Knowledge of the psychophysiological responses that characterize optimal motor performance is required to inform biofeedback interventions. This experiment compared cortical, cardiac, muscular, and kinematic activity in 10 experts and 10 novices as they performed golf putts in low- and high-pressure conditions. Results revealed that in the final seconds preceding movement, experts displayed a greater reduction in heart rate and EEG theta, high-alpha, and beta power, when compared to novices. EEG high-alpha power also predicted success, with participants producing less high-alpha power in the seconds preceding putts that were holed compared to those that were missed. Increased pressure had little impact on psychophysiological activity. It was concluded that greater reductions in EEG high-alpha power during preparation for action reflect more resources being devoted to response programming, and could underlie successful accuracy-based performance.

It is well established that performance is influenced by pressure, but the underlying mechanisms of the pressure‐performance relationship are poorly understood. To address this important issue, the current experiment evaluated psychological, physiological, and kinematic factors as mediators of the pressure‐performance relationship. Psychological, physiological, and kinematic responses to three levels of competitive pressure were measured in 23 males and 35 females during a golf putting task. Pressure manipulations impaired putting performance. Self‐reported anxiety, effort, and perceived pressure were increased. Heart rate, heart rate variability, muscle activity, and lateral clubhead acceleration were also elevated. Mediation analyses revealed that effort, muscle activity, and lateral acceleration partially mediated the decline in performance. Results confirmed that pressure elicits effects on performance through multiple pathways.

Catastrophizing is reliably associated with increased reports of clinical and experimental pain. To test the hypothesis that catastrophizing may heighten pain experience by increasing nociceptive transmission through spinal gating mechanisms, the present study examined catastrophizing as a predictor of pain ratings and nociceptive flexion reflex (NFR) thresholds in 88 young adult men (n = 47) and women (n = 41). The NFR threshold was defined as the intensity of electrocutaneous sural nerve stimulation required to elicit a withdrawal response from the biceps femoris muscle of the ipsilateral leg. Participants completed an assessment of their NFR threshold and then provided pain ratings using both a numerical rating scale (NRS) and the short-form McGill pain questionnaire (SF-MPQ). Pain catastrophizing was assessed using the catastrophizing subscale of the coping strategies questionnaire (CSQ). Although catastrophizing was positively related to both NRS and SF-MPQ pain ratings, catastrophizing was not significantly related to NFR threshold. These findings suggest that differential modulation of spinal nociceptive input may not account for the relationship between catastrophizing and increased pain.

Carotid baroreceptor stimulation has been shown to dampen pain. This study tested, in 40 normotensive adults, the hypothesis that pain is lower during systole when arterial baroreceptor stimulation is maximal than diastole when stimulation is minimal. The sural nerve was stimulated electrocutaneously to obtain a nociceptive flexion reflex (NFR) threshold, and then stimulation was delivered for 28 trials at 100% NFR threshold at seven intervals after the R-wave. Nociceptive responding was indexed by electromyographic (EMG) activity elicited in the biceps femoris. Significant variations in EMG activity occurred across the cardiac cycle, with less activity midcycle, indicating that the NFR response was attenuated during systole compared to diastole. Stimulation of baroreceptors by natural changes in blood pressure during the cardiac cycle dampened nociception, and accordingly, the data support the arterial baroreflex mechanism of hypertensive hypoalgesia.

The arterial baroreflex may mediate hypertensive hypoalgesia. Carotid baroreceptors can be artificially stimulated by neck suction and inhibited by compression. Effects of brief neck suction and compression on nociceptive responding and pain were studied in 25 normotensive adults. The sural nerve was electrocutaneously stimulated at threshold intensity during systole or diastole combined with neck suction, neck compression, or no pressure. Nociceptive responding was indexed by electromyographic activity elicited in the biceps femoris. Participants rated the intensity of sural stimulation. Although artificial baroreceptor stimulation (suction) did not affect nociceptive responding, baroreceptor inhibition (compression) reduced pain ratings. In contrast, natural baroreceptor stimulation during systole reduced nociceptive responding compared to diastole, but did not affect pain ratings. The data provide partial support for baroreflex modulation of pain.