Pelvic floor electromyographic dysfunction as a novel physiological indicator for subclassifying sexual dysfunction in patients with chronic prostatitis/chronic pelvic pain syndrome

Abstract

Background

Sexual dysfunction (SD) is a common complication in patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), and there remains a lack of objective diagnostic physiological indicators in clinical practice.

Objective

This study aimed to explore the value of pelvic floor electromyography (PF-EMG) parameters as novel physiological indicators for SD in CP/CPPS patients.

Methods

A total of 116 CP/CPPS patients were enrolled and stratified into PE and ED subgroups based on validated questionnaires (C-ISFPE and IIEF-5). All participants underwent standardized PF-EMG assessment to evaluate resting tone, fast-twitch, and slow-twitch functions. Statistical analyses included t-tests, logistic regression, and ROC curve analysis.

Results

In the PE subgroup (n = 66), resting tone was significantly elevated (anterior baseline: 6.49 ± 3.42 µV vs. 3.78 ± 2.79 µV in the non-PE group, P < 0.001) and served as an independent predictor of PE (OR = 1.428, P = 0.003). In the ED subgroup (n = 45), fast-twitch function was severely impaired (rapid contraction: 37.87 ± 18.36 µV vs. 69.92 ± 25.78 µV in the non-ED group, P < 0.001). With a cut-off value of < 45.41 µV for rapid contraction, the area under the curve (AUC) for ED diagnosis was 0.866, with a sensitivity of 92.6%.

Conclusion

PF-EMG parameters serve as objective, non-invasive physiological indicators that can effectively distinguish between PE and ED subtypes in CP/CPPS patients, paving the way for targeted therapies.

Introduction

CP/CPPS is a common urological disease with a prevalence ranging from 2.7 to 16% [1], involving the combined effects of multiple factors, including autoimmunity, oxidative stress, urinary reflux, and pelvic floor dysfunction [2], However, its etiology and pathogenesis remain unclear, and the primary clinical goal is to improve patients’ quality of life [3], which is often compromised by depressive symptoms [4, 5]. An updated systematic review and meta-analysis of 20,127 patients revealed that 59% of men with CP/CPPS suffer from at least one form of sexual dysfunction, with pooled prevalence rates of 34% for ED and 35% for PE [6]. Currently, the diagnosis and treatment of sexual dysfunction in CP/CPPS face a dilemma: psychological scales fail to distinguish somatic etiologies, whereas invasive examinations exacerbate patient discomfort. Therefore, there is an urgent need for non-invasive physiological indicators to elucidate the pathological mechanisms of sexual dysfunction in CP/CPPS.

Recent studies have indicated that pelvic floor dysfunction may be a key factor in sexual dysfunction secondary to CP/CPPS [7], The pelvic floor muscle complex consists of fast-twitch muscle fibers (e.g., the bulbocavernosus muscle, involved in rapid erection) and slow-twitch muscle fibers (e.g., the puborectalis muscle, involved in ejaculatory control), and regulates sexual response through multiple electrophysiological and vascular regulatory mechanisms [8, 9]. The pathophysiological link between pelvic floor muscle (PFM) dysfunction and sexual symptoms in CP/CPPS involves distinct mechanisms for erectile dysfunction (ED) and premature ejaculation (PE). ED primarily stems from impaired fast-twitch fiber function in muscles like the bulbocavernosus, which are crucial for the rapid, forceful contractions required for the penile “veno-occlusive mechanism” that maintains erection. Conversely, PE is largely driven by elevated resting tone (hypertonicity) of the slow-twitch fibers, often resulting from a chronic pelvic “pain-spasm cycle,” which predisposes the pelvic floor to a hyperexcitable state and shortens ejaculatory latency [10, 11]. The causal link between PFM function and sexual performance is further supported by interventional evidence. A systematic review concluded that pelvic floor muscle training is an effective treatment for both ED and PE, reinforcing the role of musculoskeletal rehabilitation in managing these conditions. This provides a strong rationale for objectively quantifying PFM function as a basis for targeted therapy [12]. However, previous analyses of pelvic floor muscles have been relatively general (only distinguishing conditions such as reduced muscle tone), lacking electromyography-based refined subtyping and correlation analysis with specific sexual dysfunction phenotypes [13, 14]. This study hypothesizes that CP/CPPS-related sexual dysfunction stems from distinct patterns of abnormal pelvic floor electromyographic function—premature ejaculation is caused by high resting tone, while erectile dysfunction originates from fast-twitch failure. To test this hypothesis, we conducted a multimodal study that integrated quantitative analysis of pelvic floor electromyography with validated sexual dysfunction scales, and for the first time established electromyographic diagnostic thresholds for subtyping sexual dysfunction.

