The effect of high‐intensity training on mitochondrial fat oxidation in skeletal muscle and subcutaneous adipose tissue

Abstract

High-intensity interval training (HIT) is known to increase mitochondrial content in a similar way as endurance training [60-90% of maximal oxygen uptake (VO2peak)]. Whether HIT increases the mitochondria's ability to oxidize lipids is currently debated. We investigated the effect of HIT on mitochondrial fat oxidation in skeletal muscle and adipose tissue. Mitochondrial oxidative phosphorylation (OXPHOS) capacity, mitochondrial substrate sensitivity (K(m)(app)), and mitochondrial content were measured in skeletal muscle and adipose tissue in healthy overweight subjects before and after 6 weeks of HIT (three times per week at 298 ± 21 W). HIT significantly increased VO2peak from 2.9 ± 0.2 to 3.1 ± 0.2 L/min. No differences were seen in maximal fat oxidation in either skeletal muscle or adipose tissue. K(m)(app) for octanoyl carnitine or palmitoyl carnitine were similar after training in skeletal muscle and adipose tissue. Maximal OXPHOS capacity with complex I- and II-linked substrates was increased after training in skeletal muscle but not in adipose tissue. In conclusion, 6 weeks of HIT increased VO2peak. Mitochondrial content and mitochondrial OXPHOS capacity were increased in skeletal muscle, but not in adipose tissue. Furthermore, mitochondrial fat oxidation was not improved in either skeletal muscle or adipose tissue.

Determinants of maximal whole‐body fat oxidation in elite cross‐country skiers: Role of skeletal muscle mitochondria

“…Beyond O 2 , also substrates have to be transported and/or diffuse across the mitochondrial membrane and perhaps this is where the mitochondrial adaptations play a role. While increased OXPHOS p following increased Mito VD is a consistent finding after endurance training (Figure A), FAO p respiration has only been reported in a few studies (untrained moderately trained) with no clear trend emerging thus far . However, as FAO p was substantially higher (51%) in the endurance athletes, the present study demonstrates that highly endurance‐trained athletes indeed have a higher FAO p compared to untrained individuals.…”

Effects of one‐legged high‐intensity interval training on insulin‐mediated skeletal muscle glucose homeostasis in patients with type 2 diabetes

“…However, in absolute terms, mass‐specific mitochondrial respiratory capacity (ie not corrected for mitochondrial content) may increase with a training‐induced mitochondrial biogenesis. The plasticity of mitochondria has been known since the mid‐sixties, and an increase in biomarkers of mitochondrial content in response to high‐intensity training in human muscle has also been shown . In the present study, we found only small increases in some of these biomarkers (Figures and ), but if the mitochondrial biogenesis had been of substantial magnitude, the higher lactate release from the trained legs may not have been seen.…”

An evaluation of low volume high-intensity intermittent training (HIIT) for health risk reduction in overweight and obese men

“…Data is inconclusive as to whether training at intensities above those utilised in the current study lead to better outcomes in aerobic capacity. A number of studies [16, 24, 57–60] in similar populations to those in this work have demonstrated improvements comparable to those at lower intensities [41, 53–56]. It may be interesting to speculate therefore, that a threshold for potential adaptation is reached at approximately 80% V̇O 2max , with further improvements governed by training volume.…”