Pelvic floor training can help active women avoid exercise-related symptoms
If the answer is no, now's the time to start. It's never too late to protect yourself from pelvic floor dysfunction – and the benefits go far beyond avoiding leaks.
The pelvic floor is a complex hammock of muscles and ligaments stretching from the front of your pelvis to your tailbone. It weaves around the urethra, vagina and anus, supporting the pelvic organs and helping them stay in the right place.
These muscles are essential for bladder and bowel control, sexual function and core stability. In fact, your pelvic floor works alongside the diaphragm, abdominal muscles, and back muscles in what's known as the 'core canister' or 'core rectangle.' Together, they help stabilise the spine, protect internal organs, and support movement, especially in high-impact or strength-based activities.
How does sport affect pelvic floor health?
Many sports rely heavily on core strength. Running, jumping, lifting and full-contact sports like rugby all demand stability, control and muscular endurance. But they also place significant strain on the pelvic floor.
That's why pelvic floor dysfunction is surprisingly common among sportswomen. Around one in two women in the UK will experience pelvic floor symptoms at some point in their lives – but rates are even higher among female athletes. A 2024 study of female rugby players found that 63% experienced pelvic floor dysfunction serious enough to affect both their performance and daily life, often requiring physiotherapy or specialist support.
Movements such as jumping, running, landing and breath-holding during exertion all increase intra-abdominal pressure, which pushes down on the pelvic floor. Without proper conditioning, these muscles can become strained or fatigued, especially if they're weaker than the surrounding core muscles.
Endurance sports can also take their toll, causing the pelvic floor to repeatedly contract under pressure. Like any muscle, the pelvic floor is susceptible to overuse injuries and needs time to recover.
Pelvic floor dysfunction can show up in several ways, including leaking urine or faeces during exercise, coughing or sneezing; disrupted bowel habits; a heavy or dragging feeling in the lower abdomen or vagina; pain during sex; a bulging sensation or visible tissue in the vaginal area; and pelvic organ prolapse.
These symptoms may appear during exercise – or at rest – and often worsen over time without the right support or training.
Exercise can help with pelvic floor dysfunction – only if the pelvic floor is actively and effectively engaged. Many workouts target the abs or general core, but if the pelvic floor isn't included with the same intensity, muscular imbalances can develop. Combined with gravity and high-impact movement, this puts the pelvic floor at greater risk of dysfunction.
The good news? The pelvic floor responds well to training. With regular, focused practice, these muscles become stronger, more coordinated and more resilient – helping to prevent dysfunction and even aiding recovery after childbirth.
How to train your pelvic floor
Not sure where to start? Here's a simple exercise:
Imagine you're holding in wind – gently contract your anus.
Next, squeeze your urethra as if stopping a flow of urine.
Now, lift upwards through the vagina.
Hold the contraction for a few seconds (or as long as you comfortably can), then release.
That's one pelvic floor contraction: well done!
Try doing a few reps at a time, and gradually build up. You can incorporate these into your run, add them to your core workout, or practise them during rest days or cool-downs. The goal is to make pelvic floor training a regular part of your routine.
Your pelvic floor deserves just as much attention as your abs, glutes or quads. If you're a woman who exercises, training these deep core muscles can boost your performance, reduce your risk of injury and support your overall health now and in the future.
So next time you lace up your trainers or hit the gym, don't forget your pelvic floor. Your body will thank you.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Holly Ingram does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.
