Evaluation of muscle metaboreflex function through graded reduction in forearm blood flow during rhythmic handgrip exercise in humans

2011 ◽  
Vol 301 (2) ◽  
pp. H609-H616 ◽  
Author(s):  
Masashi Ichinose ◽  
Stephane Delliaux ◽  
Kazuhito Watanabe ◽  
Naoto Fujii ◽  
Takeshi Nishiyasu
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Voluntary Contraction ◽  
Open Loop ◽  
Handgrip Exercise ◽  
Hemodynamic Responses ◽  
Muscle Metaboreflex ◽  
Arterial Blood

Hypoperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex. Our aim was to determine the muscle metaboreflex threshold and gain in humans by creating an open-loop relationship between active muscle blood flow and hemodynamic responses during a rhythmic handgrip exercise. Eleven healthy subjects performed the exercise at 5 or 15% of maximal voluntary contraction (MVC) in random order. During the exercise, forearm blood flow (FBF), which was continuously measured using Doppler ultrasound, was reduced in five steps by manipulating the inner pressure of an occlusion cuff on the upper arm. The FBF at each level was maintained for 3 min. The initial reductions in FBF elicited no hemodynamic changes, but once FBF fell below a threshold, mean arterial blood pressure (MAP) and heart rate (HR) increased and total vascular conductance (TVC) decreased in a linear manner. The threshold FBF during the 15% MVC trial was significantly higher than during the 5% MVC trial. The gain was then estimated as the slope of the relationship between the hemodynamic responses and FBFs below the threshold. The gains for the MAP and TVC responses did not differ between workloads, but the gain for the HR response was greater in the 15% MVC trial. Our findings thus indicate that increasing the workload shifts the threshold for the muscle metaboreflex to higher blood flows without changing the gain of the reflex for the MAP and TVC responses, whereas it enhances the gain for the HR response.

scholarly journals Absence of compensatory vasodilation with perfusion pressure challenge in exercise: evidence for and implications of the noncompensator phenotype

2018 ◽  
Vol 124 (2) ◽  
pp. 374-387 ◽  
Author(s):  
Robert F. Bentley ◽  
Jeremy J. Walsh ◽  
Patrick J. Drouin ◽  
Aleksandra Velickovic ◽  
Sarah J. Kitner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Delivery ◽  
Exercise Tolerance ◽  
Forearm Blood Flow ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Interindividual Differences ◽  
Arterial Blood ◽  
Pressor Responses

Compromising oxygen delivery (O2D) during exercise requires compensatory vasodilatory and/or pressor responses to protect O2D:demand matching. The purpose of the study was to determine whether compensatory vasodilation is absent in some healthy young individuals in the face of a sudden reduction in exercising forearm perfusion pressure and whether this affects the exercise pressor response. Twenty-one healthy young men (21.6 ± 2.0 yr) completed rhythmic forearm exercise at a work rate equivalent to 70% of their own maximal exercise vasodilation. During steady-state exercise, the exercising arm was rapidly adjusted from below to above heart level, resulting in a reduction in forearm perfusion pressure of −30.7 ± 0.9 mmHg. Forearm blood flow (ml/min; brachial artery Doppler and echo ultrasound), mean arterial blood pressure (mmHg; finger photoplethysmography), and exercising forearm venous effluent (antecubital vein catheter) measurements revealed distinct compensatory vasodilatory differences. Thirteen individuals responded with compensatory vasodilation (509 ± 128 vs. 632 ± 136 ml·min−1·100 mmHg−1; P < 0.001), while eight individuals did not (663 ± 165 vs. 667 ± 167 ml·min−1·100 mmHg−1; P = 0.6). Compensatory pressor responses between groups were not different (5.5 ± 5.5 and 9.7 ± 9.5 mmHg; P = 0.2). Forearm blood flow, O2D, and oxygen consumption were all protected in compensators (all P > 0.05) but not in noncompensators, who therefore suffered compromises to exercise performance (6 ± 14 vs. −36 ± 29 N; P = 0.004). Phenotypic differences were not explained by potassium or nitric oxide bioavailability. In conclusion, both compensator and noncompensator vasodilator phenotype responses to a sudden compromise to exercising muscle blood flow are evident. Interindividual differences in the mechanisms governing O2D:demand matching should be considered as factors influencing exercise tolerance. NEW & NOTEWORTHY In healthy young individuals, compromising submaximally exercising muscle perfusion appears to evoke compensatory vasodilation to defend oxygen delivery. Here we report the absence of compensatory vasodilation in 8 of 21 such individuals, despite their vasodilatory capacity and increases in perfusion with increasing exercise intensity being indistinguishable from compensators. The absence of compensation impaired exercise tolerance. These findings suggest that interindividual differences in oxygen delivery:demand matching efficacy affect exercise tolerance and depend on the nature of a delivery:demand matching challenge.

