Zone 2 Training Is Getting More Credit Than it Deserves
Popular media built a compelling case for low-intensity training as the key to metabolic health, but the studies behind that claim tell a far more complicated story.
Zone 2 training has become one of the most talked-about topics in health and fitness media. Podcasters and popular health commentators have positioned it as the optimal intensity for improving mitochondrial capacity, fat oxidation, and long-term cardiometabolic health. The argument is compelling, and the health effects and benefits of aerobic fitness are undeniable. But, a new narrative review published in Sports Medicine from researchers at Queen's University and McMaster University asks if the science backs it all up?
Aims and Methods
The researchers set out to critically evaluate the evidence supporting Zone 2 training as the optimal exercise intensity for improving mitochondrial capacity and cardiorespiratory fitness (CRF) in the general population, meaning non-elite, non-endurance-trained people.
Zone 2 in this context refers to low-to-moderate intensity exercise performed below the first lactate threshold (LT1), roughly where you can maintain a comfortable conversation. Popular definitions also tie it to the maximal rate of fat oxidation (Fatmax) and blood lactate concentrations just below where the body starts to accumulate lactate more rapidly.
Rather than conducting a systematic review, the authors conducted a narrative review, pulling together studies on low-intensity endurance training, mitochondrial biogenesis signalling, fatty acid oxidative (FAO) capacity, and cardiorespiratory fitness outcomes. They looked at acute exercise studies examining what happens inside the muscle during Zone 2, as well as longer-term training studies measuring actual adaptations.
A notable finding at the outset was that very few studies have actually examined Zone 2 as it is commonly defined. The authors had to work with studies that approximated Zone 2 intensity based on available physiological markers.
Results
The mitochondrial signalling case for Zone 2 is weak. The key driver of mitochondrial biogenesis is metabolic stress inside the muscle, specifically changes in the AMP/ADP:ATP ratio, which activates a signaling molecule called AMPK. Zone 2 exercise produces minimal and inconsistent changes in these intramuscular signals. AMPK activation following Zone 2 exercise is generally absent or negligible, and the downstream gene expression responses that lead to new mitochondrial development, including PGC-1a, are mixed at best. Higher exercise intensities, those above Zone 2, consistently produce greater activation of these pathways.