Exercising before bed has long been discouraged as the body doesn’t have time to wind down before the lights go out.

But new research has found breaking up a quiet, sedentary evening of watching television with short bursts of resistance exercise can lead to longer periods of sleep.

Adults spend almost one third of the 24-hour day sleeping. But the quality and length of sleep can affect long-term health. Sleeping too little or waking often in the night is associated with an increased risk of heart disease and diabetes.

Physical activity during the day can help improve sleep. However, current recommendations discourage intense exercise before going to bed as it can increase a person’s heart rate and core temperature, which can ultimately disrupt sleep.

Nighttime habits

For many, the longest period of uninterrupted sitting happens at home in the evening. People also usually consume their largest meal during this time (or snack throughout the evening).

Insulin (the hormone that helps to remove sugar from the blood stream) tends to be at a lower level in the evening than in the morning.

Together these factors promote elevated blood sugar levels, which over the long term can be bad for a person’s health.

Our previous research found interrupting evening sitting every 30 minutes with three minutes of resistance exercise reduces the amount of sugar in the bloodstream after eating a meal.

But because sleep guidelines currently discourage exercising in the hours before going to sleep, we wanted to know if frequently performing these short bursts of light activity in the evening would affect sleep.

Activity breaks for better sleep

In our latest research, we asked 30 adults to complete two sessions based in a laboratory.

During one session the adults sat continuously for a four-hour period while watching streaming services. During the other session, they interrupted sitting by performing three minutes of body-weight resistance exercises (squats, calf raises and hip extensions) every 30 minutes.

After these sessions, participants went home to their normal life routines. Their sleep that evening was measured using a wrist monitor.

Our research found the quality of sleep (measured by how many times they woke in the night and the length of these awakenings) was the same after the two sessions. But the night after the participants did the exercise “activity breaks” they slept for almost 30 minutes longer.

Identifying the biological reasons for the extended sleep in our study requires further research.

But regardless of the reason, if activity breaks can extend sleep duration, then getting up and moving at regular intervals in the evening is likely to have clear health benefits.

Time to revisit guidelines

These results add to earlier work suggesting current sleep guidelines, which discourage evening exercise before bed, may need to be reviewed.

As the activity breaks were performed in a highly controlled laboratory environment, future research should explore how activity breaks performed in real life affect peoples sleep.

We selected simple, body-weight exercises to use in this study as they don’t require people to interrupt the show they may be watching, and don’t require a large space or equipment.

If people wanted to incorporate activity breaks in their own evening routines, they could probably get the same benefit from other types of exercise. For example, marching on the spot, walking up and down stairs, or even dancing in the living room.

The key is to frequently interrupt evening sitting time, with a little bit of whole-body movement at regular intervals.

In the long run, performing activity breaks may improve health by improving sleep and post-meal blood sugar levels. The most important thing is to get up frequently and move the body, in a way the works best for a person’s individual household.

Jennifer Gale, PhD candidate, Department of Human Nutrition, University of Otago and Meredith Peddie, Senior Lecturer, Department of Human Nutrition, University of Otago

This article is republished from The Conversation under a Creative Commons license. Read the original article.

The core experiences of depression – changes in energy, activity, thinking and mood – have been described for more than 10,000 years. The word “depression” has been used for about 350 years.

Given this long history, it may surprise you that experts don’t agree about what depression is, how to define it or what causes it.

But many experts do agree that depression is not one thing. It’s a large family of illnesses with different causes and mechanisms. This makes choosing the best treatment for each person challenging.

Reactive vs endogenous depression

One strategy is to search for sub-types of depression and see whether they might do better with different kinds of treatments. One example is contrasting “reactive” depression with “endogenous” depression.

Reactive depression (also thought of as social or psychological depression) is presented as being triggered by exposure to stressful life events. These might be being assaulted or losing a loved one – an understandable reaction to an outside trigger.

Endogenous depression (also thought of as biological or genetic depression) is proposed to be caused by something inside, such as genes or brain chemistry.

Many people working clinically in mental health accept this sub-typing. You might have read about this online.

But we think this approach is way too simple.

While stressful life events and genes may, individually, contribute to causing depression, they also interact to increase the risk of someone developing depression. And evidence shows that there is a genetic component to being exposed to stressors. Some genes affect things such as personality. Some affect how we interact with our environments.

What we did and what we found

Our team set out to look at the role of genes and stressors to see if classifying depression as reactive or endogenous was valid.

In the Australian Genetics of Depression Study, people with depression answered surveys about exposure to stressful life events. We analysed DNA from their saliva samples to calculate their genetic risk for mental disorders.

Our question was simple. Does genetic risk for depression, bipolar disorder, schizophrenia, ADHD, anxiety and neuroticism (a personality trait) influence people’s reported exposure to stressful life events?

You may be wondering why we bothered calculating the genetic risk for mental disorders in people who already have depression. Every person has genetic variants linked to mental disorders. Some people have more, some less. Even people who already have depression might have a low genetic risk for it. These people may have developed their particular depression from some other constellation of causes.

We looked at the genetic risk of conditions other than depression for a couple of reasons. First, genetic variants linked to depression overlap with those linked to other mental disorders. Second, two people with depression may have completely different genetic variants. So we wanted to cast a wide net to look at a wider spectrum of genetic variants linked to mental disorders.

If reactive and endogenous depression sub-types are valid, we’d expect people with a lower genetic component to their depression (the reactive group) would report more stressful life events. And we’d expect those with a higher genetic component (the endogenous group) would report fewer stressful life events.

But after studying more than 14,000 people with depression we found the opposite.

We found people at higher genetic risk for depression, anxiety, ADHD or schizophrenia say they’ve been exposed to more stressors.

Assault with a weapon, sexual assault, accidents, legal and financial troubles, and childhood abuse and neglect, were all more common in people with a higher genetic risk of depression, anxiety, ADHD or schizophrenia.

These associations were not strongly influenced by people’s age, sex or relationships with family. We didn’t look at other factors that may influence these associations, such as socioeconomic status. We also relied on people’s memory of past events, which may not be accurate.

How do genes play a role?

Genetic risk for mental disorders changes people’s sensitivity to the environment.

Imagine two people, one with a high genetic risk for depression, one with a low risk. They both lose their jobs. The genetically vulnerable person experiences the job loss as a threat to their self-worth and social status. There is a sense of shame and despair. They can’t bring themselves to look for another job for fear of losing it too. For the other, the job loss feels less about them and more about the company. These two people internalise the event differently and remember it differently.

Genetic risk for mental disorders also might make it more likely people find themselves in environments where bad things happen. For example, a higher genetic risk for depression might affect self-worth, making people more likely to get into dysfunctional relationships which then go badly.

What does our study mean for depression?

First, it confirms genes and environments are not independent. Genes influence the environments we end up in, and what then happens. Genes also influence how we react to those events.

Second, our study doesn’t support a distinction between reactive and endogenous depression. Genes and environments have a complex interplay. Most cases of depression are a mix of genetics, biology and stressors.

Third, people with depression who appear to have a stronger genetic component to their depression report their lives are punctuated by more serious stressors.

So clinically, people with higher genetic vulnerability might benefit from learning specific techniques to manage their stress. This might help some people reduce their chance of developing depression in the first place. It might also help some people with depression reduce their ongoing exposure to stressors.

If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.

Jacob Crouse, Research Fellow in Youth Mental Health, Brain and Mind Centre, University of Sydney and Ian Hickie, Co-Director, Health and Policy, Brain and Mind Centre, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.