Exercise is medicine: a new perspective for health promotion in bipolar disorder

ABSTRACT

Introduction

Similar effects in reducing the symptoms of the mood disorder are reported in the literature compared the action of drugs and aerobic exercise sessions, demonstrating the potential of exercise in the control and mood stabilization. Therefore, there are many reasons to believe that the increased cardiorespiratory fitness (VO_2max) can be an important means of protection and a reducing potential of physical and mental damage in bipolar disorders (BD). This review will highlight the current pattern of response of exercise on the pathophysiology of BD, relating the possible mechanisms, and hypotheses based on exercises.

Areas covered

The mechanism of monoaminergic action and its relationship with exercise, role of physical conditioning and increased VO_2Max on neurotrophin release, and new perspectives on long-term exercise will be reviewed.

Expert opinion

The adaptations to training, although little explored in the context of BD, can induce the expression of substances that co-regulate several processes related to the pathophysiology of BD. Furthermore, high intensity interval training (HIIT) can also be adjusted to improve the physical fitness and health in patients with BD. Future research is needed to adopt a training strategy that is both time efficient and adequate for the population in question.

KEYWORDS:

• Bipolar disorder
• monoaminergic system
• catecholamines
• exercise
• high intensity interval training

Article highlights

• In BD, changes in physical and neurological status are observed;

• Bipolar patients have low level of physical activity, therefore, low tolerance and ability to adhere to training;

• Exercise intervention causes anxiolytic and antidepressant effects similar to drug therapy but without additional side effects.

• Exercise seems to be an effective and economical alternative to the treatment of mood disorders, and this can be extrapolated to BD.

• Trophic factors such as BDNF, NGF, GDNF, and IGF-I have been widely explored in the pathogenesis and pathophysiology of neurodegenerative disorders.

The improvement in VO_2Max could be an interesting channel to be stimulated in BD.

Acknowledgments

The authors wish to thank Professor Rodolfo Valentini for assistance with translation, and for their help in reviewing the document.

Declaration of interest

The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or conflict with the subject matter or materials discussed in this manuscript apart from those disclosed.

Reviewer disclosures

One of the reviewers on this manuscript reports personal fees from the Neuroscience Education Institute and grants from Assurex, Genome Canada, Sage Therapeutics, Stanley Medical Research Institute, and Sunovion Pharmaceuticals, and participation on the advisory boards for Sunovion Pharmaceuticals and Otsuka, outside the submitted work. Peer reviewers on this manuscript have no other relevant financial relationships or otherwise to disclose.

Additional information

Funding

S Machado was supported by grant from Carlos Chagas Foundation for the Research Support in the State of Rio de Janeiro (FAPERJ), Young Scientists from the State of Rio de Janeiro, E −26/203.295/2017.