Min Of Isometric Handgrip Exercise Research Articles

Low Ocular Perfusion Pressure Values at Rest and during Resistance Exercise in Offspring of Glaucoma Patients.

To compare the ocular perfusion pressure (OPP) response during physical exercise in individuals with and without a family history (FH+, FH-) of glaucoma. Thirty-four subjects, divided into FH+ and FH- groups, realized 3 min at rest, 3 min of isometric handgrip exercise at 30% of maximal voluntary contraction, followed by 3 min of recovery. Blood pressure (Dixtal® automatic device) and intraocular pressure (Goldmann applanation tonometer) were measured during rest, exercise, and recovery. The mean OPP (mOPP) was calculated. In the FH+ group (17 subjects), baseline mOPP values were significantly lower than in the FH- group (17 subjects) (right eye: P < 0.001, left eye: P < 0.001, respectively). During exercise, both the FH+ and FH- groups showed a similar increase in mOPP in both eyes (right eye: FH+: 38 ± 4 mmHg vs. 51 ± 7 mmHg, FH-: 48 ± 5 mmHg vs. 57 ± 9 mmHg, P < 0.001; left eye: FH+: 39 ± 3 mmHg vs. 51 ± 7 mmHg; FH-: 46 ± 5 mmHg vs. 58 ± 8 mmHg, P < 0.001, respectively). However, the FH+ group maintained significantly lower mOPP values compared to the FH- group in the right and left eyes (group effect: P = 0.002, P = 0.002, respectively). The percentage of increase in mOPP in the FH+ group was greater compared to the FH- group during exercise (right eye: 34.1% ± 15.9% vs. 22.1% ± 13.2%, respectively; P = 0.025; left eye: 33.2% ± 17.7% vs. 22.4% ± 13.7%, respectively, P = 0.056). mOPP increased during physical exercise in both groups, but the FH+ group had lower absolute values. In addition, the FH+ group appears to demonstrate a higher percentage increase in mOPP compared to the FH- group.

Muscle Metaboreflex Control of Sympathetic Activity Is Preserved after Acute Intermittent Hypercapnic Hypoxia.

In normotensive patients with obstructive sleep apnea (OSA), the muscle sympathetic nerve activity (MSNA) response to exercise is increased while metaboreflex control of MSNA is decreased. We tested the hypotheses that acute intermittent hypercapnic hypoxia (IHH) in males free from OSA and associated comorbidities would augment the MSNA response to exercise but attenuate the change in MSNA during metaboreflex activation. Thirteen healthy males (age = 24 ± 4 yr) were exposed to 40 min of IHH. Before and after IHH, the pressor response to exercise was studied during 2 min of isometric handgrip exercise (at 30% maximal voluntary contraction), whereas the metaboreflex was studied during 4 min of postexercise circulatory occlusion (PECO). Mean arterial pressure (MAP), heart rate (HR), and fibular MSNA were recorded continuously. MSNA was quantified as burst frequency (BF) and total activity (TA). Mixed effects linear models were used to compare the exercise pressor and metaboreflex before and after IHH. As expected, IHH led to significant increases in MSNA BF, TA, and MAP at baseline and throughout exercise and PECO. However, during handgrip exercise, the change from baseline in MAP, HR, MSNA BF, and TA was similar before and after IHH (All P > 0.31). During PECO, the change from baseline in MSNA BF and TA was similar after IHH, whereas the change from baseline in MAP (Δ14 mm Hg, 95% CI = 7-19, vs Δ16 mm Hg, 95% CI = 10-21; P < 0.01) was modestly increased. After acute IHH, MSNA response to handgrip exercise and metaboreflex activation were preserved in healthy young males despite overall increases in resting MSNA and MAP. Chronic IHH and comorbidities often associated with OSA may be required to modulate the exercise pressor reflex and metaboreflex.

Hemodynamic Response to Isometric Handgrip Exercise in Adults with Intellectual Disability.

