Many athletes throughout a wide range of sports will often require various training adaptations to achieve success (9). Habitually, the vast majority of competitive athletes, specifically field-based participants, require a high level of strength and endurance capacity to improve and/or maintain an elitist competitive status (20). However, both characteristics implicate a large amount of diverse adaptation. Strength training approaches involve traditional heavy resistance modalities, primarily focussing on skeletal muscle tissue hypertrophy and an increase in neural motor unit recruitment (13, 32). On the contrary, endurance training aims to increase an athlete’s VO2 max (16), focusing on improving muscle fibre oxidative capacity and mitochondrial density (18). Implementing both strength and endurance training interventions, often described as concurrent training (14), has revealed increases in endurance related performance, partly due to greater running economy (13). However, research has also revealed that concurrent training may have detrimental effects to strength-related and skeletal muscle hypertrophic adaptation compared to strength training alone (17, 23, 34). This is identified as the Interference Effect (IE) (17). For the vast majority of athletes in invasion-based environments – where there is perhaps a larger emphasis on strength-related adaptations – deficiencies in strength development from concurrently incorporating frequent and intense endurance-like technical training, could promote the interference effect. Therefore this review aims to highlight and critically discuss potential causes for this incompatibility with concurrent strength and endurance training.
Both strength-related and endurance training approaches initiate DNA translation and transcription by upregulating gene expression through a series of distinct pathways (4). Despite both methods of training utilising several primary signals, strength-related interventions primarily stimulate protein synthesis through phosphorylation, subsequently upregulating insulin-like growth factor-1 (IGF-1), phosphoinositide dependent kinase (PDK-1) and mammalian target of Rapamycin (mTOR) (7). Endurance stimuli typically cultivates a depletion of energy and a release of calcium ions into the functioning skeletal muscle tissues via the sarcoplasmic reticulum (3, 19). Throughout this signalling pathway (figure 1), energy depletion and calcium release activity signals an upregulation of adenosine monophosphate-activated kinase (AMPK) and calcium-calmodulin-dependent-kinases. These two gene expressions elicit an increase in peroxisome proliferator co-activator-1 (PGC-1) and further ensues an upsurge in mitochondrial activity and mitochondrial biogenesis – one of the prime physiological adaptations from endurance training (7). It has been theorised that AMPK inhibits the strength-related pathway, blocking the upregulation of mTOR via the tuberous sclerosis complex (TSC2) and suppressing further increases in protein synthesis (27). This blunting of the strength-related pathway theorises the interruption of muscle tissue hypertrophy, possibly adding to the decrease in strength-like characteristics compared to adaptations traditionally seen in strength training, alone. However, additional research has contested the likelihood of an interference effect and presented strength and endurance improvements throughout concurrent training (1, 2, 9). Conversely, these positive findings may be accountable due to several factors – mainly the relatively new training status in participants, the length of study and strength intervention method (for instance, isolated elbow extension instead of multi-joint compound movements). Hickson (1980) theorised that individuals undertaking concurrent training will see positive adaptations from both stimuli for the first 7 weeks, then a plateau and a gradual decline as concurrent training continues. Sedentary individuals relatively new to either training stimulus will often see benefits in concurrent training due to a novice training status, provided they control excessive overreaching (29).
Figure 1. Molecular pathways in resistance and endurance exercise.
Acute and chronic fatigue
Acute fatigue, the immediate deficiency of contractile force due to high volumes of activity, is another speculated strength adaptation inhibitor (22). It’s hypothesised that strength training proceeding endurance activity causes a reduction in strength training performance, likely depressing further gains in strength related qualities (26). Higher motor unit recruitment adaptations are a result of intense, high tension contractions (33) and therefor a decrease in force output could lead to a supressed motor unit recruitment in strength sessions. In 1991, Craig, Lucas, Pohlman & Stelling revealed that introducing an endurance activity prior to a weightlifting session found a decrease in lower body power output. Whilst acute fatigue may contribute to a decrease in strength performance in concurrent training, separating training sessions throughout a microcycle may alleviate this impairment, providing there is sufficient rest and adequate carbohydrate intake (20).
Chronic fatigue is often a result of continual imbalance between phases of intense training and periods of recovery (4). With concurrent training utilising several stimuli, chronic fatigue may also induce an interference effect in training programmes with progressively heavy resistance workloads. Although concurrent training appears to decrease strength-like adaptations, endurance adaptations appear to be unaffected when chronically corresponded with strength stimuli (11). There is also existing research disproving chronic fatigue as a major influence overall (5, 21). If appropriate recovery is managed correctly between endurance and strength bouts, acute and chronic fatigue may produce less of a factor in decreasing strength training adaptations. Possible training recommendations involve separating endurance and strength training with a 6-24 hour rest period to help recover for intense strength sessions, thus maximising possible adaptations (4).
Research examining high amounts of endurance exercise has revealed catabolic environments in the working muscles (10) leading to a negative nitrogen balance and a decrease in protein synthesis (28). Muscle cell hypertrophy requires a positive nitrogen balance in order to maintain or upregulate anabolic mechanisms, often seen in the working muscles as a response to strength training (31). Despite the catabolic effects of endurance training, sufficient dietary protein and adequate recovery can minimise the onset of a catabolic interference effect and help improve strength adaptations in concurrently trained individuals.
Muscle phenotype transformation
Another variable that could potentially encourage the interference effect is muscle fibre transformation within skeletal muscle structures. Hakkinen, Pakarinen, Allen, Kauhanen & Komi (1987) stated that Type II muscle fibres possess the greatest potential for cell hypertrophy (30). Endurance approaches physiologically target Type I muscle fibre recruitment, also altering Type IIa fibres to possess Type I oxydative characteristics (24). Luginbuhl, Dudley & Staron (1984) previously revealed endurance training initiated an increase in Type I fibre percentage throughout the muscle structures. With less fibres exhibiting Type II strength characteristics, this could potentially explain a reduction in hypertrophy when an individual participant includes endurance training alongside strength focussed protocals. Contrary to this, it has been found that a prominant result of strength training reduces mitochondrial density and decreases oxydative enzymes which can impeed endurance capacity, but there is minimal conversion of type II to type I muscle fibres (27). These contradictions suggest further research is needed on the investigation of complete fibre transformation to examine the potential effects on concurrent training (13).
In summary, successful athletes will often require high levels of endurance and strength to flourish in their sport, in particular field-based games players. However, it is evident that adopting strength training concurrently with intense endurance training leads to a decline in strength-like adaptaions in training programmes. The most influencing factor in contemporary research is the interference of molecular signalling pathways as a result of both exercise stimuli. Other influencing factors, such as acute and chronic fatigue, muscle fibre type transformation and catabolic environments can all be controlled or minimised by coaches and athletes through adequate rest and appropriate nutritional strategies – such as higher carbohydrate intake prior to strength training. Despite molecular signalling playing an important role in IE, there are several guidelines that coaches and athletes can follow to minimise the onset of IE. Athletes should avoid strength training for up to 6 hours when proceeding endurance training. Dependant on endurance intensity, this gap in strength-endurance training may increase for up to 24 hours post endurance training. A minimal IE periodisation plan should encorporate higher strength intensities in the presence of lower endurance intensities and vice-vercer. Manging training intensity will not only assist an athlete in reaching their full potential in various training adaptations, but continue to improve and maintain high performance in their chosen sport.
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