REF-1357 · Coffey & Hawley, 2007 · Sports Medicine · Paper · PubMed

Why don't lifting and riding build the same fitness?

Each switches on its own molecular programme: endurance training builds mitochondria and slower fibres, heavy lifting builds contractile protein and force (review, 2007).

Main caveat: Read from the abstract only. The studies, populations, signalling pathways and any doses or time courses could not be checked.
moderate evidenceMeasured on non-athletes to highly trained athletes

Coffey and Hawley review how skeletal muscle turns repeated disruptions of its homeostasis into lasting change. Exercise triggers signalling that activates specific genes; their messages are translated into new proteins, and the functional result of a training block depends on its volume, intensity and frequency and on how long the proteins concerned last (their half-life).

Many features of the adaptation are specific to the type of stimulus, such as the mode of exercise.

Prolonged endurance training produces metabolic and structural changes including mitochondrial biogenesis, a fast-to-slow fibre-type transformation and altered substrate metabolism; heavy resistance exercise instead stimulates the synthesis of the contractile proteins responsible for muscle hypertrophy and higher maximal force.

Because the functional outcomes differ so much, the genetic and molecular mechanisms are distinct too.

New techniques made it possible to measure signalling proteins and early-response genes in muscle after different training interventions; the authors state plainly that this work could not yet be claimed to have influenced elite training practice, but that it explains how current methods produce specific muscular adaptations and may suggest new ones.

Our reading: this is a mechanism source for "you get what you train" — endurance work and heavy lifting build different proteins through different signals — and for why the half-life of what was built matters when training stops; it does not measure transfer between endurance sports, which rests on REF-537 and trials such as REF-952.

Protocol

Design: narrative review of exercise-induced molecular and genetic adaptation in skeletal muscle.
Studies and participants: n = not given in the abstract (no search, study count or populations stated).
Topics (abstract): signalling and gene expression after exercise; determinants of the functional outcome (volume, intensity, frequency, protein half-life); endurance vs resistance adaptations; the then-new methods for measuring signalling proteins and early-response genes.
Funding and interests: PubMed indexes the review as "Research Support, Non-U.S. Gov't" without naming the funder; conflicts are not available from the abstract.

Key Results

Question (abstract)What the review states
What sets the functional result of training?Training volume, intensity and frequency, and the half-life of the protein
Is adaptation specific?Many features are specific to the type of stimulus, such as the mode of exercise
Prolonged endurance trainingmitochondrial biogenesis, fast-to-slow fibre-type transformation, changes in substrate metabolism
Heavy resistance exercisesynthesis of contractile proteins → muscle hypertrophy and higher maximal contractile force
Mechanismsgenetic and molecular mechanisms of adaptation to the two modes are distinct
Has molecular work changed elite training?"it cannot presently be claimed" (2007)
Doses, time courses, interference between modesnot in the abstract

Mechanisms

Measured (in the studies reviewed, as summarised in the abstract): endurance and resistance training produce different structural and metabolic changes in muscle, accompanied by different signalling-protein and early-response-gene responses.
Authors' interpretation: the specificity of adaptation follows from distinct molecular pathways activated by each type of exercise; the half-life of the proteins made decides, with volume, intensity and frequency, the functional consequences.
Inference: a short half-life means an adaptation must be renewed by continued training, which is one way to read why some adaptations fade within weeks of stopping (REF-374); the abstract does not give half-lives.
Inference: the review addresses the two extremes (prolonged endurance vs heavy resistance work). Whether two endurance modes such as running and cycling share enough of their signal to transfer is a separate, empirical question (REF-537, REF-1358).

Practical Application

Why don't lifting and riding build the same fitness? Each switches on its own molecular programme: endurance training builds mitochondria and slower fibres, heavy lifting builds contractile protein and force (review, 2007).
Train the adaptation the goal needs: the functional result of a block is set by its volume, intensity, frequency and mode (B+, review, from the abstract). Not from this paper; the base's own practice: race-like efforts in race-like conditions in the final weeks before an event (SYNTH-48, SYNTH-76).
Hybrid athletes: endurance and strength work build different things through different signals, so neither stands in for the other (inference); how much they interfere is a scheduling question (SYNTH-21) that this abstract does not address.
What it is good for as a source: the mechanism of training specificity at the muscle level. What it does not show: how much fitness transfers from one endurance sport to another, doses, or performance; and, by the authors' own statement, molecular findings had not changed elite practice.

Limitations

Read from the abstract only. The studies, populations, signalling pathways and any doses or time courses could not be checked.
Narrative review from 2007. No systematic method; molecular exercise physiology has moved a long way since, so the specific pathways named in the full text may be outdated (inference); the abstract's general claims are the part used here.
Extremes of the spectrum. Endurance vs heavy resistance work; mixed or sport-to-sport transfer is outside the abstract.
Mechanism, not outcome. No performance results in the abstract; the authors say the molecular work had not yet influenced elite training.
Funding and interests: funder not named (PubMed: "Research Support, Non-U.S. Gov't"); conflicts not available from the abstract. No device maker, federation or data platform is named.
How this entry was checked and changed
Why this level

an authoritative narrative review from the leading group on exercise signalling and training specificity (Hawley; RMIT Exercise Metabolism Group); no systematic method, no pooled data, and its signalling detail dates from 2007. Read from the abstract (closed access; Europe PMC holds no full text, the RMIT repository record of the article has no file, and the open RMIT item that OpenAlex merges with it is the first author's doctoral thesis, a different work, which was not used)