Subjects and methods

Study design and subjects

This cross-sectional study recruited consecutive patients diagnosed with CP/CPPS in the urology department of a tertiary hospital from January to December 2023. The diagnosis of CP/CPPS was clinically established based on the presence of chronic pelvic pain for at least 3 months, in the absence of other identifiable causes (NIH-CPSI score ≥ 15 points). All patients underwent urinalysis and urine culture to exclude active urinary tract infection. The Meares-Stamey test was not routinely performed for patients without a history or clinical symptoms suggestive of chronic bacterial prostatitis.

Exclusion criteria: ① Complicated with interfering diseases such as urinary tract infection; ② Complicated with benign prostatic hyperplasia (diagnosed based on clinical assessment, including symptoms, digital rectal examination, and/or prostate volume measurement) or other significant pelvic organ diseases (e.g., interstitial cystitis/bladder pain syndrome, significant anorectal diseases); ③ With a history of neurological or spinal cord lesions and other relevant diseases; ④ Patients taking medications for prostatitis/CPPS (e.g., alpha-blockers, anti-inflammatory agents, antibiotics) with a washout period of less than 5 half-lives before baseline; ⑤ Patients with severe mental stress, or taking psychotropic drugs, who were unable to cooperate with the investigation.

The study protocol was approved by the Ethics Committee (approval number: 2023KYLL205) and was conducted in accordance with the ethical standards of the Declaration of Helsinki.

Pelvic floor electromyography (PF-EMG) examination procedure

The pelvic floor electromyography (PF-EMG) assessment was performed using the NeuroTrac electromyography system equipped with an intra-anal probe. All examinations were conducted by a single, experienced technician to ensure consistency. Patients were placed in a standardized left lateral decubitus position.

The intra-anal probe was inserted to a depth of approximately 3–4 cm to ensure proper contact with the pelvic floor musculature, specifically targeting the puborectalis and pubococcygeus muscles. The specific detection parameters were set as follows: current 20–50 mA, frequency 40–80 Hz, and pulse width 200–400 µs.

The examination protocol quantitatively assessed the following functional domains:

Resting Tone: The anterior and posterior baseline values (in µV) were recorded over a sustained 60-second period while the patient maintained complete muscle relaxation.

Fast-Twitch Function: The maximum rapid contraction capacity was assessed by instructing the patient to perform three rapid and forceful contractions. The peak value (in µV) from these three attempts was recorded for analysis.

Slow-Twitch Function: The endurance capacity was evaluated by asking the patient to sustain a contraction for 10 s. The sustained contraction value (in µV) was recorded, and the contraction-relaxation ratio was calculated.

Subjective scales

All participants completed a series of well-validated questionnaires under the supervision of a trained researcher in a private and quiet room to ensure confidentiality and minimize distractions.

Erectile dysfunction (ED) was assessed using the International Index of Erectile Function-5 (IIEF-5). This is a globally recognized, self-administered tool with excellent reliability and validity. The IIEF-5 score ranges from 5 to 25, with a score of ≤ 21 serving as the widely accepted cut-off point for diagnosing ED [15].

Premature ejaculation (PE) was evaluated using the Chinese Index of Sexual Function for Premature Ejaculation (C-ISFPE). This is a culturally adapted and validated instrument for the Chinese population, demonstrating robust psychometric properties, including high internal consistency (Cronbach’s α >0.8) and test-retest reliability. In accordance with its validation study, a score of < 36 was used to define PE [16].

CP/CPPS Symptom Severity was measured with the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI).

Group stratification and diagnostic criteria

Patients were stratified into subgroups based on their scores from the validated questionnaires. Premature ejaculation (PE) was defined as a C-ISFPE score < 36. Erectile dysfunction (ED) was defined as an IIEF-5 score ≤ 21. Patients meeting the criteria for both conditions were included in the comorbidity analysis.

