As androgens might have rapid androgen-receptor (AR) independent action on muscle cells, we analysed the in vivo acute effect of androgens on maximal force generation capacity and electrically evoked calcium transient responsible for the excitation-contraction coupling in skeletal muscle from wild-type male mice and muscle fibre androgen receptor (AR) deficient (AR(skm-/y)) male mice. We tested the hypothesis that acute in vivo androgen treatment improves contractility and modifies calcium transient in mouse hindlimb muscles. In addition, we determined whether the reduced maximal force generation capacity of AR(skm-/y) mice is caused by an alteration in calcium transient. We found that acute dehydrotestosterone (DHT) and testosterone treatment of mice does not change in situ maximal force, power or fatigue resistance of tibialis anterior muscles. In agreement with this observation, maximal force and twitch kinetics also remained unchanged when both whole extensor digitorum longus (EDL) muscle or fibre bundles were incubated in vitro with DHT. Electrically evoked calcium transient, i.e. calcium amplitude, time to peak and decay, was also not modified by DHT treatment of EDL muscle fibre bundles. Finally, we found no difference in calcium transient between AR(skm-/y) and wild-type mice despite the reduced maximal force in EDL fibre bundles of AR(skm-/y) mice. In conclusion, acute androgen treatment has no ergogenic effect on muscle contractility and does not affect calcium transient in response to stimulation. In addition, the reduced maximal force of AR(skm-/y) mice is not related to calcium transient dysfunction.
Keywords: Androgen; Androgen receptor deficient mice; Maximal force; Rapid action; Skeletal muscle.
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