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1 The Centre for Activity and Ageing, School of Kinesiology and Departments of 2 Physiology and 3 Medical Biophysics, University of Western Ontario, London, Ontario N6A 3K7; and 4 Lawson Research Institute, St. Joseph's Health Centre, London, Ontario, Canada N6A 4V2
The
effects of acetazolamide (Acz)-induced carbonic anhydrase inhibition
(CAI) on muscle intracellular thresholds (T) for intracellular pH
(pHi) and inorganic phosphate-to-phosphate creatine ratio
(Pi/PCr) and the plasma lactate (La
)
threshold were examined in nine adult male subjects performing forearm
wrist flexion exercise to fatigue. Exercise consisted of raising and
lowering (1-s contraction, 1-s relaxation) a cylinder whose volume
increased at a rate of 200 ml/min. The protocol was performed during
control (Con) and after 45 min of CAI with Acz (10 mg/kg body wt iv).
TpHi and TPi/PCr,
determined using 31P-labeled magnetic resonance
spectroscopy (MRS), were similar in Acz (722 ± 50 and 796 ± 75 mW, respectively) and Con (855 ± 211 and 835 ± 235 mW,
respectively). The pHi was similar at end-exercise (6.38 ± 0.10 Acz and 6.43 ± 0.22 Con), but pHi
recovery was slowed in Acz. In a separate experiment, blood was sampled
from a deep arm vein at the elbow for determination of plasma lactate
concentration ([La
]pl) and
TLa
. [La
]pl was
lower (P < 0.05) in Acz than Con (3.7 ± 1.7 vs.
5.0 ± 1.7 mmol/l) at end-exercise and in early recovery, but
TLa
was higher (1,433 ± 243 vs.
1,041 ± 414 mW, respectively). These data suggest that the lower
[La
]pl seen with CAI was not due to a
delayed onset or rate of muscle La
accumulation but may
be related to impaired La
removal from muscle.
intracellular threshold; acid-base; acetazolamide; lactate; intracellular pH
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