Over the past year or so, the idea of making sure not to inhibit the training effect has risen in popularity. The old concept was that as soon as the workout was done, everything possible was done to recover for the next workout. In practicality, this made sense, as if we could recover for the next training bout, we could get more intensity and volume out of that session. Now, the pendulum is swinging to the other side.
To me, this represents a classic case of switching back and forth between two paradigms. We started with the old school notion of little worry over recovering after a workout to the hypersensitive world of always consuming your Gatorade and ice baths after every run. Now, it seems we are correcting the balance and finding some happy medium. The way it is headed is towards a paradigm of periodizing recovery. How did we get to this point?
A change in mindset with fresh new ideas in the coaching and research world, along with a knowledge base increase in what recovery actually does and how adaptation actually works. Adaptation was traditionally presented as some nebulous graph copied from some obscure Russian text about super-compensating. There is truth to this approach, but what we’ve come to realize is that adaptation is impacted a multiple levels beyond just the workout and how you recover from it. The rise in knowledge of molecular adaptation, signaling pathways, and genetics has given us a peak into what happens and what is triggered the moment after our training stress is applied.
This paradigm shift has led us to consider many traditional approaches such as:
- Antioxidants around working out.
- Training with low glycogen stores.
- Ice baths
- Inflammations role.
And in the future, I have a feeling that other aspects will be examined, such as going without carbs/protein for a few hours post workout or even recovering in a hypoxic state.
While I have covered some of these before, I’d like to focus on the role of inflammation in adaptation and injury prevention. There have been a few recent research articles that have targeted what the role of inflammation is and it’s worth a look at the latest science.
Anti-inflammatory drugs are some of the most used in the world. If something hurts, pop ibuprofen and get better. Get injured, sprain a muscle, or sprain an ankle? Take some NSAIDs, reduce the inflammation, and get better. The theory is that if we reduce the inflammation, it’ll speed healing.
The problem with that theory is that the inflammatory response is one of the body’s natural responses to actually increase healing. Let’s take a look at how that process works and what anti-inflammatories actually do.
The process of inflammation and anti-inflammatories:
When you do a damaging workout or have an acute injury, your body goes through a nice little cycle that is initially pro-inflammatory and then eventually switches to anti-inflammatory. It’s an interesting little cycle that is akin to how our medical world works. We start with an emergency first responder team (leukocytes and monocytes) that responds quickly, followed by what we might relate to as your initial hospital stay (macrophages). From there, we go into a regeneration and repair state. For the technical details I’ll turn to the study by Urso (2013):
“The first inflammatory cells to arrive to the site of injury are polymorphonuclear leukocytes, which are eventually replaced by monocytes within hours of the injury. Over the next 24-48 hours these cells transform into macrophages which phagocytose and remove necrotic tissue. Macrophages, along with fibroblasts and the extracellular matrix, also produce growth factors, cytokines, and chemokines (59, 76, 99). It is these factors that activate regenerative mechanisms such as myogenic factors and satellite cells. During the repair phase, satellite cells proliferate and differentiate into myoblasts which fuse with injured myofibers (39, 54). In cases where the injury damages the basal lamina, a connective tissue scar is formed from fibrin and fibronectin (22, 40). While this scar tissue strengthens the muscle during contractions as the muscle heals, if there is a continued injury to the muscle and excessive proliferation of fibroblasts, dense scar tissue may form which interferes with the repair process and contributes to incomplete functional recovery (89).”
Traditionally, for injury, the idea has been to limit inflammation. As Urso (2013) points out, this might not be such a good idea, and perhaps the better question is not if we should, but at what point during this cycle may it be beneficial.
Let’s look at how anti-inflammatories impact the above cycle.
Cox-1 vs. Cox-2
Most anti-inflammatory drugs work as cycloocygenase (COX) inhibitors. There are multiple forms of COX in the body. If we look at what ones are elevated post exercise, it is mostly COX-1. NSAIDs are generally non-specific COX inhibitors or COX-2 inhibitors. Therefore, depending on the drug taken, it can either have an impact on inflammation in response to exercise, or not.
When COX is inhibited, what it does is inhibits that inflammatory cascade. For example, PGE2 is decreased which in turn decreases some of the interleukin response. Some of the IL’s in turn play a role in adapting to exercise.
Blocking inflammation: Adaptation and Repair
So what’s the deal and why is it bad? The reason blocking inflammation might be bad is because of the effect on adaptation and recovery. Simply put, muscle damage is one of the key signals for adaptation. If enough damage occurs, and inflammatory markers are released, then it induces a signaling cascade that eventually results in adaptation to make sure the body/muscle is prepared for that amount of damage in the future. All those neat inflammatory markers like Interleuken’s (IL), cytokines, etc. all are potential triggers for some downstream adaptation. It’s a cascade of events that changes everything.
What the research has shown is that dampening the inflammatory response will:
- Decrease protein synthesis
- impair mitochondrial adaptations (in mice)
- impaired satellite cell increase (in animals)
- alterations in glucose metabolism (in animals)
For example, Research has shown that taking a NSAID will dampen down the increase in muscle protein synthesis post workout. An inhibition of muscle protein synthesis means less repair and regeneration. In addition it means that on the see saw between protein synthesis and degradation, the body stays on the degradation side of the balance for just a bit longer. On the same side of things, satellite cell activity (which plays a vital role in muscle growth) is inhibited if the inflammation signal is taken away.