Individuals with intellectual disability (ID) have an increased risk of cardiovascular disease and reduced work capacity, which could partly be explained by alterations to autonomic and hemodynamic regulation. The measurement of heart rate and blood pressure during isometric handgrip (HG) exercise, a sympathoexcitatory stimulus, is a noninvasive method to investigate autonomic and hemodynamic alterations. The purpose of this study was to assess alterations to autonomic and associated hemodynamic regulation between individuals with ID and a matched control group during isometric HG exercise. Individuals with ID (n = 13; 31 ± 2 yr, 27.6 ± 7.7 kg·m-2) and without ID (n = 16; 29 ± 7 yr, 24.2 ± 2.8 kg·m-2) performed 2 min of isometric HG exercise at 30% of maximal voluntary contraction (MVC) in the seated position. Blood pressure was averaged for 2 min before, during, and after HG exercise (mean arterial pressure [MAP], systolic blood pressure, and diastolic blood pressure). Heart rate variability, blood pressure variability, and baroreflex sensitivity were calculated from the continuous blood pressure and heart rate recordings. Isometric HG elicited a blunted response in systolic blood pressure, diastolic blood pressure, and MAP among individuals with ID compared with individuals without ID, even after controlling for strength (MAP: rest, HG, recovery; ID: 103 ± 7, 108 ± 9, 103 ± 7; without ID: 102 ± 7, 116 ± 10, 104 ± 10 mm Hg; interaction P < 0.05). Individuals with ID also had an attenuated baroreflex sensitivity response to HG exercise compared with individuals without ID (interaction P = 0.041), but these effects were no longer significant after controlling for maximal voluntary contraction. Indices of heart rate variability and blood pressure variability were not different between groups overall or in response to HG exercise (P > 0.05). Individuals with ID have a blunted hemodynamic and autonomic response to isometric HG exercise compared with individuals without ID.

Attenuated aortic blood pressure responses to metaboreflex activation in older adults with dynapenia.

Low muscle strength (dynapenia) is a primary characteristic of sarcopenia, the age-related loss of muscle mass and strength or low walking speed. New evidence suggests that muscle strength positively affects blood pressure (BP) responses to exercise. As older adults with lowest handgrip strength also have lowest BP at rest, those with dynapenia may experience attenuated BP responses during physical activity. The purpose of this study was to test the hypothesis that dynapenic older adults would exhibit lower BP response to post-exercise muscle ischemia (PEMI). Brachial and aortic systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP) were measured in older adults (age, 80±5 y) with dynapenia (n=16) and non-dynapenia (n=9) at rest and during PEMI following 2min of isometric handgrip exercise at 30% maximal voluntary contraction. Walking speed was assessed by an 8-foot (2.44m) walk course. Increases in aortic SBP (11±2 vs. 23±6mmHg, p=.03), DBP (6±2 vs.14±4mmHg, p=.04), and MAP (8±1 vs. 17±5mmHg, p=.02) were lower in dynapenic compared to non-dynapenic adults. Aortic MAP (r=0.52, p<.05) response to PEMI was correlated with MVC in dynapenic adults. Gait speed was correlated with aortic DBP response to PEMI (r=0.698, p=.05) in non-dynapenic adults. Our findings indicate that aortic DBP response to muscle metaboreflex activation is attenuated in older adults with dynapenia. Normal aortic DBP response during metaboreflex activation may positively affect walking performance in non-dynapenic older adults.

Effect of Isometric Handgrip Exercise on Diastolic Function in Pediatric Heart Transplant Recipients

