Electromyography (EMG) is a type of technology that is used to measure the activity of muscles.
The most common type of EMG device used is surface EMG, which utilises tools called electrodes placed on the skin, directly over the muscle(s) about which the researchers want to gather data.
Sometimes, electrode needles are used to collect data from the muscle itself (intramuscular EMG).
The signal detected by electrodes is called the electromyogram, and it shows the output from the motor neurons that supply axons to the muscle(s) being analysed.
From this signal, researchers can see which muscles are active during movement, when and how hard the various muscles contract, and if other muscles are also activating during movement.
While surface EMG is the most common technique used in electromyography studies (probably because it's easier to recruit study participants when you're not jabbing them with needles!), it does a poor job of differentiating between various muscles that are active at a given moment in time.
Many authors of EMG research articles equate the size of the EMG signal with the amount of active tension produced by a muscle during contraction, but it's essential to keep in mind several variables that can confuse interpretations of EMG measurements.
These variables include the accuracy of electrode placement on the skin, the muscle length's when EMG is measured, the speed of muscle lengthening, and passive tension arising from the layers of tissue between the muscle and electrode (fascia, fat, skin, etc.).
For these reasons, researchers generally try to avoid comparing EMG signal sizes of a given muscle across different people or over several days in the same test subject.
Unfortunately, many authors make erroneous conclusions about levels of activation and the amount of force generated by the muscle.
Activation refers to the energetic state of the muscle, and it is related to the size of the force that the muscle produces relative to the muscle's maximum ability to produce force. (Understand that 'activation' describes active conditions and thus does not include contributions of tension from passive structures like connective tissues.)
Force is related to activation, but they are not the same thing.
As stated, activation refers only to contributions of tension created by the utilisation of chemical energy, and it ignores the passive elements of the muscle-tendon unit.
Therefore, we cannot use activation to indicate the muscle's total force production capabilities (total force is a combination of both active and passive tension).
It's also important to remember that activation is not affected by a muscle's length and its speed of lengthening, but the muscle's ability to produce force is highly dependent upon length and velocity.
Activation does not account for the dynamics of muscle contractions, such as force-velocity and force-length relationships, which have been discussed in some detail in previous blog entries.
Therefore, activation relates to the number of activated fibres - not the force-generating capacity of those fibres.
This helps to explain why EMG studies that cited increased levels of muscle activation following isometric contractions during static active (PNF) stretching are not necessarily a reliable counterargument against the premise of autogenic inhibition.
Autogenic inhibition is the supposed relaxation of a stretched muscle caused by stimulation of Golgi tendon organs; in simple terms, the resistance felt during a stretch is suppressed by contraction of the stretched muscle, thus reducing the sensitivity of the stretch reflex and enabling the muscle to be stretched further.
If the stretch reflex was suppressed as the theory of autogenic inhibition suggests, a decrease in active tension (muscle force) would follow the release of the isometric contraction.
Opponents of autogenic inhibition (which some training providers have erroneously referred to as reciprocal inhibition) point to the EMG studies demonstrating increased muscle activation following isometric contractions.
However, as this blog entry points out, activation and muscle force are not the same thing, and many of the EMG studies used in arguments against autogenic inhibition have suffered from methodological flaws, such as comparing output signals at disparate muscle lengths.
Another flaw of many EMG studies is that authors do not differentiate between muscle activation and muscle excitation.
Surface EMG measures changes in the polarity of muscle fibre membranes caused by nervous system excitation, and they are not the same thing.
Excitation occurs before activation, and activation accounts for excitation-contraction dynamics, whereas excitation does not.
Unfortunately, many authors use the term "muscle activation" when they are actually referring to muscle excitation or the amount of neural excitability that occurs before activation.
It is vital to be aware of the differences between excitation, activation, and muscle force when reading research articles, and to ensure the authors clarify how they define these terms in their published works.