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O2 during low- and high-intensity
contractions
1 School of Rehabilitation Therapy, 2 Department of Physiology, and 3 Department of Surgery, Queen's University, Kingston, Ontario, Canada K7L 3N6
In the present
study, we determined whether endothelin (ET)-1 contributed to the
observed reduction in muscle blood flow (
) during contractions
with nitric oxide synthase (NOS) inhibition and whether muscle
O2 uptake (
O2) would
be affected by the decrease in muscle
with NOS inhibition at
different contraction intensities. Muscle
,
O2, O2 extraction ratio
(OER), and tension development (TD) were studied in the in situ
gastrocnemius muscle preparation in anesthetized dogs. A decrease in
the
O2-to-TD ratio
(
O2/TD) was used as an indicator
of O2 limitation. Three contraction protocols were used:
1) isometric twitch contractions at 2 twitches (tw)/s, 2) the same contractions at 4 tw/s, and 3)
pretreatment with an ETA-receptor antagonist (BQ-123)
before 2 tw/s contractions. The muscle was stimulated to contract, and
measures were obtained at steady state (~5-8 min). NOS
inhibition (N
-nitro-L-arginine
methyl ester) was then induced, and measures were repeated at 2, 5, 10, and 15 min. During 2 tw/s contractions, NOS inhibition reduced
with and without ETA-receptor blockade. In both groups, OER
increased in response to the fall in
, with the result being no
change in
O2/TD. NOS inhibition
also decreased
during 4 tw/s contractions, but OER did not
increase, resulting in a reduction in
O2/TD 5 and 15 min after
N
-nitro-L-arginine methyl ester.
These data indicated that 1) a reciprocal increase in ET-1
during NOS inhibition does not influence active hyperemia in skeletal
muscle, and 2) during 4 tw/s contractions, the
ischemia with NOS inhibition was associated with either an O2 limitation or an alteration in the efficiency of muscle contractions.
fatigue; oxygen extraction; tension development; oxygen demand
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