Pelvic floor dysfunction (PFD) is under-reported, under-recognized, and under-treated in female athletes, despite the fact that high impact, repetitive sport can put women at risk for developing PFD (Casey & Temme 2017).
Introduction
The prevalence of urinary incontinence (UI) in female nulliparous athletes can range between 5-80%, with the highest prevalence in women participating in high-impact sport. Pires et al. (2020) reported that the prevalence of UI among female athletes was 25% and when stress urinary incontinence (SUI) was analyzed separately, the prevalence was 20%. The prevalence in high impact sports was 25.%, with the highest prevalence observed in volleyball namely, 75%; 72% for trampolining; 50% for indoor soccer; 45% for cross-country skiers and runners; 44% for running; 34% for basketball; 20% for athletics and 20% for handball (Pires et al. 2020).
Mechanisms
The pelvic floor works in concert with the abdominal and spinal stabilizing muscles as well as the diaphragm to transfer forces between the upper and lower body, maintain upright posture and dynamic stabilization and to support forces that the skeleton alone could not withstand.
High impact activities are defined as those involving the performance of several jumps and actions related to maximum abdominal contractions. The increase in intra-abdominal pressure exert an impact force directly on the pelvic floor muscles (PFM), (Bø, 2004; Casey and Temme, 2017; Reis et al., 2011; Santos et al., 2018; Teixeira et al., 2018).
High impact activities can be classified as follows:
• Impact grade 3 (>4 times body weight, e.g., jumping);
• Impact grade 2 (2–4 times body weight, e.g., sports involving sprinting activities and rotational movements);
• Impact grade 1 (1–2 times body weight, e.g., such as lifting light weights);
• Impact grade 0 (<1 times body weight, e.g. swimming).
Specifically running, jumping, and landing have been highlighted as activities that is associated with increased intra-abdominal pressure in the pelvic organs and tissues (Rebullido et al. 2021).
Hypotheses
Different hypotheses have been investigated as possible reasons and mechanisms why high impact activities may lead to PFD in female athletes. The first hypothesis is that athletes normally should have strong pelvic floor muscles, as strenuous exercise increases abdominal pressure, which may lead to a simultaneous or pre-contraction of the pelvic floor muscles, which may act as a training stimulus (Ree, Nygaard, & Bo 2007). The second main hypothesis contradicts the first, as a recent systematic review found that strenuous activity may actually overload, stretch and weaken the pelvic floor due to the chronic and repeated increase of abdominal pressure.
A study by Da Roza, Brandão, Oliveira, et al. (2015) found that an incontinent group of athletes had a thicker pubovisceral muscle at the mid-vaginal level, suggesting that SUI is not necessarily associated with the strength or displacement of the PFM. SUI could rather be associated with a decreased response or delayed reaction of the pubovisceral muscle. The muscle becomes thicker to try to counteract decreased responsiveness of the sphincter urethrae. The delayed response could occur due to alterations in the intrafusal fibres as a consequence of many years of sports training (Da Roza, Brandão, Oliveira, et al., 2015).
Another explanation may be that high impact activities produce higher forces, and that forces are transmitted through tissue, where an injury may occur. The remodelled tissue after repair may be malformed and dysfunctional (Southon, 2008) which can create problems in transmitting muscular forces to the urethra and consequent failure of the continence mechanism. In addition, the repeated intra-abdominal pressure during sport may fatigue the pelvic floor, and this may further reduce the effectiveness of the continence mechanism.
A couple of alternative hypotheses have also been published:
• Keane et al. (1997) have linked a decrease in collagen in the pubovesical ligament to the development of UI.
• Genetic predisposition has also been postulated to be a risk factor for PFD in female athletes.
• A different personal fatigue threshold exists for each female athlete. When this fatigue level is reached the continence mechanism may malfunction (Eliasson, Nordlander, Larson, Hammarström, & Mattsson, 2005).
• More athletes experience leakage during training rather than competition (95.2 vs. 51.2%). It is postulated that higher catecholamine levels during competition may be the reason for this. The catecholamine act on the urethral α-receptors to maintain its closure during activities which take place at competition level (Goldstick and Constantini, 2014; Thyssen et al., 2002).
• Low body mass index (BMI), low energy availability (RED-s), estrogen changes, and hypermobility joint syndrome have also been postulated to be contributing factors to the development of PFD in female athletes.
• Lastly, the risk for leakage in conditioned athletes may occur at the muscle spindle level. Recurrent or prolonged, increased intra-abdominal pressure may lengthen the pelvic floor muscles and negatively impact the intra-fusal muscle fibre function and responsiveness over time (Casey & Telle 2017).
Clinical implications
A couple of clinical implications can be highlighted based on current evidence. Firstly, coaches should be informed of PFD that may occur in high performance female athletes, as the athlete is not likely to report this or seek treatment for the problem. Female athletes should therefore be screened for these dysfunctions as they have a risk of developing PFD. Together with this, preventative measures should also be taken in young female athletes, especially those with REDs.
PFD among female athletes is multifactorial, treatment and advice should therefore be focused on the endurance of the muscles to reduce fatigue – together with other contributing factors which have been identified during assessment. This may include factors such as imbalances in the closed kinetic chain or stabilising mechanisms, other injuries or pain, medical factors and genetic predisposition.
It is important to emphasize that according to current literature, but contrary to standard practice, PFM strength does not seem to be the major issue – although it cannot be ruled out until assessed.
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