The reflex responses to static contraction are augmented by ischemia. The metabolic 'error signals' that are responsible for these observed responses are unknown. Therefore this study was designed to test the hypothesis that static contraction-induced pressor responses, which are enhanced during muscle ischemia, are the result of alterations in muscle oxygenation, acid-base balance, and K+. Thus, in 36 cats, the pressor response, active muscle blood flow, and muscle venous pH, PCO2, PO2, lactate, and K+ were compared during light and intense static contractions with and without arterial occlusion. During light contraction (15-16% of maximal), active muscle blood flow increased without and decreased with arterial occlusion (+35 ± 12 vs. -60 ± 11%). Arterial occlusion augmented these pressor responses by 132 ± 25%. Without arterial occlusion, changes (P < 0.05) were seen in PO2, O2 content, PCO2, and K+. Lactate and pH were unchanged. With arterial occlusion, changes in muscle PCO2 were augmented and significant changes were seen in pH and lactate. During intense static contraction (67-69% of maximal), muscle blood flow decreased without arterial occlusion (-39 ± 9%) and decreased further during occlusion (-81 ± 6%). Arterial occlusion augmented the pressor responses by 39 ± 12%. All metabolic variables increased during contraction without arterial occlusion, but occlusion failed to augment any of these changes. These data suggest that light static ischemic contractions cause increases in muscle PCO2 and lactate and decreases in pH that may signal compensatory reflex-induced changes in arterial blood pressure. On the other hand, intense ischemic static contractions may cause changes in other unidentified ischemic muscle metabolites that contribute to this metabolic error signal.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Applied Physiology|
|State||Published - 1989|
ASJC Scopus subject areas
- Orthopedics and Sports Medicine
- Physical Therapy, Sports Therapy and Rehabilitation