Pediatric heart transplant recipients (HTR) have reduced exercise tolerance and diastolic dysfunction at rest despite normal ejection fraction. In adult HTR the impaired diastolic function is related to peak exercise tolerance, but this relationship is poorly understood in pediatric HTR. To determine the effects of low‐grade exercise stress on diastolic function in pediatric HTR, we tested the hypothesis that diastolic function would be augmented during isometric handgrip exercise.MethodsSeven pediatric HTRs were studied (mean±SD age: 10±3 yrs; sex: 3F, 4M; time since transplant: 5.4±2.1 yrs; left ventricular mass: 68±19 g/m2; end‐diastolic volume: 42±6 mL; end‐systolic volume: 12±2 mL; ejection fraction: 71±9 %). Pulsed Doppler was used to quantify early (E) and late (A) diastolic inflow velocities, deceleration time and slope. Tissue Doppler imaging of the lateral mitral annulus was used to assess velocity during early diastole (e′) and late diastole (a′). Left ventricular filling pressure responses were estimated using the early diastolic mitral valve inflow velocity/early diastolic lateral wall tissue velocity ratio (E/e′). Resting diastolic assessment was performed followed by 2 min of isometric handgrip exercise at 30% maximal voluntary contraction with diastolic function re‐assessed during the last 30 s of exercise.ResultsHeart rate (92±10 to 105±13 bpm; P=0.01) and mean arterial pressure (73±7 to 90±21 mmHg; P=0.035) increased from rest to exercise. There was no significant change in E/A (2.2±0.8 to 2.2±1.1; P=0.831), deceleration time (0.183±0.031 to 0.173±0.035 s; P=0.529), deceleration slope (613±152 to 619±169 cm/s2; P=0.926), e′/a′ (2.8±0.7 to 2.5±1.2 cm/s2; P=0.433), or E/e′ (7.02±1.37 to 7.13±1.71; P=0.709) from rest to exercise.ConclusionPediatric HTR have diastolic dysfunction at rest that is not augmented during low‐grade handgrip exercise stress.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Abstract 17249: Impacts of Isometric Handgrip Exercise and Post-Exercise Circulatory Arrest on Hemodynamics and Left Ventricular Function in Heart Failure With Preserved Ejection Fraction

Introduction: Isometric handgrip (IHG) training at 30% maximal voluntary contraction (MVC) lowers blood pressure (BP) in patients with hypertension and healthy individuals. However, impacts of IHG and post-exercise circulatory arrest (PECA), which isolates the metaboreflex control, on left ventricular (LV) function and hemodynamics have been unclear in patients with heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). Methods: Sixteen patients with HF (age 63±13 years, 5M:11F, 10HFpEF:6HFrEF) underwent invasive LV pressure-volume assessments using conductance catheter with microtip-manometer during 3min of IHG exercise at 30% MVC, followed by 3 min of PECA. Impacts of IHG and PECA on LV function and hemodynamics were evaluated and compared between HFpEF and HFrEF. Results: During 3 min of IHG at 30% MCV, heart rate increased by 10±8 bpm in HFpEF and by 14±6 bpm in HFrEF. IHG elevated LV end-systolic BP in both HFpEF (134±21 vs. 158±30 mmHg, p&lt;0.01) and HFrEF (119±30 vs. 142±31 mmHg, p&lt;0.01) with no change in stroke volume. There was a trend towards an increase in LV end-diastolic pressure in both groups (HFpEF:14±5 vs. 19±10 mmHg, HFrEF: 15±12 vs. 23±11 mmHg). Time constant of LV relaxation was unchanged by 3 min of IHG in HFpEF (52±14 vs. 54±15 ms), while it was prolonged in HFrEF (48±7 vs. 60±9 ms, p&lt;0.01, groupхtime interaction effect p=0.08). During PECA, LV end-systolic BP decreased in both groups and was maintained higher than baseline throughout PECA only in HFpEF. Conclusions: Although IHG exercise at 30% MVC for 3 min would elevate LV end-systolic and end-diastolic pressures, this IHG exercise has no detrimental effect on LV systolic and diastolic function, especially in HFpEF patients. Chronic effect of IHG training on BP and hemodynamics will need to be evaluated in HFpEF patients who often suffer from arterial hypertension.

