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Training to Failure

One of the most controversial areas of resistance training, especially where bodybuilding is concerned, is should an athlete train to failure in order to realise muscular gains and strength improvements. This article will look at the rationale behind the premise and attempt to arrive at a scientific conclusion to the time honoured question.

 

Before we attempt to analyse and rationalise the science behind this theory we should first arrive at a definition of what ‘failure’ implies. Our definition of 'training to failure' will be ‘decreased ability to generate appropriate amounts of muscle force or power during on-going contractile activity’. At this juncture, the lifter would have to be rescued by a spotter if on a bench exercise or would have to rack the weight in a standing exercise. This inability to further perform a repetition i.e. achieve failure could be due to a number of physiological factors which are encompassed under the banner of ‘fatigue’. Such factors could include some of the following:

  • Reduced Intracellular pH - Lactic acid builds-up in the muscle cell causing a reduced intracellular pH (increased acidity causes failure of Ca2+ release and inhibition of contractile proteins) which affects force development. (Mainwood, G.W. et al, 1987; Chin E.R., 1998)

  • Reduced Intramuscular ATP - When ATP stores deplete, muscles might not have enough energy to contract. (Karatzaferi C., et al, 2001). ATP and PCr utilization is greater in type II compared with type I fibres (Casey et al, 1996) and total restoration of ATP will not occur in the first four minutes of rest for the type II fibres. However, in type I fibres four minutes are sufficient to allow full ATP restoration to occur. Therefore if a second set were carried out within a four or five minute period the type II fibres would be incapable of significant force production. (Casey et al, 1996).

  • Accumulation of Inorganic Phosphate (Pi) - Concentration of Pi increases during intense skeletal muscle activity, mainly due to the breakdown of PCr.  High force production in cross bridges within the sarcomere of the muscle cell is hindered by this increased Pi. (Westerblad, H., 2002)

  • Reduced Creating Phosphate – Creatine phosphate (PCr) is a high energy compound used in anaerobic metabolism to re-synthesise ATP. There are limited stores of PCr in the muscles. This high energy ‘molecule’ is predominantly used by FTb fibres.  The rate of depletion will be dictated by the intensity of the exercise. If PCr is depleted complete fatigue will occur in the working muscles.  (Hirvonen, J. et al, 1992; Karatzaferi C., et al, 2001)

  • PNS Fatigue – Peripheral nervous system fatigue occurs differently for low intensity and high-intensity exercise. Similarly to CNS fatigue; PNS fatigue may be due to a number of complex physiological reasons. Factors such as ionic adaptations i.e. Ca2+, NA+ and K+; decreases in substrate availability i.e.  PCr and glycogen; hypoxia, acidosis and accumulation of inorganic Pi might all be influential influences behind PNS fatigue. These metabolic changes can cause fatigue by acting on nerve processes that activate muscles.

  • CNS Fatigue – Unwillingness to generate and maintain adequate CNS drive to the working muscle during exercise, is the most likely explanation of fatigue for most people during normal activities. It is believed that several neurotransmitters and the influence they exert on the brain are influential to the fatigued state.  Davis J.M. and Bailey S.P. (1997) also asserted that ‘Accumulation of ammonia in the blood and brain during exercise could also negatively affect the CNS function and fatigue’.  Serotonin levels are also increased during intense exercise and these higher levels can increase perceptions of effort and peripheral muscle fatigue (Young, S. N. 1996). CNS fatigue is a highly complex area of significance.

  • Increased Heat – As exercise ensues and intensifies, the requirement for energy will be increased.  This increased metabolism and mechanical muscular effort will increase heat within the body. Indeed up to 80% of the oxygen consumed in exercise ends up as heat rather than facilitating mechanical work.  If the environment is both hot and humid the core body temperature can rise significantly and this hypothermic environment can result in an impedance of several physiological mechanisms including the CNS and PNS which are involved with development of muscle force. (Nybo & Secher, 2004).

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Ahtiainen et al (2003) asserted that

 

‘forced repetition exercise system induced greater acute hormonal and neuromuscular responses than a traditional maximum repetition exercise system’.

 

Schoenfeld B.J. (2013) postulated that

 

‘Current research indicates that low-load exercise taken to failure can indeed promote increases in muscle growth in untrained subjects and that these gains may be functional, metabolically, and/or aesthetically meaningful’. The suggestion is that this low load training method closely mimics blood flow restriction training which has been shown to have positive ‘marked effects on muscle hypertrophy’.

 

Rooney et al, 1994, carried out research on the roles of fatigue in weight training and concluded that

 

‘the processes associated with fatigue contribute to the strength training stimulus’.

 

Other studies have supported training to failure (Goto et al, 2007; Willardson, 2007) but there is also some opposing research.           

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Failure is Not Volitional. Failure is induced!

