Venous blood gas and metabolite response to low-intensity muscle contractions with external limb compression.
The effect of low-intensity resistance exercise with external limb compression (100 [EC100] and 160 [EC160] mm Hg) on limb blood flow and venous blood gas-metabolite response was investigated and compared with that of high-intensity resistance exercise (no external compression). Unilateral elbow flexion muscle contractions were performed at 20% (75 repetitions, 4 sets, 30-second rest intervals) and 70% of 1-repetition maximum (1-RM; 3 sets, each set was until failure, 3-minute rest intervals). Precontraction brachial arterial blood flow (Doppler ultrasound) was reduced with EC100 or EC160 (56% and 39% of baseline value, respectively) compared with no external compression (control). At 20% 1-RM, brachial arterial blood flow increased after contractions performed with EC160 (190%), but not with the others. Decreases in venous oxygen partial pressure (P(v)O(2)) and venous oxygen saturation (S(v)O(2)) were greater during EC100 and EC160 than control (mean [SE]: P(v)O(2), 28 [3] vs 26 [2] vs 33 [2] mm Hg; S(v)O(2), 41% [5%] vs 34% [4%] vs 52% [5%], respectively). Changes in venous pH (pH(v)), venous carbon dioxide partial pressure (P(v)CO(2)), and venous lactate concentration ([L(-)](v)) were greater with EC160 than EC100 and/or control (pH(v), 7.19 [0.01] vs 7.25 [0.01] vs 7.27 [0.02]; P(v)CO(2), 72 [3] vs 64 [2] vs 60 [3] mm Hg; [L(-)](v), 5.4 [0.6] vs 3.7 [0.4] vs 3.0 [0.4] mmol/L, respectively). Seventy percent 1-RM contractions resulted in greater changes in pH(v) (7.14 [0.02]), P(v)CO(2) (91 [5] mm Hg), and [L(-)](v) (7.0 [0.5] mmol/L) than EC100 and EC160, but P(v)O(2) (30 [4] mm Hg) and S(v)O(2) (40% [3%]) were similar. In conclusion, changes in pH(v), P(v)CO(2), and [L(-)](v), but not in P(v)O(2) and S(v)O(2), are sensitive to changes in relative, "internal" intensity of low-intensity muscle contractions caused by reduced blood flow (EC160) or high-intensity muscle contractions. Given the magnitude of the changes in pH(v), P(v)CO(2), and [L(-)](v), it appears plausible that they may be involved in stimulating the observed increase in muscle activation via group III and IV afferents.
Yasuda
Tomohiro
T
Department of Ischemic Circulatory Physiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. yasuda@h.k.u-tokyo.ac.jp
Abe
Takashi
T
Brechue
William F
WF
Iida
Haruko
H
Takano
Haruhito
H
Meguro
Kentaro
K
Kurano
Miwa
M
Fujita
Satoshi
S
Nakajima
Toshiaki
T
D000328:Adult; D001784:Blood Gas Analysis; D001916:Brachial Artery / Q000737:chemistry / Q000473:pathology; D003251:Constriction, Pathologic / Q000097:blood; D005121:Extremities / Q000098:blood supply* / Q000473:pathology* / Q000502:physiology; D005740:Gases / Q000032:analysis / Q000097:blood* / Q000378:metabolism*; D006801:Humans; D008297:Male; D055442:Metabolome / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology*; D005082:Physical Exertion / Q000502:physiology; D011312:Pressure; D012039:Regional Blood Flow / Q000502:physiology; D055070:Resistance Training; D014680:Veins / Q000737:chemistry / Q000502:physiology; D055815:Young Adult
D005740:Gases