Evidence of an Exaggerated Muscle Metaboreflex Response in Heart Failure with Preserved Ejection Fraction

BackgroundExercise intolerance is the primary chronic symptom in heart failure patients with preserved ejection fraction (HFpEF), and often persists even with optimized treatment. Though there are many mechanisms that may contribute to this deficit, disease‐related changes in the muscle metaboreflex may play a role. Indeed, it has been previously shown that in heart failure with reduced ejection fraction (HFrEF), input from group III/IV muscle afferents contributes to the development of fatigue and exercise intolerance. Therefore, the purpose of this study was to examine metaboreflex modulation of heart rate (HR) and mean arterial pressure (MAP) in HFpEF patients.MethodsEight HFpEF patients (6M, 2F; age 67 ± 4 yrs; BMI 35 ± 3 kg/m2; ejection fraction 63 ± 3%) and seven healthy controls (4M, 3F; age 59 ± 3 yrs; BMI 30 ± 1 kg/m2) participated in this study. Patients were studied under their normal pharmacotherapy. After 30 min of supine rest, participants performed 2 min of isometric handgrip exercise at 30% and 40% of maximal voluntary contraction (MVC), followed by 2 min of post‐exercise circulatory occlusion (PECO) to isolate the muscle metaboreflex response. HR (3‐lead ECG) and arterial blood pressure (Finapres Medical Systems BV) were measured continuously, and the last 30 sec of exercise and PECO was averaged to determine peak changes in HR and MAP.ResultsBaseline HR and MAP were not different between HFpEF and controls (70 ± 7 vs. 68 ± 5 bpm; 97 ± 4 vs. 103 ± 5 mmHg, respectively). At 30% MVC, comparable ΔHR were observed between groups during handgrip (6 ± 1 vs. 4 ± 2 bpm, HFpEF vs. control) and PECO (2 ± 1 vs. 2 ± 1 bpm, HFpEF vs. control). While ΔMAP was similar between groups during handgrip (15 ± 2 vs. 14 ± 3 mmHg, HFpEF vs. control), HFpEF patients exhibited a greater ΔMAP during PECO (16 ± 2 vs. 8 ± 3 mmHg, HFpEF vs. control, p&lt;0.05). At 40% MVC, ΔHR was not significantly different between HFpEF and controls during handgrip (7 ± 3 vs. 12 ± 2 bpm, respectively) or PECO (1 ± 1 vs. 1 ± 2 bpm, respectively). Similarly, ΔMAP at 40% MVC was comparable between the groups during handgrip (24 ± 5 vs. 24 ± 2 mmHg, HFpEF vs. control), whereas there was a trend towards a greater ΔMAP during PECO in the HFpEF patients (24 ± 5 vs. 16 ± 3 mmHg, p=0.16).ConclusionsWhile the overall pressor response during handgrip was comparable between groups, a notable elevation in blood pressure was observed during PECO in the HFpEF patients. It is important to note that these differences occurred with the patients maintaining their normal pharmacotherapy, which often includes antihypertensive agents. These preliminary findings suggest that the muscle metaboreflex is exaggerated in patients with HFpEF, and this may be involved in the exercise intolerance observed in this patient population.Support or Funding InformationFunded in part by the National Institutes of Health (HL118313) and the U.S. Department of Veterans Affairs (RX001697, RX001418, E6910R)

Sex difference in the influence of central blood volume mobilization on the exercise pressor response.

To determine the sex difference in the impact of central venous pressure (CVP) on the pressor response induced by ischemic handgrip exercise. Twelve young healthy individuals (six males, 25 ± 3 years) performed ischemic handgrip exercise during mild levels of lower body negative pressure (LBNP, -5 mmHg) and during a 10° head-down tilt (HDT) to lower and increase CVP, respectively. The protocol consisted of 3 min of baseline ischemia, followed by 2 min of isometric handgrip exercise at 35 % of maximal voluntary contraction force, and 2 min of post-exercise circulatory occlusion. Mean arterial pressure (MAP) was assessed continuously by finger plethysmography and CVP was estimated from the venous pressure of the non-exercising dependent arm. Baseline CVP was greater during HDT than LBNP (8.4 ± 1.8 vs. 6.5 ± 1.8 mmHg, p < 0.01). MAP was greater during LBNP than HDT throughout the protocol (p = 0.05). During ischemic handgrip exercise, CVP increased in males but not in females (Group × protocol interaction: p = 0.01). A group × condition interaction was also observed for MAP, with males showing a greater MAP during LBNP than HDT (110 ± 2 vs. 103 ± 2 mmHg, p < 0.01). Baseline CVP inversely affected the pressor response to handgrip exercise in all individuals, with a greater MAP response observed during LBNP than HDT. Increase in CVP in males may be due to a greater splanchnic vasoconstrictor response to ischemic handgrip exercise. Therefore, combined baseline CVP and changes in CVP likely contributed to the greater MAP response observed during LBNP in males.