The above studies have asserted that ‘failure’ training indeed is a positive method of training for a strength athlete or a bodybuilder. However, much of the research into this specific area is contrary to the claim that this method of training is an effective strategy for strength and muscular development. Willardson, J. (2007) stated that training to failure,

 

’is not essential for increases in muscular characteristics such as strength and hypertrophy’.

 

Izquierdo, M. et al (2006) also concurred with this statement when their research indicated that there was ‘a potential beneficial stimulus of non-failure training for improving strength and power’. Sanborn et al (2000) in a study comparing the effectiveness of multiple set training and a single set taken to failure, established that ‘Body mass did not change significantly over time’ and that ‘results generally show a superior adaptation for the multiples sets group’. Kramer et al, 1997, carried out a similar research programme to Sanborn in that they compared two multiple non- failure sets to a single set taken to failure. They found that ‘multiple sets not performed to failure produce superior gains in the 1-RM squat’. Folland et al, (2002) established that

 

‘Fatigue and metabolite accumulation do not appear to be critical stimuli for strength gain, and resistance training can be effective without the severe discomfort and acute physical effort associated with fatiguing contractions’.

 

So further compounding the premise that training to failure is not necessarily an inherent requirement where stimulation for adaptation is required.   

So where does that leave the trainee who is looking for an answer to this question? The following guidelines address some of the ways in which training to failure may be beneficial if employed in a training regimen:

 

  • Use failure training as part of a ‘periodization’ training year.

  • Only use failure sets in one or two exercises for the last two sets.

  • Allow adequate acute recovery periods between work sets when using failure.

  • Allow adequate chronic recovery periods between workouts to avoid injury or overtraining.

  • Use a wide expanse of repetition ranges to stimulate all muscle fibres.

  • Where possible use machine-based resistance to guide technique during the fatigue stages.

  • Use a ‘spotter’ whenever possible to ensure safety.

  • Do not use failure training for beginners or early intermediate trainees.

Training to Failure. Freind or Foe?

When an organism is stressed beyond its physiological ‘normal’ capabilities; then that organism will potentially realise adaptation; to ensure that it can more fully cope with the stressor if it is experienced again.  A realisation of absolute muscular fatigue i.e. repetition failure is the stressor utilised to enforce this physiological response and thus chronic adaptation. This is the premise behind ‘training to failure’. 

 

It is theorised that when the working muscles are taken to muscular failure any or all of the following factors may be influenced. Increased muscle activation i.e. greater motor unit recruitment (Stone et al., 1996 and Tan, 1999); more mechanical stressed based protein damage which would result in increased synthesis (Stone et al, 1996); increased anabolic hormone levels (Kraemer & Ratamess, 2005) or fibre transitioning i.e. ST fibres taking on FT fibre capabilities (Fry, 2004).  Adaptation in any of these areas could result in increased strength gains and indeed increased muscle fibre cross-sectional area.

 

Now we have established the relationships between the physiological systems and total muscular fatigue, let us now look at the evidence that supports muscular failure training. 

MMA

Is training to failure effective or not? Some notable studies have supported the effectiveness of ‘failure’ training. In a study carried out on a number of elite basketball and football players, the researchers found that

 

‘Bench press training that leads to repetition failure induced greater strength gains than non-failure training in the bench press exercise for elite junior team sport athletes’ (Drinkwater et al , 2005).  

References

 

Ahtiainen J.P., Pakarinen A., Kraemer W.J., Häkkinen K. (2003) Acute Hormonal And Neuromuscular Responses And Recovery To Forced Vs Maximum Repetitions Multiple Resistance Exercises. International Journal of Sports Medicine.  24(6): 410-8.

 

Baudry S., Duchateau J. (2004) Post-Activation Potentiation In Human Muscle Is Not Related To The Type Of Maximal Conditioning Contraction. Muscle & Nerve. Journal of Applied Physiology. 30: 328-36.

 

Casey, A., D. Constantin-Teodosiu, S. Howell, E. Hultman, and P.L. Greenhaff (1996). Metabolic response of type I and II muscle fibres during repeated bouts of maximal exercise in humans. American Journal of Physiology. 271: 38-43.

 

Chin E.R. and Allen D.G. (1998) The Contribution Of Ph-Dependent Mechanisms To Fatigue At Different Intensities In Mammalian Single Muscle Fibres. Journal of Physiology. 1;512 :831-40

 

Davis J.M. and Bailey S.P. (1997) Possible Mechanisms Of Central Nervous System Fatigue During Exercise. Medicine and Science in Sport and Exercise. 29(1):45-57.

