TY - JOUR
T1 - Contribution of pH, diprotonated phosphate and potassium for the reflex increase in blood pressure during handgrip
AU - Boushel, R.
AU - Madsen, P.
AU - Nielsen, H. B.
AU - Quistorff, B.
AU - Secher, N. H.
PY - 1998
Y1 - 1998
N2 - The relative importance of pH, diprotonated phosphate (H2PO4-) and potassium (K+) for the reflex increase in mean arterial pressure (MAP) during exercise was evaluated in seven subjects during rhythmic handgrip at 15 and 30% maximal voluntary contraction (MVC), followed by post-exercise muscle ischaemia (PEMI). During 15% MVC, MAP rose from 92 ± 1 to 103 ± 2 mmHg, [K+] from 4.1 ± 0.1 to 5.1 ± 0.1 mmol L-1, while the intracellular (7.00 ± 0.01 to 6.80 ± 0.06) and venous pH fell (7.39 ± 0.01 to 7.30 ± 0.01) (P < 0.05). The intracellular [H2PO4-] increased 8.4 ± 2 mmol kg-1 and the venous [H2PO4-] from 0.14 ± 0.01 to 0.16 ± 0.01 mmol L-1 (P < 0.05). During PEMI, MAP remained elevated along with the intracellular [H2PO4-] as well as a low intracellular and venous pH. However, venous [K+] and [H2PO4-] returned to the level at rest. During 30% MVC handgrip, MAP rose to 130 ± 3 mmHg, [K+] to 5.8 ± 0.2 mmol L-1, the intracellular and extracellular [H2PO4-] by 20 ± 5 mmol kg-1 and to 0.20 ± 0.02 mmol L-1, respectively, while the intracellular (6.33 ± 0.06) and venous pH fell (7.23 ± 0.02) (P < 0.05). During post-exercise muscle ischaemia all variables remained close to the exercise levels. Analysis of each variable as a predictor of blood pressure indicated that only the intracellular pH and diprotonated phosphate were linked to the reflex elevation of blood pressure during handgrip.
AB - The relative importance of pH, diprotonated phosphate (H2PO4-) and potassium (K+) for the reflex increase in mean arterial pressure (MAP) during exercise was evaluated in seven subjects during rhythmic handgrip at 15 and 30% maximal voluntary contraction (MVC), followed by post-exercise muscle ischaemia (PEMI). During 15% MVC, MAP rose from 92 ± 1 to 103 ± 2 mmHg, [K+] from 4.1 ± 0.1 to 5.1 ± 0.1 mmol L-1, while the intracellular (7.00 ± 0.01 to 6.80 ± 0.06) and venous pH fell (7.39 ± 0.01 to 7.30 ± 0.01) (P < 0.05). The intracellular [H2PO4-] increased 8.4 ± 2 mmol kg-1 and the venous [H2PO4-] from 0.14 ± 0.01 to 0.16 ± 0.01 mmol L-1 (P < 0.05). During PEMI, MAP remained elevated along with the intracellular [H2PO4-] as well as a low intracellular and venous pH. However, venous [K+] and [H2PO4-] returned to the level at rest. During 30% MVC handgrip, MAP rose to 130 ± 3 mmHg, [K+] to 5.8 ± 0.2 mmol L-1, the intracellular and extracellular [H2PO4-] by 20 ± 5 mmol kg-1 and to 0.20 ± 0.02 mmol L-1, respectively, while the intracellular (6.33 ± 0.06) and venous pH fell (7.23 ± 0.02) (P < 0.05). During post-exercise muscle ischaemia all variables remained close to the exercise levels. Analysis of each variable as a predictor of blood pressure indicated that only the intracellular pH and diprotonated phosphate were linked to the reflex elevation of blood pressure during handgrip.
KW - Blood pressure
KW - Exercise
KW - Heart rate
KW - Nuclear magnetic resonance
UR - http://www.scopus.com/inward/record.url?scp=0031736681&partnerID=8YFLogxK
U2 - 10.1046/j.1365-201X.1998.00429.x
DO - 10.1046/j.1365-201X.1998.00429.x
M3 - Journal article
C2 - 9853014
AN - SCOPUS:0031736681
SN - 0001-6772
VL - 164
SP - 269
EP - 275
JO - Acta Physiologica Scandinavica
JF - Acta Physiologica Scandinavica
IS - 3
ER -