Mitochondrial gene expression in elite cyclists: effects of high-intensity interval exercise

Abstract

Little is known about the effect of training on genetic markers for mitochondrial biogenesis in elite athletes. We tested the hypothesis that low-volume sprint interval exercise (SIE) would be as effective as high-volume interval exercise (IE). Ten male cyclists competing on national elite level (W (max) 403 ± 13 W, VO(2peak) 68 ± 1 mL kg(-1) min(-1)) performed two interval exercise protocols: 7 × 30-s "all-out" bouts (SIE) and 3 × 20-min bouts at ~87% of VO(2peak) (IE). During IE, the work was eightfold larger (1,095 ± 43 vs. 135 ± 5 kJ) and the exercise duration 17 times longer (60 vs. 3.5 min) than during SIE. Muscle samples were taken before and 3 h after exercise. The mRNA of upstream markers of mitochondrial biogenesis [peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1α), PGC-1α-related coactivator (PRC) and peroxisome proliferator-activated receptor δ (PPARδ)] increased to the same extent after SIE and IE (6-, 1.5- and 1.5-fold increase, respectively). Of the downstream targets of PGC-1α, mitochondrial transcription factor A (Tfam) increased only after SIE and was significantly different from that after IE (P < 0.05), whereas others increased to the same extent (pyruvate dehydrogenase kinase, PDK4) or was unchanged (nuclear respiratory factor 2, NRF2). We conclude that upstream genetic markers of mitochondrial biogenesis increase in a similar way in elite athletes after one exercise session of SIE and IE. However, since the volume and duration of work was considerably lower during SIE and since Tfam, the downstream target of PGC-1α, increased only after SIE, we conclude that SIE might be a time-efficient training strategy for highly trained individuals.

Sprint-interval but not continuous exercise increases PGC-1α protein content and p53 phosphorylation in nuclear fractions of human skeletal muscle

“…Similarly, only SIE, and not CE, increased nuclear PGC-1α protein content post-exercise. Although the differential response to SIE and CE may be due to differences in the degree and time course of nuclear p53 and PGC-1α protein accumulation, our findings suggest that SIE may represent a more potent stimulus than CE to induce some of the early molecular events associated with mitochondrial biogenesis, as previously suggested31. An additional novel finding was that the exercise-induced increase in the nuclear content of p53 protein in human skeletal muscle was also accompanied by an increase in the nuclear content of PHF20, a protein that stabilises and activates p5329, but was not differentially regulated by the two types of exercise investigated.…”

The Order of Exercise during Concurrent Training for Rehabilitation Does Not Alter Acute Genetic Expression, Mitochondrial Enzyme Activity or Improvements in Muscle Function

“…Two additional coactivators of mitochondrial biogenesis are PRC [33] and PGC-1β [34] . Acting in a similar manner to PGC-1α, PRC expression is increased with endurance exercise [35] , [36] and enhanced when performed concurrently with resistance exercise [37] . To the contrary, chronic endurance exercise appears to attenuate resting PGC-1β protein content [38] though acute exercise does not affect mRNA values [39] .…”

Pronounced Effects of Acute Endurance Exercise on Gene Expression in Resting and Exercising Human Skeletal Muscle

“…In addition, regulation at the mRNA level importantly contributes to the acute response and chronic adaptations to exercise. A large number of studies have shown that acute exercise induces genes involved in a variety of processes, including energy metabolism, hypertrophy and signalling [13], [14], [15], [16], [17], [18], [19], [20], [21]. Whole genome mRNA profiling has confirmed these findings, revealing major changes in skeletal muscle gene expression from 1 hour to even 48 hours after cessation of exercise [22], [23], [24], [25].…”