Learned Industriousness as a Translational Mechanism of Excess Goal Pursuit: An Example in Eating Disorders

Researchers have long grappled to understand the persistence of behaviors that are non-hedonic and, ostensibly, aversive. At times, such behaviors can be taken to excess in the form of psychopathology. Eating disorders characterize a prototype of psychiatric disorders in which behaviors that most people find unpleasant (e.g., restrictive eating, excessive exercise) are rigidly and repeatedly performed. The learned industriousness theory, which has roots in behavioral neuroscience, provides a theoretical account for such phenomena. Informed by humans and animal data, this theory posits that effort (intense physical or mental activity) can be conditioned to acquire secondary rewarding properties through repeatedly pairing high-effort behavior with reward. Over time, effort sensations would become less aversive and more appetitive because they signal impending reward, increasing eagerness to engage in effortful behavior. In this manuscript we: 1) review biobehavioral data supporting learned industriousness; 2) highlight evidence that this theory may account for persistence of certain eating disorder behaviors; and 3) consider clinical and research implications of this model, including the translation to other psychiatric presentations.

Androgen receptor regulates the proliferation of myoblasts under appropriate or excessive stretch through IGF-1 receptor mediated p38 and ERK1/2 pathways

Background Androgen receptor (AR) exerts important roles in exercise-induced alterations of muscle mass, in which the proliferation and differentiation of satellite cells or myoblasts are crucial. Our previous study in C2C12 myoblasts demonstrated that 15% (mimic appropriate exercise) and 20% (mimic excessive exercise) stretches promoted and inhibited the proliferation respectively; and AR played a crucial role in 15% stretch-induced pro-proliferation through IGF-1-modulated PI3K/Akt, p38 and ERK1/2 pathways, but AR’s role in stretches-modulated proliferation of general myoblasts, especially 20% stretch, remains unclear, and the mechanisms need to be further clarified. Methods Firstly, the discrepancy in proliferation and the above indicators between L6 (without AR) and C2C12 (with AR) myoblasts were compared under 15% or 20% stretch. Then the influences of transfection AR or exogenous IGF-1 treatment on proliferation and these indicators were detected in stretched L6 myoblasts. Results (1) Under un-stretched state, the proliferation of L6 was slower than C2C12 cells. Furthermore, AR knockdown in C2C12 myoblasts repressed, while AR overexpression in L6 myoblasts promoted the proliferation. (2) 15% stretch-induced increases in the proliferation and activities of p38 and ERK1/2 were lower in L6 than C2C12 cells; AR overexpression enhanced the proliferation of 15% stretched L6 cells accompanied with the increases of p38 and ERK1/2 activities. (3) 20% stretch-induced anti-proliferation and inhibition of p38 activity were severer in L6 than C2C12 myoblasts; AR overexpression reversed the anti-proliferation of 20% stretch and enhanced p38 activity in L6 myoblasts. (4) In stretched L6 myoblasts, AR overexpression increased IGF-1R level despite no detectable IGF-1; and recombinant IGF-1 increased the proliferation, the level of IGF-1R, and the activities of p38 and ERK1/2 in 15% stretched L6 myoblasts. Conclusions The study demonstrated AR's crucial roles in stretches-regulated proliferation of myoblasts, and increased AR fulfilled 15% stretch's pro-proliferation via activating IGF-1R- p38 and ERK1/2 pathways while decreased AR achieved 20% stretch's anti-proliferation via inhibiting IGF-1R- p38 pathway, which is useful to understand in depth the role and mechanisms of AR in appropriate exercise increasing while excessive exercise decreasing muscle mass.

Exercise Professionals’ Knowledge and Understanding of Eating Disorders and Excessive Exercise

Background: Eating Disorders (ED) are complex mental health problems requiring early recognition and treatment. Exercise Professionals (EP) are in close contact with people who suffer from ED and/or Excessive Exercise (EE) and play a role in early intervention and ensuring safe behaviors. We examined the ability of EP to identify eating and exercise issues and to intervene if appropriate. Methods: Participants were recruited via anonymous online survey advertised through industry channels. A chi-square test of independence examined the associations between socio-demographic characteristics and responses to specific questions (significance level alpha=0.05). Results: Of 414 respondents, 80.4% were female, mean age 44.8 years, with 13.3 years’ work experience in the fitness sector. More than half (57.2%) did not receive any ED/EE instruction during training and the vast majority (93.0%) indicated a need of further ED/ EE education. While more than three quarters (76.3%) of respondents had suspected an ED/EE in a client, only 25.1% felt confident to address the client about this matter. Approximately one third (30.7%) of respondents reported having a personal experience of an ED and/or EE. Conclusions: These results highlight a need for better education concerning ED and EE among EP to facilitate early identification and safe industry practice.

