Editing Exercise physiology (section)

=== Intense activity ===
Researchers once attributed fatigue to a build-up of lactic acid in muscles.<ref>{{Cite book |last=Hermansen |first=L |title=Ciba Foundation Symposium 82 - Human Muscle Fatigue: Physiological Mechanisms |work=Ciba Foundation Symposium |year=1981 |isbn=9780470715420 |series=Novartis Foundation Symposia |volume=82 |pages=75–88 |chapter=Effect of Metabolic Changes on Force Generation in Skeletal Muscle During Maximal Exercise |doi=10.1002/9780470715420.ch5 |pmid=6913479}}</ref> However, this is no longer believed.<ref>{{Cite journal |last=Brooks |first=GA |year=2001 |title=Lactate doesn't necessarily cause fatigue: Why are we surprised? |journal=The Journal of Physiology |volume=536 |issue=Pt 1 |pages=1 |doi=10.1111/j.1469-7793.2001.t01-1-00001.x |pmc=2278833 |pmid=11579151}}</ref><ref>{{Cite journal |last=Gladden |first=LB |year=2004 |title=Lactate metabolism: A new paradigm for the third millennium |journal=The Journal of Physiology |volume=558 |issue=Pt 1 |pages=5–30 |doi=10.1113/jphysiol.2003.058701 |pmc=1664920 |pmid=15131240}}</ref> Rather, lactate may stop muscle fatigue by keeping muscles fully responding to nerve signals.<ref>{{Cite journal |vauthors=Pedersen TH, Nielsen OB, Lamb GD, Stephenson DG |year=2004 |title=Intracellular acidosis enhances the excitability of working muscle |journal=Science |volume=305 |issue=5687 |pages=1144–7 |bibcode=2004Sci...305.1144P |doi=10.1126/science.1101141 |pmid=15326352 |s2cid=24228666}}</ref> The available oxygen and energy supply, and disturbances of muscle ion homeostasis are the main factors determining exercise performance, at least during brief very intense exercise.{{cn|date=April 2025}}

Each [[muscle contraction#Skeletal muscle|muscle contraction]] involves an [[action potential]] that activates voltage sensors, and so releases [[Voltage-dependent calcium channel|Ca<sup>2+</sup> ions]] from the [[muscle fibre]]'s [[Sarcoplasmic reticulum#Sarcoplasmic reticulum|sarcoplasmic reticulum]]. The action potentials that cause this also require ion changes:  [[Sodium channel#Voltage-gated|Na influxes]] during the [[depolarization]] phase and K effluxes for the [[repolarization]] phase. [[Chloride channel|Cl<sup>−</sup> ions]] also diffuse into the sarcoplasm to aid the repolarization phase. During intense muscle contraction, the ion pumps that maintain homeostasis of these ions are inactivated and this (with other ion related disruption) causes ionic disturbances. This causes cellular membrane depolarization, inexcitability, and so muscle weakness.<ref>{{Cite journal |last=McKenna |first=MJ |last2=Bangsbo |first2=J |last3=Renaud |first3=JM |year=2008 |title=Muscle K<sup>+</sup>, Na<sup>+</sup>, and Cl disturbances and Na<sup>+</sup>-K<sup>+</sup> pump inactivation: Implications for fatigue |journal=Journal of Applied Physiology |volume=104 |issue=1 |pages=288–95 |doi=10.1152/japplphysiol.01037.2007 |pmid=17962569 |s2cid=25190764}}</ref> Ca<sup>2+</sup> leakage from type 1 [[ryanodine receptor]]) channels has also been identified with fatigue.<ref>{{Cite journal |last=Bellinger |first=AM |last2=Reiken |first2=S |last3=Dura |first3=M |last4=Murphy |first4=PW |last5=Deng |first5=SX |last6=Landry |first6=DW |last7=Nieman |first7=D |last8=Lehnart |first8=SE |last9=Samaru |first9=M |last10=Lacampagne |first10=A. |last11=Marks |first11=A. R. |display-authors=8 |year=2008 |title=Remodeling of ryanodine receptor complex causes "leaky" channels: A molecular mechanism for decreased exercise capacity |journal=Proceedings of the National Academy of Sciences of the United States of America |volume=105 |issue=6 |pages=2198–202 |bibcode=2008PNAS..105.2198B |doi=10.1073/pnas.0711074105 |pmc=2538898 |pmid=18268335 |doi-access=free}}</ref>

[[File:Dorando Pietri 1908.jpg|right|thumb|300px|[[Dorando Pietri]] about to collapse at the Marathon finish at the 1908 London Olympic Games]]