Statistical analysis

Data normality was assessed using the Shapiro-Wilk test. Continuous variables with normal distribution were presented as mean ± standard deviation and compared using independent samples t-test; otherwise, the Mann-Whitney U test was applied. Categorical data were compared using the Chi-square test. Univariate analyses (including t-test, Mann-Whitney U, or Chi-square test as appropriate) were first performed to identify potential risk factors (including demographic and clinical variables such as age and disease duration) associated with sexual dysfunction. Variables with a P value < 0.1 in these univariate analyses were then entered into a binary logistic regression model (forward stepwise, likelihood ratio method) to identify independent predictors, with adjustments made for age and disease duration. Receiver operating characteristic (ROC) curve analysis was performed to evaluate diagnostic efficacy, where the optimal cut-off value was determined by maximizing the Youden index. Confidence intervals for the areas under the ROC curves (AUCs) were computed using the DeLong method. All statistical analyses were conducted using SPSS 24.0, and the ROC curves were generated with the same software. A two-tailed P value < 0.05 was considered statistically significant. A post-hoc power analysis was performed using G*Power software. With an effect size of 0.5, α error of 0.05, and a sample size of 116, the achieved power for detecting group differences exceeded 90%.

Results

A total of 116 CP/CPPS patients were included in the final analysis. Based on validated questionnaires, 66 patients were classified into the premature ejaculation (PE) subgroup and 45 into the erectile dysfunction (ED) subgroup, with some patients presenting both conditions.

The baseline characteristics and univariate comparisons are summarized in Tables 1 and 2. Patients in both the PE and ED subgroups were significantly older and had a longer disease duration compared to their respective control groups (all P < 0.05). As expected, the PE subgroup had significantly lower C-ISFPE scores, while the ED subgroup had lower IIEF-5 scores.

Table 1.

Comparison of clinical characteristics and pelvic floor electromyography (EMG) parameters between premature ejaculation group and Non-Premature ejaculation group

Variable	Premature ejaculation group (n = 66)	Non-premature ejaculation group (n = 50)	P value
Age/years	31.56 ± 7.54	26.58 ± 7.87	< 0.001
BMI	23.98 ± 2.35	23.18 ± 2.42	0.076
Duration of disease/months	19.09 ± 15.31	11.10 ± 10.54	0.001
C-ISFPE	28.09 ± 8.41	42.12 ± 1.08	< 0.001
IIEF-5	18.70 ± 4.24	21.34 ± 2.84	0.001
Pre-baseline value/µV	6.49 ± 3.42	3.78 ± 2.79	< 0.001
Rapid contraction value/µV	57.00 ± 27.88	56.21 ± 28.12	0.880
Contraction-relaxation value/µV	27.52 ± 14.28	28.85 ± 15.08	0.629
Sustained contraction value/µV	34.60 ± 20.08	31.63 ± 21.06	0.442
Post-baseline value/µV	7.25 ± 3.93	5.07 ± 2.90	< 0.001
Total score of NIH-CPSI	24.80 ± 4.82	21.84 ± 5.38	0.002

Data presented as mean ± standard deviation. P values in bold indicate statistical significance (P < 0.05)

Table 2.

Comparison of clinical characteristics and pelvic floor electromyography (EMG) parameters between erectile dysfunction group and Non-Erectile dysfunction group

Variable	Erectile dysfunction group (n = 45)	Non-erectile dysfunction group (n = 71)	P value
Age/years	34.63 ± 8.80	25.74 ± 4.84	< 0.001
BMI	23.69 ± 2.31	23.60 ± 2.48	0.846
Duration of disease/months	21.63 ± 16.00	11.43 ± 10.61	< 0.001
C-ISFPE	31.85 ± 9.11	35.75 ± 9.40	0.028
IIEF-5	15.52 ± 2.79	22.60 ± 0.79	< 0.001
Pre-baseline value/µV	5.06 ± 3.24	5.52 ± 3.56	0.478
Rapid contraction value/µV	37.87 ± 18.36	69.92 ± 25.78	< 0.001
Contraction-relaxation value/µV	21.51 ± 9.66	32.74 ± 15.70	< 0.001
Sustained contraction value/µV	28.18 ± 16.29	36.95 ± 22.38	0.022
Post-baseline value/µV	6.05 ± 3.38	6.49 ± 3.88	0.522
Total score of NIH-CPSI	23.92 ± 5.12	23.25 ± 5.37	0.243