Exercise Professionals’ Knowledge and Understanding of Eating Disorders and Excessive Exercise

Background: Eating Disorders (ED) are complex mental health problems requiring early recognition and treatment. Exercise Professionals (EP) are in close contact with people who suffer from ED and/or Excessive Exercise (EE) and play a role in early intervention and ensuring safe behaviors. We examined the ability of EP to identify eating and exercise issues and to intervene if appropriate. Methods: Participants were recruited via anonymous online survey advertised through industry channels. A chi-square test of independence examined the associations between socio-demographic characteristics and responses to specific questions (significance level alpha=0.05). Results: Of 414 respondents, 80.4% were female, mean age 44.8 years, with 13.3 years’ work experience in the fitness sector. More than half (57.2%) did not receive any ED/EE instruction during training and the vast majority (93.0%) indicated a need of further ED/ EE education. While more than three quarters (76.3%) of respondents had suspected an ED/EE in a client, only 25.1% felt confident to address the client about this matter. Approximately one third (30.7%) of respondents reported having a personal experience of an ED and/or EE. Conclusions: These results highlight a need for better education concerning ED and EE among EP to facilitate early identification and safe industry practice.

Identification of Potentially Related Genes and Mechanisms Involved in Skeletal Muscle Atrophy Induced by Excessive Exercise in Zebrafish

Long-term imbalance between fatigue and recovery may eventually lead to muscle weakness or even atrophy. We previously reported that excessive exercise induces pathological cardiac hypertrophy. However, the effect of excessive exercise on the skeletal muscles remains unclear. In the present study, we successfully established an excessive-exercise-induced skeletal muscle atrophy zebrafish model, with decreased muscle fiber size, critical swimming speed, and maximal oxygen consumption. High-throughput RNA-seq analysis identified differentially expressed genes in the model system compared with control zebrafish. Gene ontology and KEGG enrichment analysis revealed that the upregulated genes were enriched in autophagy, homeostasis, circadian rhythm, response to oxidative stress, apoptosis, the p53 signaling pathway, and the FoxO signaling pathway. Protein–protein interaction network analysis identified several hub genes, including keap1b, per3, ulk1b, socs2, esrp1, bcl2l1, hsp70, igf2r, mdm2, rab18a, col1a1a, fn1a, ppih, tpx2, uba5, nhlrc2, mcm4, tac1, b3gat3, and ddost, that correlate with the pathogenesis of skeletal muscle atrophy induced by excessive exercise. The underlying regulatory pathways and muscle-pressure-response-related genes identified in the present study will provide valuable insights for prescribing safe and accurate exercise programs for athletes and the supervision and clinical treatment of muscle atrophy induced by excessive exercise.

Childhood onset exercise addiction or atypical anorexia nervosa during Covid-19: case report

Background Childhood-onset Anorexia Nervosa (AN) is recognised to be atypical in presentation, both in terms of extent and nature of eating pathology, exercise and compensatory behaviours with many falling short of full diagnostic criteria. Failure to consider an eating disorder diagnosis in youth who present with extreme weight loss may have serious immediate and long term implications. However, failure to consider other non-organic causes of weight loss may be equally detrimental to the child’s health. Case presentation This case reports on the acute presentation of a 12-year old boy, who presented to hospital in a severely malnourished state eight weeks into lockdown. To compensate for Covid-19 induced restrictions on sporting activity, this boy had followed a self-imposed daily schedule of arduous exercise, without increasing his nutritional intake. This report examines the clinical features suggestive of AN and other differential diagnosis. A discussion on the specific diagnostic differential of exercise addiction and challenges faced by youth during Covid-19 restrictions are presented. Conclusion Accepting that AN may present atypically in pre-pubertal youth, it is important that clinicians maintain an open mind in youth presenting without goal directed weight loss. Although weight loss was significant in this case, it was due to an excessive exercise regime. This may have commenced as a coping strategy in response to Covid-19 restrictions but subsequently became excessive and impairing in nature. The collateral damage of Covid-19 mandated restrictions, aimed at containing the spread of the virus, are evident in this case. Clinicians need to be alert to potentially maladaptive coping strategies and unusual or altered pathways of presentation, especially in younger children during these challenging times.

