<\/p>\n Its conclusions were tantalising. Not only was exercise capacity, represented by VO2max<\/a>, increased by almost 4%, but inflammation was markedly reduced, making the treatment attractive for both performance and recovery<\/a>. It caught my attention because I was already using tVNS, doing my own kind of experiment. For the past seven months, I\u2019d been relaxing for an hour every morning with an electrical current gently pulsing through my ear. If the study was right, could this be a no-brainer performance gain for pros and amateurs alike?<\/p>\n Article continues below <\/p>\n You may like<\/p>\n The tVNS trial was published in the European Heart Journal in February 2025 but wasn\u2019t picked up by the mainstream media until the summer, at which point it gained considerable interest, including my own. The study, led by Professor Gareth Ackland of the William Harvey Research Institute, Queen Mary, University of London, recruited 28 healthy adults (14 men and 14 women) to receive tVNS for 30 minutes daily for two week-long periods.<\/p>\n Small study size<\/p>\n The vagus nerve is a major communication pathway between the brain and the body, involved in regulating heart rate,<\/a> breathing, inflammation and stress. Stimulating it via non-invasive tVNS means using a transcutaneous electrical nerve stimulation (TENS) machine, with electrodes clipped to the tragus of both ears. The ear contains specific zones where one branch of the vagus nerve projects; these areas, the tragus and cymba concha, provide an accessible conduit to the brain. Most scientific studies use one ear, but Ackland chose bilateral stimulation because contemporary research suggested this protocol is more effective in inducing brain plasticity and repair.<\/p>\n Its small sample size of 28 healthy adults, with an average age of 34, was a significant limitation of the study. That said, it was diligently executed. Professor Ackland and his team ensured that there was a blind randomised allocation of sham and active tVNS, with all participants receiving both over two seven-day periods, separated by a two-week washout interval. On average, work rate increased by six watts, respiratory rate by four breaths a minute at peak exercise, and VO2max by 1.04ml\/kg\/min, versus no increase in VO2max with the sham treatment. Markers of inflammation were also significantly reduced.<\/p>\n Pre-clinical research<\/p>\n \n (Image credit: Simon Fellows for Future)<\/p>\n Tempering my enthusiasm for using tVNS to boost my VO2max from the comfort of my sofa was the nagging acceptance that this study was not intended for cyclists, amateur or pro. \u201cIt\u2019s a proof-of-concept trial, funded by the British Heart Foundation,\u201d says Ackland, \u201cexamining how tVNS might bring the health benefits of exercise<\/a> to those who struggle to keep active.\u201d As most cyclists know, greater exercise capacity is strongly associated with a reduced risk of a range of serious conditions, from cardiovascular issues to neurodegenerative diseases. Even so, not everyone is willing or able to exercise regularly.<\/p>\n \u201cIf you\u2019ve just had chemotherapy before a major operation,\u201d says Ackland, \u201cthe last thing you want to do is visit the gym. Similarly, neural control is a fundamental part of exercise, which probably explains why some people find it harder than others. Seeing whether we could hijack the autonomic nervous system to gain the benefits of exercise seemed worth pursuing.\u201d Over the past few decades, doubt has been cast on the assumption that lower heart rates (higher vagal tone) associated with fitter people are entirely a product of exercise. Contemporary data suggest the brain plays a role too. \u201cWe were able to test that idea directly,\u201d says Ackland, \u201cand found three plausible physiological effects \u2013 changes in exercise capacity, changes in peripheral blood signatures to inflammation, and changes in resting heart rate. Our research demonstrates that vagal activity determines an individual\u2019s ability to exercise.\u201d<\/p>\n A 3.8% increase in VO2max may sound modest, but it compares very favourably with a 2007 study that found that high-intensity aerobic interval training<\/a> performed three times per week for eight weeks increased VO2max by 5.5-7.2%, while long, slow distance running and lactate threshold training yielded no effect at all. \u201cI would not want your readers to over-interpret this proof-of-concept study data,\u201d cautions Ackland, quick to rein in my enthusiasm. \u201cMuch more research is needed; it\u2019s not even close to adoption in either clinical work or by athletes. We are currently exploring the link between the neural influence on exercise and the eff ect that exercise has on that neural control, but that\u2019s still work in progress.\u201d<\/p>\n I ask Ackland whether there\u2019s any potential gain for pro cyclists, who already have finely tuned vagal tone. \u201cWell-trained athletes have optimal autonomic function,\u201d he says, \u201cbut there\u2019s a strong influence of neuroplasticity in the autonomic nervous system that underpins this. So, it\u2019s very likely that athletes could further benefit\u2026 Our work has put enhanced athletic performance on the menu of possibilities.\u201d<\/p>\n What to read next<\/p>\n DIY protocol<\/p>\n \n Simon trialled the device, did it make him faster on the bike? <\/p>\n (Image credit: Simon Fellows for Future)<\/p>\n I started using tVNS a month before the Daily Mail piece, having heard about research suggesting that vagus nerve stimulation, administered for an hour a day, could reduce atrial fibrillation <\/a>(AF) burden by 85%. I\u2019d recently undergone an ablation for AF, and my hope was that tVNS would reduce post-operative ectopic beats.