Is the muscle metaboreflex important in control of blood flow to ischemic active skeletal muscle in dogs?

1995 ◽  
Vol 268 (3) ◽  
pp. H980-H986 ◽  
Author(s):  
D. S. O'Leary ◽  
D. D. Sheriff
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Vascular Occlusion ◽  
Systemic Arterial Pressure ◽  
Initial Increase ◽  
Aortic Blood Flow ◽  
Muscle Metaboreflex

Ischemia of active skeletal muscle induces a reflex increase in sympathetic activity, heart rate, cardiac output, and arterial pressure, termed the muscle metaboreflex. Whether this pressor response contributes importantly in the regulation of blood flow to the ischemic active skeletal muscle is not well understood. If the pressor response is achieved without substantial vasoconstriction in the ischemic muscle, this increase in arterial pressure would act to improve muscle blood flow. Dogs performed treadmill exercise at mild (3.2 km/h, 0% grade) and moderate (6.4 km/h, 10% grade) workloads. During each workload, resistance to blood flow in the hindlimbs (Rh) was increased via graded partial inflation of a vascular occluder implanted on the terminal aorta. The closed-loop gain of the muscle metaboreflex (Gcl) was calculated, based on the steady-state changes in terminal aortic blood flow (TAQ). If no pressor response occurred, then TAQ should decrease in proportion to the increase in total Rh (the sum of resistance due to partial vascular occlusion and hindlimb vascular resistance); i.e., no reflex restoration of hindlimb blood flow would occur. However, with a reflex increase in systemic arterial pressure, TAQ could rise above the level predicted on the basis of the increase in Rh. We observed that with the initial increase in Rh during mild exercise, Gcl was not significantly different from zero (P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

2014 ◽  
Vol 306 (2) ◽  
pp. H251-H260 ◽  
Author(s):  
Kazuhito Watanabe ◽  
Masashi Ichinose ◽  
Rei Tahara ◽  
Takeshi Nishiyasu
Keyword(s):  
Individual Differences ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Coefficients Of Variation ◽  
Isometric Handgrip Exercise ◽  
Induced Changes

We tested the hypotheses that, in humans, changes in cardiac output (CO) and total peripheral vascular resistance (TPR) occurring in response to isometric handgrip exercise vary considerably among individuals and that those individual differences are related to differences in muscle metaboreflex and arterial baroreflex function. Thirty-nine healthy subjects performed a 1-min isometric handgrip exercise at 50% of maximal voluntary contraction. This was followed by a 4-min postexercise muscle ischemia (PEMI) period to selectively maintain activation of the muscle metaboreflex. All subjects showed increases in arterial pressure during exercise. Interindividual coefficients of variation (CVs) for the changes in CO and TPR between rest and exercise periods (CO: 95.1% and TPR: 87.8%) were more than twofold greater than CVs for changes in mean arterial pressure (39.7%). There was a negative correlation between CO and TPR responses during exercise ( r = −0.751, P < 0.01), but these CO and TPR responses correlated positively with the corresponding responses during PEMI ( r = 0.568 and 0.512, respectively, P < 0.01). The CO response during exercise did not correlate with PEMI-induced changes in an index of cardiac parasympathetic tone and cardiac baroreflex sensitivity. These findings demonstrate that the changes in CO and TPR that occur in response to isometric handgrip exercise vary considerably among individuals and that the two responses have an inverse relationship. They also suggest that individual differences in components of the pressor response are attributable in part to variations in muscle metaboreflex-mediated cardioaccelerator and vasoconstrictor responses.