Functional Hypothalamic Amenorrhea: A Stress-Based Disease

The aim of the study is to present the problem of functional hypothalamic amenorrhea, taking into account any disease and treatment, diagnosis, and consequences of this disease. We searched PubMed (MEDLINE) and included 38 original and review articles concerning functional hypothalamic amenorrhea. Functional hypothalamic amenorrhea is the most common cause of secondary amenorrhea in women of childbearing age. It is a reversible disorder caused by stress related to weight loss, excessive exercise and/or traumatic mental experiences. The basis of functional hypothalamic amenorrhea is hormonal, based on impaired pulsatile GnRH secretion in the hypothalamus, then decreased secretion of gonadotropins, and, consequently, impaired hormonal function of the ovaries. This disorder leads to hypoestrogenism, manifested by a disturbance of the menstrual cycle in the form of amenorrhea, leading to anovulation. Prolonged state of hypoestrogenism can be very detrimental to general health, leading to many harmful short- and long-term consequences. Treatment of functional hypothalamic amenorrhea should be started as soon as possible, and it should primarily involve lifestyle modification. Only then should pharmacological treatment be applied. Importantly, treatment is most often long-term, but it results in recovery for the majority of patients. Effective therapy, based on multidirectional action, can protect patients from numerous negative impacts on fertility, cardiovascular system and bone health, as well as reducing mental morbidity.

Complex Probiotics Supplementation Improves Overtraining-Induced Muscle Inflammatory Response and Antioxidant Status Via LPS-TLR4/NF-κb Signalling Pathway in Rats

Background: Prolonged endurance and intensive exercise has shown detrimental effects on muscle health as well as causes intestinal dysbiosis. Probiotics are known as live microorganisms effective in improving gut microbiota and immunity to warrant health and well-being, which exert global and local biological functions on gut and muscle comprising of anti-oxidative stress, anti-inflammatory and anti-apoptosis, etc,. This research was conducted to investigate whether complex probiotics supplementation could alleviate excessive exercise-induced muscle damage and underlying signaling mechanism in rats.Methods: Thirty-two male SD rats were randomly allocated to four groups: control (SC), exercise (EC), probiotics (SP) and exercise with probiotics (EP) (n = 8 each). In the overtraining model, rats were arranged to an incremental load training on the treadmill 6 days/week for 8 weeks and gavaged with complex-probiotic-preparation (4 × 109 CFU/g) containing maltodextrin or maltodextrin only once a day. Serum and soleus were collected at the end of experiment. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities, the levels of lipopolysaccharide (LPS), interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), and muscle total antioxidant capacity (T-AOC), glutathione peroxidase (GPx), catalase (CAT) in soleus were measured. Furthermore, soleus protein expression of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), p-p65/p65, Bax, Bcl-2, caspase-9 and caspase-3 were determined by western blotting assay. Results: The findings indicated that excessive exercise induced a significant increased CK and LDH activities, LPS levels, relative protein expression of TLR4, MyD88, p-p65/p65, inflammatory cytokines and lipid peroxidation (p < 0.05). Simultaneously, the antioxidant elements including T-AOC, GPx, CAT were markedly decreased in the muscle of EC group (p < 0.05). In addition, up-regulated the protein expression of Bax/Bcl-2, cleaved caspase-9/procaspase-9 and cleaved caspase-3/procaspase-3 in muscle (p < 0.05). Administration of complex probiotics attenuated overtraining-induced inflammatory response, oxidative injury and TLR4/nuclear factor-kappa B (NF-kB) signaling factors expression as a result of reversing the most of above altered biochemical parameters (p < 0.05), and there was only tendency downregulation in the expression of apoptosis-regulated proteins (p > 0.05). Conclusions: Administration of complex probiotics could improve capability of the anti-oxidant, anti-inflammatory status induced by excessive exercise in rat skeletal muscle possibly via protecting the gut mucosal barrier, inhibiting the outflow of endotoxin, attenuating the action of TLR4-mediated NF-kB pathway.