REF-1189 · Bathgate et al., 2018 · European Journal of Applied Physiology · Paper · PubMed

Can 30 years of endurance training make one identical twin very different?

In one pair aged 52, the trained twin had 12.4 ml/kg/min more VO2max and 8.6% lower body-fat % but smaller, weaker muscle. One pair: what is possible, not typical.

C+thin evidenceMeasured on trained athletes

Bathgate, Galpin and colleagues (California State University, Fullerton, with San Francisco State University and California State Polytechnic University, Pomona) studied one pair of male monozygotic twins aged 52: a trained twin (TT) with more than 30 years of chronic endurance training and an untrained twin (UT) with "no specific/consistent exercise".

They compared anthropometry and blood profiles, cardiovascular and pulmonary markers, skeletal muscle size, strength and power, and molecular markers in muscle.

TT had lower body mass, body fat, resting heart rate, blood pressure, cholesterol, triglycerides and plasma glucose; greater relative cycling power, anaerobic endurance and VO2max; but lower muscle size and strength and poorer muscle quality; more MHC I (slow-twitch) and fewer MHC IIa (fast-twitch) fibres; greater AMPK protein; and greater PAX7, IGF1Ec, IGF1Ea and FN14 mRNA.

The authors highlight three differences as the largest reported between monozygotic twins: 55% more MHC I fibres, a 12.4 ml/kg/min higher VO2max and 8.6% lower body fat in TT. They conclude that the data support chronic endurance training for body composition and cardiovascular health and suggest that the cardiovascular and muscle systems are more plastic than thought.

Our reading: a vivid demonstration of how far two people with the same genes can diverge, with a clear trade-off (aerobic and metabolic health up, muscle size and strength down); one pair cannot say how much of this the training caused, why one twin trained, or how common such a gap is.

Protocol

Participants (from the abstract): one pair of male monozygotic twins, age 52. TT: more than 30 years of chronic endurance training. UT: no specific or consistent exercise. Training modes, volume and competition history are not in the abstract.
Measurements: (1) anthropometry and blood profiles; (2) cardiovascular and pulmonary health markers; (3) skeletal muscle size, strength and power, and molecular markers of muscle health (fibre type by myosin heavy chain, AMPK protein, mRNA of PAX7, IGF1Ec, IGF1Ea, FN14). Methods for each are not detailed in the abstract.
Comparator: the co-twin only; no reference group and no statistics are possible on one pair.
Funding and conflicts: not stated in the abstract; the Europe PMC record lists a San Francisco State University "Development of Research & Creativity" grant. Conflicts of interest not checked (full text not read).

Key Results

Outcome (TT vs UT, from the abstract)DirectionMagnitude given
VO2maxhigher in TT12.4 ml/kg/min
Body-fat percentagelower in TT8.6% (units not specified)
MHC I (slow-twitch) fibresmore in TT"55% more" (not specified whether percentage points or relative)
MHC IIa (fast-twitch) fibresfewer in TTnot given
Body mass, resting HR, blood pressure, cholesterol, triglycerides, plasma glucoselower in TTnot given
Relative cycling power, anaerobic endurancegreater in TTnot given
Muscle size and strength; muscle qualitylower and poorer in TTnot given
AMPK protein; PAX7, IGF1Ec, IGF1Ea, FN14 mRNAgreater in TTnot given
n: one pair. No variance, no confidence intervals, no tests between the two men.

Mechanisms

Measured: the endurance-trained twin had more slow-twitch and fewer type IIa fibres, smaller and weaker muscle, and a higher VO2max and better cardiometabolic profile than his identical co-twin.
Authors' interpretation: the cardiovascular and skeletal muscle systems "exhibit greater plasticity than previously thought", and chronic endurance training improves body composition and cardiovascular health.
Inference: the fibre-type gap fits other long-term data, with a caution: in former distance runners re-biopsied after 20 years, the type I share rose in the men who had cut back or stopped training, not in those who stayed highly trained (REF-311), and lifelong runners in their 70s had a lower type II share than lifelong strength athletes, a tendency by fibre number (P = 0.063) and significant by area (P = 0.016) (REF-1190).A rising type I share with age is at least partly an ageing signature, not only a training effect. A slow-twitch muscle is not itself unhealthy; what the case links to it is lower muscle size and strength, which matter for function with age.
Inference: relative cycling power and VO2max per kilogram favour the lighter twin by arithmetic as well as by physiology; the abstract does not give absolute values.
Inference: why one twin trained for 30 years and the other did not (health, injury, job, temperament) is unknown, so the gap is not attributable to training alone even though genes are matched.

Practical Application

Can 30 years of endurance training make one identical twin very different? In one pair aged 52, the trained twin had 12.4 ml/kg/min more VO2max and 8.6% lower body-fat % but smaller, weaker muscle. One pair: what is possible, not typical.
The trade-off is the useful part (C+, one case): endurance-only training for decades went with a big aerobic and cardiometabolic advantage and with less muscle and strength than the untrained twin ("no specific/consistent exercise"). For a masters endurance athlete this is the case for keeping heavy strength work in the week; the trial evidence for that is in REF-597 and REF-1086, not here.
Do not quote the 55% figure as a rate: the abstract does not say whether it is percentage points or a relative difference, and one pair gives no estimate of what training does on average.
Genes still matter: one pair diverging widely does not mean training overrides genetics in general; the population-level evidence is that response is wide and partly inherited (REF-429, SYNTH-13).

Limitations

One pair (n = 1 comparison): no statistics, no estimate of typical effect, no generalisation.
Read from the abstract only; methods, absolute values and training history are not checked.
Observational and retrospective: why one twin trained is unknown; lifetime diet, occupation, illness and other exposures are not controlled by the twin design.
Several abstract figures are ambiguous in units ("55% more MHC I fibers", "8.6% lower body fat%").
Men only, aged 52; endurance modes and volume not given in the abstract.
Funding and conflicts of interest not stated in the abstract.
How this entry was checked and changed
Why this level

single case study (the rubric puts a single case at C+), one pair, read from the abstract only (the publisher version is closed and no repository copy was found). It shows what is possible within one genome; it cannot show what is typical, and the differences cannot be attributed to training alone