Post-activation Potentiation Versus Post-activation Performance Enhancement in Humans: Historical Perspective, Underlying Mechanisms, and Current Issues

Abstract

Post-activation potentiation (PAP) is a well-described phenomenon with a short half-life (~28 s) that enhances muscle force production at submaximal levels of calcium saturation (i.e., submaximal levels of muscle activation). It has been largely explained by an increased myosin light chain phosphorylation occurring in type II muscle fibers, and its effects have been quantified in humans by measuring muscle twitch force responses to a bout of muscular activity. However, enhancements in (sometimes maximal) voluntary force production detected several minutes after high-intensity muscle contractions are also observed, which are also most prominent in muscles with a high proportion of type II fibers. This effect has been considered to reflect PAP. Nonetheless, the time course of myosin light chain phosphorylation (underpinning "classic" PAP) rarely matches that of voluntary force enhancement and, unlike PAP, changes in muscle temperature, muscle/cellular water content, and muscle activation may at least partly underpin voluntary force enhancement; this enhancement has thus recently been called post-activation performance enhancement (PAPE) to distinguish it from "classical" PAP. In fact, since PAPE is often undetectable at time points where PAP is maximal (or substantial), some researchers have questioned whether PAP contributes to PAPE under most conditions in vivo in humans. Equally, minimal evidence has been presented that PAP is of significant practical importance in cases where multiple physiological processes have already been upregulated by a preceding, comprehensive, active muscle warm-up. Given that confusion exists with respect to the mechanisms leading to acute enhancement of both electrically evoked (twitch force; PAP) and voluntary (PAPE) muscle function in humans after acute muscle activity, the first purpose of the present narrative review is to recount the history of PAP/PAPE research to locate definitions and determine whether they are the same phenomena. To further investigate the possibility of these phenomena being distinct as well as to better understand their potential functional benefits, possible mechanisms underpinning their effects will be examined in detail. Finally, research design issues will be addressed which might contribute to confusion relating to PAP/PAPE effects, before the contexts in which these phenomena may (or may not) benefit voluntary muscle function are considered.

Keywords: methodology; muscle; myosin phosphorylation; neuromuscular; performance; temperature; warm-up.

Figure 1

Many forms of potentiation have been described in human (and other) muscles (top bar). Staircase and treppe, post-tetanic potentiation, and post-activation potentiation have been well described and are observed as an increase in forces produced during muscle twitch (or low-frequency tetanic) stimulations. Post-activation performance enhancement has been studied more recently (our definition was first used in Cuenca-Fernandez et al., 2017), and is observed as an increase in voluntary [sometimes maximal (MVC)] muscle force, and has a different time course of action compared to other forms of potentiation (bottom bar).

Figure 2

Time course (with example error bars) of post-activation potentiation (PAP) measured as the torque evoked during a twitch contraction (T_Tw) versus post-activation performance enhancement (PAPE) measured as the torque produced during a voluntary contraction (T_Vol). PAP and PAPE exhibit different temporal profiles, suggesting that they are at least partly different phenomena. Data for illustrative purposes only; experimental data can be seen in Seitz et al. (2015); gray solid line indicates that PAP would be higher at time points < 1 min (>80% according to Hamada et al., 2000). Note: functions are plotted from 1 min because the first experimental data were collected at this time point.

Figure 3

Proposed mechanism of (classic) post-activation potentiation (PAP). (A) Calcium ions activate myosin light chain kinase (MLCK) subsequent to calcium-calmodulin interaction. MLCK then phosphorylates the myosin regulatory light chain (MRLC), which is believed to trigger the rotation of the myosin head away from the thick filament (myosin backbone) toward the thin filament (light color myosin head in panel B). Removal or reuptake of calcium triggers the dissociation of calmodulin and inactivation of MLCK. Dephosphorylation of the MRLC by myosin light chain phosphatase (MLCP) completes the process of potentiation removal. (B) MRLC phosphorylation and subsequent rotation of the myosin head (light color) increases the probability of the head attaching to actin, and thus force production. At submaximal (i.e., below saturating) levels of calcium, this process increases force output at a given calcium concentration, i.e., calcium sensitivity. Since phosphorylation is rapid but dephosphorylation is relatively slow, a period of contractile activity (e.g., a warm-up period) is sufficient to augment contractile properties in subsequent contractions, even if a short period of rest is imposed (e.g., contractions are intermittent) (Manning and Stull, 1979).

Figure 4

Potential factors influencing post-activation potentiation (PAP) and post-activation performance enhancement (PAPE). The smaller and more transient PAP effect (left circle) is largely explained by myosin regulatory light chain phosphorylation (although other factors may play a small role), and may be briefly inhibited by factors associated with fatigue. The longer-lasting PAPE effect (right circle) may potentially be associated with increases in muscle temperature and muscle water, although enhancements in muscle activation (partly through motivation) may influence performance, while it may be inhibited for several minutes by residual fatigue or motor pattern interference (perseveration) effects. Thus, there may be minimal commonality of mechanism. However, while the mechanisms underpinning PAP are thought to be relatively well defined, there is a lack of evidence regarding the mechanisms that contribute to PAPE.