Why the study?
Does venous occlusion to the lower limb attenuate vasoconstriction in the nonexercised limb during posthandgrip muscle ischemia?
Does venous occlusion to the lower limb attenuate vasoconstriction in the nonexercised limb during posthandgrip muscle ischemia?
Increases in calf volume via venous occlusion attenuate the increase in vascular resistance in the nonexercised limb induced by muscle chemoreflex activation.
Venous occlusion may attenuate chemoreflex vasoconstriction in nonexercised limbs; leaves open whether this mechanism applies beyond acute physiology experiments.
We investigated the effects of increases in calf volume on cardiovascular responses during handgrip (HG) exercise and post-HG exercise muscle ischemia (PEMI). Seven subjects completed two trials: one control (no occlusion) and one venous occlusion (VO) session. Both trials included a baseline measurement followed by 15 min of rest (REST), 2 min of HG, and 2 min of PEMI. VO was applied at 100 mmHg via cuffs placed around both distal thighs during REST, HG, and PEMI. Mean arterial pressure, heart rate, forearm blood flow (FBF) in the nonexercised arm, and forearm vascular resistance (FVR) in the nonexercised arm (FVR) were measured. During REST and HG, there were no significant differences between trials in all parameters. During PEMI in the control trial, mean arterial pressure and FVR were significantly greater and FBF was significantly lower than baseline values (P < 0.05 for each). In contrast, in the VO trial, FBF and FVR responses were different from control responses. In the VO trial, FBF was significantly greater than in the control trial (4.7 +/- 0.5 vs. 2.5 +/- 0.3 ml x 100 ml(-1) x min(-1), P < 0.05) and FVR was significantly lower (28.0 +/- 4.8 vs. 49.1 +/- 4.6 units, respectively, P < 0.05). These results indicate that increases in vascular resistance in the nonexercised limb induced by activation of the muscle chemoreflex can be attenuated by increases in calf volume.
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Tokizawa et al. (2004) studied this question.
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