Relative Roles of Central Command and the Skeletal Muscle Pump During Recovery Following Vigorous Exercise

We sought to determine the relative contributions of cessation of skeletal muscle pumping and withdrawal of central command to the rapid decrease in arterial pressure during recovery from exercise. Twelve healthy volunteers underwent three exercise sessions, each consisting of a warm-up, 3 min of cycling at 60% of maximal heart rate, and 5 min of one of the following recovery modes: seated (inactive), loadless pedaling (active), and passive cycling. Mean arterial pressure (MAP), cardiac output, thoracic impedance, and heart rate were measured. When measured 15 s after exercise, MAP decreased less ( P < 0.05) during the active (−3 ± 1 mmHg) and passive (−6 ± 1 mmHg) recovery modes than during inactive (−18 ± 2 mmHg) recovery. These differences in MAP persisted for the first 4 min of recovery from exercise. Significant maintenance of central blood volume (thoracic impedance), stroke volume, and cardiac output paralleled the maintenance of MAP during active and passive conditions during 5 min of recovery. These data indicate that engaging the skeletal muscle pump by loadless or passive pedaling helps maintain MAP during recovery from submaximal exercise. The lack of differences between loadless and passive pedaling suggests that cessation of central command is not as important.

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Decreased skeletal muscle pump activity in patients with postural tachycardia syndrome and low peripheral blood flow

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00738.2003 ◽

2004 ◽

Vol 286 (3) ◽

pp. H1216-H1222 ◽

Cited By ~ 42

Author(s):

Julian M. Stewart ◽

Marvin S. Medow ◽

Leslie D. Montgomery ◽

Kenneth McLeod

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Blood Volume ◽

Orthostatic Intolerance ◽

Low Flow ◽

Peripheral Blood Flow ◽

Muscle Pump ◽

Postural Tachycardia ◽

Calf Blood Flow ◽

Skeletal Muscle Pump

Standing translocates thoracic blood volume into the dependent body. The skeletal muscle pump participates in preventing orthostatic intolerance by enhancing venous return. We investigated the hypothesis that skeletal muscle pump function is impaired in postural tachycardia (POTS) associated with low calf blood flow (low-flow POTS) and depends in general on muscle blood flow. We compared 12 subjects that have low-flow POTS with 10 controls and 7 patients that have POTS and normal calf blood flow using strain-gauge plethysmography to measure peripheral blood flow, venous capacitance, and calf muscle pump function. Blood volume was estimated by dye dilution. We found that calf circumference was reduced in low-flow POTS (32 ± 1 vs. 39 ± 3 and 43 ± 3 cm) and, compared with controls and POTS patients with normal blood flow, is related to the reduced fraction of calf venous capacity emptied during voluntary muscle contraction (ejection fraction, 0.52 ± 0.07 vs. 0.76 ± 0.07 and 0.80 ± 0.06). We found that blood flow was linearly correlated ( rp = 0.69) with calf circumference (used as a surrogate for muscle mass). Blood volume measurements were 2.2 ± 0.3 in low-flow POTS vs. 2.6 ± 0.5 in controls ( P = 0.17) and 2.4 ± 0.7 in normal-flow POTS patients. Decreased calf blood flow may reduce calf size in POTS and thereby impair the upright ejective ability of the skeletal muscle pump and further contribute to overall reduced blood flow and orthostatic intolerance in these patients.

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