Key PF-EMG findings from univariate analysis were as follows:

PE Subgroup: Patients with PE exhibited significantly elevated pelvic floor resting tone, demonstrated by higher anterior baseline (6.49 ± 3.42 µV vs. 3.78 ± 2.79 µV, P < 0.001) and posterior baseline values (7.25 ± 3.93 µV vs. 5.07 ± 2.90 µV, P < 0.001), compared to the non-PE group. No significant differences were found in fast-twitch or slow-twitch contractile parameters.

ED Subgroup: Patients with ED showed severe impairment in both fast-twitch and slow-twitch functions. Their rapid contraction value (37.87 ± 18.36 µV vs. 69.92 ± 25.78 µV, P < 0.001), contraction-relaxation ratio (21.51 ± 9.66 µV vs. 32.74 ± 15.70 µV, P < 0.001), and sustained contraction value (28.18 ± 16.29 µV vs. 36.95 ± 22.38 µV, P = 0.022) were all significantly reduced compared to the non-ED group.

Correlation analysis (Table 3) revealed that PE severity (C-ISFPE score) was moderately to strongly negatively correlated with anterior and posterior baseline values (r = −0.450 and r = −0.338, respectively; both P < 0.001), indicating that elevated resting tone was associated with worse ejaculatory control. Conversely, ED severity (IIEF-5 score) was strongly positively correlated with rapid contraction (r = 0.658, P < 0.001), and moderately correlated with contraction-relaxation ratio and sustained contraction values (r = 0.456 and r = 0.339, respectively; both P < 0.001).

Table 3.

Correlation analysis between electromyographic parameters and sexual dysfunction

Variable	Premature ejaculation group	P value	Erectile dysfunction group	P value
Pre-baseline value/µV	−0.450	< 0.001	0.060	0.522
Rapid contraction value/µV	0.046	0.626	0.658	< 0.001
Contraction-relaxation value/µV	0.017	0.853	0.456	< 0.001
Sustained contraction value/µV	−0.065	0.486	0.339	< 0.001
Post-baseline value/µV	−0.338	< 0.001	−0.002	0.985

P values in bold indicate statistical significance (P < 0.05)

The anterior baseline value and contraction-relaxation value were independent predictors of premature ejaculation (p < 0.05). For every 1 µV increase in resting tone, the risk of PE increased by 42.8% (Adjusted OR = 1.428, 95% CI 1.131–1.804). The lower bound of the confidence interval (1.131) indicates that even in a conservative estimate, the risk increase is at least 13.1%, confirming the robustness of this association.Such an elevation indicates a state of high pelvic floor muscle tone, which may shorten ejaculatory latency through the “pain-spasm cycle” (Table 4). The rapid contraction value and sustained contraction value were independent predictors of erectile dysfunction (p < 0.05). For every 1µV increase in the rapid contraction value, the risk of erectile dysfunction decreased by 8.3% (OR < 1); the 95% CI was far from 1 with a significant p-value, suggesting that an increase in the rapid contraction value is a strong protective factor for erectile function. The rapid contraction value reflects the transient contraction capacity of fast-twitch muscle fibers (e.g., bulbocavernosus muscle); its elevation can enhance cavernous venous compression, maintain erectile pressure, and directly support the mechanism of “the association between fast-twitch failure and ED” (Table 5).

Table 4.

Multivariate logistic regression analysis for independent predictors of PE and ED

Predictor	β	OR (95%CI)	P value
Pre-baseline value/µV	0.356	1.428 (1.131–1.804)	0.003
Rapid contraction value/µV	0.003	1.003 (0.983–1.024)	0.751
Contraction-relaxation value/µV	−0.052	0.949 (0.901–1.000.901.000)	0.049
Sustained contraction value/µV	0.017	1.017 (0.983–1.051)	0.328
Post-baseline value/µV	−0.022	0.978 (0.806–1.187)	0.821

Analysis adjusted for age and disease duration. Analysis adjusted for age and disease duration

OR odds ratio, CI confidence interval

Table 5.

