Immediate force loss after eccentric contractions is increased with L-NAME administration, a nitric oxide synthase inhibitor.
BACKGROUND
Nitric oxide (NO) signaling regulates many biological processes in skeletal muscle, wherein aberrant signaling contributes to myopathic conditions (e.g., Duchenne muscular dystrophy). NO has been shown to play a role in muscle regeneration after injury. However, less is known about its role during injury. In this study we aimed to determine whether NO synthase (NOS) inhibition exacerbates functional deficits immediately after the performance of eccentric contractions.


METHODS
Wild-type mouse extensor digitorum longus (EDL) muscles underwent in vitro functional testing in the presence or absence of a non-specific NOS inhibitor (L-NAME, 10 mM) before and after performance of 10 eccentric contractions.


RESULTS
After eccentric contractions, P(o) was reduced by ∽25% for muscle in regular physiological solution but by ∽50% with the addition of L-NAME (P = 0.009).


CONCLUSIONS
Non-specific blockade of NOS exacerbates functional deficits immediately after eccentric contractions, suggesting that NO signaling protects skeletal muscle from excessive injury in healthy muscle.
Muscle Biology Laboratory, Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia, USA. benjamin.t.corona.ctr@us.army.mil
Benjamin T
BT
Corona
Christopher P
CP
Ingalls
D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D008297:Male; D051379:Mice; D009119:Muscle Contraction / Q000187:drug effects* / Q000502:physiology; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*
D004791:Enzyme Inhibitors; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester