It is Friday, the sun is back and it is one of those clear crisp cold spring days here in Uppsala. Tomorrow the trail race season in Sweden will really start with Ursvik Ultra, a 75 km (47 mile) night race starting in the middle of the night between Saturday and Sunday. It is the 15th time the race is held and it has grown tremendously in the past years and there are over 100 registered runner’s for this year - there is really a running boom of shorter trail and ultra trail races like this in Sweden. I elaborated for a long time whether I should run Ursvik Ultra, I really feel strong now, but decided to do like last year and focus all my training on the year’s overreaching goal and not be distracted by races early in the season, however tempting it may be. Last year my goal was Tor des Géants in the beginning of September and this year it will be La PetiteTrotte à Léon (PTL) in the end of August.
Feeling the urge to run and race, and realizing that I share these feelings with an increasingly large number of people in the “running boom”, made me think about the similarities between running and addiction and whether you can become dependent on running. I have previously mentioned in a blog post that if I used the normal diagnostic criteria for a substance use disorder according to DSM-5 and changed the word substance to running I clearly scored high (fulfilling 9/11 criteria) in having a “Running Use Disorder” and thus be dependent on running. I will in a later blog post review the various scales, besides DSM-5 which actually does not contain a term for exercise dependence or exercise use disorder, that have been used in the literature to define “Exercise Addiction”. The term “exercise addiction” appears to be well established and there have been a number of scientific articles published on the area (reviewed in for instance Landolfi “Exercise addiction” Sports Med. 2013; 43: 111-9; Berczik et al “Exercise Addiction: Symptoms, diagnosis, epidemiology, and etiology” Subst Use Misuse. 2012; 47: 403-17; Kerr et al “Exercise Dependence” 2007 (Book) Routledge, New York, NY, US).
It is tempting to speculate that there might be similar neuropsychological and neuropathophysiological mechanisms in dependence to running or substances. A very interesting recent study tested the hypothesis that exercise is associated with lower frequency (incidence and prevalence) of psychiatric disorders (Dakwar et al “Exercise and mental illness: results from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC)” J Clin Psychiatry 2012; 73: 960-6). Data were collected from 2001 to 2005 as part of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) and the sample consisted of 23,505 nondisabled US adults aged between 18 and 65 years. Contrary to the hypothesis, individuals who engaged in vigorous exercise were significantly more likely than were nonexercisers to be diagnosed with a current psychiatric disorder (adjusted odds ratio [AOR] = 1.22, 95% CI, 1.12-1.34 for the nationally recommended amount vs no exercise), significantly less likely to attain remission from a psychiatric disorder between waves (AOR = 0.77, 95% CI, 0.65-0.91), and significantly more likely to relapse or be newly diagnosed with a psychiatric disorder between waves (AOR = 1.15, 95% CI, 1.02-1.30). Alcohol dependence and bipolar II disorder were the disorders most strongly associated with exercise. The authors speculate that this surprising finding may be due to reward-related factors that influence both exercise engagement and the expression of certain psychiatric disorders, but that further studies are needed. Similar conclusions can be drawn from a review by
Interestingly, the findings by Dakwar and others give support to the hypothesis that exercise can serve as a reward that is particularly reinforced in individuals who have vulnerabilities in reward-related neurocircuitry and that treatment thus can be used as a treatment for substance use disorders. The benefit of exercise as a treatment for psychiatric disorders and substance use disorders have recently been reviewed by Zschucke and colleagues (Zschucke et al “Exercise and Physical Activity in the Therapy of Substance Use Disorders” Scientific World Journal 2012; 2012: 901741; Zschucke et al “Exercise and Physical Activity in Mental Disorders: Clinical and Experimental Evidence” J Prev Med Public Health. 2013; 46: S12–S21). Another mechanism besides the reward-related might be effects on underlying depression in both disorders. That exercise in general, and specifically running, has anti-depressive effects in both mice and men has been shown in many studies (reviewed in for instance Helmich et al “Neurobiological alterations induced by exercise and their impact on depressive disorders” Clin Pract Epidemiol Ment Health. 2010; 30; 6:115-25; “Running is rewarding and antidepressive” Physiol Behav. 2007; 92: 136-40).
