J., Cureton, K. J., Warren, G. L., & Prior, B. M. (1996). Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation. Journal of Applied Physiology, 81(5), 2173–2181. https://doi.org/10.1152/jappl.1996.81.5.2173
Hill, M., & Goldspink, G. (2003). Expression and Splicing of the Insulin‐Like Growth Factor Gene in Rodent Muscle is Associated with Muscle Satellite (stem) Cell Activation following Local Tissue Damage. The Journal of Physiology, 549(2), 409–418. https://doi.org/10.1113/jphysiol.2002.035832
Marcotte, G. R., West, D. W. D., & Baar, K. (2015). The Molecular Basis for Load-Induced Skeletal Muscle Hypertrophy. Calcified Tissue International, 96(3), 196–210. https://doi.org/10.1007/s00223-014-9925-9
McGlory, C., & Phillips, S. M. (2015). Exercise and the Regulation of Skeletal Muscle Hypertrophy. In Progress in Molecular Biology and Translational Science (Vol. 135, pp. 153–173). Elsevier. https://doi.org/10.1016/bs.pmbts.2015.06.018
Neufer, P. D., Ordway, G. A., Hand, G. A., Shelton, J. M., Richardson, J. A., Benjamin, I. J., & Williams, R. S. (1996). Continuous contractile activity induces fiber type specific expression of HSP70 in skeletal muscle. American Journal of Physiology-Cell Physiology. https://doi.org/10.1152/ajpcell.1996.271.6.C1828
Saunders, P., Pyne, D., Telford, R., & Hawley, J. (2004). Factors affecting running economy. 34(7), 465–485.
Suarez, D. G., Mizuguchi, S., Hornsby, W. G., Cunanan, A. J., Marsh, D. J., & Stone, M. H. (2019). Phase-Specific Changes in Rate of Force Development and Muscle Morphology Throughout a Block Periodized Training Cycle in Weightlifters. Sports, 7(6), 129. https://doi.org/10.3390/sports7060129
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. https://doi.org/10.1007/s00421-006-0238-1
Wilson, J. M., Marin, P. J., Rhea, M. R., Wilson, S. M. C., 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. https://doi.org/10.1519/JSC.0b013e31823a3e2d
Winder, W. W., Wilson, H. A., Hardie, D. G., Rasmussen, B. B., Hutber, C. A., Call, G. B., Clayton, R. D., Conley, L. M., Yoon, S., & Zhou, B. (1997). Phosphorylation of rat muscle acetyl-CoA carboxylase by AMP-activated protein kinase and protein kinase A. Journal of Applied Physiology, 82(1), 219–225. https://doi.org/10.1152/jappl.1997.82.1.219
Yu, J.-G., Carlsson, L., & Thornell, L.-E. (2004). Evidence for myofibril remodeling as opposed to myofibril damage in human muscles with DOMS: An ultrastructural and immunoelectron microscopic study. Histochemistry and Cell Biology, 121(3), 219–227. https://doi.org/10.1007/s00418-004-0625-9
Comments