There was a significant difference in the angle between testosterone-treated and control groups where testosterone caused a decrease in the passive ROM. The degree of knee joint angle (differences between passive flexion and extension) is shown in Figure 1. Additionally, the involvement of the androgen receptor and testosterone active metabolite, 5α-DHT, in mediating testosterone effect was also investigated.
In contrast to the microdialysis experiment, OC use decreased resting collagen synthesis, and neither group saw an increase in collagen incorporation into the patellar tendon after exercise (Hansen et al., 2009a). Many of these studies have focused on collagen synthesis and the interactions between estrogen and exercise. There have been a number of elegant studies performed in women that have tried to establish the mechanism underlying the effect of estrogen on tendon health. Therefore, periodic rises in estrogen levels are necessary for the protective effect on tendon and muscle health. As discussed above, an increase in muscle damage is consistent with an increase in tendon stiffness that decreases shielding of the muscle from strain injury.
Clayton and Court-Brown reported an incidence rate for quadriceps tendon ruptures of 1.37 per 100,000 person years in the United Kingdom with a mean age of 50.5 years and 51.7 years in male and female patients, respectively. These injuries occur on a spectrum, ranging from mild strains or contusions of the muscle belly to more severe quadriceps tendon ruptures that can lead to surgery. For those considering orthobiologic treatments, consulting with specialists to assess and optimize testosterone levels may be a key step in strengthening recovery and achieving optimal outcomes. In men, testosterone can enhance tendon stiffness due to an enhanced tendon collagen turnover and collagen content, but testosterone has also been linked to a reduced responsiveness to relaxin. Yet, in active young female athletes, physiological high concentration of estrogen may enhance the risk of injuries due to reduced fibrillar crosslinking and enhanced joint laxity. Alternative treatments for ligament injuries if testosterone is not an option include physical therapy, bracing, platelet-rich plasma (PRP) injections, and, in severe cases, surgery.
The ratio of each target band/β actin was calculated using Image J version 1.46j (National Institutes of Health, Bethesda, MD, USA) and was considered as the expression level of the target proteins. Patellar tendon and lateral collateral ligament from rat’s left hind leg were separated from fat and rinsed with 0.1% phosphate buffer solution. Patellar tendon and lateral collateral ligament were harvested from rat left hind limb and was kept in RNALater solution (Ambion, Calsbad, CA, USA) prior to RNA extraction. A day after the last day of treatment, rats were anaesthetized and knee passive ROM was determined using a digital miniature goniometer (Figure 6). Testosterone could affect female knee laxity as its level was reported to be the highest in the ovulatory phase of the menstrual cycle . DHT has also been reported to cause an increase in the twitch and titanic contraction of fast-twitch skeletal muscle in mice .
The authors found no significant difference in myofibrillar protein synthesis between phases (Miller et al., 2005). Beyond the metabolic roles, estrogen is clearly beneficial for muscle mass and strength, at least in animal models (McClung et al., 2006; Kitajima and Ono, 2016). Within these tissues, estrogen is known to regulate metabolism (Nelson and Bulun, 2001), however, it is still unclear whether these effects are beneficial or harmful. These pills typically maintain estradiol levels at ~25 pg/ml and decrease the ovulatory rise in estrogen (Mishell et al., 1972). Beyond the nucleus, estrogen has a variety of post-transcriptional effects such as regulating the redox state of the cell (Kumar et al., 2010), altering mitochondrial function (Yao and Brinton, 2012), and directly inhibiting the activity of specific enzymes (Lee C. A. et al., 2015). As a steroidal hormone, estrogen can freely pass through the plasma membrane and move into the nucleus where it can bind to its nuclear receptors, the estrogen receptors (ER)α and β, and modify gene expression (Heldring et al., 2007). In young women, estrogen is produced from cholesterol in a series of reactions within the ovaries.