How long does soreness after a new eccentric session last?
Typically it starts 12-24 h after, peaks at 24-72 h and is gone within 5-7 days; strength can stay down after the soreness has faded. Narrative review.
Hody, Croisier, Bury, Rogister and Leprince review what lengthening (eccentric) contractions do to muscle, from the first damage to long-term adaptation.
Eccentric actions produce high force at low metabolic cost — about fourfold lower than the same exercise done concentrically — and in unaccustomed muscle they cause more damage than other contraction types: overstretched ("popped") sarcomeres, membrane and connective-tissue disruption, then a secondary phase driven by calcium overload, protease activation, reactive oxygen species and inflammation, with abnormalities spreading and worsening 2-3 days after exercise.
Damage shows as soreness, stiffness, swelling and lost force; creatine kinase (CK) in blood varies markedly between people even after standardised protocols.
Soreness typically appears 12-24 h after unaccustomed eccentric exercise, peaks between 24 and 72 h and is gone within 5-7 days, correlates poorly with other indirect markers of damage, and disappears before muscle function has fully recovered; strength loss is named as the best indirect marker.
The proposed causes of soreness include lactic acid release, spasm, connective-tissue damage, muscle damage, inflammation and oxidative stress, and recent work (much of it in rats) points to bradykinin, nerve growth factor and GDNF sensitising nerve endings.
The repeated-bout effect is described as unequivocal: one bout protects against the next, more completely after several sessions, for several weeks and up to 6 months, even when the first bouts were not damaging; its mechanism is neural, mechanical and cellular with no unified theory.
The authors' practical line is to introduce eccentric training with submaximal, progressively loaded sessions (citing REF-1346), to avoid explosive efforts while damage persists, and to avoid anti-inflammatory drugs in healthy people.
Our reading: the review supplies the base's time course of soreness and two statements the base held only as inference — that soreness tracks damage poorly and that it resolves before function does; its weakest lines are an uncited advice to avoid stretching during damage (the base's meta-analysis found stretching simply ineffective, REF-385) and the rodent basis of the soreness mechanism.
Protocol
Key Results
The authors' synthesis, with the sources they cite (numbers as printed in the full text):
| Topic | Statement | Cited by the authors |
|---|---|---|
| Time course of soreness | appears 12-24 h after unaccustomed eccentric exercise, peaks at 24-72 h, gone within 5-7 days | no citation for the time course itself |
| Soreness vs damage | soreness intensity is poorly correlated with the other indirect markers and does not seem to reflect the magnitude of damage | Nosaka et al. 2002 |
| Soreness vs function | soreness disappears before muscle function has fully recovered; function may stay down after the pain has resolved | Strojnik et al. 2001; Damas et al. 2016 |
| Best indirect marker | the fall in muscle strength; leukocyte invasion relates to force loss, not necessarily to soreness | Paulsen et al. 2010 |
| CK | marked inter-individual variability even under standardised eccentric protocols; extreme CK and myoglobin rises can, exceptionally, cause kidney tubulopathy | Clarkson 1992; Nosaka & Clarkson 1996; Sayers 1999 |
| Damage course | abnormalities spread to more fibres and are worse 2-3 days after exercise (primary and secondary damage); type II fibres more affected | Fridén et al. 1983 |
| What worsens damage | high vs low eccentric torque, long vs short muscle length, more contractions; arm muscles more than leg muscles, knee flexors more than knee extensors; untrained status, genetic variants, ageing, chronic disease | Nosaka & Newton 2002; Chen et al. 2011 |
| Repeated-bout effect | a first bout protects against the next; more complete after several sessions; persists for several weeks and up to 6 months, fading over time; repeated "non-damaging" bouts also protect | Nosaka et al. 2001, 2005; Chen et al. 2013 |
| RBE mechanism | neural, mechanical and cellular theories; protection in the other, unexercised limb is smaller than in the exercised one; RBE also after electrically stimulated contractions; "a unified theory is not yet available" | McHugh 2003; Howatson & van Someren 2007; Black & McCully 2008 |
| Prevention | the most useful strategy is repeated submaximal eccentric sessions of progressively increasing intensity; few evidence-based guidelines exist for stretching, cryotherapy, electric or manual therapy, vibration, nutrition or drugs | Cheung et al. 2003 (REF-1345) among others |
| Progressive programs (rehabilitation ergometers) | start at 50-75 W, target 400-500 W (over 1,200 W in competitive athletes); 2-4 days between steps up; 5-10 min rising to 20-30 min; two sessions a week the lower limit for measurable gains | Hoppeler 2016; Mueller et al. 2009 |
| Athletes | vulnerable at the start of the season, on return after injury and after an unaccustomed eccentric session; while damage persists avoid high-intensity, particularly explosive, efforts; avoid stretching; avoid NSAIDs in healthy subjects | Cheung et al. 2003; Mackey et al. 2007; Paulsen et al. 2012; stretching: no citation |
Mechanisms
Practical Application
Limitations
How this entry was checked and changed
a narrative review without a systematic method, from a group (University of Liège) that works on eccentric damage but is not the field's leading laboratory; its statements are the authors' synthesis of cited studies, several of the mechanistic ones in rodents, and a few practical lines carry no citation