Sympathetic reactivity in young women with a family history of hypertension (680.11)

Young adults with a family history of hypertension (+FH) have an increased risk of developing hypertension. Further, the blood pressure (BP) response to sympatho‐excitatory stimuli in young adults can predict the future development of hypertension. Therefore, we hypothesized young women +FH (n=7, 22±1 yrs, 21±1 kg/m2, 81±2 mmHg resting mean BP) will have exaggerated sympathetic reactivity compared to young women without a family history of hypertension (‐FH; n=9, 23±2 yrs, 22±1 kg/m2, 80±2 mmHg resting mean BP). BP and muscle sympathetic nerve activity (MSNA) were measured during three sympatho‐excitatory maneuvers: 2 min of isometric handgrip exercise at 30% of maximal voluntary contraction (EX), 3 min of post‐exercise ischemia (PEI), and a cold pressor test (CPT). The increase in BP was greater in +FH during the last minute of EX (ΔMean BP: +FH 19±3 vs. ‐FH 11±2 mmHg, P=0.03) and during PEI (ΔMean BP: +FH 14±3 vs. ‐FH 6±1 mmHg, P=0.03). The increase in MSNA was greater in +FH during EX (ΔMSNA: +FH 15±4 vs. ‐FH 8±2 burst/min, P=0.13) and PEI (ΔMSNA: +FH 15±2 vs. ‐FH 5±2 burst/min, P&lt;0.01). In a subset of women (+FH n=6, ‐FH n=5), +FH tended to have a greater increase in BP during CPT (ΔMean BP: +FH 12±2 vs. ‐FH 8±2 mmHg, P=0.21), but ΔMSNA was not different (P&gt;0.05). These preliminary data suggest that +FH women may have greater sympathetic reactivity compared to ‐FH women.

Muscle metaboreflex activation speeds the recovery of arterial blood pressure following acute hypotension in humans

It has been suggested that the arterial baroreflex and muscle metaboreflex are both activated during heavy exercise and that they interact to modulate primary cardiovascular reflex responses. This proposed interaction and its consequences are not fully understood, however. The purpose of present study was to test our hypothesis that dynamic arterial baroreflex-mediated cardiovascular responses to acute systemic hypotension in humans are augmented when the muscle metaboreflex is active and that this results in a faster recovery of arterial blood pressure. Acute hypotension was induced nonpharmacologically in 12 healthy subjects by releasing bilateral thigh cuffs after 9 min of suprasystolic resting ischemia, with and without muscle metaboreflex activation via postexercise muscle ischemia (PEMI) after 1 min of isometric handgrip exercise at 50% maximum voluntary contraction. The thigh-cuff release evoked rapid reductions in mean arterial pressure (MAP) and increases in heart rate, cardiac output (Doppler), and total vascular conductance (TVC) under control conditions and during PEMI. The reductions in MAP from baseline were greater and the increases in TVC were smaller during PEMI than control. In addition, arterial baroreflex-mediated peripheral vasoconstriction was augmented during PEMI, as evidenced by a near doubling of the rate of recovery of MAP and TVC. These results show that when the muscle metaboreflex is activated in humans, arterial baroreflex-mediated peripheral vasoconstriction elicited in response to acute hypotension is augmented, which halves the time needed for MAP recovery. Such modulation of baroreflex function would be advantageous for maintaining an elevated arterial blood pressure during activation of the muscle metaboreflex.

