Bursts of high-intensity exercise improve mitochondrial function

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A few minutes of high-intensity interval or sprinting exercise may be as effective as much longer exercise sessions in spurring beneficial improvements in mitochondrial function, according to research.

Mitochondria, the energy centres of the cells, are essential for good health. Previous research has found that exercise creates new mitochondria and improves the function of existing mitochondria. Altered mitochondrial function in response to a single session of exercise generates signals that may lead to beneficial changes in the cells, lowering the risk for chronic disease. High-intensity interval exercise consists of short bursts of high-intensity aerobic exercise – a physical activity that raises the heart rate – alternating with brief recovery periods. Whether the intensity of a workout affects mitochondrial response is unclear.

A team of researchers led by Nigel Stepto at the Institute for Health and Sport, Victoria University, Australia, studied eight young adult volunteers as they participated in cycling workouts of varying intensity. Moderate intensity consisted of 30 minutes of continuous exercise at 50% peak effort. High-intensity interval exercise consisted of five four-minute cycling sessions at 75% peak effort, each separated by one minute of rest. Sprint cycling consisted of four 30-second sessions at maximum effort, each separated by 4.5 minutes of recovery time.

The research team measured the amount of energy the volunteers spent on each workout and compared mitochondrial changes in the participants’ thigh muscles before and after each exercise session. The researchers found that levels of hydrogen peroxide – a type of molecule involved in cell signalling called “reactive oxygen species” that contains oxygen and hydrogen – in different parts of the mitochondria change after exercise. While too much reactive oxygen species can be damaging to the cells, the researchers noted that the volunteers’ levels were an appropriate amount to potentially promote cell responses that benefit metabolic function rather than cause damage.

In addition, the research team found that fewer minutes of higher-intensity exercise produced similar mitochondrial responses compared to a longer moderate-intensity activity. “A total of only two minutes of sprint interval exercise was sufficient to elicit similar responses as 30 minutes of continuous moderate-intensity aerobic exercise,” the researchers wrote.

“This suggests that exercise may be prescribed according to individual preferences while still generating similar signals known to confer beneficial metabolic adaptions. These findings have important implications for improving our understanding of how exercise can be used to enhance metabolic health in the general population.”

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), metabolic and redox signaling responses. In a randomized, repeated measures crossover design, eight recreationally active individuals (24 ± 5 years; VO2peak 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 post-exercise for high-resolution mitochondrial respirometry (JO2) and H2O2 emission (JH2O2), gene and protein expression analysis. Immediately post-exercise and irrespective of protocol, JO2 increased during complex I+II leak/state-4 respiration but JH2O2 decreased (p<0.05). AMP-activated protein kinase (AMPK) and acetyl co-A carboxylase (ACC) 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 hours post-exercise, 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); 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.

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

American Physiological Society material
American Journal of Physiology – Regulatory, Integrative and Comparative Physiology abstract


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