Training raised peak VO2 by 2.3 in 205 patients with a thickened heart
In short
A meta-analysis of 8 studies (3 randomised controlled trials) covering 205 low-to-moderate-risk hypertrophic cardiomyopathy patients found individualised training raised peak VO2 by 2.3 mL/kg/min (95% CI 0.76–3.83), predicted peak VO2 by 8.1% (2.7–13.4) and exercise time by 1.0 min (0.5–1.5), and lowered resting heart rate by 3.1 bpm (-5.7 to -0.4), all P<0.05. Endurance training and concurrent training that included resistance work produced no different results, and no adverse events were reported in these cohorts.
Hypertrophic cardiomyopathy (HCM) has long functioned as a diagnosis that means exercise less. This meta-analysis tested that premise head-on, and in low-to-moderate-risk patients the numbers ran the other way.
The pool is 8 studies (3 randomised controlled trials) and 205 adult patients, drawn from PubMed, Web of Science and Cochrane through December 2025. Both obstructive and non-obstructive HCM were included, and eligibility was restricted to individualised endurance or concurrent (endurance plus resistance) interventions that reported both cardiopulmonary exercise testing and echocardiographic measures. Risk of bias was assessed with ROBINS-I V2.
How much actually improved?
Everything below improved significantly with training (all P<0.05). Peak VO2 +2.3 mL/kg/min (95% CI 0.76–3.83), predicted peak VO2 +8.1% (2.7–13.4), exercise time +1.0 min (0.5–1.5), peak heart rate +5.2 bpm (0.04–10.3), heart rate reserve +5.5 bpm (2.5–8.5). In the other direction, body mass index fell 1.12 kg/m² (-2.13 to -0.11) and resting heart rate fell 3.1 bpm (-5.7 to -0.4).
The 5.5 bpm gain in heart rate reserve means more than general fitness. Chronotropic incompetence — a heart rate that will not climb enough during effort — is common in HCM, and training partially reversed it.
Does adding resistance work make it riskier?
In this analysis there was no difference between endurance-only and concurrent training. Including a resistance component neither worsened nor improved the outcome, and no adverse events were reported in these cohorts. With 205 patients total this is not a sample sized to detect rare events — but the reflex of automatically excluding all resistance work has less to stand on.
One echocardiographic result stands out. Across the 3 studies with controlled data, maximal wall thickness was 0.9 mm lower than usual care (-1.7 to -0.1, P<0.05). Every other echocardiographic feature, blood pressure and NT-proBNP were unchanged. Nothing pointed in the direction of training worsening the disease.
Who gained the most?
The meta-regression is the most practically useful part of the paper. Every 10-unit lower baseline heart rate reserve was associated with a 1.3 mL/kg/min larger peak VO2 gain (0.8–1.9, R=0.86, P<0.05). The worse the starting point, the more came back — the same shape that turns up in the exercise dose for blood pressure and in exercise for sarcopenia.
These results apply to low-to-moderate-risk phenotypes in individualised, guided, mostly on-site supervised programmes. The number of interventions is small, the populations are heterogeneous, and only 3 were randomised controlled trials; the authors state explicitly that the findings should be read cautiously. If you have a cardiac condition, this article is not clearance to start training — it is evidence to bring to the decision you make with your doctor. How beta-blockers affect heart rate reserve and the training response is still unresolved.
What a lifter without heart disease takes from it
One confusion is worth clearing first. HCM is a genetic disease of the heart muscle, distinct from the remodelling a heart undergoes in response to training. This paper says nothing about whether lifting causes HCM. What it addresses is whether someone already diagnosed can train.
From a fairlift standpoint, what the paper changes is what you log. For anyone with a cardiac restriction, Big 3 1RMs and a Muscle Index score are the wrong progress markers. The numbers that actually moved here were resting heart rate (-3.1 bpm) and heart rate reserve (+5.5 bpm). One line of resting heart rate, taken under the same conditions each morning, will tell you more honestly whether three months of training worked than a 1RM will.
Frequently asked questions
Should people with hypertrophic cardiomyopathy avoid exercise?
In a meta-analysis of 8 studies covering 205 low-to-moderate-risk patients, individualised exercise raised peak VO2 by 2.3 mL/kg/min with no adverse events reported. Those results come from risk-stratified, mostly supervised programmes, so whether and how hard to train is a decision to make with your cardiologist.
Is resistance training more dangerous than cardio here?
This meta-analysis found no difference in outcomes between endurance-only training and concurrent training that included resistance work. With 205 patients in total, though, the pool is not large enough to detect rare adverse events.
Does exercise thicken the heart wall further?
It went the other way in this analysis. Across the 3 studies with controlled data, maximal wall thickness was 0.9 mm lower than usual care (P<0.05), while other echocardiographic measures, blood pressure and NT-proBNP were unchanged.
Who saw the biggest effect?
The meta-regression found that every 10-unit lower baseline heart rate reserve was associated with a 1.3 mL/kg/min larger peak VO2 gain (R=0.86, P<0.05). Patients with the worst starting capacity improved the most.
Do these findings transfer to healthy lifters?
No. The population is low-to-moderate-risk HCM patients on individualised, mostly supervised programmes. The transferable point is narrower: when a cardiac restriction is in play, track resting heart rate and heart rate reserve rather than 1RM.
Source: PubMed