Apples and oranges in the basket of a clinical model for exercise addiction: Rebuttal to Brevers et al. (2022).

This note is a reply to Brevers et al.'s (2022) the commentary. We first explain that the commentary's title is in discord with the theoretical implications of the Expanded Interactional Model of Exercise Addiction (EIMEA; Dinardi et al., 2021). Subsequently, we argue that in contrast to Brevers et al.'s arguments, exercise volume or intensive physical exercise is not even mentioned in the revised EIMEA. Most importantly, we point out that the commentary's reference to assessment scales of exercise addiction is irrelevant, because the EIMEA is intended for idiographic clinical cases rather than nomothetic research. Furthermore, we discuss how the ELMEA cannot account for secondary exercise addiction and motivational incentives due to its individual-specific orientation. Finally, we conclude our reply by highlighting that Brevers et al.'s commentary seems to revolve around nomothetic research assessing a certain level of 'risk' of exercise addiction, while the EIMEA accounts for specific clinically dysfunctional cases presented in the limited number of case studies published in the literature.

The expanded interactional model of exercise addiction.

BACKGROUND AND AIMS: Cited in over 100 articles, the interactional model of exercise addiction (Egorov & Szabo, 2013) forms the theoretical foundation of many studies on the risk of exercise addiction. Still, the inclusion of previously omitted determinants could make it more useful. Therefore, this review presents the expanded version of the original model. METHOD: We added 'self-concept' as another determinant in the 'personal factors' domain and 'attractive alternatives' to the 'situational factors' domain. Further, we doubled the reasons for exercise in the 'incentives for exercise domain.' Last, we added a new domain, the 'exercise-related stressors,' to illustrate that exercise itself might be a source of stress. RESULTS: The expanded model is more inclusive and accounts for a greater combination of interactions playing roles in exercise addiction. Overlooking the eventuality that stress resulting from exercise might also fuel the dysfunction was a significant omission from the original model, rectified in the current update. Finally, the new expansions make the model more applicable to competitive situations too. CONCLUSION: The expanded interactional model of exercise addiction is more comprehensive than its original version. It also accounts for the exercise or sport-related stress as possible fuel in addictive exercise behavior.

Endogenous Bufadienolide, Blood Pressure and Alcohol Withdrawal.

BACKGROUND AND OBJECTIVE: Previously, it was demonstrated that marinobufagenin (MBG) is implicated in the development of ethanol withdrawal in rats. It has been shown that ethanol withdrawal is associated with a pressor response in the alcoholics. We hypothesized that elevated levels of sodium pump ligand, MBG, would underline the increase in systolic blood pressure during alcohol withdrawal in humans. METHODS: The cohort included 9 patients with the diagnosis "alcohol dependence syndrome" (F10.(1-3) according to ICD-10). The blood samples for measurement of MBG concentration were collected from the subjects on the first day of withdrawal and after 7 days treatment of the abstinence. Arterial blood pressure was measured via plethysmography at the same time points. RESULTS: The beginning of the alcoholic abstinence was associated with the rise of arterial blood pressure with enhanced levels of plasma MBG. At day 7 following withdrawal, the systolic blood pressure and MBG levels were decreased to normal values. CONCLUSION: The development of alcohol withdrawal is accompanied by an increase in arterial blood pressure, which is associated with increased plasma MBG concentration.

Marinobufagenin in Urine: A Potential Marker of Predisposition to Ethanol and a Target for Spironolactone.

BACKGROUND AND OBJECTIVE: Previously it was demonstrated that digitalis-like cardiotonic steroid, marinobufagenin (MBG), is implicated in the development of ethanol addiction in rats. We hypothesized that (i) levels of sodium pump ligand, MBG, would be negatively correlated with the amount of ethanol consumed by rats, and (ii) that spironolactone would oppose the MBG induced ethanol-seeking behavior and blood pressure in rats. METHODS: Voluntary consumption of 9% alcohol (vs. water) during 10 days period by 11 adult male Wistar rats was studied. Eight weeks after the beginning of the experiment, the animals were divided into two treatment subgroups: high alcohol drinkers (HAD, n=6, daily consumption of ethanol > 4 g/kg) and low alcohol drinkers (LAD, n=5, daily consumption of ethanol < 4 g/kg) rats. Spironolactone treatment (7 days) was started following 3-day habituation to intragastric vehicle administration. Consumption of ethanol and blood pressure were recorded daily. RESULTS: Urinary MBG excretion at baseline was 11.2±0.6 pmoles in HAD rats and 19.1±2.9 pmoles (p<0.05) in LAD rats, respectively. Seven days of spironolactone treatment was associated with reduction in ethanol intake (2.9 g/kg/24 hr), reduction in systolic blood pressure (5 mm Hg), and increase in sodium excretion (1 mmol/24 hr). CONCLUSION: Levels of MBG may be a predisposing factor to voluntary ethanol intake. Spironolactone, along with antihypertensive effect, decreases ethanol intake.

The exercise paradox: An interactional model for a clearer conceptualization of exercise addiction.

BACKGROUND AND AIMS: Exercise addiction receives substantial attention in the field of behavioral addictions. It is a unique form of addiction because in contrast to other addictive disorders it is carried out with major physical-effort and high energy expenditure. METHODS: A critical literature review was performed. RESULTS: The literature evaluation shows that most published accounts report the levels of risk for exercise addiction rather than actual cases or morbidities. The inconsistent prevalence of exercise addiction, ranging from 0.3% to 77.0%, reported in the literature may be ascribed to incomplete conceptual models for the morbidity. Current explanations of exercise addiction may suggest that the disorder is progressive from healthy to unhealthy exercise pattern. This approach drives research into the wrong direction. DISCUSSION: An interactional model is offered accounting for the adoption, maintenance, and transformation of exercise behavior. The here proposed model has an idiosyncratic black-box containing the antecedents and characteristics that are unique to the individual, which cannot be researched via the nomothetic approach. Subjective aspects in the black-box interact with stressful life events that force the person to cope. The range of coping may be wide. Escape into exercise depends on personal (subjective) and situational (objective) factors, but the subjective components are inaccessible for a priori scholastic scrutiny. It is our view that currently only this dual interactional model may account for the fact that exercise addiction emerges suddenly and only in a few individuals from among those at high risk, estimated to be around 3.0% of the exercising population.