Abhinandan Batra1, Ravneet Vohra2, Steve Chrzanowski1, Donovan J Lott1, Glenn A Walter1, Krista Vandenborne1, and Sean C Forbes1
1University of Florida, Gainesville, FL, United States, 2University of Washington, Seattle, WA, United States
Synopsis
This study examined the effects of phosphodiesterase 5A inhibition with sildenafil citrate on skeletal muscle 1H2O T2 in dystrophic mice (mdx) following downhill running and during four weeks of low-intensity treadmill training. Skeletal muscle 1H2O T2 was measured from spectra acquired with a single voxel 1H-MRS STEAM sequence. Our findings showed less altered T2 after downhill running with sildenafil citrate treatment indicating less muscle damage and improved running performance during endurance training. Collectively, the results support the use of sildenafil citrate when combined with acute and chronic bouts of exercise as a potential therapeutic intervention in muscular dystrophies.
Introduction
Duchenne muscular dystrophy (DMD) is characterized by the absence of dystrophin, which is accompanied by lack of sarcolemma localized neuronal nitric oxide synthase (nNOS). This lack of nNOS impairs the ability to blunt sympathetic vasoconstriction, reduces local blood flow, and increases susceptibility to damage in dystrophic muscle(1, 2). To compensate for lack of nNOS, treatments that inhibit phosphodiesterase-5A (PDE5A) have been proposed(3). In this study, we utilized transverse relaxation time constant (T2) of 1H2O, an in vivo marker of skeletal muscle damage(4), to test the hypothesis that a PDE5A inhibitor (sildenafil citrate) will reduce muscle damage following an acute bout of downhill running and during four weeks of progressive low-intensity endurance training in dystrophic (mdx) mice. Methods
Single voxel 1H-MRS data were
acquired using stimulated echo acquisition mode (STEAM; TR 9 s, 10-128 TE’s
exponentially spaced: 5-288 ms, 4 phase cycles) with a 4.7 T Varian/Agilent MR
system to evaluate 1H2O T2 of skeletal muscle
in mdx and wild-type mice (Figure 1). Mice
treated with sildenafil citrate (mdx-sil:
n=14) were compared to untreated mice (mdx:
n=14; wild-type: n=5) before and 24 hours after downhill running and in a subset of mice (5-10/group) were compared weekly during four weeks of horizontal treadmill
running (5 days/week). Data were
acquired from the deep medial compartment (MC) in the lower hindlimbs; this
region has previously been established to be consistently susceptible to muscle
damage following downhill running in mdx
mice(4).
Downhill treadmill running was performed for 30-60 minutes at 6-12 m/min with a
14% grade. Also, a low-intensity
treadmill running program was performed five days/week for four weeks with
weekly increases in intensity and volume (8-12m/min; 25-60min;0o
incline). Spectra were fit with
principal component analysis and 1H2O T2 was
calculated using a monoexponential model. Results
At baseline, 1H2O T2
was greater (p<0.05) in treated and untreated mdx than wild-type mice (Con: 25.5±0.8ms; mdx: 29.4±0.7ms; mdx-sil:
30.4±1.6ms). Following downhill running,
T2 increased (p<0.05) by, on average, 11% in the MC of untreated mdx mice compared to baseline, whereas in
the treated mdx mice, there was no
increase in T2 of the MC (Figure 2).
Also, wild-type mice did not show an increase in T2 following
this downhill running protocol. During four
weeks of treadmill training, T2 did not increase from baseline during
training in wild-type, mdx, or mdx treated with sildenafil; however, the
prescribed distance completed during training was greater in sildenafil treated
mdx mice (98%) and wild-type (100%)
than untreated mdx mice (60%) (Figure
3).Conclusions
Overall, sildenafil citrate diminished the
increase in T2 of skeletal muscles 24 hours after an acute bout of downhill
running in mdx mice, suggesting
reduced muscle damage, possibly by enhancing local blood flow following exercise. Furthermore, sildenafil citrate resulted in
an increase in exercise performance during treadmill training without an associated
increase in muscle T2. Collectively, these results support the use of
sildenafil citrate when combined with acute and chronic bouts of exercise as a
potential therapeutic intervention in DMD.Acknowledgements
This research study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health (R01AR070101), Muscular Dystrophy Association development grant, and the National High Magnetic Field Laboratory.
References
1. Thomas GD, Sander M, Lau KS, Huang PL,
Stull JT, Victor RG. Impaired metabolic modulation of alpha-adrenergic
vasoconstriction in dystrophin-deficient skeletal muscle. Proc Natl Acad Sci U
S A. 1998;95(25):15090-5.
2. Kobayashi YM, Rader EP, Crawford RW,
Iyengar NK, Thedens DR, Faulkner JA, Parikh SV, Weiss RM, Chamberlain JS, Moore
SA, Campbell KP. Sarcolemma-localized nNOS is required to maintain activity
after mild exercise. Nature. 2008;27(456(7221)):511-5.
3. Victor RG, Sweeney HL, Finkel R,
McDonald CM, Byrne B, Eagle M, Goemans N, Vandenborne K, Dubrovsky AL,
Topaloglu H, Miceli MC, Furlong P, Landry J, Elashoff R, Cox D, Group. TDS. A
phase 3 randomized placebo-controlled trial of tadalafil for Duchenne muscular
dystrophy. Neurology. 2017;89(17):1811-20.
4. Mathur S, Vohra RS, Germain SA, Forbes
S, Bryant ND, Vandenborne K, Walter GA. Changes in muscle T2 and tissue damage
after downhill running in mdx Mice. Muscle Nerve. 2011;43(6):878-86.