Depressed Na+-K+-ATPase activity in skeletal muscle at fatigue is correlated with increased Na+-K+-ATPase mRNA expression following intense exercise

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Abstract
We investigated whether depressed muscle Na+-K+-ATPase activity with exercise reflected a loss of Na+-K+-ATPase units, the time course of its recovery postexercise, and whether this depressed activity was related to increased Na+-K+-ATPase isoform gene expression. Fifteen subjects performed fatiguing, knee extensor exercise at ∼40% maximal work output per contraction. A vastus lateralis muscle biopsy was taken at rest, fatigue, 3 h, and 24 h postexercise and analyzed for maximal Na+-K+-ATPase activity via 3-O-methylfluorescein phosphatase (3-O-MFPase) activity, Na+-K+-ATPase content via [3H]ouabain binding sites, and Na+-K+-ATPase α1-, α2-, α3-, β1-, β2- and β3-isoform mRNA expression by real-time RT-PCR. Exercise [352 (SD 267) s] did not affect [3H]ouabain binding sites but decreased 3-O-MFPase activity by 10.7 (SD 8)% (P < 0.05), which had recovered by 3 h postexercise, without further change at 24 h. Exercise elevated α1-isoform mRNA by 1.5-fold at fatigue (P < 0.05). This increase was inversely correlated with the percent change in 3-O-MFPase activity from rest to fatigue (%Δ3-O-MFPaserest-fatigue) (r = −0.60, P < 0.05). The average postexercise (fatigue, 3 h, 24 h) α1-isoform mRNA was increased 1.4-fold (P < 0.05) and approached a significant inverse correlation with %Δ3-O-MFPaserest-fatigue (r = −0.56, P = 0.08). Exercise elevated α2-isoform mRNA at fatigue 2.5-fold (P < 0.05), which was inversely correlated with %Δ3-O-MFPaserest-fatigue (r = −0.60, P = 0.05). The average postexercise α2-isoform mRNA was increased 2.2-fold (P < 0.05) and was inversely correlated with the %Δ3-O-MFPaserest-fatigue (r = −0.68, P < 0.05). Nonsignificant correlations were found between %Δ3-O-MFPaserest-fatigue and other isoforms. Thus acute exercise transiently decreased Na+-K+-ATPase activity, which was correlated with increased Na+-K+-ATPase gene expression. This suggests a possible signal-transduction role for depressed muscle Na+-K+-ATPase activity with exercise.