Does Ozempic Improve Your Fitness?

Evidence on whether GLP-1 receptor agonists improve cardiorespiratory fitness in adults with obesity.

The evidence does not support it. In a randomised trial of 193 adults with obesity and without diabetes, aged 18 to 65 with a BMI of 32 to 43, cardiorespiratory fitness improved when a structured moderate-to-vigorous exercise programme was added and did not improve from the GLP-1 receptor agonist alone. These drugs also cause notable reductions in fat-free mass alongside the fat loss, and their effect on cardiorespiratory fitness is not yet understood, reported in the Journal of Clinical Endocrinology and Metabolism in 2025. KnowYourPrime's VO2 max desk rates this claim Unsupported. The complication is that your wearable will probably show the number going up anyway, because VO2 max is reported per kilogram of body weight, so removing kilograms raises the ratio while your actual oxygen uptake stays where it was.

Why the number rises when the capacity does not

VO2 max is conventionally expressed in millilitres of oxygen per kilogram of body weight per minute. Body weight is the denominator. A person who loses 15 percent of their body mass and whose absolute oxygen uptake is completely unchanged will show a VO2 max roughly 15 percent higher, because the same numerator is being divided by a smaller number.

That is not an error in the metric and it is not a wearable problem. Relative VO2 max is the right measure for most purposes precisely because moving your own body costs energy proportional to its mass, and a lighter person genuinely does have more aerobic capacity available per kilogram carried. The point is narrower: a rising per-kilogram figure after weight loss is evidence of weight loss. It is not, on its own, evidence that the heart, lungs and muscles got better at using oxygen.

This is where a reader checking Cardio Fitness on a watch and a reader checking a laboratory test can reach different conclusions from the same physiology. The published trial measured fitness directly rather than inferring it from heart rate against pace, which is what a consumer wearable does.

What the randomised evidence found

The trial was a secondary analysis of a randomised controlled trial in 193 adults with obesity, aged 18 to 65, with a body mass index of 32 to 43 and without diabetes. After a period of diet-induced weight loss, participants entered weight maintenance on one of four arms: a moderate-to-vigorous intensity exercise programme, a GLP-1 receptor agonist, both together, or neither. The outcomes were physical functional performance and cardiorespiratory fitness.

The separation between arms is the finding. Cardiorespiratory fitness improved where structured exercise was part of the arm. It did not improve from the drug on its own. A design that gives one group the drug and another group the drug plus exercise is the design that can tell those two apart, and when it did, the exercise carried the result.

The fat-free mass problem

Alongside the fat loss, these drugs are associated with notable reductions in fat-free mass, which is the category that includes skeletal muscle. The review raising this stated plainly that how the drugs affect cardiorespiratory fitness is not yet understood, and set that question against the fact that cardiorespiratory fitness is an independent predictor of all-cause and cardiovascular mortality.

So there are two directions in play rather than one. Weight falls, which raises the per-kilogram figure. Fat-free mass also falls, and muscle is where oxygen is consumed, which pushes the absolute figure the other way. Nothing published measures the net effect on absolute oxygen uptake over a long enough period to settle it, which is why the rating here is Unsupported rather than negative. Unsupported means the evidence does not support the claim, not that the opposite has been demonstrated.

What the mechanism research establishes, and what it does not

There is a laboratory finding pointing the other way, and it belongs in the record with its limits attached. In differentiated mouse muscle cells, treatment with exendin-4, a GLP-1 receptor agonist, reduced lipid accumulation and triglyceride content and raised the oxygen consumption rate compared with untreated cells.

That is a cell culture result in a mouse cell line. It establishes that GLP-1 receptor activation can act on muscle energy metabolism, which is a real mechanistic observation and a reason the question was worth asking. It is several steps away from a person's whole-body oxygen uptake during maximal exercise, and the randomised trial that did measure whole-body fitness in people found no drug effect without exercise. Where a mechanism study and an outcome trial disagree, the outcome trial is answering the question a reader is asking.

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