<\/p>\n Vagal nerve stimulation has been used to treat epilepsy for decades (using implanted devices), so there\u2019s a good body of evidence to suggest it\u2019s safe. However, if, like me, you choose the DIY route, there is no guarantee, no safety net. To Professor Ackland\u2019s point, there isn\u2019t currently enough research to demonstrate that tVNS is effective or entirely safe for use by the wider public.<\/p>\n That said, my experience has been positive. Using a sub-\u00a350 TENS device from my local pharmacy, dialled in with settings scraped from the internet (low-frequency pulse rate 20-30Hz, to match natural electrical impulses) my daily, hour-long, tVNS ritual has been without incident, bar the mild, tingling sensation of an electrical current passing through my ear. My AF symptoms disappeared within two days and haven\u2019t reappeared, which is great, but beyond that, I haven\u2019t noticed any changes. Is my improvement in health just a coincidence? Possibly. Has my VO2max increased by so subtle a degree that it hasn\u2019t been noticeable while cycling? Maybe.<\/p>\n My dedicated but utterly unscientific use of tVNS demonstrates why more robust studies are needed. There are just too many variables to account for. The settings I\u2019m using are generic, rather than individualised, and whereas Ackland\u2019s team used bilateral tVNS, I\u2019m hooking up just my left ear, which is less likely to introduce cardiac side effects, but is possibly less potent too. Unlike Ackland\u2019s strict protocols, I only have my Garmin watch to estimate my exercise capacity.<\/p>\n For now, then, the lab research is still chasing the clinical potential, but if this technology fulfi ls its promise, it could be transformative \u2013 off ering a vital lifeline for those physically unable to train, and a supercharged marginal gain for the pros. I, for one, will be keeping tabs on the research with interest.<\/p>\n Vagus nerve stimulation explained <\/p>\n \n (Image credit: Simon Fellows for Future)<\/p>\n To understand the significance of the vagus nerve, we need to explore the role of the body\u2019s autonomic nervous system (ANS). This is the \u2018autopilot\u2019 that constantly runs vital functions, such as heartbeat, breathing and temperature regulation \u2013 the physiological processes we don\u2019t consciously control.<\/p>\n The brain maintains a delicate balance between our sympathetic system \u2013 fight-or-flight mode \u2013 which mobilises energy for high-intensity efforts<\/a>, and our parasympathetic system \u2013 rest-and-digest mode \u2013 which handles digestion and tissue repair.<\/p>\n \u201cBoth systems have a major role in cardiovascular function,\u201d explains Dr Mark Burnley, senior lecturer in exercise physiology at Loughborough University, \u201cas well as influence over the respiratory system and digestion. The sympathetic nervous system innervates the heart by acting on its sinoatrial (SA) node \u2013 the heart\u2019s natural pacemaker \u2013 releasing noradrenaline, which speeds up the heart\u2019s rate.\u201d<\/p>\n The parasympathetic nervous system also acts on the SA node, slowing it down. It does this by releasing acetylcholine, which opens specific channels that allow potassium to leak out of the cells, making them less excitable. \u201cThe vagus nerve is the main conduit of the parasympathetic nervous system,\u201d continues Dr Burnley, \u201ca vast network of nerves that branches from the brainstem to the lowest part of the intestines. It sends eff erent [outward] information from the brain down to peripheral organs, but about 80% of its traffi c is aff erent [inward], sending signals back to the brain.\u201d<\/p>\n Fundamentally, the vagus nerve continuously monitors the body and reports back to the brain when it\u2019s time to calm down. \u201cA fitter, stronger heart has to beat less often at a given cardiac output due to increased stroke volume,\u201d says Burnley, \u201cbut other processes are at play. When you train consistently, a part of the brain called the medulla oblongata becomes more active at rest, sending a stronger, more continuous electrical signal via the vagus nerve to the heart. More acetylcholine is released onto the SA node, which causes the potassium channels to be held open for longer, creating a lower resting heart rate.\u201d<\/p>\n In a nutshell, for the well-trained, the brain compensates for increased sympathetic outflow during efforts by boosting parasympathetic outflow during recovery. Fitter individuals have higher vagal tone, resulting in a slower resting heart rate. \u201cAdditionally,\u201d continues Burnley, \u201clong-term endurance training like cycling can remodel the SA node, leading to a decrease in certain ion channels, specifically HCN4. This slows the intrinsic rhythm of the heart regardless of autonomic input.\u201d<\/p>\n Transcutaneous vagal nerve stimulation (tVNS) doesn\u2019t directly affect the SA node. Instead, by stimulating the auricular branch of the vagus nerve in the ear, electrical signals travel to the brainstem. Interpreted as a call for \u2018rest and digest,\u2019 this prompts the medulla oblongata to send calming signals back down the main vagal trunk to the heart\u2019s SA node.<\/p>\n![\"Simon](\"https:\/\/www.newsbeep.com\/ie\/wp-content\/uploads\/2026\/04\/Xm5GsyAj3y7vUuDNqF6Min.jpg\")
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