Heat stress attenuates the increase in arterial blood pressure during isometric handgrip exercise

The purpose of this study was to examine arterial blood pressure responses during isometric handgrip (IHG) exercise performed at increasing levels of heat stress. Ten male subjects performed 1 min of IHG exercise at 60 % of maximal voluntary contraction under no heat stress (NHS), moderate heat stress [MHS, 0.6 °C increase in esophageal temperature (T (es))] and high heat stress (HHS, 1.4 °C increase in T (es)). For all conditions, IHG exercise significantly elevated mean arterial pressure (MAP) (NHS: 124 ± 6 vs. 90 ± 4 mmHg, MHS: 112 ± 6 vs. 89 ± 6 mmHg, HHS: 107 ± 7 vs. 91 ± 5 mmHg, P ≤ 0.05) and cardiac output (CO) (NHS: 9.0 ± 1.5 vs. 6.1 ± 0.6 L/min, MHS: 9.8 ± 1.8 vs. 7.6 ± 1.3 L/min, HHS: 10.0 ± 2.0 vs. 8.5 ± 1.9 L/min, P ≤ 0.05) relative to baseline, whereas no differences in total peripheral resistance (TPR) were observed (P > 0.05). However, the relative increases in MAP and CO were significantly reduced during MHS (MAP: 23 ± 6 mmHg, CO: 2.1 ± 0.9 L/min) and HHS (MAP: 16 ± 7 mmHg, CO: 1.5 ± 0.8 L/min) compared to NHS (34 ± 5 mmHg, CO: 2.9 ± 1.1 L/min, P ≤ 0.05). Furthermore, these elevations were significantly attenuated during HHS compared to MHS (P ≤ 0.05). Our findings show that heat stress attenuates the increase in arterial blood pressure during isometric handgrip exercise and this attenuation is cardiac output dependent, since TPR did not change during exercise for all heat stress conditions.

A respiratory response to the activation of the muscle metaboreflex during concurrent hypercapnia in man

In this study, we aimed to assess the ventilatory and cardiovascular responses to the combined activation of the muscle metaboreflex and the ventilatory chemoreflex, achieved by postexercise circulatory occlusion (PECO) and euoxic hypercapnia (end-tidal partial pressure of CO2 7 mmHg above normal), respectively. Eleven healthy subjects (4 women and 7 men; 29 +/- 4.4 years old; mean +/- S.D.) undertook the following four trials, in random order: 2 min of isometric handgrip exercise followed by 2 min of PECO with hypercapnia; 2 min of isometric handgrip exercise followed by 2 min of PECO while breathing room air; 4 min of rest with hypercapnia; and 4 min of rest while breathing room air. Ventilation was significantly increased during exercise in both the hypercapnic (+3.17 +/- 0.82 l min(-1)) and the room air breathing trials (+2.90 +/- 0.26 l min(-1); all P < 0.05). During PECO, ventilation returned to pre-exercise levels when breathing room air (+0.52 +/- 0.37 l min(-1); P > 0.05), but it remained elevated during hypercapnia (+3.77 +/- 0.23 l min(-1); P < 0.05). The results indicate that the muscle metaboreflex stimulates ventilation with concurrent chemoreflex activation. These findings have implications for disease states where effort intolerance and breathlessness are linked.

Neural and non‐neural control of skin blood flow during isometric handgrip exercise in the heat stressed human

