Do blood cells mimic gene expression profile alterations known to occur in muscular adaptation to endurance training?

Exercise is known to upregulate mRNA synthesis for carnitine palmitoyl transferase1 (CPT1) and possibly also other mitochondrial carnitine acyltransferases in muscle tissue. The aim of this study was to test whether such an adaptation of oxidative metabolism in skeletal muscle is a systemic process and consequently, also affects other cells. Messenger RNA levels of five genes [carnitine palmitoyl transferases 1 and 2 (CPT1 and CPT2), carnitine acetyltransferase (CRAT), carnitine palmitoyltransferase 2 (CPT2), microsomal carnitine palmitoyltransferase (GRP58) and organic cation transporter (OCTN2)] were determined with quantitative real time polymerase chain reaction (PCR) in blood cells and in muscle biopsy samples from six cross country skiers before and 6 months after a high volume/low intensity exercise training, when training had elicited a significantly slower rate of lactate accumulation. Quantitative real time PCR showed that levels of mRNA in blood cells correlated significantly (CPT1B: P< 0.001) with those in muscle tissue from the same donors. After 6-months training, there was a 15-fold upregulation of CPT1B mRNA, a six to ninefold increase of CRAT mRNA, of CPT2 mRNA, GRP58 mRNA, and of OCTN2 mRNA. The observation of a concordant stimulation of CPT1, CPT2, CRAT, GRP58 and OCTN2 transcription in blood cells and muscle tissue after 6-month-endurance training leads the hypothesis of a common stimulation mechanism other than direct mechanical stress or local chemical environment, but rather humoral factors.