Potentiation of the exercise pressor reflex by muscle ischemia

1989 ◽  
Vol 66 (3) ◽  
pp. 1046-1053 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Flow ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Arterial Occlusion ◽  
Acid Base Balance ◽  
Active Muscle ◽  
Arterial Blood ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Static Contraction

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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Acute ascorbic acid ingestion increases skeletal muscle blood flow and oxygen consumption via local vasodilation during graded handgrip exercise in older adults

2015 ◽  
Vol 309 (2) ◽  
pp. H360-H368 ◽  
Author(s):  
Jennifer C. Richards ◽  
Anne R. Crecelius ◽  
Dennis G. Larson ◽  
Frank A. Dinenno
Keyword(s):  
Older Adults ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Ascorbic Acid ◽  
Oxygen Consumption ◽  
Lower Body Negative Pressure ◽  
Muscle Blood Flow ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Forearm Vascular Conductance

Human aging is associated with reduced skeletal muscle perfusion during exercise, which may be a result of impaired endothelium-dependent dilation and/or attenuated ability to blunt sympathetically mediated vasoconstriction. Intra-arterial infusion of ascorbic acid (AA) increases nitric oxide-mediated vasodilation and forearm blood flow (FBF) during handgrip exercise in older adults, yet it remains unknown whether an acute oral dose can similarly improve FBF or enhance the ability to blunt sympathetic vasoconstriction during exercise. We hypothesized that 1) acute oral AA would improve FBF (Doppler ultrasound) and oxygen consumption (V̇o2) via local vasodilation during graded rhythmic handgrip exercise in older adults ( protocol 1), and 2) AA ingestion would not enhance sympatholysis in older adults during handgrip exercise ( protocol 2). In protocol 1 ( n = 8; 65 ± 3 yr), AA did not influence FBF or V̇o2 during rest or 5% maximal voluntary contraction (MVC) exercise, but increased FBF (199 ± 13 vs. 248 ± 16 ml/min and 343 ± 24 vs. 403 ± 33 ml/min; P < 0.05) and V̇o2 (26 ± 2 vs. 34 ± 3 ml/min and 43 ± 4 vs. 50 ± 5 ml/min; P < 0.05) at both 15 and 25% MVC, respectively. The increased FBF was due to elevations in forearm vascular conductance (FVC). In protocol 2 ( n = 10; 63 ± 2 yr), following AA, FBF was similarly elevated during 15% MVC (∼20%); however, vasoconstriction to reflex increases in sympathetic activity during −40 mmHg lower-body negative pressure at rest (ΔFVC: −16 ± 3 vs. −16 ± 2%) or during 15% MVC (ΔFVC: −12 ± 2 vs. −11 ± 4%) was unchanged. Our collective results indicate that acute oral ingestion of AA improves muscle blood flow and V̇o2 during exercise in older adults via local vasodilation.

Maintained exercise pressor response in heart failure

1998 ◽  
Vol 85 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Allen R. Kunselman ◽  
David H. Silber ◽  
Lawrence I. Sinoway
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Ambient Pressure ◽  
Muscle Blood Flow ◽  
Positive Pressure ◽  
Arterial Blood ◽  
Muscle Reflex ◽  
The Impact

The impact of forearm blood flow limitation on muscle reflex (metaboreflex) activation during exercise was examined in 10 heart failure (HF) (NYHA class III and IV) and 9 control (Ctl) subjects. Rhythmic handgrip contractions (25% maximal voluntary contraction, 30 contractions/min) were performed over 5 min under conditions of ambient pressure or with +50 mmHg positive pressure about the exercising forearm. Mean arterial blood pressure (MAP) and venous effluent hemoglobin (Hb) O2 saturation, lactate and H+ concentrations ([La] and [H+], respectively) were measured at baseline and during exercise. For ambient contractions, the increase (Δ) in MAP by end exercise (ΔMAP; i.e., the exercise pressor response) was the same in both groups (10.1 ± 1.2 vs. 7.33 ± 1.3 mmHg, HF vs. Ctl, respectively) despite larger Δ[La] and Δ[H+] for the HF group ( P < 0.05). With ischemic exercise, the ΔMAP for HF (21.7 ± 2.7 mmHg) exceeded that of Ctl subjects (12.2 ± 2.8 mmHg) ( P < 0.0001). Also, for HF, Δ[La] (2.94 ± 0.4 mmol) and Δ[H+] (24.8 ± 2.7 nmol) in the ischemic trial were greater than in Ctl (1.63 ± 0.4 mmol and 15.3 ± 2.8 nmol; [La] and [H+], respectively) ( P < 0.02). Hb O2 saturation was reduced in Ctl from ∼43% in the ambient trial to ∼27% with ischemia ( P < 0.0001). O2 extraction was maximized under ambient exercise conditions for HF but not for Ctl. Despite progressive increases in blood perfusion pressure over the course of ischemic exercise, no improvement in Hb O2saturation or muscle metabolism was observed in either group. These data suggest that muscle reflex activation of the pressor response is intact in HF subjects but the resulting improvement in perfusion pressure does not appear to enhance muscle oxidative metabolism or muscle blood flow, possibly because of associated increases in sympathetic vasoconstriction of active skeletal muscle.