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The comparator or control group was 2000 steps. Compared to that those who reported or documented with counter 7000 steps per day had a: 47% reduction in all-cause death (HR 0.53 [95% CI, 0.46–0.60]; I 2 =36.3; 14 studies) 25% reduction in CV disease incidence (HR 0·75 [0·67–0·85]; I 2 =38·3%; 6 studies) 47% reduction in CV mortality (HR 0·53 [0·37–0·77]; I 2 =78·2%; 3 studies) 37% reduction in cancer mortality (HR 0·63 [0·55–0·72]; I 2 =64·5%; 3 studies) 14% reduction type 2 diabetes (HR 0·86 [0·74–0·99]; I 2 =48·5%; 4 studies) 38% reduction in dementia (HR 0·62 [0·53–0·73]; I 2 =0%; 2 studies) 28% reduction in falls (HR 0·72 [0·65–0·81]; I 2=47·5%; four studies) My issue with this study is that when you go to the main figure, the plots with hazard ratio (HR) on the y-axis and step counts on the x-axis, you see a clear dose response of steps and specific outcomes. 2000 steps is where the HR is 0. If it's less than 2000 steps, the outcomes are actually higher, but as the step count increases the HR drops. The authors pick 7000, I assume because that is where the slope of benefit seems to plateau, but when you look at the curves, the HR keeps dropping with more steps. The authors quantify the added benefit of > 7000 steps per day in Table 8 of the supplement. For all-cause death, there is an added 10% lower HR with 10,000 vs 7000. Same for cancer mortality and depressive symptoms—an added 10% lower relative risk. So I don't think any myths were busted. 7000 is fine. 7000 steps per day is associated with lower bad health outcomes. But for many, including all-cause death, 10,000 is better. The added benefits reached statistical significance. So if a patient asks, the number is still 10,000. Though 7000 is also good. And 5000 is better than 4000, which is better than 3000. After reviewing this study, the thought about European vs American life popped into my head. We have probably 2000 people working at my hospital. Less than 5 of them walk to work; less than 10 of them ride their bike. When I visited the team at Basel, Switzerland last fall, it looked like more than 75% walked or cycled to work. Very few American cities are set up for walking. That's sad. So Americans have to make an effort to be active. I think it's worth it. And I recommend it in the clinic. For my height, 7000 steps is about 3 miles. 10,000 steps is nearly 5 miles. The optimal dose is the longer one. But some is better than none. Everyone Deserves a Shot at the American Dream: Sinus Rhythm Let me say a few words here about rate vs rhythm control, because this may actually be the number one issue in all of electrophysiology. The stimulus for writing such a review piece I think comes from the PRAGUE 25 trial of lifestyle modification vs AF ablation. I have opined on that in my July 11 podcast. In sum, AF ablation led to less AF than risk factor (RF) modification alone, though 35% (or 1 in 3 patients) in the risk factor modification group had sinus rhythm (SR) without ablation. And RF modification led to more weight loss, better glycemic control, and better fitness as measured by VO 2 max. PRAGUE 25 also found no statistical differences in AF burden nor quality of life measures. The sits in the literature as a 'positive' ablation trial, but I actually think, healthwise, it is a 'positive' trial for RF modification. The Medscape article cites a 'hybrid' approach wherein all patients who pursue rhythm control also get risk factor modification, which I totally agree with, and I have to say, is underused, at least in my zip code. The absolute wrong thing to do is ablate the AF and not help the patient lose weight and improve cardiometabolic health. Because if you do this, you have merely reduced a surrogate marker — AF episodes. Health is not improved if obesity, hypertension, diabetes, and poor exercise tolerance remain. You succeed as a proceduralist but fail as a doctor in this scenario. The Medscape article goes on to celebrate the benefits of SR over AF. The next logical step is to laud rhythm control over rate control. And here I have a problem. And I somewhat disagree with friend and colleague Eric Prystowsky, MD. Eric is well known for his criticism of AFFIRM and how that trial set EP back years. But I had the pleasure of speaking in Calgary and met the late Dr. George Wyse, the principal investigator of AFFIRM. AFFIRM is one of those landmark trials that deserves your attention. Published in 2002, a total of 4060 patients with AF were randomized to rate or rhythm control. Mortality was the primary endpoint. Patients in AFFIRM were like those we see every day. 70 years old. Most with hypertension, a third with CAD. At 5 years, 23.8% in the rhythm control arm died vs 21.3% in the rate control arm. The HR was 1.15, or 15% worse for rhythm control. CIs were 0.99-1.34 so the P value for arm was just outside 0.05 but the upper bound or worse case was a 34% higher rate of death in the rhythm control arm. More patients in the rhythm-control group than in the rate-control group were hospitalized, and there were more adverse drug effects in the rhythm-control group as well. AFFIRM was largely interpreted as showing no differences in the two strategies. But, really, there was a strong trend for worse outcomes in the rhythm-control arm. One of the major changes in knowledge that came from AFFIRM is the importance of maintaining oral anticoagulation (AC). In AFFIRM, patients in the rhythm control arm who were maintaining SR could stop their oral AC. This led to a difference in AC use 85% vs 70% rate vs rhythm control. In fact, AFFIRM largely changed the view that patients with AF with either strategy should remain on oral AC. The Sherman et