Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Standard

Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle. / Søndergård, Stine D; Dela, Flemming; Helge, Jørn W; Larsen, Steen.

I: European Journal of Sport Science, Bind 16, Nr. 7, 10.2016, s. 801-807.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Søndergård, SD, Dela, F, Helge, JW & Larsen, S 2016, 'Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle', European Journal of Sport Science, bind 16, nr. 7, s. 801-807. https://doi.org/10.1080/17461391.2015.1130750

APA

Søndergård, S. D., Dela, F., Helge, J. W., & Larsen, S. (2016). Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle. European Journal of Sport Science, 16(7), 801-807. https://doi.org/10.1080/17461391.2015.1130750

Vancouver

Søndergård SD, Dela F, Helge JW, Larsen S. Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle. European Journal of Sport Science. 2016 okt.;16(7):801-807. https://doi.org/10.1080/17461391.2015.1130750

Author

Søndergård, Stine D ; Dela, Flemming ; Helge, Jørn W ; Larsen, Steen. / Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle. I: European Journal of Sport Science. 2016 ; Bind 16, Nr. 7. s. 801-807.

Bibtex

@article{6ae677df58f44c26b3590ffcbf872d09,
title = "Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle",
abstract = "Actovegin, a deproteinized haemodialysate of calf blood, is suggested to have ergogenic properties, but this potential effect has never been investigated in human skeletal muscle. To investigate this purported ergogenic effect, we measured the mitochondrial respiratory capacity in permeabilized human skeletal muscle fibres acutely exposed to Actovegin in a low and in a high dose. We found that Actovegin, in the presence of complex I-linked substrates increased the oxidative phosphorylation (OXPHOS) capacity significantly in a concentration-dependent manner (19 ± 3, 31 ± 4 and 45 ± 4 pmol/mg/s). Maximal OXPHOS capacity with complex I and II-linked substrate was increased when the fibres were exposed to the high dose of Actovegin (62 ± 6 and 77 ± 6 pmol/mg/s) (p < .05). The respiratory capacity of the electron transfer system as well as Vmax and Km were also increased in a concentration-dependent manner after Actovegin exposure (70 ± 6, 79 ± 6 and 88 ± 7 pmol/mg/s; 13 ± 2, 25 ± 3 and 37 ± 4 pmol/mg/s; 0.08 ± 0.02, 0.21 ± 0.03 and 0.36 ± 0.03 mM, respectively) (p < .05). In summary, we report for the first time that Actovegin has a marked effect on mitochondrial oxidative function in human skeletal muscle. Mitochondrial adaptations like this are also seen after a training program in human subjects. Whether this improvement translates into an ergogenic effect in athletes and thus reiterates the need to include Actovegin on the World Anti-Doping Agency's active list remains to be investigated.",
author = "S{\o}nderg{\aa}rd, {Stine D} and Flemming Dela and Helge, {J{\o}rn W} and Steen Larsen",
year = "2016",
month = oct,
doi = "10.1080/17461391.2015.1130750",
language = "English",
volume = "16",
pages = "801--807",
journal = "European Journal of Sport Science",
issn = "1746-1391",
publisher = "Taylor & Francis",
number = "7",

}

RIS

TY - JOUR

T1 - Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle

AU - Søndergård, Stine D

AU - Dela, Flemming

AU - Helge, Jørn W

AU - Larsen, Steen

PY - 2016/10

Y1 - 2016/10

N2 - Actovegin, a deproteinized haemodialysate of calf blood, is suggested to have ergogenic properties, but this potential effect has never been investigated in human skeletal muscle. To investigate this purported ergogenic effect, we measured the mitochondrial respiratory capacity in permeabilized human skeletal muscle fibres acutely exposed to Actovegin in a low and in a high dose. We found that Actovegin, in the presence of complex I-linked substrates increased the oxidative phosphorylation (OXPHOS) capacity significantly in a concentration-dependent manner (19 ± 3, 31 ± 4 and 45 ± 4 pmol/mg/s). Maximal OXPHOS capacity with complex I and II-linked substrate was increased when the fibres were exposed to the high dose of Actovegin (62 ± 6 and 77 ± 6 pmol/mg/s) (p < .05). The respiratory capacity of the electron transfer system as well as Vmax and Km were also increased in a concentration-dependent manner after Actovegin exposure (70 ± 6, 79 ± 6 and 88 ± 7 pmol/mg/s; 13 ± 2, 25 ± 3 and 37 ± 4 pmol/mg/s; 0.08 ± 0.02, 0.21 ± 0.03 and 0.36 ± 0.03 mM, respectively) (p < .05). In summary, we report for the first time that Actovegin has a marked effect on mitochondrial oxidative function in human skeletal muscle. Mitochondrial adaptations like this are also seen after a training program in human subjects. Whether this improvement translates into an ergogenic effect in athletes and thus reiterates the need to include Actovegin on the World Anti-Doping Agency's active list remains to be investigated.

AB - Actovegin, a deproteinized haemodialysate of calf blood, is suggested to have ergogenic properties, but this potential effect has never been investigated in human skeletal muscle. To investigate this purported ergogenic effect, we measured the mitochondrial respiratory capacity in permeabilized human skeletal muscle fibres acutely exposed to Actovegin in a low and in a high dose. We found that Actovegin, in the presence of complex I-linked substrates increased the oxidative phosphorylation (OXPHOS) capacity significantly in a concentration-dependent manner (19 ± 3, 31 ± 4 and 45 ± 4 pmol/mg/s). Maximal OXPHOS capacity with complex I and II-linked substrate was increased when the fibres were exposed to the high dose of Actovegin (62 ± 6 and 77 ± 6 pmol/mg/s) (p < .05). The respiratory capacity of the electron transfer system as well as Vmax and Km were also increased in a concentration-dependent manner after Actovegin exposure (70 ± 6, 79 ± 6 and 88 ± 7 pmol/mg/s; 13 ± 2, 25 ± 3 and 37 ± 4 pmol/mg/s; 0.08 ± 0.02, 0.21 ± 0.03 and 0.36 ± 0.03 mM, respectively) (p < .05). In summary, we report for the first time that Actovegin has a marked effect on mitochondrial oxidative function in human skeletal muscle. Mitochondrial adaptations like this are also seen after a training program in human subjects. Whether this improvement translates into an ergogenic effect in athletes and thus reiterates the need to include Actovegin on the World Anti-Doping Agency's active list remains to be investigated.

U2 - 10.1080/17461391.2015.1130750

DO - 10.1080/17461391.2015.1130750

M3 - Journal article

C2 - 26744809

VL - 16

SP - 801

EP - 807

JO - European Journal of Sport Science

JF - European Journal of Sport Science

SN - 1746-1391

IS - 7

ER -

ID: 167805902