Wang Y, Henry R P, Wright P M, Heigenhauser G J, Wood C M
Division of Marine Biology and Fisheries, Rosenstiel School of Marine and Atmospheric Science, University of Miami, Miami, Florida 33149, USA.
Am J Physiol. 1998 Dec;275(6):R1766-79. doi: 10.1152/ajpregu.1998.275.6.R1766.
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 NH+4 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 HCO-3-dependent pathway(s) may be involved in glyconeogenesis.
对用盐水灌注的鳟鱼躯干标本进行电刺激，所引发的代谢和呼吸反应与在体内进行力竭运动后出现的反应相当。细胞内酸碱状态的恢复和糖原再合成比在体内更快。与静息肌肉的先前研究相反，与未处理的运动后对照组相比，细胞内碳酸酐酶（ICF CA）阻断使细胞内PCO2升高，而细胞外CA（ECF CA）阻断则没有这种作用。ECF CA阻断对运动后CO2和氨流出仅有短暂影响。相对较小的膜相关CA池似乎被运动诱导的肌肉CO2产生所淹没。跨膜氨流出似乎从静息时主要以NH3形式扩散（由ECF CA促进）转变为运动后主要以NH+4形式移动（与CA无关）。由ECF和ICF CA抑制中的一种或两种引起的细胞内pH恢复延迟与肌肉代谢酸和乳酸排泄减少一致。CA抑制使磷酸肌酸再合成延迟，而ATP补充不受影响。糖原恢复延迟表明HCO-3依赖性途径可能参与糖原异生。