Multivariate logistic regression analysis for independent predictors of ED

Predictor	β	OR (95%CI)	P value
Pre-baseline value/µV	−0.041	0.960 (0.752–1.226)	0.744
Rapid contraction value/µV	−0.087	0.917 (0.883–0.952)	< 0.001
Contraction-relaxation value/µV	−0.066	0.936 (0.869–1.007)	0.078
Sustained contraction value/µV	0.053	1.054 (1.001–1.110)	0.044
Post-baseline value/µV	0.037	1.037 (0.794–1.355)	0.789

Analysis adjusted for age and disease duratio. Analysis adjusted for age and disease duration

OR odds ratio, CI confidence interval

The diagnostic performance of these key PF-EMG parameters was further evaluated using ROC curve analysis (Tables 6 and 7). The anterior baseline value demonstrated a significant ability to identify patients with PE, with an area under the curve (AUC) of 0.749 (95% CI 0.658–0.841). For ED, the rapid contraction value proved to be an excellent biomarker, with an AUC of 0.866 (95% CI 0.789–0.934). At an optimal cut-off value of < 45.41 µV, the sensitivity for diagnosing ED was 92.6%.

Table 6.

Diagnostic efficacy of electromyographic parameters in the premature ejaculation group

Diagnostic indicator	AUC	95%CI	Cut-off value	Sensitivity	Specificity
Pre-baseline value/µV	0.749	0.658–0.841	> 4.39µV	0.742	0.740
Rapid contraction value/µV	0.487	0.378–0.596	> 28.03µV	0.924	0.200
Contraction-relaxation value/µV	0.485	0.376–0.593	< 9.41µV	1.000	0.080
Sustained contraction value/µV	0.567	0.460–0.675	> 23.59µV	0.773	0.420
Post-baseline value/µV	0.681	0.583–0.779	> 4.50µV	0.788	0.600

 ROC receiver operating characteristic, AUC area under the curve

Table 7.

Diagnostic efficacy of electromyographic parameters in the erectile dysfunction group

Diagnostic indicator	AUC	95%CI	Cut-off value	Sensitivity	Specificity
Pre-baseline value/µV	0.533	0.426–0.640	> 6.73µV	0.382	0.792
Rapid contraction value/µV	0.866	0.789–0.934	< 45.41µV	0.926	0.687
Contraction-relaxation value/µV	0.723	0.631–0.815	< 26.60µV	0.618	0.771
Sustained contraction value/µV	0.612	0.508–0.715	< 20.43µV	0.294	0.917
Post-baseline value/µV	0.508	0.400–0.615	> 12.03µV	0.103	0.979

ROC receiver operating characteristic, AUC area under the curve

Of the 116 patients, 28 (24.1%) were identified as having both PE and ED. This comorbidity subgroup exhibited a mixed PF-EMG profile, characterized by both significantly elevated resting tone (similar to the isolated PE group) and impaired rapid contraction capacity (similar to the isolated ED group). This pattern supports the hypothesis that PE and ED in CP/CPPS can have distinct but co-existing pathophysiological mechanisms related to pelvic floor muscle dysfunction (Fig. 1).

Fig. 1.

Distinct pelvic floor electromyographic profiles in CP/CPPS patients with sexual dysfunction. A The anterior baseline value, reflecting resting muscle tone, was significantly elevated in patients with premature ejaculation (PE) compared to those without PE (****, P < 0.0001), B The rapid contraction value, reflecting fast-twitch muscle function, was severely impaired in patients with erectile dysfunction (ED) compared to those without ED (****, P < 0.0001). Data are presented as box plots; the central line represents the median, the box shows the interquartile range (25th to 75th percentile), and the whiskers extend to the minimum and maximum values. Group sample sizes are indicated below the X-axis

