Oestrogen and progesterone are the primary reproductive hormones in females, and are known for their neuroactive properties, with oestrogen typically exhibiting excitatory effects and progesterone exerting inhibitory effects [1]. However, existing research investigating the effects of hormonal fluctuations throughout the menstrual cycle (MC) on neuromuscular function and performance has yielded inconsistent results [2]. Muscle force production depends on the recruitment of progressively larger motor units (MUs) and an increase in MU discharge rate. The ability to control force production is critical for functional tasks such as walking, dexterity, and fall prevention. These are particularly relevant in clinical settings and sports, for example non-contact anterior cruciate ligament (ACL) injuries are more common in female athletes and are partly linked to neuromuscular control [3]. No studies have yet quantified the MU adaptations in both the vastus medialis (VM) and vastus lateralis (VL) in conjunction with reproductive hormone fluctuations across the MC. Therefore, this study aimed to assess knee-extensor strength, force steadiness, and VM and VL activation using high density surface electromyography (HDsEMG) across different timepoints of the MC.
Ten recreationally active, eumenorrheic females (age: 30 ± 8 years; BMI: 24 ± 2.8 kg/m2) were recruited. Their MCs were tracked (mean cycle length: 28 ± 3 days; luteinizing hormone surge detected on 14 ± 2 days) prior to and during participation. Blood samples were collected at the early follicular (EF), pre-ovulatory (Ov), and mid-luteal (ML) phases to determine circulating levels of 17β-oestradiol and progesterone. Knee extensor maximum voluntary contraction (MVC) was recorded, and neuromuscular control was assessed through isometric trapezoid contractions at 40% and 75% MVC, with real-time visual target feedback. A 64-channel HDsEMG electrode was placed over the VM and VL during contractions and root mean square (RMS) EMG (activation) was calculated as the highest amplitude within a 50ms window and reported as a ratio of maximum RMS EMG. One-way ANOVA and a mixed-effect model were used to assess differences between MC timepoints, with p < 0.05 indicating statistical significance.
Serum concentrations of 17β-oestradiol and progesterone varied significantly across the MC (17β-oestradiol: EF, 159pg/ml; Ov, 200pg/ml; ML, 208pg/ml; p=0.028; progesterone: EF, 11.96ng/ml; Ov, 12.11ng/ml; ML, 39.27ng/ml; p=0.036). Despite these hormonal fluctuations, no significant differences were observed in knee extensor maximal strength (EF:408N, Ov:395N, ML:419N, p=0.393). Similarly, no differences were found in normalised VM and VL RMS EMG (VM: EF, 58%; Ov, 49%; ML, 55%, p=0.324; VL: EF, 54%; Ov, 60%; ML, 50%, p=0.775) or in neuromuscular control during the hold phase at 40% (p=0.756) and 75% MVC (p=0.895), during the ascent phase at 40% (p=1.096) and 75% (p=0.739), or the descent phase at 40% (p=0.097) and 75% (p=0.604).
These findings suggest that fluctuations in reproductive hormones across the MC have minimal influence on VM and VL activation and knee extensor neuromuscular performance. However, further research is necessary to investigate additional factors of neuromuscular performance, such as individual MU characteristics across varying contraction levels and performance measures, to better understand the disparity in non-contact ACL injury rates between males and females.