Interesting read:
maybe not? “However, in aggregate such observations give rise to the idea that while acute, but intermittent lactate exposure as occurs in physical exercise is adaptive, prolonged cellular exposure to lactate, as occurs in chronic inflammatory diseases, may be maladaptive” so I wonder… can anyone exercise to cause 48 hours of high lactate? Though Dr San Milan may be able to shed light on whether this study has implications for exercise and intensity, it probably does strengthen the low intensity is good narrative. What would interest me is how much (time) is needed to see mitochondrial impact for low intensity exercise?
I think it’s another argument for not doing HIIT type exercise most days of the week. A little high intensity each week is healthy, but don’t overdo it, as it may lead to chronic inflammation.
@scooter The study does indeed not reflect normal training behavior.
I always assumed high-intensity can hurt endurance as the fatigue and damage prevents the endurance training.
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The methods used were surely not a great reflection of normal training conditions, but I wonder if any of the conclusions could be significant for people struggling with type2 diabetes. Should we suggest that people dealing with type2 diabetes restrain from high-intensity training when they, for example, are working out to lose some weight? Would the low-intensity training, leading to elevate mitochondrial density, be a right choice to “balance” the problems associated with chronically increased lactate levels?
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Really cool study! I feel it sheds more light on those with poor metabolic health than it does trained athletes. It really gets at that route cause of metabolic syndrome being mitochondrial dysfunction. As a healthcare provider working primarily with patients with metabolic syndrome, besides dietary intake improvements, I find that prescribing Z2 cardio with resistance training is a powerful lever to pull. Talk about really improving mitochondrial function and improving insulin sensitivity!