Training the breathing muscles (primarily the diaphragm which plays a vital role in breathing) could have longer lasting benefits than previously thought. The strength gains to the muscles from five weeks of inspiratory muscle training (a form of weight training to strengthen the muscles used to breathe) persist for five weeks after the training has stopped, according to new research published in Experimental Physiology.

Stronger breathing muscles may improve the distribution of blood flow during exercise, which allows a person to undergo physical activity for longer periods before tiring and becoming less breathless. Enhancing breathing muscle function can potentially help people manage and slow down the progression of chronic obstructive pulmonary disease (COPD), a group of lung conditions including emphysema and bronchitis. The disease is the third leading cause of death worldwide¹ but is helped with pulmonary rehabilitation which can include inspiratory muscle training. Healthcare needs and the frequency of hospital visits depends on a person’s symptoms and how regularly they worsen. For people with weak breathing muscles, the training may help relieve the symptoms.

Muscles can lose function or weaken over time with disuse, particularly the respiratory muscles which may weaken faster than the other muscles in the body. The researchers from University of Waterloo, Canada foundthat the breathing muscles remain stronger after an equal amount of time without training, in this case five weeks. By observing similar muscle gains between weight training of the breathing muscles with that of the tibialis anterior (the muscle that runs down the front of the shin) indicates that the respiratory muscles can be trained like other skeletal muscles.  

Paolo Dominelli, University of Waterloo, Canada, a researcher on the study, said, “Inspiratory muscle training can be beneficial to people with breathing difficulties and can be part of pulmonary rehabilitation. Knowing the time frame before muscle function loss occurs could help inform treatment programs, determining how frequently an individual would need to train and the length of the programme.”

Inspiratory muscle training also caused a positive change to the respiratory muscle metaboreflex, a process where the body restricts the blood flow to the limbs when the breathing muscles tire. Typically during exercise when the limb muscles are working hard, the respiratory metaboreflex prioritises blood flow to the breathing muscles to ensure breathing is maintained. As a result, heart rate and blood pressure rise. However, inspiratory muscle training reduces the metaboreflex, which lowers the heart rate and blood pressure. Reducing the metaboreflex may improves a person’s endurance during exercise, meaning they can workout for longer before reaching exhaustion. The researchers found that the effects on the metaboreflex were preserved after five weeks in the absence of training.

Paolo Dominelli said, “By showing that the strength of the breathing muscles persisted, along with the retained reductions in the respiratory metaboreflex after five weeks without training suggests that the training itself may not need to be continuous. We would need to carry out subsequent clinical trails to test the appropriate frequency and length of training required to evaluate how long the health benefits persist.”

A group of 16 young healthy adults were randomly assigned into either the control group (seven male, one female) or the experimental group (six male, two female). Over 10-weeks their respiratory muscle strength and muscle strength of their lower leg (via the ability to flex the ankle upwards) were tested in a laboratory, and their blood pressure and heart rate were measured at pre-training (zero weeks), post-training (five weeks) and post-detraining (10 weeks) while their respiratory muscles were working hard to elicit the metaboreflex.

Over five weeks the experimental group performed inspiratory muscle training twice a day for five days a week. This was then followed by five weeks of undergoing normal physical activity but no inspiratory muscle training (post-detraining). The control group did not take part in inspiratory muscle training. All participants engaged in regularly physical activity (approximately three days per week) throughout the 10-week study period.

Paolo Dominelli cautions, “Firstly, our study was done in young healthy individuals who are not limited by their respiratory muscles. Follow-up studies needs to be completed in those with lung disease such as COPD. Secondly, the main limitation of the study was the duration of the detraining (no training) period. It was only for five weeks, the same amount of time as the training, where we did not see any decreases in breathing muscle strength. Further studies should extend the detraining phase to see if the reduction in the metaboreflex still persists with decreases in muscle strength.”

Poor blood sugar control could be associated with higher core body temperature and increased heart rate for physically active men with type 2 diabetes. The research published in Experimental Physiology found that while a common marker of long-term blood sugar control, haemoglobin A1c (also called glycated haemoglobin), was not associated with differences in the amount of heat lost  from the body, heart rate rose by six beats per minute and core body temperature increased by 0.2°C with each percentage point rise in haemoglobin A1c (from 5.1% to 9.1%) in men with type 2 diabetes during cycling in a heated chamber.

People with type 2 diabetes can have a reduced ability to lose heat, which can heighten their risk of developing a heat-related injury during a heat stress. However, the cause of the reduced capacity to dissipate heat is not well understood. This health issue is becoming more relevant as countries around the globe experience more frequent and enduring temperature extremes as well as hotter average summer temperatures, such as the global heat waves of 2022.

Researchers from University of Ottawa, Canada sought to identify whether blood sugar control affects the body’s ability to lose heat during exercise in the heat. Although worse blood sugar control did not seem to impair whole-body heat loss, the association between chronically elevated blood sugar (indexed via haemoglobin A1c) with higher body core temperatures and heart rate could implicate its role in thermoregulation. Importantly, this effect did not appear to be related to the physical fitness of the participants. The findings suggest that among people with type 2 diabetes, poor blood sugar control could lead to a greater risk of reaching dangerously high core body temperatures and greater strain on the heart during physical activity in the heat. However, more research is needed to confirm this link and understand why these impairments are observed even when heat loss is not compromised.

