Abstract
We have previously reported that there are inter-individual differences in the cardiovascular responses to experimental muscle pain, which are consistent over time: intramuscular infusion of hypertonic saline, causing pain lasting ~60 min, increases muscle sympathetic nerve activity (MSNA)—as well as blood pressure and heart rate—in certain subjects, but decrease it in others. Here, we tested the hypothesis that baseline physiological parameters (resting MSNA, heart rate, blood pressure, heart rate variability) determine the cardiovascular responses to long-lasting muscle pain. MSNA was recorded from the common peroneal nerve, together with heart rate and blood pressure, during a 45-min intramuscular infusion of hypertonic saline solution into the tibialis anterior of 50 awake human subjects (25 females and 25 males). Twenty-four subjects showed a sustained increase in mean amplitude of MSNA (160.9 ± 7.3%), while 26 showed a sustained decrease (55.1 ± 3.5%). Between the increasing and decreasing groups there were no differences in baseline MSNA (19.0 ± 1.5 vs. 18.9 ± 1.2 bursts/min), mean BP (88.1 ± 5.2 vs. 88.0 ± 3.8 mmHg), HR (74.7 ± 2.0 vs. 72.8 ± 1.8 beats/min) or heart rate variability (LF/HF 1.8 ± 0.2 vs. 2.2 ± 0.3). Furthermore, neither sex nor body mass index had any effect on whether MSNA increased or decreased during tonic muscle pain. We conclude that the measured baseline physiological parameters cannot account for the divergent sympathetic responses during tonic muscle pain.
Highlights
Pain is important for survival by helping to avoid tissue damage, mobilizing all relevant homeostatic systems for a fight-and-flight response or, alternatively, promoting conservation of energy, and promoting healing (Craig, 2002)
We showed that a bolus (0.5 ml) injection of hypertonic saline into the tibialis anterior muscle caused a sustained increase in muscle sympathetic nerve activity (MSNA), and a modest increase in blood pressure and heart rate (Burton et al, 2009a), while there was only a transient increase in skin sympathetic nerve activity (SSNA)—the latter being consistent with an arousal rather than reflex response (Burton et al, 2009b)
Muscle sympathetic nerve activity (MSNA) increased during tonic pain in the subject depicted in Figure 1; it is apparent that blood pressure increased
Summary
Pain is important for survival by helping to avoid tissue damage, mobilizing all relevant homeostatic systems for a fight-and-flight response or, alternatively, promoting conservation of energy, and promoting healing (Craig, 2002). Subsequent studies confirmed Lewis’ findings that muscle pain was associated with a fall in blood pressure and bradycardia in awake human subjects (Feinstein et al, 1954). Since these early observations by Lewis and Feinstein, very few studies have examined the effects of pain on the cardiovascular system in awake human subjects. We have been using subcutaneous or intramuscular injection of hypertonic saline—a specific stimulus for nociceptors (Graven-Nielsen and Mense, 2001)—to study the effects of acute pain on the cardiovascular system in awake human subjects. We showed that about half of the subjects showed a sustained increase in MSNA, blood pressure, and heart rate during tonic muscle pain, while the other half showed sustained decreases (Fazalbhoy et al, 2012, 2014)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
