Dr Johannes Fleckenstein (Goethe University Frankfurt) presented in the lecture "Pain Triggers: When Movement/Sport Hurts" at the Sports, Medicine and Health-Summit 2021. The session centred on the question: What happens when we suffer pain despite, or precisely because of a sport activity?
The reason for painkiller use in sports is the hope to anticipate pain. Every third person who takes painkillers hopes to reduce the risk of missing a training session or game. Behind this is, for example, the fear of losing a regular place in team sports. There is evidence that the level of athletic performance correlates with other substance abuse such as nicotine, alcohol and other substances.
Preventive analgesia refers to taking a painkiller before a pain stimulus occurs. If we compare ultramarathon runners (160 km) who took the entire dose of 1800 mg ibuprofen, with a control group, there is no pain:
Painkillers are taken more for psychological reasons as there is no benefit for physiological or performance-enhancing reasons. Acute and chronic pain are to be differentiated. Acute pain is characterised by a sudden appearance, for example during a marathon, and it is a warning signal. It is supposed to encourage people to stop a certain movement. This includes muscle soreness, defined as minor damage to muscle tissue after unaccustomed exercise. On the one hand, there is muscle soreness, which most people in popular sports are familiar with. Structural damage is more likely to result from a strain that occurs above the stress limit, for example, from overtraining, with a corresponding loss of function.
Chronic, persistent pain over months or longer, no longer has the warning function of acute pain. It causes increased suffering and reduces the quality of life. A study (Fett et al) illustrates its consequences:
But the basic problem is that acute pain fulfils a protective and warning function. Chronic pain however does not have this function.
The trauma, the injury, the overtraining is the initial stress. It leads to inflammation on a neurogenic and cellular, local level. This in turn leads to peripheral sensitisation, which causes an initial painful sensation (Gierthmühlen et al). In addition, a secondary process develops, which primarily causes stress, activating the autonomic nervous system. This leads to a feedback, a sympatho-afferent coupling, which in turn supports the inflammation process. In addition, there are contextual factors from the biopsychosocial aspect, i.e. psychological, social experience, which can additionally trigger the stress situation. And the pain takes on a life of its own.
Laboratory studies with rats have shown that pain is switched off when the sympathetic nerve is severed. This is therefore eminently important for the nociceptor’s inflammatory sensitisation to be possible at all. But the sympathetic nerve is needed in sports. In a way, it makes high performance possible and a problem arises when the pain becomes very intense and enters a worsening dynamic.
What happens in the chronic course of pain development is that the HPA axis is excessively activated by maladaptation. Cortisol no longer has its anti-inflammatory function, and cortisol dysfunction occurs, where inflammation can no longer be controlled. We experience the reflex of pain and inflammation, and in addition, the psychosocial experience that can be called depression. The vicious circle is activated and self-reinforcing.