Discussion

Prostatitis is a group of diseases encompassing acute and chronic prostatitis, often manifesting with lower urinary tract symptoms, pain, and sexual dysfunction. Chronic prostatitis is one of the most common forms, whose symptoms are often refractory to treatment and are closely linked to pelvic floor muscle function [14]. PF-EMG is commonly used to clinically assess pelvic floor muscle function. Clinical studies have reported that early-onset muscle dysfunction in patients is mainly characterized by abnormal electromyographic signals [17, 18]. Relevant studies have shown that pelvic floor muscles (PFM) are closely related to male sexual dysfunction. Strengthening the pelvic floor muscle groups through the combination of manual physical therapy and PFM training can effectively improve erectile dysfunction (ED) and premature ejaculation (PE) [10].The pelvic floor muscles are muscle groups that support pelvic organs (such as the bladder, prostate, and rectum). The pelvic floor (PF) is a multifunctional complex composed of muscle fibers, fascia, ligaments, and connective tissues, forming a hammock at the base of the abdominopelvic cavity. The pelvic floor muscles include superficial muscles, such as the bulbocavernosus muscle, ischiocavernosus muscle, perineal muscles, and external anal sphincter. The deep pelvic floor muscles are the levator ani muscles, consisting of the puborectalis, pubococcygeus, and iliococcygeus muscles. The pelvic floor provides anatomical support for the pelvic and abdominal viscera and is involved in urination, defecation, and sexual function [10]. The relationship between prostatitis and pelvic floor muscles is relatively complex. A growing body of evidence suggests that pelvic floor exercises and manual physical therapy may improve premature ejaculation (PE) and erectile dysfunction (ED) in men [19], Clinically, extracorporeal shock wave therapy (ESWT) treats symptoms of premature ejaculation by enhancing the strength of pelvic floor muscles [20]. The functional status of male pelvic floor muscles can be assessed via electrophysiological tests (e.g., EMG). Studies have found that patients with chronic pelvic pain are accompanied by increased resting tone of pelvic floor muscles and decreased fast-twitch muscle endurance, which indicates that pelvic floor muscle function plays an important role in CP/CPPS [21]. Pelvic floor muscles (PFM) are important muscles involved in male sexual function. It has been reported that weakening of PFM may be one of the causes of erectile dysfunction (ED). When males are sexually stimulated, the bulbocavernosus and ischiocavernosus muscles, which are part of the PFM, contract strongly, increasing blood flow to the penis and thereby maintaining penile erection and rigidity [10]. Pelvic floor muscles play a role in sexual activity. The contraction of the ischiocavernosus and bulbocavernosus muscles leads to an increase in intracavernous pressure. The bulbocavernosus muscle compresses the deep dorsal vein of the penis to prevent blood from flowing out of the engorged penis, ultimately resulting in male erection. This indicates that PFM play an important role in normal erection, and dysfunction of pelvic floor muscles leads to erectile dysfunction [22].

Another significant finding of our study is the identification of a substantial patient subgroup (24.1%) exhibiting both PE and ED. The PF-EMG profile of these patients was characterized by a combination of elevated resting tone and impaired rapid contraction—a ‘mixed’ dysfunction pattern. This observation provides direct electrophysiological evidence that the previously hypothesized distinct pathophysiological mechanisms for PE and ED in CP/CPPS [10, 23] are not mutually exclusive and can co-exist in the same individual. This has profound clinical implications. It suggests that a one-size-fits-all approach to managing CP/CPPS-related SD is inadequate. Instead, PF-EMG can serve as a precision diagnostic tool to identify such patients with complex, mixed dysfunction, guiding a more tailored and potentially sequential treatment strategy—for instance, initially focusing on relaxing hypertonic muscles for PE, followed by strengthening fast-twitch fibers for ED.

CP/CPPS is often accompanied by changes in pelvic floor muscle function, including muscle tension, contractile ability, and relaxation ability, which play an important role in supporting and protecting the morphology and function of the prostate. Patients with prostatitis are often accompanied by persistent pain, which leads to excessive tension of the pelvic floor muscles.