al substudy in JAMA Internal Medicine found that patients who remained on warfarin were 68% less likely to have stroke. A large proportion of ischemic strokes (113 of 157) occurred in patients in whom anticoagulation had been stopped (on the basis of re-established normal sinus rhythm) and who had a subtherapeutic international normalized ratio. Eric's point about AFFIRM is it led to too many patients with AF being told that there was no reason to try to get into SR, and if you don't try, and you leave patients in AF, it becomes impossible to restore SR after a year or so. The other problems (or criticisms) of AFFIRM were that patients had to be able to tolerate rate-control. So highly symptomatic patients were excluded. AFFIRM should never have been applied to these patients. Many of these symptomatic patients were younger, and it is a serious error to just leave a symptomatic younger person with AF forever in AF. Another criticism of AFFIRM was that it only included antiarrhythmic drugs (AAD), and amiodarone was the most common one used. AAD were all that was available at the time. We now know that AF ablation is far more effective at rhythm control than drugs. So there is a like a bridge to SR early on, and many patients can be put into SR with rhythm control. Proponents of aggressive rhythm control also cite the EAST-AF trial, a rhythm vs rate control trial, which strongly favored rhythm control. But EAST-AF suffered from serious performance bias issues wherein the rhythm control arm got oodles more interactions with the health system. Here is my take of the decision: AFFIRM still applies. If you have an older person with minimal to no symptoms from AF, rate control is not only fine but maybe preferred. But if there are a) symptoms, and b) clues that rhythm control is possible (e.g., the LA size is not ginormous, or the patient can cooperate, and maybe the AF is not more than 2 years persistent), I try rhythm control. But I tell patients that while there is benefit from SR (in terms of quality of life) rhythm control is hard. It costs a lot, not only in money, but investment in their time and effort. Patients have to know that RF modification is crucial, they will also have to spend a few days in the hospital (for cardioversions, maybe drug initiation or ablation). Remember, when you are getting cardioversions and AAD and ablations you are not at work or on a bike. You are being a patient. It's fine. It's an investment but patients need to know that rhythm control is unlike a gallbladder operation or an appendectomy. Rhythm control is a process that requires a friendship with a cardiologist. It's not one and done. There are also risks to rhythm control. Drug side effects and ablation complications do occur. My friends, be careful flying close to the sun with rhythm control. One of the biggest mistakes I see in general cardiology is leaping to cardioversion without a plan. CV of AF is fine, but you have to have a plan for what will happen in a week or month when the patient is back in AF. CV doesn't modify the problem of AF. It just resets the heart. In the end: EP is here to help. Get us involved. Especially when there are symptoms. And doubly especially, when there is heart failure. But don't dismiss AFFIRM. It is important trial that shows that rate control is not a terrible strategy in selected patients. GLP-1 RAs Protective Against Stroke, Neurodegeneration? A GLP-1 study purports to show benefit in cerebrovascular health. It actually shows how observational studies can mislead you. The title of the study is, 'Neurodegeneration and Stroke After Semaglutide and Tirzepatide in Patients With Diabetes and Obesity.' 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BMI on average 40, and 70 % with hypertension. Here were the main results: During a 7-year follow-up, GLP-1 RA users had a lower risk of dementia (HR, 0.63; 95% CI, 0.50-0.81) lower risk of stroke (HR, 0.81; 95% CI, 0.70-0.93) lower all-cause mortality (HR, 0.70; 95% CI, 0.63-0.78) and had no significant differences in the risk of Parkinson disease or intracerebral hemorrhage. The authors concluded: 'These findings suggest potential neuroprotective and cerebrovascular benefits of GLP-1 receptor agonists beyond glycemic control, warranting further trials to confirm these outcomes.' Maybe these drugs are beneficial for cerebrovascular health, especially in young people (age 57 and diabetes and BMI of 40) But this is a hopelessly confounded study where healthier patients got the more pricey and newer drug. How do I know that? There are two clues. First, is that the Kaplan-Meier curve diverges immediately and continues in parallel. That's what you expect when healthier patients get one treatment. Immediately better outcomes. If the GLP-1 was better than other drugs, you'd see gradually increasing benefit. Second reason: the mortality benefit is huge. A 30% reduction in death. In the SELECT trial of semaglutide vs placebo in patients with heart disease and obesity, semaglutide only reduced CV mortality by 15%. In the SUSTAIN-6 trial of semaglutide vs placebo, semaglutide had no sig reduction in death or CV death and required a composite endpoint to drive positive results. My overall take, therefore, is that GLP-1 drugs induce weight loss. They do modify disease in patients with obesity and diabetes and patients with obesity and atherosclerotic disease. But whether they reduce important cerebrovascular outcomes like dementia cannot be answered by these confounded observational studies. I am not sure it's worth doing these studies because the only value is to show readers the signs of bias in non-random, retrospective comparison studies.
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