Mitochondrial Adaptations to Endurance Training
Aerobic training increases muscle mitochondrial content, by a similar amount across endurance, interval and sprint training.
- Chest pain, pressure, or unusual shortness of breath during exertion
- Fainting, dizziness, or palpitations with exercise
- Known or suspected cardiovascular, metabolic, or renal disease without medical clearance
What the evidence says
The sources on this entry studied skeletal muscle mitochondrial content, capillarisation and fat oxidation in response to endurance, interval and sprint training: two meta-analyses, one randomised trial and three narrative reviews. Mølmen 2024 (meta-analysis, 5973 participants, 353 studies for mitochondrial content and 131 for capillary content) reports that mitochondrial content increased by 23% with endurance training, 27% with HIT and 27% with SIT, capillaries per fibre by 15%, 13% and 10%, and VO2max similarly with all training types, and concludes that the magnitude of change is largely determined by initial fitness level, with greater changes in individuals with lower initial fitness. Lundby 2016 (narrative review) highlights altering intensity and duration within a training program, with low-to-moderate endurance training for fat oxidation and high-intensity intervals for global respiratory capacity, to maximise mitochondrial function and performance. Atakan 2022 (meta-analysis, 18 studies, 511 participants) reports that HIIT or SIT can improve fat oxidation during exercise, with larger effects expected for longer regimens and individuals with overweight or obesity, and Venables 2008 (randomised trial) reports that fat oxidation increased by 44% and insulin sensitivity by 27% with a continuous low-intensity protocol, significantly more than with a eucaloric interval protocol. Maffetone 2020 (narrative review) describes the MAF approach of personalised low-intensity exercise to promote maximal fat oxidation, and Despres 1994 (narrative review) calls prolonged, low-intensity endurance exercise on an almost daily basis probably the most feasible exercise prescription with considerable potential to reduce coronary heart disease risk.
- 'Only long slow distance builds mitochondria' (intervals also drive adaptation)
- (myth: One optimal protocol exists) CORRECTION: (mitochondrial content rises by a similar amount across endurance, interval and sprint training)
- No cure claims for any disease
- No guaranteed outcomes or fixed numeric results for any individual
- Does not replace prescribed medical treatment
- Supplements are not required to gain mitochondrial adaptations
- Agreement
- The review summary this entry was written from does not say whether its sources agree at this claim. All 6 sources state a direction. A review summary is the written synthesis this entry was first built from; it is not one of the sources counted here.
- The claim's outcome
- Outcome not yet recorded
- Certainty
- A source states a certainty rating for 1 outcome.
What each source measured and concluded (6)
- What it measured
- Fat oxidation during exercise (FatOx)
- How it measured it
- Indirect calorimetry during a continuous submaximal or an incremental graded exercise test
- Direction it states for the claim's outcome
- Improved
- How it was read
- read in full text
- What the review says it includes
- systematic review and meta-analysis
- Studies and participants, as stated
- N = 511 participants across 18 studies
- Heterogeneity, as stated
- Low certainty of evidence due to methodological issues and heterogeneity
- What it measured
- Fat oxidation
- How it measured it
- Clinician-measured outcomes (blood and urine laboratory testing), user-reported outcomes, field tests (MAF test)
- Direction it states for the claim's outcome
- Improved
- How it was read
- read in full text
- What it measured
- Fat oxidation rates and whole-body insulin sensitivity index.
- How it measured it
- Fat oxidation: breath-by-breath measurements during a graded exercise test; Insulin sensitivity: plasma glucose and insulin concentrations during OGTT.
- Direction it states for the claim's outcome
- Improved
- How it was read
- read in full text
- What it measured
- Mitochondrial volume density (Mito VD), fat oxidation capacity, global respiratory capacity.
- How it measured it
- Laboratory tests (biochemical and morphological analyses).
- Direction it states for the claim's outcome
- Improved
- How it was read
- read in full text
- What it measured
- Changes in skeletal muscle mitochondrial content and capillarization.
- How it measured it
- Transmission electron microscopy for mitochondrial content; immunohistochemical analysis for capillarization.
- Direction it states for the claim's outcome
- Improved
- How it was read
- read in full text
- What the review says it includes
- systematic review and meta-analysis
- Studies and participants, as stated
- N = 5973 participants across 353 studies for mitochondrial content and 131 studies for capillary content
- What it measured
- Metabolic variables relevant to CHD risk (e.g., weight, body fat percentage, VO2max, insulin/glucose ratio, triglycerides, cholesterol, LDL-C, HDL-C, apolipoproteins).
- Direction it states for the claim's outcome
- Improved
- How it was read
- read in full text
Certainty ratings the sources state (1)
- Rating, as the source states it
- Low
- Framework
- not named by the source
- Applies to
- Low certainty of evidence due to methodological issues and heterogeneity
- Stated by
- Atakan et al. (2022)
Every source below is shown with its study design and links to the original study. This is the audit trail.