Long-term muscle tension is hypothesized to potentially impair local blood circulation and contribute to a persistent inflammatory or pain-sensitized state [24–26]. Pelvic floor muscles are not exclusive to women; they play an important role in andrological diseases. For example, pelvic floor muscle weakness is closely associated with the occurrence of premature ejaculation, erectile dysfunction, and prostatitis [23], Exercising pelvic floor muscles can reduce congestion and edema in prostatitis, enhance erectile hardness, improve sexual function, and other benefits, thereby alleviating symptoms in CP/CPPS patients and helping men prevent and treat erectile dysfunction and premature ejaculation. The present study found that slow-twitch muscle fatigue leads to decreased ejaculatory control, while high tension (elevated baseline value) reflects pelvic floor muscle spasm, which is consistent with the “pelvic floor muscle hyperactivity” model proposed by Padoa [23]. Fast-twitch muscle failure (e.g., of the bulbocavernosus muscle) impairs the function of the “venous occlusion pump” during erection. The bulbocavernosus muscle is a key component of the “venous occlusion pump” in the process of erection. Contraction of its fast-twitch fibers (type II muscle fibers) compresses the deep dorsal vein of the penis and cavernous sinuses, reducing venous return and thereby maintaining erectile hardness. The rapid contraction value reflects the transient contractile capacity of fast-twitch fibers (such as those of the bulbocavernosus muscle); an increase in this value can enhance cavernous venous compression and maintain erectile pressure.

This study has several limitations that should be considered when interpreting the findings. First, the cross-sectional design precludes the establishment of causality. Second, the diagnoses of erectile dysfunction (ED) and premature ejaculation (PE) relied solely on validated questionnaires, without comprehensive assessments (e.g., penile Doppler ultrasound, hormonal profiles) to exclude all potential organic causes. This is particularly relevant as our univariate analysis identified older age as a significant risk factor for both conditions. While this may reflect the natural progression of CP/CPPS, it also raises the possibility that older patients had a higher burden of undiagnosed vascular or endocrine etiologies, which could confound the results. Third, it is important to acknowledge the heterogeneity of CP/CPPS; we did not subclassify patients into inflammatory (category IIIa) and non-inflammatory (category IIIb) subtypes, which might represent different pathophysiological entities. This very heterogeneity, however, underscores that the neuromuscular dysfunction quantified by PF-EMG in our study may represent a key pathophysiological mechanism underlying sexual dysfunction in a substantial subset of CP/CPPS patients, independent of overt prostatic inflammation. Finally, potential biases associated with the PF-EMG technique itself must be acknowledged, including inter-operator variability in probe placement and signal interpretation, as well as concerns regarding measurement reproducibility. Although all assessments were performed by a single experienced technician to maximize consistency, future studies would benefit from multiple blinded assessors to formally evaluate inter-rater reliability. These limitations highlight the need for future longitudinal research that incorporates more comprehensive organic work-ups and refined patient stratification to better disentangle the contributions of neuromuscular dysfunction from other pathologies. Additionally, the single-center design and relatively modest sample size may limit the generalizability of our findings. Future multi-center studies with larger cohorts are necessary to validate and extend our conclusions.

Conclusion

Patterns of pelvic floor electromyographic dysfunction represent the first objective biomarker for classifying sexual dysfunction subtypes, which can define sexual dysfunction subtypes in CP/CPPS patients: premature ejaculation (PE) is characterized by high tension, while erectile dysfunction (ED) involves fast-twitch muscle failure. This provides the possibility for precise treatment. In the future, attention should be paid to the pelvic floor muscle function status in CP/CPPS patients.

Author contributions

Shiwei SONG: Conceptualization, Methodology, Investigation, Data Curation, Formal Analysis, Writing - Original Draft, Writing - Review & Editing. Bin ZHANG: Resources, Validation, Writing - Review & Editing. Chang YU: Investigation, Data Collection. Jinlong YIN: Investigation, Data Collection. Dehui CHANG: Supervision, Project Administration, Funding Acquisition, Writing - Review & Editing.All authors have read and agreed to the published version of the manuscript.

Funding

This work was supported by the Key Project of University Collaborative Innovation (HXLH-XTCX11), the Central University Project (31920240072), the Natural Science Foundation of Gansu Province (22JR5RA001, 22KYLL195, 23JRRA531, 23JRRA001) and the Science and Technology Project of Lanzhou City (2023-2-63). The funders had no role in the design of the study, data collection, analysis, decision to publish, or preparation of the manuscript.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Conflict of interest

The authors declare no competing interests.