High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle

Abstract

The effect of high‐intensity training (HIT) on mitochondrial ADP sensitivity and respiratory capacity was investigated in human skeletal muscle and subcutaneous adipose tissue (SAT). Twelve men and women underwent 6 weeks of HIT (7 × 1 min at app. 100% of maximal oxygen uptake (VO 2max)). Mitochondrial respiration was measured in permeabilized muscle fibers and in abdominal SAT. Mitochondrial ADP sensitivity was determined using Michaelis Menten enzyme kinetics. VO 2max, body composition and citrate synthase (CS) activity (skeletal muscle) and mtDNA (SAT) were measured before and after training. VO 2max increased from 2.6 ± 0.2 to 2.8 ± 0.2 L O2/min (P = 0.011) accompanied by a decreased mitochondrial ADP sensitivity in skeletal muscle (K m: 0.14 ± 0.02 to 0.29 ± 0.03 mmol/L ADP (P = 0.002)), with no changes in SAT (K m: 0.12 ± 0.02 to 0.16 ± 0.05 mmol/L ADP; P = 0.186), following training. Mitochondrial respiratory capacity increased in skeletal muscle from 57 ± 4 to 67 ± 4 pmol O2·mg−1·sec−1 (P < 0.001), but decreased with training in SAT from 1.3 ± 0.1 to 1.0 ± 0.1 pmol O2·mg−1·sec−1 (P < 0.001). CS activity increased (P = 0.027) and mtDNA was unchanged following training. Intrinsic mitochondrial respiratory capacity was unchanged in skeletal muscle, but increased in SAT after HIT. In summary, our results demonstrate that mitochondrial adaptations to HIT in skeletal muscle are comparable to adaptations to endurance training, with an increased mitochondrial respiratory capacity and CS activity. However, mitochondria in SAT adapts differently compared to skeletal muscle mitochondria, where mitochondrial respiratory capacity decreased and mtDNA remained unchanged after HIT.

Mitochondrial respiration variability and simulations in human skeletal muscle: The Gene SMART study

“…This means that it would be a challenge to observe true changes in mitochondrial capacity using the OROBOROS technology, since most studies do not report such large increases following exercise training (−9% to 20%). 18,19,32,[34][35][36][37][38] We acknowledge that some of the studies have observed significant changes in mitochondrial respiration without reaching the effect sizes we presented here. This implies that although such studies were significant, the sample sizes were too low to detect the magnitude of changes they reported at 80% power.…”

“…Experiments with less than 15 individuals would require a change of at least 13% to achieve 80% power. The triangles represent real effect sizes and sample sizes reported in different studies 8,[10][11][12]14,20,35 a minimum of 23 participants to detect changes for CI + CII P and CI + CII E at 80% power. Our results suggest that with the typical sample size in exercise training studies (n = 12), only changes of >15% in mitochondrial respiration following training would be detectable at 80% power.…”

Blood flow restricted resistance exercise and reductions in oxygen tension attenuate mitochondrial H2O2 emission rates in human skeletal muscle

“…; Dohlmann et al . ; Petrick & Holloway, ), an effect that appears required for cellular adaptations to occur (Miotto & Holloway, ). As a closely linked control point (Holloway, ), evidence also suggests that an increase in mitochondrial reactive oxygen species (ROS) emission rates in the presence of physiological ADP concentrations occurs acutely in response to aerobic exercise (Barbeau et al .…”

NADPH-oxidase 2 is required for molecular adaptations to high-intensity interval training in skeletal muscle.

“…HIIT has been associated with an increase in both mitochondrial content and function [25]. ROS could regulate training-induced mitochondrial biogenesis [26, 27].…”

“…Endurance exercise training is associated with an elongated mitochondrial network [29] and decreased mitochondrial fragmentation [30] in the trained musculature in rodents and humans [44]. HIIT has been reported to increase the respiratory capacity of mitochondria [25, 45] but the HIIT-associated changes in mitochondrial morphology have, as far as we are aware, not been investigated in any species. Our data show for the first time that these responses also occur with HIIT.…”