I think one common mechanism in both cases might be the benefical psycophysical effects exercise and in particular indurance training can induce, such as stress reduction (Rosch “Exercise and stress reduction”. Compr Ther. 1985; 11: 10—15), anxiolysis (Morgan “ Affective beneficence of vigorous physical activity” Med Sci Sports Exerc. 1985; 17: 94—100), mood elevation (Janal et al “Pain sensitivity, mood and plasma endocrine levels in man following long-distance running: effects of naloxone” Pain. 1984; 19: 13—25) and reduced pain perception (Janal et al “Pain sensitivity, mood and plasma endocrine levels in man following long-distance running: effects of naloxone” Pain. 1984; 19: 13—25). There are numerous reports in both popular and scientific press regarding a state of euphoria associated with in particular running, often referred to as “Runner’s High” (Wagemaker & Goldstein “The runner’s high” J Sports Med Phys Fitness 1980; 20: 227—229; Partin 1983 “Runner’s ‘‘high’’” JAMA. 1983; 249: 21). A number of studies have attributed runner’s high to changes in central opioidergic transmission caused by increased levels of endorphin’s in the brain, the so called “endorphin hypothesis”. This hypothesis has however been questioned as it was based mainly on elevated levels of endorphins in circulating peripheral blood and not the brain (Dietrich & McDaniel “Endocannabinoids and exercise” Br J Sports Med. 2004; 38: 536—541). In addition there are other neurotransmitters implicated in Runner’s High, such as endocannabinoids (Raichlen et al “Exercise-induced endocannabinoid signaling is modulated by intensity” Eur J Appl Physiol 2013; 113: 869-75).
A seminal study providing support for the existence of “Runner’s High” and that it is at least partly caused by endogenous opioids in the brain was published in 2008 where 10 trained male athletes ran for 2 hours before undergoing positron emission tomography (PET) analysis of opioid receptor occupancy and scoring of euphoria (Boecker et al “The runner's high: opioidergic mechanisms in the human brain” Cereb Cortex 2008; 18: 2523-31). Reductions in opioid receptor availability were identified preferentially in prefrontal and limbic/paralimbic brain structures. The level of euphoria was significantly increased after running and was inversely correlated with opioid binding in prefrontal/orbitofrontal cortices, the anterior cingulate cortex, bilateral insula, parainsular cortex, and temporoparietal regions. That short term running influences brain biochemistry is further corroborated by the findings of brain changes and plasticity after a long term ultrarunning exertion in participants of the 4500 km long Trans Europe Foot Race project, which I previously have posted a blog post about (Perrey & Mandrick “Evidence from neuroimaging to explore brain plasticity in humans during an ultra-endurance burden” BMC Med 2012; 10: 171).
|From Boecker et al “The runner's high: opioidergic mechanisms in the human brain” Cereb Cortex 2008; 18: 2523-31|
Finally, a very interesting recent study by Raichlen and colleagues tested the hypothesis that it is neurobiological rewards, i.e. runner’s high, that motivate human endurance exercise in general from an evolutionary perspective. They studied endocannabinoid signaling (eCB) in in humans, dogs (another cursorial mammal) and ferrets (a non-cursorial mammal) before and after treadmill exercise to test the hypothesis that neurobiological rewards are linked to high-intensity exercise in cursorial mammals. They show that humans and dogs share significantly increased exercise-induced eCB signaling following high-intensity endurance running. eCB signaling does not significantly increase following low-intensity walking in these taxa, and eCB signaling does not significantly increase in the non-cursorial ferrets following exercise at any intensity. The study thus indicate that inter-specific variation in neurotransmitter signaling may explain differences in locomotor behavior among mammals. The authors speculate that the fact that “running, and endurance exercise in general, remains an enjoyable and psychologically beneficial recreational activity for tens of millions of humans today suggests that we still may respond to a neurobiological trait that evolved early in our lineage”. Time to go out running and get high.