Taurine supplementation increases skeletal muscle force production and protects muscle function during and after high-frequency in vitro stimulation.
Recent studies report that depletion and repletion of muscle taurine (Tau) to endogenous levels affects skeletal muscle contractility in vitro. In this study, muscle Tau content was raised above endogenous levels by supplementing male Sprague-Dawley rats with 2.5% (wt/vol) Tau in drinking water for 2 wk, after which extensor digitorum longus (EDL) muscles were examined for in vitro contractile properties, fatigue resistance, and recovery from fatigue after two different high-frequency stimulation bouts. Tau supplementation increased muscle Tau content by approximately 40% and isometric twitch force by 19%, shifted the force-frequency relationship upward and to the left, increased specific force by 4.2%, and increased muscle calsequestrin protein content by 49%. Force at the end of a 10-s (100 Hz) continuous tetanic stimulation was 6% greater than controls, while force at the end of the 3-min intermittent high-frequency stimulation bout was significantly higher than controls, with a 12% greater area under the force curve. For 1 h after the 10-s continuous stimulation, tetanic force in Tau-supplemented muscles remained relatively stable while control muscle force gradually deteriorated. After the 3-min intermittent bout, tetanic force continued to slowly recover over the next 1 h, while control muscle force again began to decline. Tau supplementation attenuated F(2)-isoprostane production (a sensitive indicator of reactive oxygen species-induced lipid peroxidation) during the 3-min intermittent stimulation bout. Finally, Tau transporter protein expression was not altered by the Tau supplementation. Our results demonstrate that raising Tau content above endogenous levels increases twitch and subtetanic and specific force in rat fast-twitch skeletal muscle. Also, we demonstrate that raising Tau protects muscle function during high-frequency in vitro stimulation and the ensuing recovery period and helps reduce oxidative stress during prolonged stimulation.
Goodman
Craig A
CA
School of Human Movement, Recreation and Performance, Victoria University, Melbourne, Victoria, Australia. goodmanc@unimelb.edu.au
Horvath
Deanna
D
Stathis
Christos
C
Mori
Trevor
T
Croft
Kevin
K
Murphy
Robyn M
RM
Hayes
Alan
A
D000818:Animals; D002135:Calcium-Binding Proteins; D002155:Calsequestrin; D002352:Carrier Proteins / Q000032:analysis / Q000378:metabolism; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis / Q000378:metabolism; D026901:Membrane Transport Proteins / Q000032:analysis / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects* / Q000502:physiology; D018763:Muscle Fatigue / Q000187:drug effects* / Q000502:physiology; D018656:Muscle Fibers, Fast-Twitch / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000737:chemistry / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013654:Taurine / Q000008:administration & dosage* / Q000032:analysis; D014881:Water Supply; D000099247:Taurine Transporters
D002135:Calcium-Binding Proteins; D002155:Calsequestrin; D002352:Carrier Proteins; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins; D013654:Taurine; D000099247:Taurine Transporters; C057137:Casq1 protein, rat