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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: J Mol Cell Cardiol. 2012 Jul 21;53(4):532–541. doi: 10.1016/j.yjmcc.2012.07.004

Figure 3. Increased ventricular K+ current amplitudes with chronic exercise training in animals lacking Akt1 is accompanied by transcriptional upregulation of channel subunits.

Figure 3

The amplitudes of the individual Kv current components, Ito,f, IK,slow, and Iss, as well as of IK1, in the LV apex myocytes from swim-trained and untrained Akt1−/− animals were determined (as described in Methods). Mean ± SEM Ito,f and Iss (at +40 mV) and IK1 (at −120 mV) amplitudes (A) and densities (B) were significantly (‡P<0.05, #P<0.01, *P<0.001) higher in LV apex myocytes from swim-trained, compared with untrained, Akt1−/− animals. Expression levels of the transcripts encoding repolarizing K+ (C–F), as well as depolarizing Na+ and Ca2+ (G), channel subunits were measured in individual LV samples from swim-trained (n=6) and untrained (n=6) Akt1−/− LV, normalized to Hprt and subsequently to the mean value of the untrained Akt1−/− LV samples. The mean ± SEM relative expression levels of many ion channel subunit transcripts were significantly (‡P<0.05, #P<0.01,*P<0.001) higher in swim-trained, than in untrained, Akt1−/− LV.