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

Abstract

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.

Effect of intermittent hypoxic training on HIF gene expression in human skeletal muscle and leukocytes

“…As suggested by a past study performed on rats adapted to chronic hypobaric hypoxia, the mechanism of HIF-1 gene activation depends on the diVerences in vascular perfusion and oxygen-carrying functions particular to the tissue being studied . This diVerence in RNA regulation between muscle and blood compartment contradicts previous Wndings reporting similar adaptations (correlations) in serum and muscle with exercise in normoxia (Zeibig et al 2005). Indeed, the authors found a concomitant stimulation of Wve genes in blood cells and muscle tissue after a period of endurance training.…”

“…Furthermore, the subjects followed a low-intensity training program. Given the diVerences between biopsy sampling protocols do not justify the discrepancy, the present results suggest the relationships identiWed by Zeibig et al (2005) are not universally valid for training eVects. The current results indicate a rejection of the proposed use of RNA measures in blood as a replacement of muscle biopsies for diagnostic measures on muscle adaptations to exercise.…”

“…Finally, Zeibig et al (2005) showed levels of mRNA in blood cells correlated signiWcantly with those in muscle tissue from the same donors after 6-month endurance training. The objective of our laboratory was to determine the impact of IHE on hif, ahif, vegf, and mct4 gene expression in skeletal muscle and to compare these data with gene expression at the leukocytes level.…”

A Combination of (ω–3) Polyunsaturated Fatty Acids, Polyphenols and <i>L</i>-Carnitine Reduces the Plasma Lipid Levels and Increases the Expression of Genes Involved in Fatty Acid Oxidation in Human Peripheral Blood Mononuclear Cells and HepG2 Cells

“…As previously shown, PBMCs mimic mitochondrial gene expression profile alterations in muscle after 6 months of endurance training in young athletes [11]. Moreover, fasting has a profound effect on gene expression in PBMCs, in particular on PPARα [17,18].…”

“…This has been shown in distinct models of glucose intolerance like aging, high-fat feeding and genetic diabetes [6]. In cell culture experiments, in animal studies, as well as in human trials we demonstrated that L -carnitine administration significantly increased the relative mRNA abundances of genes involved in fatty acid (FA) catabolism, such as carnitine palmitoyltransferases-1 (CPT1) and carnitine acetyltransferase (CrAT) [9,10,11]. CPT1 is the rate-limiting enzyme for FA oxidation in all tissues and exists in at least three isoforms, a liver form (CPT1A) expressed in liver and many other tissues, a smaller counterpart (CPT1B) found in adipose tissue, testis, cardiac and skeletal muscle, and CPT1C in the brain [12].…”