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Acute HIIE elicits similar changes in human skeletal muscle mitochondrial H 2 O 2 release, respiration, and cell signaling as endurance exercise even with less work

Adam J Trewin, Lewan Parker, Christopher S Shaw, Danielle S Hiam, Andrew Garnham, Itamar Levinger, Glenn K McConell, Nigel K Stepto

Am J Physiol Regul Integr Comp Physiol. 2018 Nov 1;315(5):R1003-R1016.

PMID: 30183338

Abstract:

It remains unclear whether high-intensity interval exercise (HIIE) elicits distinct molecular responses to traditional endurance exercise relative to the total work performed. We aimed to investigate the influence of exercise intensity on acute perturbations to skeletal muscle mitochondrial function (respiration and reactive oxygen species) and metabolic and redox signaling responses. In a randomized, repeated measures crossover design, eight recreationally active individuals (24 ± 5 yr; V̇o2peak: 48 ± 11 ml·kg-1·min-1) undertook continuous moderate-intensity [CMIE: 30 min, 50% peak power output (PPO)], high-intensity interval (HIIE: 5 × 4 min, 75% PPO, work matched to CMIE), and low-volume sprint interval (SIE: 4 × 30 s) exercise, ≥7 days apart. Each session included muscle biopsies at baseline, immediately, and 3 h postexercise for high-resolution mitochondrial respirometry ( Jo2) and H2O2 emission ( Jh2o2) and gene and protein expression analysis. Immediately postexercise and irrespective of protocol, Jo2 increased during complex I + II leak/state 4 respiration but Jh2o2 decreased ( P < 0.05). AMP-activated protein kinase and acetyl co-A carboxylase phosphorylation increased ~1.5 and 2.5-fold respectively, while thioredoxin-reductase-1 protein abundance was ~35% lower after CMIE vs. SIE ( P < 0.05). At 3 h postexercise, regardless of protocol, Jo2 was lower during both ADP-stimulated state 3 OXPHOS and uncoupled respiration ( P < 0.05) but Jh2o2 trended higher ( P < 0.08) and PPARGC1A mRNA increased ~13-fold, and peroxiredoxin-1 protein decreased ~35%. In conclusion, intermittent exercise performed at high intensities has similar dynamic effects on muscle mitochondrial function compared with endurance exercise, irrespective of whether total workload is matched. This suggests exercise prescription can accommodate individual preferences while generating comparable molecular signals known to promote beneficial metabolic adaptations.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
IAR42414861 Peroxiredoxin II Active human Peroxiredoxin II Active human Price
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