Respiratory and metabolic functions of carbonic anhydrase in exercised white muscle of trout

Yuxiang Wang, Raymond P. Henry, Pamela M. Wright, George J.F. Heigenhauser, Chris M. Wood

Research output: Contribution to journalArticle

25 Scopus citations

Abstract

Electrical stimulation of a trout saline-perfused trunk preparation resulted in metabolic and respiratory responses comparable to those occurring after exhaustive exercise in vivo. Recovery of intracellular acid-base status and glycogen resynthesis were faster than in vivo. Intracellular carbonic anhydrase (ICF CA) blockade elevated intracellular PCO2 relative to untreated postexercise controls, whereas extracellular CA (ECF CA) blockade did not, in contrast to previous work with muscle at rest. ECF CA blockade had only a transient effect on postexercise CO2 and ammonia efflux. The relatively small pool of membrane-associated CA appears to be overwhelmed by exercise-induced CO2 production in muscle. Transmembrane ammonia efflux appears to shift from diffusion primarily as NH3 at rest, which is facilitated by ECF CA, to movement predominantly as NH4/+ after exercise, which is independent of CA. The postponed recovery of intracellular pH caused by either or both ECF and ICF CA inhibition was consistent with reduced metabolic acid and lactate excretion from muscle. Creatine phosphate resynthesis was delayed by CA inhibition, whereas ATP replenishment was not affected. Delayed glycogen recovery indicates that HCO3/--dependent pathway(s) may be involved in glyconeogenesis.

Original languageEnglish (US)
Pages (from-to)R1766-R1779
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume275
Issue number6 44-6
StatePublished - Dec 1 1998

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Keywords

  • Acetazolamide
  • Acid-base regulation
  • Ammonia
  • Benzolamide
  • Carbonic anhydrase inhibition
  • Energy-rich phosphates
  • Glycolytic metabolism

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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