TY  - JOUR
A1  - Stratos, Ioannis
A1  - Rinas, Ingmar
A1  - Schröpfer, Konrad
A1  - Hink, Katharina
A1  - Herlyn, Philipp
A1  - Bäumler, Mario
A1  - Histing, Tina
A1  - Bruhn, Sven
A1  - Müller-Hilke, Brigitte
A1  - Menger, Michael D.
A1  - Vollmar, Brigitte
A1  - Mittlmeier, Thomas
T1  - Effects on bone and muscle upon treadmill interval training in hypogonadal male rats
JF  - Biomedicines
N2  - Testosterone deficiency in males is linked to various pathological conditions, including muscle and bone loss. This study evaluated the potential of different training modalities to counteract these losses in hypogonadal male rats. A total of 54 male Wistar rats underwent either castration (ORX, n = 18) or sham castration (n = 18), with 18 castrated rats engaging in uphill, level, or downhill interval treadmill training. Analyses were conducted at 4, 8, and 12 weeks postsurgery. Muscle force of the soleus muscle, muscle tissue samples, and bone characteristics were analyzed. No significant differences were observed in cortical bone characteristics. Castrated rats experienced decreased trabecular bone mineral density compared to sham-operated rats. However, 12 weeks of training increased trabecular bone mineral density, with no significant differences among groups. Muscle force measurements revealed decreased tetanic force in castrated rats at week 12, while uphill and downhill interval training restored force to sham group levels and led to muscle hypertrophy compared to ORX animals. Linear regression analyses showed a positive correlation between bone biomechanical characteristics and muscle force. The findings suggest that running exercise can prevent bone loss in osteoporosis, with similar bone restoration effects observed across different training modalities.
KW  - osteoporosis
KW  - muscle
KW  - force
KW  - bone
KW  - micro-CT
KW  - training
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-319266
SN  - 2227-9059
VL  - 11
IS  - 5
ER  - 
TY  - JOUR
A1  - Stratos, Ioannis
A1  - Behrendt, Ann-Kathrin
A1  - Anselm, Christian
A1  - Gonzalez, Aldebarani
A1  - Mittlmeier, Thomas
A1  - Vollmar, Brigitte
T1  - Inhibition of TNF-α restores muscle force, inhibits inflammation, and reduces apoptosis of traumatized skeletal muscles
JF  - Cells
N2  - Background: Muscle injuries are common in humans and are often associated with irrecoverable damage and disability. Upon muscle injury, TNF-α signaling pathways modulate the healing process and are predominantly associated with tissue degradation. In this study we assumed that TNF-α inhibition could reduce the TNF-α-associated tissue degradation after muscle injury. Materials and methods: Therefore, the left soleus muscle of 42 male Wistar rats was injured using a standardized open muscle injury model. All rats were treated immediately after injury either with infliximab (single i.p. injection; 10 mg/kg b.w.) or saline solution i.p. Final measurements were conducted at day one, four, and 14 post injury. The muscle force, the muscle cell proliferation, the muscle cell coverage as well as the myofiber diameter served as read out parameters of our experiment. Results: Systemic application of infliximab could significantly reduce the TNF-α levels in the injured muscle at day four upon trauma compared to saline treated animals. The ratio of muscle weight to body weight was increased and the twitch muscle force showed a significant rise 14 days after trauma and TNF-α inhibition. Quantification of myofiber diameter in the penumbra zone showed a significant difference between both groups at day one and four after injury, indicated by muscle hypertrophy in the infliximab group. Planimetric analysis of the injured muscle at day 14 revealed increased muscle tissue fraction in the infliximab group compared to the control animals. Muscle cell proliferation did not differ between both groups. Conclusions: These data provide evidence that the TNF-α blockade positively regulates the restauration of skeletal muscles upon injury.
KW  - muscle injury
KW  - regeneration
KW  - infliximab
KW  - tumor necrosis factor alpha
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-286094
SN  - 2073-4409
VL  - 11
IS  - 15
ER  -