Muscle lost during treatment is usually regained with resistance training and enough protein, over months rather than weeks. Muscle lost to cancer cachexia is different: while the cancer is active, training and food slow the loss but rarely reverse it, and the consensus definition says so plainly.
Two different things are called muscle loss. The first is disuse and treatment atrophy: weeks in hospital, a major operation, steroids, hormone therapy and the sheer tiredness of chemotherapy. That muscle responds to progressive resistance training and adequate protein in the ordinary way, and the randomised exercise trials that improved physical functioning were largely doing this.
The second is cancer cachexia, defined by the 2011 international consensus as "a multifactorial syndrome defined by an ongoing loss of skeletal muscle mass (with or without loss of fat mass) that cannot be fully reversed by conventional nutritional support and leads to progressive functional impairment". That sentence is the honest answer to the question people ask: while the driving cancer is active, feeding and training do not restore the muscle. Drugs aimed at the underlying signal are the current attempt on it, including GDF-15 blockade with ponsegromab.
Androgen deprivation for prostate cancer and long courses of steroids both cause measurable muscle loss on top of either of the above, and resistance training is the counter-measure with the best evidence in those settings.
What comes back, and when: for disuse and treatment atrophy, recovery is usual with training, over three to six months of consistent work; the ACSM dose is the one to use. For cachexia with active cancer, recovery is unlikely until the cancer is controlled, and the consensus definition says in its own words that conventional nutritional support cannot fully reverse it. Telling someone who is losing weight that eating more will put it back is not what the evidence says.
Resistance training raises muscle protein synthesis and, with sufficient dietary protein, net protein balance. In cachexia, tumour and host inflammatory signalling (including GDF-15, IL-6 and the ubiquitin-proteasome pathway) holds net balance negative regardless of intake, which is why nutrition alone does not restore mass.
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