Coexistence of potentiation and fatigue in skeletal muscle

Abstract

Twitch potentiation and fatigue in skeletal muscle are two conditions in which force production is affected by the stimulation history. Twitch potentiation is the increase in the twitch active force observed after a tetanic contraction or during and following low-frequency stimulation. There is evidence that the mechanism responsible for potentiation is phosphorylation of the regulatory light chains of myosin, a Ca 2+ -dependent process. Fatigue is the force decrease observed after a period of repeated muscle stimulation. Fatigue has also been associated with a Ca 2+ -related mechanism: decreased peak Ca 2+ concentration in the myoplasm is observed during fatigue. This decrease is probably due to an inhibition of Ca 2+ release from the sarcoplasmic reticulum. Although potentiation and fatigue have opposing effects on force production in skeletal muscle, these two presumed mechanisms can coexist. When peak myoplasmic Ca 2+ concentration is depressed, but myosin light chains are relatively phosphorylated, the force response can be attenuated, not different, or enhanced, relative to previous values. In circumstances where there is interaction between potentiation and fatigue, care must be taken in interpreting the contractile responses.

Effects of acute fatigue on the volitional and magnetically-evoked electromechanical delay of the knee flexors in males and females

“…It is plausible that these changes facilitate a biological conservation of resources during energy-costly volitional exercise efforts, while simultaneously offering enhanced reflex and 'emergency' capabilities to resist mechanical threats to musculoskeletal integrity. While metabolically mediated increases in sensitivity of muscle contractile proteins to Ca 2+ may represent the processes underlying potentiated muscle force characteristics (Rassier and MacIntosh 2000), exercise-related changes to the compliance characteristics of the musculoskeletal system may represent the principal potentiating processes in the present study. This may be particularly true considering that the major proportion of EMD is accounted for by lengthening of the SEC (Komi 1979;Zhou et al 1995).…”

“…Improvements of electrically-evoked peak twitch force (Rassier and MacIntosh 2000) and EMD (Sahlin and Seger 1995) have been described following acute and prolonged exercise protocols, respectively. It is plausible that these changes facilitate a biological conservation of resources during energy-costly volitional exercise efforts, while simultaneously offering enhanced reflex and 'emergency' capabilities to resist mechanical threats to musculoskeletal integrity.…”

Repeated exercise stress impairs volitional but not magnetically evoked electromechanical delay of the knee flexors

“…For example, while PF V performance was almost fully-restored within 6-minutes of the cessation of fatiguing exercise, the recovery of EMD V to baseline performance was not achieved during the same time period. The differential patterns of restoration to estimates of PF V and EMD V performance throughout exercise and acute recovery may reflect varying degrees of adaptation and interactions within conductive (Zhou et al, 1998; O'Leary, Hope, Sale, 1997), contractile, and elastic properties (Rassier & Macintosh, 2000;Stone, 1992). Alongside fatigue-related limitations to the peripheral processes involved in the conversion of excitation into muscle force (Kent-Braun, 1999), increased intra-muscular temperature with correspondingly greater tissue compliance and increased time to stretch the series elastic component (Zhou et al, 1998) Peak twitch force (PTFE) was reduced by up to 23 % compared to baseline performance following the fourth episode of exercise (200s) (21.4 ± 13.8 vs. 16.4 ± 14.6 N) and remained impaired at this level throughout the cessation of exercise and recovery (500s).…”

Postactivation Potentiation Following Different Modes of Exercise

“…Increased muscular activity results in decreased neuromuscular force generation and fatigue (20), having a negative impact on subsequent strength and power performance. In contrast, optimal previous muscular activity can increase force generation and improve subsequent strength and power performance, a phenomenon termed post-activation potentiation (PAP,22).…”

“…This enhancement has been primarily attributed to two mechanisms; regulatory light chains phosphorylation and increased recruitment of motor units. Regulatory light chains phosphorylation has been shown to increase the sensitivity of the actin-myosin interaction to the Ca 2+ released from the sarcoplasmic reticulum and alter the structure of the myosin head, resulting in a higher force-producing state for the myosin cross-bridges (20). For the second mechanism, it is postulated that previous contractions increase the excitation potential across the spinal cord, which lasts for several minutes following the initial contractions, resulting in increased post-synaptic potentials and, subsequently, increased force generation capacity (8).…”