REF-452 · Bergström & Hultman, 1967 · Scandinavian Journal of Clinical and Laboratory Investigation, Vol. · Paper · PubMed

A study of the glycogen metabolism during exercise in man

The foundational needle-biopsy study tying muscle glycogen depletion to loss of working capacity

Blimited evidenceMeasured on recreational to trained athletesWritten before October 2026, being re-checked

Historical Significance

One of the first needle-biopsy studies tying muscle glycogen depletion to the loss of working capacity during exercise. Together with the companion 1967 diet experiments (Bergström, Hermansen, Hultman & Saltin — a different paper, not this DOI) it laid the rationale for carbohydrate loading in endurance sport.

Method

Glycogen content of the quadriceps femoris determined in needle biopsy specimens from normal subjects, taken in connection with muscular work (bicycle-ergometer work — full text; not checked against the abstract)
Work performed both in the fasting state and during continuous intravenous glucose infusion
Liver carbohydrate metabolism also studied before and during exercise
Sample size is not stated in the abstract (small group; the exact n is not traced here)

Protocol

Uncontrolled physiological study in normal subjects (number not stated in the abstract): glycogen content of the quadriceps femoris determined in needle biopsy specimens taken in connexion with muscular work (from the abstract).
Work performed both in the fasting state and during intravenous infusion of glucose; glycogen of resting muscle compared with muscle groups emptied by exercise in the same subject.
Carbohydrate metabolism of the liver (glucose production) studied before and during periods of exercise.

Key Findings (the abstract's four inferences)

1

During work, muscle glycogen falls successively to values approaching zero, and working capacity decreases when the glycogen store is depleted

2

Glycogen in a resting muscle stays unchanged while other muscle groups in the same subject are being emptied by exercise — depletion is local to the working muscle

3

With continuous glucose infusion during work, glycogen consumption is significantly lower than without glucose — but the difference is small, and muscle glycogen still supplies the greater part of the energy even when blood sugar is high

4

Liver glucose production increases toward the end of continuous work, but is small relative to total carbohydrate metabolism

Mechanism (later work, not from this paper)

Glycogen depletion in active fibres → reduced ATP supply capacity; modern compartment-level mechanism in Ørtenblad 2013 REF-472
Fibre-type-specific depletion patterns and central feedback from falling blood glucose are later findings, not tested here

Practical Application

Needle biopsies of the quadriceps in normal subjects during work (Bergström & Hultman 1967): muscle glycogen fell successively toward zero and working capacity dropped once the store was depleted; a continuous glucose infusion lowered glycogen use only slightly — muscle glycogen still supplied most of the energy even with high blood sugar — and liver glucose output rose late but stayed small. Meaning: the in-muscle store, not blood glucose, is the limiting fuel in hard sustained work; exogenous carbohydrate helps at the margin, it does not replace the store.
Why endurance events need a full glycogen store at the start and fueling during: substrate physics, shown directly in muscle
Not from this paper: carbohydrate intake during exercise (REF-066) and race-day fueling (SYNTH-02) — the doses live there; the diet–glycogen–endurance experiments are the companion 1967 paper, not this one
Not from this paper: training with low glycogen (train-low) as an adaptive stimulus — REF-157

Limitations

1967 methodology — exercise testing crude by modern standards
Small sample, n not stated in the abstract; normal subjects, not athletes
No control group; the diet manipulations belong to a companion paper
Doesn't address protein/fat substrate interactions in detail
Type I/II fibre discrimination not yet developed
How this entry was checked and changed
Why this level

regraded 2026-09-27 from A: small uncontrolled physiological study (n not stated in the abstract), no control group

Content correction 2026-09-27
"Fatigue coincides with glycogen depletion to ~25% of starting level" -> abstract: glycogen falls "to values approaching zero" and working capacity decreases when the store is depleted.
"High-CHO diet → higher starting glycogen → longer time to exhaustion", "Low-CHO diet → premature fatigue", "Replenishment depends on CHO intake" -> not in this abstract (companion 1967 diet paper); removed from Findings. Added the abstract's own findings on glucose infusion (glycogen use only slightly lower) and liver glucose output (small).
"60+ years", "carb-loading 36-48 h", "post-exercise CHO 1-1.2 g/kg/h" -> not from this paper; removed, pointed to REF-066/SYNTH-02.
Level A -> B (small uncontrolled physiological study); added Tier/Sport lines.
2026-09-28: added Protocol from the abstract (abstract via OpenAlex; record via Europe PMC, DOI 10.3109/00365516709090629). The abstract states no sample size, so no n was added.
2026-09-28: PMID 6049917 belonged to an unrelated paper; replaced with 6048626, the PubMed record for this entry's own DOI.
2026-09-29: race-day fuelling cross-references pointed at SYNTH-04 (heat acclimation); repointed to SYNTH-02 (fuelling by duration).