 

Drinkwater E.J., Lawton T.W., Lindsell R.P., Pyne D.B., Hunt P.H., McKenna M.J. (2005) Training Leading To Repetition Failure Enhances Bench Press Strength Gains In Elite Junior Athletes. Journal of Strength and Conditioning Research.  19(2): 382-8

 

Folland J.P., Irish C.S., Roberts J.C., Tarr J.E., Jones D.A. (2002) Fatigue Is Not A Necessary Stimulus For Strength Gains During Resistance Training. British Journal of Sports Medicine.  36(5):370-3

 

Fry A.C. (2004) The Role Of Resistance Exercise Intensity On Muscle Fibre Adaptations. Sports Medicine 34:663-679.

 

Goto K, Nagasawa M, Yanagisawa O, Kizuka T, Ishii N, Takamatsu K. (2004) Muscular Adaptations To Combinations Of High And Low-Intensity Resistance Exercises. Journal of Strength and Conditioning Research. 2004; 18:730-737.

 

Gorostiaga E.M., Navarro-Amezqueta I., Calbet J.A., Hellsten Y., Cusso R., Guerrero M., Granados C., Gonzalez-Izal M., Ibanez J., & Izquierdo M.(2012)  Energy Metabolism During Repeated Sets Of Leg Press Exercise Leading To Failure Or Not. PloS One.  7(7): e40621.

 

Hirvonen, J., Nummella, T., Rusko, H. Rehunen, S. Harkonen, N. (1992) Fatigue And Changes Of ATP, Creatine Phosphate, And Lactate During The 400-M Sprint. Canadian Journal of Sports Science.  17(2):141-4.

 

Izquierdo, M.  Ibañez , J.,  José J.,  Badillo G., Häkkinen, K.,  Ratamess, N.,  Kraemer, W.  French, D.  Eslava, J.  Altadill, A.  Asiain, X. (2006) Differential Effects Of Strength Training Leading To Failure Versus Not To Failure On Hormonal Responses, Strength, And Muscle Power Gains. Journal of Applied Physiology. 100. 5: 1647-1656

Holm, L. Reitelseder, S., Pedersen, T. Doessing, S., Petersen S.,  Flyvbjerg, A., Andersen, J.  Aagaard, P., Kjaer, M.  (2008) Changes In Muscle Size And MHC Composition In Response To Resistance Exercise With Heavy And Light Loading Intensity. Journal of Applied Physiology. 105: 5, 1454-1461

 

Karatzaferi C., de Haan A., Ferguson R.A., van Mechelen W., Sargeant A.J. (2001) Phosphocreatine And ATP Content In Human Single Muscle Fibres Before And After Maximum Dynamic Exercise. European Journal of Physiology.  442(3):467-74

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Kramer J.B., Stone M.H., O Bryant H.S., Conley M.S., Johnson R.L., Nieman, D.C., Honeycutt D.  (1997) Effects Of Single Vs Multiple Set Of Weight Training: Impact Of Volume, Intensity And Variation. Journal of Strength and Conditioning Research.  11:143-147.

 

Mainwood G.W., Renaud J.M., Mason M.J. (1987) The pH Dependence Of The Contractile Response Of Fatigued Skeletal Muscle. Canadian Journal of Physiology and Pharmacology. 65(4):648-58

 

Nybo, L., and N.H. Secher (2004). Cerebral Perturbations Provoked By Prolonged Exercise. Progress in Neurobioolgy. 72: 223-261.

 

Ratamess N., Alvar B., Evetoch T.K., Housch T.J., Kibler B., Kraemer W.J., Triplett N.T.  (2009) Progression Models In Resistance Training For Healthy Adults.  Medicine and Science in Sports and Exercise. 41:687-708.

 

Rooney K.J., Herbert R.D., Balnave R.J. (1994) Fatigue Contributes To The Strength Training Stimulus. Medicine and Science in Sports and Exercise.  26(9):1160-4.

 

Schoenfeld BJ. (2013) Potential Mechanisms For A Role Of Metabolic Stress In Hypertrophic Adaptations To Resistance Training. Sports Medicine. 43(3):179-94.

 

Schoenfeld BJ. (2013) Is There A Minimum Intensity Threshold For Resistance Training-Induced Hypertrophic Adaptations? Sports Medicine.  43(12):1279-88

 

Stone MH, Chandler TJ, Conley MS, Kraemer JB, Stone ME. (1996) Training To Muscular Failure: Is It Necessary? Strength Conditioning Journal.  18:44-48.

 

Tan B. (1999) Manipulating Resistance Training Program Variable To Optimize Maximum Strength In Men: A Review.  Journal of Strength and Conditioning Research.  13:289-304.

 

Westerblad , H., Allen D.G., and Lännergren, J. (2002)  Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause?. American Physiological Society. 17:1, 17-21

 

Willardson, J.M. (2007) The Application Of Training To Failure In Periodized Multiple-Set Resistance Exercise Programs. Journal of Strength and Conditioning Research. 21(2):628-31

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