Why the study?
Does static handgrip and postcontraction muscle ischemia alter sympathetic outflow to resting muscles in healthy subjects?
Does static handgrip and postcontraction muscle ischemia alter sympathetic outflow to resting muscles in healthy subjects?
Stimulation of chemosensitive endings in forearm muscles induces differentiation of sympathetic neural outflow to muscles in the leg and the contralateral arm.
Answers are grounded in this paper and cite their sources.
Reveals differential sympathetic outflow to leg versus arm muscles during ischemia; extends autonomic physiology models but leaves clinical relevance open.
Simultaneous microneurographic recordings were made of muscle sympathetic activity (MSA) in the radial and the peroneal nerves of seven healthy subjects during 2-min static handgrip (30% of maximal voluntary contraction) followed by 2 min of forearm ischemia induced by arterial occlusion. At rest sympathetic burst frequency was similar in both nerves, but relative burst strengths differed between the two neurograms, suggesting that sympathetic outflows to arm and leg were not identical. Both radial and peroneal MSA were unchanged during the first minute of handgrip and increased to a similar degree during the second minute. Thus previously reported differences in vascular resistance between forearm and calf during static handgrip cannot be explained by differences in MSA to arm and leg muscles. During forearm ischemia after handgrip, peroneal MSA remained at the same level as during the second minute of handgrip but there was a further increase of radial MSA. This shows that stimulation of chemosensitive endings in forearm muscles induces differentiation of sympathetic neural outflow to muscles in the leg and the contralateral arm.
No takes yet. Share an insight, caveat, or question.
Wallin et al. (1989) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: