Why does my heart rate drift up at the same watts — blood to the skin, or the heart itself?
Unsettled: one account blames blood shifted to the skin, the other a rising heart rate shortening filling. This review sets out both (C+).
Souissi, Haddad, Dergaa, Ben Saad and Chamari review why heart rate rises and stroke volume falls over prolonged exercise. They start from the two predominant theories.
The first, "the hypothesis of Rowell" (cited to Rowell's 1986 book), holds that a progressive rise in skin blood flow as body temperature rises increases cutaneous venous volume and so lowers mean arterial pressure and stroke volume, the heart rate rising in response.
The second, from Fritzsche, Coyle and colleagues (REF-1340), holds that drift after about 15 min is primarily due to the rising heart rate, which shortens ventricular filling time, because stroke volume keeps falling after skin blood flow has plateaued.
The authors argue that neither suffices: diastolic filling can rise despite a shorter filling period when the heart relaxes faster, post-exercise diastolic dysfunction did not track the elevated heart rate in one study and recovered within 24 h in another, and they question the beta-blocker experiment behind the heart-rate account.
They propose instead that drift is time-dependent and multifactorial — nitric-oxide-driven vasodilation (about 40-50% of cutaneous vasodilation in a cited study) in the first ~15 min, a shorter filling time as heart rate rises, and, in long high-intensity exercise, a falling cardiac force-frequency relationship (rising rate with falling force) linked to adrenergic desensitisation, beta-3-adrenergic activation, calcium overload, nitric oxide and inflammation.
Their "new perspective" is that drift, in some conditions and time windows, may protect the heart from damage by intense, prolonged contraction. The authors themselves note that no study has yet tested nitric oxide's effect on drift, and call for those tests.
Our reading: the base cites this review for one thing — a sourced statement that the cause of drift is disputed between the skin-blood-flow and the heart-rate accounts (PHYS-11); its own proposals are hypotheses, and its attribution of the skin-blood-flow account is to Rowell's 1986 book, while Rowell's 1974 review (Physiol Rev 54:75-159, not in the base) is cited here only for heart rate rising together with skin blood flow and cardiac output.
Protocol
Key Results
The two standing theories, as the review states them:
| Theory | Claim | Source cited by the review | The review's objection |
|---|---|---|---|
| Skin blood flow ("the hypothesis of Rowell") | rising skin blood flow with body temperature raises cutaneous venous volume, lowering mean arterial pressure and stroke volume; heart rate rises in response | Rowell 1986 (book); Shaffrath & Adams on airflow | stroke volume keeps falling after skin blood flow plateaus at ~15 min (the other side's argument) |
| Heart rate (Fritzsche, Coyle and González-Alonso) | after ~15 min a sympathetically driven heart-rate rise shortens diastole and filling, lowering stroke volume | Fritzsche et al.; REF-1340 | faster relaxation can enhance filling despite a shorter filling period; diastolic dysfunction did not correlate with heart rate and was restored 24 h later; the low-dose beta-blocker results run against other literature |
The authors' own proposals (hypotheses, untested):
| Phase | Proposal | Supporting observations cited |
|---|---|---|
| First ~15 min | nitric-oxide-induced vasodilation contributes to the early fall in pressure and stroke volume and the rise in heart rate | circulating nitric oxide rises after 10 min of moderate exercise; nitric oxide accounts for ~40-50% of cutaneous vasodilation; NOS inhibition (L-NAME) blunted the early heart-rate rise. "There is no study yet that has assessed the influence of nitric oxide on cardiovascular drift" |
| Long, hard exercise | a biphasic cardiac force-frequency relationship: above a "critical heart rate" force falls as rate rises (negative inotropy), via beta-1/beta-2 desensitisation, beta-3 activation, calcium overload, nitric oxide and inflammation | ejection fraction fell at the end of prolonged high-intensity, not moderate, exercise; heart rate and change in ejection fraction correlated (r = 0.38); cardiac dysfunction typically after ≥2 h, sooner (~1 h) near maximal intensity, and over 10 h before systolic changes in trained people (a cited meta-analysis) |
| Overall | drift, in some conditions and time windows, may be a strategy that protects the myocardium from damage by intense, prolonged contraction | none tested; "a call to investigators" |
| Spinal cord injury | no drift observed in trained people with spinal cord injury, possibly through lower catecholamines and less sympathetic skin-vascular control | one cited study |
Mechanisms
Practical Application
Limitations
How this entry was checked and changed
narrative review without systematic method, not from a leading drift laboratory; useful for stating both standing theories and their sources, while its own nitric-oxide, force-frequency and "protective drift" proposals are untested hypotheses