Ask Dr Adam: Can Post-Workout Muscle Soreness Ever Be a Good Thing?
For a long time, people have focussed on the potential harm that exercise can do, manifesting itself as muscle soreness, inflammation and possibly even muscle damage. For example, delayed onset muscle soreness, or DOMs, is considered an unwanted and concerning side effect of exercise. Consequently, a significant focus is often to minimise these detrimental effects while also aggressively tackling the symptoms, often advocating the use of anti-inflammatories or dosing up on antioxidants.
However, viewed from a different perspective, these side effects of exercise are representative of the very processes that are helping the muscle to “get better” and improve you in the long run. To explain, we can look at the two main types of exercise.
Endurance Exercise
Endurance exercise, sometimes referred to as cardio or aerobic exercise, describes a moderate intensity of exercise sustained over a prolonged period. Endurance exercise requires continual energy (ATP) production in the muscle, mainly through oxidative processes in the mitochondria. However, the rate at which you can generate ATP is dependent on the respiratory chain — a series of redox reactions moving electrons from one molecule to another to end up combining with oxygen ultimately — and is reliant on a supply of oxygen.
When demand for energy production increases, some electrons will inevitably “leak” out of the respiratory chain. Given that more oxygen is in the muscle, these electrons can interact with the present oxygen and nitrogen. They are creating free radicals, specifically reactive oxygen species (ROS) and reactive nitrogen species (RNS).
These ROS and RNS are natural byproducts of mitochondrial respiration and are produced in significant amounts during exercise when energy production is high. However, levels are still within a manageable range in the muscle and will not necessarily cause damage. Instead, they act as a helpful trigger in the muscle to orchestrate cellular changes. Through mediators such as nuclear kappa beta and mitogen activating protein kinases, changes in gene transcription instruct the cell to alter manufacturing.
The goals are to trigger changes such as increased muscle fibre production, metabolic enzymes, and the creation of more mitochondria. All of which will adapt the muscle to better cope next time.
In addition, other cell signalling mechanisms are initiated in response to more free radicals and energy depletion. AMP kinase, in particular, is activated when the energy status of the cell is low. Via the cellular survival mechanism of PGC1a and SIRT1, this can further enhance mitochondrial production and better glucose uptake (increased GLUT4) and improved insulin receptor function (i.e. insulin sensitivity) in the muscle.
It may also help with the uptake and temporary storage of fat in the muscle, as an additional fuel reserve, with a greater ability to oxidise fat due to the increasing mitochondria and other metabolic adaptations — all helpful to import and utilise fuel better next time.
Resistance (+ High Intensity) Exercise
With resistance exercise, similar mechanisms to those described with endurance exercise will also occur, and also in higher intensity exercise to some extent. However, resistance exercise is also conducive to the physical strain on the muscle and potential damage to muscle fibres, particular when that exercise has some concentric features like unfavourable lengthening of the muscle and muscle ‘micro-tears’.
In essence, you damage the muscle fibres through the physical load or pull them apart. Such stress will trigger a traditional inflammatory response to facilitate repair, by example, increasing blood flow and fluid to the muscle — which makes your muscles look artificially more significant after a heavy workout — and releasing inflammatory cytokines.
This collective inflammatory response triggers the same cell signalling response described for endurance, with gene transcription changes altering manufacturing and an increase in importing materials and energy. In this case, the emphasis is on increasing protein synthesis of myofibrillar proteins for muscle fibre repair, rather than mitochondrial proteins in endurance exercise.
There is, therefore, a more pronounced trigger of the mTOR pathway to drive this protein synthesis. In keeping with this, the uptake of amino acids and glucose is enhanced, helped by the general inflammatory response that has already increased blood flow to the muscle.
Help Or Hindrance?
Appreciating these natural adaptation processes can help decide how best to achieve the benefits of exercise. With endurance exercise, the energy crisis created is an essential initiator of improvement. Hence, there is the suggestion that over fuelling the muscle, can potentially blunt some of the cell signalling that facilitates metabolic adaptation. In addition, free radicals are not necessarily bad guys, and levels produced do not necessarily represent oxidative stress which can be damaging.
There is some evidence to suggest that overdosing on antioxidants may also have a blunting effect, particularly in the pharmacological doses found in many supplements. This may be more apparent when the overall volume of exercise is low such as in the amateur athlete or average exerciser.
Nevertheless, there is some suggestion that more natural provision of antioxidants through diet, and certain polyphenols like curcumin for example may be of benefit. Plus, if the training volume is very high, a consideration of antioxidant supplementation may be more appropriate.
For the resistance exercisers, the muscle soreness experienced is likely a signal that your muscle is repairing, and while you should rest and refrain from straining the muscle again in the short term, this is not to say you should stop exercising altogether. However, don’t ignore the soreness; repeated damage and stress on the muscle without time to repair will ultimately lead to declines in muscle function and ultimately gains in performance.
