Mechanisms of force depression caused by different types of physical exercise studied by direct electrical stimulation of human quadriceps muscle

Abstract

PurposeForce production frequently remains depressed for several hours or even days after various types of strenuous physical exercise. We hypothesized that the pattern of force changes during the first hour after exercise can be used to reveal muscular mechanisms likely to underlie the decline in muscle performance during exercise as well as factors involved in the triggering the prolonged force depression after exercise.MethodsNine groups of recreationally active male volunteers performed one of the following types of exercise: single prolonged or repeated short maximum voluntary contractions (MVCs); single or repeated all-out cycling bouts; repeated drop jumps. The isometric force of the right quadriceps muscle was measured during stimulation with brief 20 and 100 Hz trains of electrical pulses given before and at regular intervals for 60 min after exercise.ResultsAll exercises resulted in a prolonged force depression, which was more marked at 20 Hz than at 100 Hz. Short-lasting (≤2 min) MVC and all-out cycling exercises showed an initial force recovery (peak after ~ 5 min) followed by a secondary force depression. The repeated drop jumps, which involve eccentric contractions, resulted in a stable force depression with the 20 Hz force being markedly more decreased after 100 than 10 jumps.ConclusionsIn accordance with our hypothesis, the results propose at least three different mechanisms that influence force production after exercise: (1) a transiently recovering process followed by (2) a prolonged force depression after metabolically demanding exercise, and (3) a stable force depression after mechanically demanding contractions.

Impaired sarcoplasmic reticulum Ca2+ release is the major cause of fatigue‐induced force loss in intact single fibres from human intercostal muscle

“…; Skurvydas et al . ). High‐intensity exercise‐induced ROS production has been implicated in the development of PLFFD (Bruton et al .…”

“…; Skurvydas et al . ; Watanabe & Wada, ). Studies in intact single fibres of rodent and amphibian skeletal muscle have revealed the underlying cellular mechanisms of fatigue to be (i) a reduced maximal myofibrillar force‐producing capacity, (ii) an impaired sarcoplasmic reticulum (SR) Ca 2+ release, and (iii) a reduced myofibrillar Ca 2+ sensitivity (Allen et al .…”

The Effect of Three Different Strategies Based on Motor Task Performance on Neuromuscular Fatigue in Healthy Men and Men with Multiple Sclerosis

“…Moreover, peripheral fatigue, i.e., decreases in electrically induced force, also depends on two processes: interactions of muscle potentiation, and fatigue [4,29]. Previous studies have shown that the performance of 100 repetitive maximal voluntary quadriceps muscle contractions leads to assertion of post-tetanic potentiation, low-frequency fatigue, and post-contractile depression [29].…”

“…Increased muscle temperature evokes a decrease in involuntary muscle force [27]. In addition, during the time of recovery, an increase in the P20/P100 factor was observed in both groups, indicating a muscle potentiation mechanism before evidential fatigue [4]. This muscle potentiation mechanism may conceal an increase in fatigue-based muscle force sensation, i.e., a higher potentiation leads to a lower force sensation [30].…”

Low frequency fatigue and changes in muscle fascicle length following eccentric exercise of the knee extensors

“…Skeletal muscle that has been subjected to eccentric exercise shows a disproportionate loss of force when electrically stimulated at low, compared to higher, frequencies (Davies & White, 1981;Kamandulis et al, 2017;Newham, Jones, & Clarkson, 1987;Skurvydas et al, 2016). This feature is relatively slow to recover and is often described as long lasting or low frequency fatigue (LFF) and may be a consequence of reduced calcium release in response to individual action potentials (Balnave & Allen, 1995;Edwards, Hill, Jones, & Merton, 1977) indicating some deficit in the mechanism of excitationcontraction (EC) coupling.…”