During heat stress, isometric handgrip (IHG) exercise causes cutaneous vasoconstriction, but it remains controversial whether neural mechanisms are responsible for this observation. The objective of this study was to test the hypothesis that cutaneous vasoconstriction during IHG exercise in heat stressed individuals occurs via a neural mechanism. An axillary nerve blockade was performed to block efferent nerve traffic to the left forearm in seven healthy subjects. Two intradermal microdialysis probes were placed within forearm skin of the blocked area. Forearm skin blood flow was measured by laser-Doppler flowmetry over the microdialysis probes as well as from skin of the contralateral (unblocked) forearm. Cutaneous vascular conductance (CVC) was calculated from the ratio of skin blood flow to mean arterial pressure. Effectiveness of nerve blockade was verified by the absence of tactile sensation, as well as an absence of sweating and cutaneous vasodilatation during a whole-body heat stress. Upon this confirmation, adenosine was perfused through one of the microdialysis probes to increase skin blood flow similar to that of the unblocked site. After internal temperature increased approximately 0.7 degrees C, subjects performed 2 min of IHG exercise at 35% of maximal voluntary contraction using the non-blocked arm. IHG exercise significantly decreased CVC at the unblocked site (82.3 +/- 5.7 to 70.9 +/- 5.4%max, P = 0.005, means +/- S.E.M.) and the adenosine treated site of the blocked arm (75.2 +/- 7.2 to 68.3 +/- 6.6%max, P = 0.005), whereas CVC was unchanged at the blocked site that did not receive adenosine (15.7 +/- 2.8 to 13.7 +/- 2.0%max, P = 0.10). Importantly, the reduction in CVC was greater at the unblocked site than at the adenosine treated site (11.4 +/- 2.6 vs. 6.9 +/- 1.6%max, respectively, P = 0.01). These findings suggest that neural and non-neural mechanisms contribute to the reduction in forearm CVC during IHG exercise in heat stressed humans.

Effects of enoximone on peripheral and central chemoreflex responses in humans

cAMP plays an important role in peripheral chemoreflex function in animals. We tested the hypothesis that the phosphodiesterase inhibitor and inotropic medication enoximone increases peripheral chemoreflex function in humans. In a single-blind, randomized, placebo-controlled crossover study of 15 men, we measured ventilatory, muscle sympathetic nerve activity, and hemodynamic responses to 5 min of isocapnic hypoxia, 5 min of hyperoxic hypercapnia, and 3 min of isometric handgrip exercise, separated by 1 wk, with enoximone and placebo administration. Enoximone increased cardiac output by 120 +/- 3.7% from baseline (P < 0.001); it also increased the ventilatory response to acute hypoxia [13.6 +/- 1 vs. 11.2 +/- 0.7 l/min at 5 min of hypoxia, P = 0.03 vs. placebo (by ANOVA)]. Despite a larger minute ventilation and a smaller decrease in O(2) desaturation (83 +/- 1 vs. 79 +/- 2%, P = 0.003), the muscle sympathetic nerve response to hypoxia was similar between enoximone and placebo (123 +/- 6 and 117 +/- 6%, respectively, P = 0.28). In multivariate regression analyses, enoximone enhanced the ventilatory (P < 0.001) and sympathetic responses to isocapnic hypoxia. Hyperoxic hypercapnia and isometric handgrip responses were not different between enoximone and placebo (P = 0.13). Enoximone increases modestly the chemoreflex responses to isocapnic hypoxia. Moreover, this effect is specific for the peripheral chemoreflex, inasmuch as central chemoreflex and isometric handgrip responses were not altered by enoximone.

Central command and the cutaneous vascular response to isometric exercise in heated humans

Cutaneous vascular conductance (CVC) decreases during isometric handgrip exercise in heat stressed individuals, and we hypothesized that central command is involved in this response. Seven subjects performed 2 min of isometric handgrip exercise (35% of maximal voluntary contraction) followed by postexercise ischaemia in normothermia and during heat stress (increase in internal temperature approximately 1 degrees C). To augment the contribution of central command independent of force generation, on a separate day the protocol was repeated following partial neuromuscular blockade (PNB; i.v. cisatracurium). Forearm skin blood flow was measured by laser-Doppler flowmetry, and CVC was the ratio of skin blood flow to mean arterial pressure. The PNB attenuated force production despite encouragement to attain the same workload. During the heat stress trials, isometric exercise decreased CVC by approximately 12% for both conditions, but did not change CVC in either of the normothermic trials. During isometric exercise in the heat, the increase in mean arterial pressure (MAP) was greater during the control trial relative to the PNB trial (31.0+/-9.8 versus 18.6+/-6.4 mmHg, P<0.01), while the elevation of heart rate tended to be lower (19.4+/-10.4 versus 27.4+/-8.1 b.p.m., P=0.15). During postexercise ischaemia, CVC and MAP returned to pre-exercise levels in the PNB trial but remained reduced in the control trial. These findings suggest that central command, as well as muscle metabo-sensitive afferent stimulation, contributes to forearm cutaneous vascular responses in heat stressed humans.