Dr. Glen Kenny, University of Ottawa, Canada, who leads the team said, “Previous research showed ageing is associated with a decay in the body’s ability to dissipate heat, which is more pronounced in individuals with type 2 diabetes.  However, it remained unclear to what extent long-term blood sugar control may mediate this response. By examining whole-body heat exchange using our one-of-a-kind whole-body air calorimeter (a device that provides a precise measurement of the heat dissipated by the human body), we were able to gain a better understanding of the association between long-term blood sugar control and the body’s physiological capacity to dissipate heat in individuals with type 2 diabetes.”

Regular exercise is generally recommended to manage and improve blood sugar control. However, rising global temperatures and enduring heat waves make it challenging for people living with type 2 diabetes to manage the disease because current health guidelines advise to avoid exercising in hot weather. People with type 2 diabetes are also at greater risk of heat-related stress, the risk of which increases with age.

The researchers monitored blood sugar control by measuring the proportion of glycated haemoglobin in the blood. This is haemoglobin (a protein molecule in red blood cells that carry oxygen) with sugar molecules attached to it and reflects the last approximate 3 months of blood sugar control. A normal healthy glycated haemoglobin level is 4-6%, while a good level for an individual with diabetes is ≤7%.

26 physically active men aged 43-73 years, who had been diagnosed with type 2 diabetes for 5 years or more, performed an exercise heat stress test, which involved cycling in the calorimeter set to 40°C. After 30 minutes of seated at rest, they completed three 30-minute bouts of cycling, with 15-minutes rest period in between each bout, at light, moderate, and vigorous exercise intensities. Intensities were set based on a fixed rate of metabolic heat production relative to body size, so that each participant was given the same heat load and therefore amount of heat to lose.

The researchers caution that the findings are based on a male-only cohort of physically active individuals (at least 150-minutes of exercise per week). This might not represent the most heat-vulnerable among those living with type 2 diabetes. Further investigations are needed to understand the changes in the body’s physiological capacity to dissipate heat when sedentary and more vulnerable individuals exercise in the heat.

Dr. Glen Kenny, University of Ottawa, Canada, said, “Type 2 diabetes is associated with higher rates of heat illness and death during heat stress when compared to the general population. By defining the levels of heat stress where diabetes-related impairments in the body’s ability to lose heat cause dangerous increases in core temperature, we can provide better heat-protection advice to safeguard the health and well-being of these heat-vulnerable individuals.  This includes guidance that can assist their health-care providers to manage heat stress in their patients who may be engaged in leisure, athletic activities or job-related activities in the heat.”

Regularly eating a high fat/calorie diet could reduce the brain’s ability to regulate calorie intake. New research in rats published in The Journal of Physiology found that after short periods of being fed a high fat/high calorie diet, the brain adapts to react to what is being ingested and reduces the amount of food eaten to balance calorie intake. The researchers from Penn State College of Medicine, US, suggest that calorie intake is regulated in the short-term by cells called astrocytes (large star-shaped cells in the brain that regulate many different functions of neurons in the brain) that control the signalling pathway between the brain and the gut. Continuously eating a high fat/calorie diet seems to disrupt this signalling pathway.

Understanding the brain’s role and the complex mechanisms that lead to overeating, a behaviour that can lead to weight gain and obesity, could help develop therapies to treat it. Obesity is a global public-health concern because it is associated with increased risk of cardiovascular diseases and type 2 diabetes. In England, 63% of adults are considered above a healthy weight and around half of these are living with obesity. One in three children leaving primary school are overweight or obese¹.

Dr Kirsteen Browning, Penn State College of Medicine, US, said, “Calorie intake seems to be regulated in the short-term by astrocytes. We found that a brief exposure (three to five days) of high fat/calorie diet has the greatest effect on astrocytes, triggering the normal signalling pathway to control the stomach. Over time, astrocytes seem to desensitise to the high fat food. Around 10-14 days of eating high fat/calorie diet, astrocytes seem to fail to react and the brain’s ability to regulate calorie intake seems to be lost. This disrupts the signalling to the stomach and delays how it empties.”

Astrocytes initially react when high fat/calorie food is ingested. Their activation triggers the release of gliotransmitters, chemicals (including glutamate and ATP) that excite nerve cells and enable normal signalling pathways to stimulate neurons that control how the stomach works. This ensures the stomach contracts correctly to fill and empty in response to food passing through the digestive system. When astrocytes are inhibited, the cascade is disrupted. The decrease in signalling chemicals leads to a delay in digestion because the stomach doesn’t fill and empty appropriately.

The vigorous investigation used behavioural observation to monitor food intake in rats (N=205, 133 males, 72 females) which were fed a control or high fat/calorie diet for one, three, five or 14 days. This was combined with pharmacological and specialist genetic approaches (both in vivo and in vitro) to target distinct neural circuits. Enabling the researchers to specifically inhibit astrocytes in a particular region of the brainstem (the posterior part of the brain that connects the brain to the spinal cord), so they could assess how individual neurons behaved to studying rats’ behaviour when awake.

Human studies will need to be carried out to confirm if the same mechanism occurs in humans. If this is the case, further testing will be required to assess if the mechanism could be safely targeted without disrupting other neural pathways.

The researchers have plans to further explore the mechanism. Dr Kirsteen Browning said, “We have yet to find out whether the loss of astrocyte activity and the signalling mechanism is the cause of overeating or that it occurs in response to the overeating. We are eager to find out whether it is possible to reactivate the brain’s apparent lost ability to regulate calorie intake. If this is the case, it could lead to interventions to help restore calorie regulation in humans.”