Muscle Stiffness and Efficiency During Movement.

Part II:The Hip Extensors


When it comes to the biomechanics of the hip extensors, our understanding still has a long way to go. This is in no small part due to the redundant problem in biomechanics. The redundant problem refers to the way in which multiple muscles interact to produce a movement, with many muscles able to contribute to the same movement, but very few actually doing so. Thus, when it comes to the biomechanical and kinematic assessment of a movement, such as hip flexion during gait, we are challenged when we want to assign a specific contribution of the movement to a specific muscle.

During gait, the work of the bi-articular long head of the biceps femoris is reduced as knee flexion angle increases. This occurs during the initial stance phase of gait, before reducing as stance phase progresses towards toe-off. During the swing phase the knee moves from flexion towards extension, being approximately fully extended at or before heel strike. As the knee flexes, so the contribution of biceps femoris is reduced, whilst that of gluteus maximus increases. The relative contribution of each muscle involved in hip extension is poorly understood, and challenging to measure.

Electromyography (EMG) can be used to quantify the timing and magnitude of muscle activation, but its use is extremely limited. Surface EMG electrodes only measure the activity directly beneath them, and so cannot detect activity of deep muscles or muscles away from the electrode. Noise is easily introduced, whilst signal quality will differ according to the amount of hair and oils on the skin (so can be removed prior to testing), subcutaneous fat, skin movement relative to muscle, and proximity of contracting fibres (amongst other things).

Video marker systems - such as Vicon - and force plates, are the gold standard of biomechanical and kinematic assessments. Inverse dynamics calculations can be applied - based upon the Newton-Euler equations - to assess joint moments, angles and velocities and muscle forces. However, the muscle forces calculated are the composite for each joint, with attempts to assign values to specific muscles liable to errors. What complicates this further is our limited knowledge of passive-elastic contributions to joint moments, muscle forces and movement.


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When walking, the bi-articular biceps femoris contracts eccentrically to decelerate the shank and stabilise the hip joint. Too little resistance, and the shank would accelerate forwards too rapidly, and there would be a risk of injury to the knee. Too much resistance, and the hip flexors would have to contract more forcefully to compensate. The efficiency of movement is optimised by a contribution of the passive-elastic properties of the hip extensors. That is, the resistance offered by the muscles during lengthening contributes to the total resistance offered by the muscle.

We can experience the passive resistance from our hamstrings when we stretch them. The resistance to stretch increases exponentially until we reach the end of our range of motion. At around that point, we might experience pain, discomfort and/or a stretch reflex. Although it is unlikely that a conscious stretch can be entirely passive, it is nevertheless considered a passive assessment, and our most practical means of assessment.

During gait, the hip flexes to approximately 30 degrees during the swing phase, terminating at heel strike. At 30 degrees, the amount of passive resistance offered by the hip extensors is very low, but it does contribute something. An area of growing interest (including that of your humble author) is quantifying the passive contribution to movement. This is where it gets interesting…

The average person with low back pain (LBP) will move more slowly and with a reduced stride length than someone without LBP. It is important to understand whether this difference in gait is due to passive or active contributions. If it is passive resistance, this implies that the muscles have either shortened or physically tightened (tightness/stiffness refers to resistance to stretch, rather than simply flexibility). The active resistance is a property of contractility, and so is neuromuscular adaptation, rather than a structural one.

It is plausible that the initial response to pain is a neuromuscular adaptation, whilst longer-term it becomes structural. If so, this has huge ramifications for how therapy should be applied. It might be that structural changes can be altered by static stretching and strengthening, whilst neuromuscular changes result from mobility and power training. Before we can explore these possibilities, it is first necessary to expand the research on how the body responds to pain and injuries, and how training influences muscle properties.

At the moment, there is interest in establishing what forms of exercise influence passive muscle properties. Only one group of researchers (Marshall et al) has published studies showing that stretching can reduce muscle stiffness, whereas all the other researchers (and there are many) show that stretching has no effect. More specifically, the other researchers have found that stretching influences stretch tolerance, so the reason flexibility increases is because we 'feel' the stretch less, and permit a greater range of motion (ROM).

At some point, this consideration becomes counter-intuitive. A dancer cannot be achieving phenomenal hip ROM, simply because he or she tolerates being stretched more than a rugby player, who might have a ROM of 45 degrees or less. Future research can explore just how much stretching is required to reduce stiffness in the long term. How dynamic stretching might be involved is yet to be investigated.

Some strengthening exercises have been found to increase muscle stiffness, such as heavy eccentric loading, with minimal or no such relationship for plyometrics, concentric or isometric contractions. However, where there are effects, these tend to last only a matter of hours, or a couple of days at the most. As with the research on stretching, investigators have a long way to go before any sort of prescription can be based on evidence. There is potential for both stretching and strengthening work to influence passive properties, but these might be long term adaptations that take years.

In a 7-day week of 24-hour days, just how many hours are being spent doing something that might create a change, compared to the number of hours where the body is already efficient at what it is doing? It is likely that the body adapts to ensure efficiency, but if any lifestyle or exercise behaviours demonstrate inefficiency for a total of 5 hours out of a 168-hour week, is this sufficient impact for change? Realistically, even if exercising for 5 hours, how much of those 5 hours is the 'working set', or stressing the body's end ROM? How many years might it actually take, and what can we recommend for the individual at risk of injury who is about to engage in his or her sport? Clearly we have a long way to go and an awful lot to learn.

When it comes to the relationship between passive and active contributions to movement, we are in the very infancy of scientific exploration. We have no idea of what 'optimal' is for an individual, and, whatever it is, it will be a property of gender, age, limb length, muscle mass and fibre type, body mass, and lifestyle and exercise habits. What is 'optimal' for an endurance runner will not be optimal for a sprinter. What is optimal for a weightlifter might not be optimal for a powerlifter.

Too much passive, active or net stiffness in the hip extensors might increase risk of hip flexor injuries, whereas too little will increase the risk of knee injuries. Too little or too much both promote inefficiencies in bioenergetics. This has important ramifications for cross-training, and whether doing might decrease sport-specific efficiency, in favour of a Jack-of-all-trades muscle with an increased risk of injury.

Clearly we have a long, long way to go. We need to better assess passive and active contributions to movement. We need to better understand how pain and injuries influence these, and over what sort of timeline. We need to establish how to influence muscle properties, so as to undo anomalies caused by pain or injury, to reduce injury risk and to promote sports performance. The last 30 years of related research has brought us a long way, and it has given us a valuable insight into just how far we still have to go.



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