Influence of muscle mass on sympathetic neural activation during isometric exercise

The primary purpose of this study was to determine whether the sympathetic neural activation induced by isometric exercise is influenced by the size of the contracting muscle mass. To address this, in nine healthy subjects (aged 19-27 yr) we measured heart rate, systolic arterial blood pressure, and muscle sympathetic nerve activity in the leg (MSNA; peroneal nerve) before (control) and during 2.5 min of isometric handgrip exercise (30% of maximal voluntary force). Exercise was performed with the right and left arms separately and with both arms simultaneously (random order). During exercise, heart rate, systolic pressure, and MSNA increased above control under all conditions (P less than 0.05). For each variable, the magnitudes of the increases from control to the end of exercise were significantly greater when exercise was performed with two arms compared with either arm alone (P less than 0.05). In general, the increases in heart rate, systolic pressure, and MSNA elicited during two-arm exercise were significantly less than the simple sums of the responses evoked during exercise of each arm separately. These findings indicate that the magnitude of the sympathetic neural activation evoked during isometric exercise in humans is determined in part by the size of the active muscle mass. In addition, our results suggest that the sympathetic cardiovascular adjustments elicited during exercise of separate limbs are not simply additive but instead exhibit an inhibitory interaction (i.e., neural occlusion).

Effects of chronic atenolol therapy on cardiovascular response to isometric exercise in essential hypertension.

Cardiovascular response to 2 min of isometric handgrip exercise at 50% of maximum voluntary contraction was studied echocardiographically in 10 essential hypertensives, before and during treatment with atenolol for a mean of 2 months. The patients responded with increases in heart rate, systolic and diastolic blood pressures, cardiac output and calculated triple product, no changes in stroke volume and total peripheral resistance, and decreases in ejection fraction, mean velocity of circumferential shortening and mean diastolic posterior wall velocity of the left ventricle before treatment. Chronic atenolol therapy attenuated the increases in heart rate, blood pressure and triple product, and the decreases in ejection fraction, mean velocity of circumferential shortening and mean diastolic posterior wall velocity of the left ventricle but resulted in a marked increase in total peripheral resistance. The pressure response and triple product rise in response to isometric handgrip exercise were also decreased. This suggests an obvious advantage to hypertensive patients who may, therefore, be protected from the risk of cardiovascular complications following isometric exercise.

Autonomic mediation of the pressor responses to isometric exercise in humans.

The purpose of this study was to determine the respective contributions of tachycardia and increases in sympathetic nerve activity (SNA) in mediating the pressor responses to fatiguing vs. nonfatiguing levels of isometric handgrip exercise (IHE) in humans. We performed direct (microneurographic) measurements of muscle SNA from the right peroneal nerve in the leg and recorded arterial pressure (AP) and heart rate (HR) in eight healthy subjects before (control), during, and after 2.5 min of IHE at 15, 25, or 35% of maximal voluntary contraction (MVC). At 15% MVC, AP increased during the initial 1.5 min of IHE (7 mmHg, P less than 0.05) and remained at this level; at 25 and 35% MVC, AP increased throughout IHE (22 and 34 mmHg vs. control, respectively, P less than 0.05). HR increased during the initial 1.5 min of IHE at all three levels (5, 12, and 19 beats/min, respectively, P less than 0.05) but did not increase further over the last minute. At 15% MVC, muscle SNA did not increase above control; during 25 and 35% MVC, muscle SNA did not increase during the 1st min of IHE but increased progressively thereafter (109 and 205% vs. control, respectively, P less than 0.05). The magnitudes of the average increases in AP and muscle SNA over the last minute of IHE were directly related (r = 0.99, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)