The drug didn’t make muscles stronger or change how much energy they used during exercise — only how fast they recovered afterward, which points to mitochondria being the target.

The muscle energy recovery speed (ViPCr) responded more clearly to IGF-I than another measure (τPCr), meaning ViPCr might be a better way to track how well muscles are making energy.

Even when accounting for differences in weight, fitness, and blood sugar, the more IGF-I went up, the better the muscle energy recovery — meaning IGF-I likely has a direct role.

The muscle energy improvement wasn’t because people lost weight or got more active — it seemed to be linked directly to IGF-I levels instead.

In people who took the placebo, IGF-I didn’t go up much, and their muscle energy recovery didn’t link to IGF-I — meaning the connection only showed up when the drug raised IGF-I.

Even when accounting for factors like age, weight, and insulin levels, higher IGF-I still links to better muscle energy recovery in obese people with low growth hormone.