Tendon structural adaptations to load exercise are inhibited by anabolic androgenic steroids.

The present study investigated the structural changes in the rat calcaneal tendon (CT), superficial flexor tendon (SFT), and deep flexor tendon (DFT) in response to jump exercises and anabolic androgenic steroids (AAS). Animals were divided into four groups: sedentary, trained, AAS-treated sedentary rats, and AAS-treated trained animals. Training increased the volume density (Vv%) of blood vessels in all regions of the CT and DFT, cell Vv% in the peritendinous sheath of the proximal and distal regions of the SFT and proximal region of DFT, and cell Vv% in the tendon proper of the proximal and distal regions of the SFT and DFT. The combination of AAS and load exercises showed little increased blood vessel Vv% at the proximal region of the CT, intermediate region of the SFT, and all regions of the DFT as opposed to an increase in adipose cell Vv% in the CT proximal region. The AAS reduced the levels of hydroxyproline in the proximal region of the DFT and in the distal region of the STF. In conclusion, exercise promoted benefits to the adaptation of the tendons to overload. These effects were absent when load exercise was combined with AAS. The abusive consumption of AAS contributes to tendon inertness and rigidity, and increases the potential risk of injury.

Nandrolone inhibits MMP-2 in the left ventricle of rats.

The indiscriminate use of anabolic-androgenic steroids has been shown to induce left ventricular dysfunctions. The main objective of the present study was to investigate the effects of nandrolone decanoate on matrix metalloprotease (MMP-2) activity and protein level in the left ventricle (LV) of rats after 7 weeks of mechanical load exercise. Wistar rats were grouped into: sedentary (S); nandrolone decanoate-treated sedentary (AAS); trained without AAS (T) and trained and treated with AAS (AAST). Exercised groups performed a 7-weeks water-jumping program. Training significantly increased the MMP-2 activity by zymography and the protein level by Western blotting analysis. However, the AAS treatment abolished both the increase in MMP activity and protein level induced by exercise. These results suggest that AAS may impair cardiac tissue remodeling which may lead to the heart malfunction.

Biomechanical responses of different rat tendons to nandrolone decanoate and load exercise.

Androgenic-anabolic steroids (AAS) have been associated with an increased incidence of tendon rupture. The aim of this study was to compare the biomechanical properties of the rat calcaneal tendon (CT), superficial flexor tendon (SFT), and deep flexor tendon (DFT), and to determine the effect of jump training in association with AAS. Animals were separated into four groups: sedentary, trained, AAS-treated sedentary rats (AAS), and AAS-treated and trained animals. Mechanical testing showed that the CT differed from the DFT and SFT, which showed similar mechanical properties. Jump caused the CT to exhibit an extended toe region, an increased resistance to tensional load, and a decreased elastic modulus, characteristics of an elastic tendon capable of storing energy. AAS caused the tendons to be less compliant, and the effects were reinforced by simultaneous training. The DFT was the most affected by training, AAS, and the interaction of both, likely because of its involvement in the toe-off step of jumping, which we suggest is related to the rapid transmission of force as opposed to energy storage. In conclusion, tendons are differently adapted to exercise, but responded equally to AAS, showing reduced flexibility, which is suggested to increase the risk of tendon rupture in AAS consumers.

MMP-2, jumping exercise and nandrolone in skeletal muscle.

Matrix metalloproteinases (MMPs) are crucial to the development and maintenance of healthy tissue. The aim of this study was to investigate MMP-2 activity in gastrocnemius, soleus, extensor digitorium longus (EDL) and tibialis anterior (TA) muscles after exercise associated with an anabolic androgenic steroid (AAS). Wistar rats were grouped into: sedentary (S); sedentary with AAS (AAS); trained without (T) and with (AAST) AAS. Exercised groups performed a 7-week water-jumping program. The exercise increased MMP-2 activity in gastrocnemius and soleus, but not in TA and EDL. The AAS treatment decreased MMP-2 activity of EDL, as compared to the S group, with no effect in gastrocnemius and soleus. The association of AAS and training restored the normal MMP activity of EDL. Training increases tissue turnover in primary motor muscles, which in turn respond differently to AAS treatment. This data may be useful for a better understanding of muscular physiology under AAS use.