So what we are taking is affecting the pathway, but how?
Acute vs. Chronic:
When we look at inflammation we can look at the acute versus chronic effects. To start with we can look at the acute versus chronic effects of severely dampening down the inflammatory response via corticosteroids. Most runners are familiar with the idea of cortisone shots. They knock out inflammation and can occasionally make things go away…for a short time.
Over the long haul though, cortisone shots generally produce some unfavorable outcomes, inhibiting the healing process of both muscle and tendon. (For more see review here)
But corticosteroids simply demonstrate an extreme case. What does taking a simple NSAID pill do? Hoffner et al. showed that taking an anti-inflammatory the day before exercise, gets rid of 90% of one of the key inflammatory markers (PGE2) after aerobic exercise. PGE2 is what eventually triggers downstream things like IL-6 which play a role in adaptation. That Is the typical response in acute models. In animal studies, take an anti-inflammatory, and the inflammatory markers are all decreased post exercise, and protein synthesis is generally impaired.
The issue is when we scale this out to the chronic side. One would think that if after each workout you got this reaction, and then if chronically taking NSAIDs, you’d get an impairment. The problem is, we just don’t have the research yet, and the research we do have is somewhat contradictory for a few reasons. Most of the chronic research has looked at taking ibuprofen or similar drugs in relation to strength and muscle growth adaptations. In animal studies, the majority confirm what happened in the acute studies.
Take NSAIDs, impair adaptation.
One particular study by Machida M and Takemasa (2010) found that giving a dose of ibuprofen to mice who were on a 4 week “running” program, blocked mitochondrial adaptations that would normally occur.
However, in humans, the results are more mixed. Several studies (Peterson et al. ) have shown no impact, while a few (Trappe et al.) have shown actual improvements in strength characteristics, particularly in older adults. Unfortunately, most of the human studies have been in regards to strength gains and not endurance adaptations.
The speculation for why the difference in outcomes rests in the participants and design of the studies. In the studies finding improvements in performance or strength, the participants were all older (50+). So there is speculation that taking a NSAID allowed for improved strength gains because of either a decrease in pain perception from taking the drug, or by impacting protein degradation. It makes sense that older people would have shift in how their bodies adapt. Older individuals generally have a higher state of inflammation, meaning they generally have low-level inflammation to some degree going on. It’s possible that by taking NSAIDs, they dampened this down so that now the body can respond like it normally would to a workout.
The age difference in limiter difference explains part of the issue but what else could be at play?
Our bodies are marvelous at adapting. Take caffeine for example. We all know that our bodies build up a sort of tolerance to it, and in fact, if we look at brain studies, there’s an increase in certain receptors in the brain with higher caffeine levels. It’s likely that something similar is going on with NSAIDs. Over time, there is likely an adaptation to it, so that the muscle does not respond in the same way, meaning that you no longer get that huge response of inhibiting inflammatory markers.
Now that we know what anti-inflammatories do, and how they impact training adaptation, a few questions arise. First, is there a timing issue?
The answer is most likely yes, but we just don’t know where in that inflammation cycle the proper timing lies. For example, you can reasonably guess with antioxidants based on how long it takes the signaling pathways to be activated. Once that process is on its way, it’s a safer bet that you can take antioxidants and not interfere.
The problem with anti-inflammatories is that it’s a complex multistep process that takes days for the body to go through, and there has been limited research into the concept.
Secondly, at what point is inflammation bad. Obviously, inflammation is needed to start the healing process. At what point do we get too much?
Urso (2013) put it best via concluding that “the question exists whether the most beneficial course of treatment should be to block inflammation or if it is sensible to allow inflammatory processes to progress naturally. Or perhaps, there is a benefit in blocking inflammation, but only for a specific time point and duration post-injury.”
The answer to those questions is unknown at the time. My feeling is we are overusing anti-inflammatory drugs. They don’t need to be taken after every time you get sore, or after small muscle strains or injuries. Instead, save it for when there actually may be too much inflammation.
In addition, there may be a better way to dampen down inflammation, if that is really needed, then to use a generic COX inhibitor. It seems like according to research that COX-1 plays a role post exercise.
In terms of adaptation, I would stay away from any NSAIDs pre-exercise or in the hours’ post exercise. It’s easy to jump to the conclusion that if we inhibit A via NSAIDs which is supposed to cause an increase in B which is supposed to lead to adaptation C, then taking NSAIDs is bad. It’s not as simple as that, but in the grand scheme of swinging from giving too much to too little, my bet would be that we are in the too much anti-inflammatory category.
Lastly, with injuries, I’ll leave it with the experts and end with another quote (Urso 2013):
“From the aforementioned examples from the literature there is compelling evidence that the release of pro-inflammatory molecules in the first hours post-injury is necessary for appropriate activation of regenerative processes. Molecules with dual inflammatory and regenerative functions in skeletal muscle seem to have the most promise as effective targets for therapeutics following traumatic muscle injury. Future research must focus on filling the gap in the scientific literature regarding the critical pro- to anti-inflammatory switch that enhances regeneration.”.
Urso (2013) Anti-Inflammatory Interventions and Skeletal Muscle Injury: Benefit or Detriment? Journal of Applied Physiology
Wong MEK, Hollinger JO, Pinero GJ. Integrated processes responsible for soft tissue healing. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996;82:475–492. [PubMed]
Speed BMJ (2001) Corticosteroid injections in tendon lesions http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1120980/