scholarly journals Measurement of muscle blood flow and O2 uptake via near-infrared spectroscopy using a novel occlusion protocol

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Joshua J. Dennis ◽  
Chad C. Wiggins ◽  
Joshua R. Smith ◽  
Jennifer M. J. Isautier ◽  
Bruce D. Johnson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Muscle Blood Flow ◽  
Arterial Occlusion ◽  
Vascular Occlusion ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Perfect Agreement

AbstractWe describe here a novel protocol that sequentially combines venous followed by arterial occlusions to determine muscle blood flow and O2 uptake from a single measurement point using near-infrared spectroscopy (NIRS) during handgrip exercise. NIRS data were obtained from the flexor digitorum superficialis (FDS) muscle on the dominant arm of 15 young, healthy adults (3 women; 26 ± 7 years; 78.6 ± 9.1 kg). Participants completed a series of 15-s static handgrip contractions at 20, 40 and 60% of maximal voluntary contraction (MVC) immediately followed by either a: (i) venous occlusion (VO); (ii); arterial occlusion (AO); or venous then arterial occlusion (COMBO). Each condition was repeated 3 times for each exercise-intensity. The concordance correlation coefficient (CCC) and robust linear mixed effects modeling were used to determine measurement agreement between vascular occlusion conditions. FDS muscle blood flow ($${\dot{\text{Q}}}_{{{\text{FDS}}}}$$ Q ˙ FDS ) and conductance ($${\text{C}}_{{{\text{FDS}}}}$$ C FDS ) demonstrated strong absolute agreement between VO and COMBO trials from rest up to 60%MVC, as evidenced by high values for CCC (> 0.82) and a linear relationship between conditions that closely approximated the line-of-identity (perfect agreement). Conversely, although FDS muscle O2 uptake ($${{\dot {\text{V}}}}{{\text{O}}_{2{\text{FDS}}}}$$ V ˙ O 2 FDS ) displayed “substantial” to “near perfect” agreement between methods across exercise intensities (i.e., CCC > 0.80), there was a tendency for COMBO trials to underestimate $${{\dot {\text{V}}}}{{\text{O}}_{2{\text{FDS}}}}$$ V ˙ O 2 FDS by up to 7%. These findings indicate that the COMBO method provides valid estimates of $${\dot {\text{Q}}}_{{\text{FDS}}}$$ Q ˙ FDS and, to a slightly lesser extent, $${{\dot {\text{V}}}}{{\text{O}}_{2{\text{FDS}}}}$$ V ˙ O 2 FDS at rest and during static handgrip exercise up to 60%MVC. Practical implications and suggested improvements of the method are discussed.

scholarly journals Muscle metaboreflex improves O2delivery to ischemic active skeletal muscle

1999 ◽  
Vol 276 (4) ◽  
pp. H1399-H1403 ◽  
Author(s):  
Donal S. O’Leary ◽  
Robert A. Augustyniak ◽  
Eric J. Ansorge ◽  
Heidi L. Collins
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Pressor Response ◽  
Systemic Arterial Pressure ◽  
Integrative Approach ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Per Se ◽  
Hb Concentration ◽  
Ischemic Muscle

Ischemia of active skeletal muscle elicits a powerful pressor response, termed the muscle metaboreflex. We recently reported that the muscle metaboreflex pressor response acts to partially restore blood flow to the ischemic active skeletal muscle. However, because this reflex is activated by reductions in O2 delivery rather than blood flow per se, gain of the muscle metaboreflex as analyzed on the basis of blood flow alone may underestimate its true strength if this reflex also acts to increase arterial O2content. In conscious dogs chronically instrumented to measure systemic arterial pressure, cardiac output, and hindlimb blood flow, we activated the muscle metaboreflex via graded, partial reductions in hindlimb blood flow during mild (3.2 km/h) and moderate (6.4 km/h, 10% grade) workloads. At rest, during free-flow exercise, and with metaboreflex activation, we analyzed arterial blood samples for Hb concentration and O2 content and compared muscle metaboreflex gain calculations based on the ability to partially restore flow with those based on the ability to partially restore O2 delivery (blood flow × arterial O2 content). During both mild and moderate exercise, metaboreflex activation caused significant increases in arterial Hb concentration and O2 content. Metaboreflex gain quantified on the ability to partially restore O2 delivery was significantly greater than that based on restoration of blood flow during both mild and moderate workloads (0.52 ± 0.10 vs. 0.39 ± 0.08, P < 0.05, and 0.61 ± 0.05 vs. 0.46 ± 0.04, P < 0.05, respectively). We conclude that the muscle metaboreflex acts to increase both arterial O2 content and blood flow to ischemic muscle such that when combined, O2 delivery is substantially increased and metaboreflex gain is greater when analyzed with a more integrative approach.

Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise

2001 ◽  
Vol 90 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Maureen J. MacDonald ◽  
Heather L. Naylor ◽  
Michael E. Tschakovsky ◽  
Richard L. Hughson
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Muscle Blood Flow ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Exercise Bout ◽  
Handgrip Exercise ◽  
Acid Base ◽  
Rate Of Increase ◽  
Forearm Exercise

We used an exercise paradigm with repeated bouts of heavy forearm exercise to test the hypothesis that alterations in local acid-base environment that remain after the first exercise result in greater blood flow and O2 delivery at the onset of the second bout of exercise. Two bouts of handgrip exercise at 75% peak workload were performed for 5 min, separated by 5 min of recovery. We continuously measured blood flow using Doppler ultrasound and sampled venous blood for O2 content, Pco 2, pH, and lactate and potassium concentrations, and we calculated muscle O2uptake (V˙o 2). Forearm blood flow was elevated before the second exercise compared with the first and remained higher during the first 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min, P < 0.05). Flow was not different at 5 min. Arteriovenous O2 content difference was lower before the second bout (4.6 ± 0.9 vs. 7.2 ± 0.7 ml O2/dl) and higher by 30 s of exercise (11.2 ± 0.7 vs. 10.8 ± 0.7 ml O2/dl, P < 0.05). Muscle V˙o 2was unchanged before the start of exercise but was elevated during the first 30 s of the transition to the second exercise bout (26.0 ± 2.1 vs. 20.0 ± 0.9 ml/min, P < 0.05). Changes in venous blood Pco 2, pH, and lactate concentration were consistent with reduced reliance on anaerobic glycolysis at the onset of the second exercise bout. These data show that limitations of muscle blood flow can restrict the adaptation of oxidative metabolism at the onset of heavy muscular exertion.

Ischemic exercise and the muscle metaboreflex

2000 ◽  
Vol 89 (4) ◽  
pp. 1432-1436 ◽  
Author(s):  
Jacob A. Cornett ◽  
Michael D. Herr ◽  
Kristen S. Gray ◽  
Michael B. Smith ◽  
Qing X. Yang ◽  
...  
Keyword(s):  
Maximum Voluntary Contraction ◽  
Random Order ◽  
Muscle Afferents ◽  
Voluntary Contraction ◽  
The Other ◽  
Reflex Response ◽  
Handgrip Exercise ◽  
Muscle Metaboreflex ◽  
Effort Level ◽  
Arterial Blood

In exercising muscle, interstitial metabolites accumulate and stimulate muscle afferents. This evokes the muscle metaboreflex and raises arterial blood pressure (BP). In this report, we examined the effects of tension generation on muscle metabolites and BP during ischemic forearm exercise in humans. Heart rate (HR), BP, Pi, H2PO4 −, and pH (31P-NMR spectroscopy) data were collected in 10 normal healthy men (age 23 ± 1 yr) during rhythmic handgrip exercise. After baseline measurements, the subjects performed rhythmic handgrip for 2 min. At 2 min, a 250-mmHg occlusion cuff was inflated, and ischemic handgrip exercise was continued until near fatigue (Borg 19). Measurements were continued for an additional 30 s of ischemia. This protocol was performed at 15, 30, 45, and 60% of the subjects' maximum voluntary contraction (MVC) in random order. As tension increased, the time to fatigue decreased. In addition, mean arterial pressure and HR were higher at 60% MVC than at any of the other lower tensions. The NMR data showed significantly greater increases in H2PO4 −, Pi, and H+at 60% than at 15 and 30% MVC. Therefore, despite the subjects working to the same perceived effort level, a greater reflex response (represented by BP and HR data) was elicited at 60% MVC than at any of the other ischemic tensions. These data are consistent with the hypothesis that, as tension increases, factors aside from insufficient blood flow contribute to the work effect on muscle metabolites and the magnitude of the reflex response.

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