Concurrently training for strength and endurance limits the strength gains, a phenomen termed the concurrent training effect. A long held belief in the concurrent training literature has been that part of the interference has come from interference from molecular signalling pathways in skeletal muscle. However, this explanation is far from adequate. How big a role is the neuromuscular component likely to play in this phenomenon?
Excellent question! I am pleased there are people recognising we have a neuromuscular system. All too often we focus on a few, what we 'think' are important molecules in the signalling cascade without fully considering the interaction of other molecules, cells or even whole systems. The answer is not straight forward, but given the stimulus is quite different between strength and endurance and is engaging vastly different neural recruitment strategies, it seems very logical to assume the neural system could be exceptionally important in the the response we see in performance (and perhaps at the very least an important synergist in the reported molecualr response). The neural system is highly plastic and changes can occur almost immedately - you just need to practice a new skill for a few minutes to see an improvement... that's adaptation. An integrated paradigm that examines the interference effect is the way forward 'from molecules to muscles to mind'... not a straightforward to design. Would love the funds to explore that one!
I think the role of residual neuromuscular fatigue from endurance exercise is certainly under-appreciated in the concurrent training literature. In my view, molecular interference must play at least a partial role in explaining the concurrent interference effect, however surely residual fatigue from endurance exercise would impact negatively on the ability to produce high levels of force/tension during subsequent resistance exercise, therefore potentially limiting the ‘quality’ of the resistance exercise stimulus itself. In turn, this might impact negatively on the ability of the muscle to respond to the resistance exercise stimulus and might manifest as a down-regulated anabolic response following resistance exercise (at least in training-accustomed individuals). Residual neuromuscular fatigue may also reduce central neural drive during resistance exercise and limit activation of higher-threshold type II motor units, which seem to be more responsive to hypertrophy. This is certainly a very complex paradigm, and given the amount of potential training variables involved there is much work to be done to improve our knowledge of the factors which worsen or reduce the interference effect!
David, have a look at the work done by Schmidtbleicher, a big focus on the importance of neuromuscular function in terms of training adaptation, especially in the area of motor unit recruitment.
The articles in a recent, special issue of Frontiers in Striated Muscle Physiology on "Muscle fatigue and muscle weakness: What we know and what we wish we did" might be of interest (http://www.frontiersin.org/Striated_Muscle_Physiology/researchtopics/Muscle_fatigue_and_muscle_weak/486).
Some good points there Will. Although I agree that Burd/Phillips et al.'s work have shown that low-load training to failure is an effective stimulus for promoting MPS, I'm not sure that this approach is effective for promoting maximal strength/power gains, particularly in trained athletes. Also, to my knowledge this approach hasn't yet been shown to translate into enhanced hypertrophy following chronic RT?
Along with hypertrophy, strength and power are also negatively effected by concurrent training and in fact probably more so than hypertrophy (see work by Hakkinen et al. 2003: http://www.ncbi.nlm.nih.gov/pubmed/12627304 and the meta-analysis by Wilson et al. 2012: http://www.ncbi.nlm.nih.gov/pubmed/?term=wilson+rhea+concurrent).
Also, if pre-fatigue augments fast-twitch fibre recruitment then this would suggest augmented hypertrophy during concurrent training which doesn't seem to be the case.
Clearly this is a complex topic with many contributing factors/variables!
It's a great question and is begging to have a study done. A quick glance at the Coffey et al 2009 paper would indeed suggest that prior to embarking upon resistance training following high intensity sprints would result in reduced intramuscular pH. Consequently, this is likely to impair action potential propagation along the sarcolemma to reduce Ca2+ release required for skeletal muscle contraction. In this study the resistance training session was matched for work load which may have resulted in compensatory increase in motor unit recruitment and firing rates. However, the study employed a protocol on just one leg extension (8 x 5 -80% 1RM) whereas a real life resistance training exercise uses a greater range of muscle groups and exercises which would likely result in reduced overall work load achieved.
One other thing I would add is that our tools for studying neuromuscular control are also pretty weak. Most of the EMG studies are far over interpreted. Let's do a better job to develop high-resolution, meaningful tools!
I agree with Dr. Lieber - it's much harder to measure, with confidence, the neuromuscular system. I think that is the primary reason that research in this area is lagging. Years ago we were hopeful that muscle functional MRI might one day become a tool for evaluation of motor unit recruitment - but the spatial resolution still isn't good enough. Without some entirely new technologies I'm not sure we'll see significant progress.
http://www.ncbi.nlm.nih.gov/pubmed/24251881 this new one looks relevant to David Lee Hamilton's question. A very interesting result.
response to concurrent training of strength & endurance will depend upon how much you want to maximize strength or endurance (usually in practice of elite endurance sport we presume that it may be some proportion or ballance of that two). Due to selection of training methods and regimens the specific training response may be "more" neuro-muscular, or structural or metabolic). And response will have several levels - tussue, system, inter-system, entire body. The task is to find out the most combatible components of strength and endurance (and, thus, corresponding methods of training), which could be developed in a single training block (say, 3-4 weeks) to provide the optimal gain of both abilities and final picking for major event.
I don't think it's really that simple. I would say the only "general" result is that early strength gains tend to be neural and later muscular. Endurance is its own thing and doesn't have clear neural/muscular divisions.
That said, one of these days, we should have a discussion about endurance. It's certainly not as straightforward as some have claimed...
In my opinion, intracellular signaling explains only 50% the effect of concurrent training. Once the muscle power and strength are influenced by neural and muscular aspects.
Studies assessing signaling pathways, are focused on skeletal muscle aspects (muscle biopsy to assess: signaling molecules → transcriptions/translations factors → protein synthesis). As show by Stuart Phillp´s lab, low intensity training to failure can increases muscle strength through muscular aspects (hypertrophy). However, if we think in magnitude of adaptative responses, it is necessary to add maximum strength and power training to increase the magnitude (neural aspects) of this process (this is why the periodized training is the best methodology).
I agree that explain the whole process of concurrent training by intramuscular signaling pathways is reducionist. But we can not deny that it is part of the whole process.
Agree, but I am not sure how you could possible come up with a number like 50%. Can you refer to published papers? It should be extremely task specific. If I were asked, I would say neuromuscular training could account for from 10-90% of a strength increase depending on many factors.
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