Muscle afferent and central command contributions to the cardiovascular response to isometric exercise of postural muscle in patients with mild chronic heart failure

2001 ◽  
Vol 100 (6) ◽  
pp. 643 ◽  
Author(s):  
C.A. CARRINGTON ◽  
W.J. FISHER ◽  
M.K. DAVIES ◽  
M.J. WHITE
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cardiovascular Response ◽  
Isometric Exercise ◽  
Central Command ◽  
Muscle Afferent ◽  
Postural Muscle

Muscle afferent and central command contributions to the cardiovascular response to isometric exercise of postural muscle in patients with mild chronic heart failure

2001 ◽  
Vol 100 (6) ◽  
pp. 643-651 ◽  
Author(s):  
C. A. CARRINGTON ◽  
W. J. FISHER ◽  
M. K. DAVIES ◽  
M. J. WHITE
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Diastolic Blood Pressure ◽  
Plantar Flexion ◽  
Isometric Exercise ◽  
Voluntary Contraction ◽  
Triceps Surae ◽  
Control Subjects ◽  
Muscle Afferent

The roles of muscle afferent activity and central drive in controlling the compromised cardiovascular system of patients with mild chronic heart failure (CHF) during isometric exercise were examined. Blood pressure and heart rate responses were recorded in eight stable CHF patients (ejection fraction 20–40%; age 62±11 years) and in nine healthy age-matched controls during voluntary and electrically evoked isometric plantar flexion and subsequent post-exercise circulatory occlusion (PECO). During voluntary contraction, control subjects had a greater mean increase in systolic blood pressure than patients (42.4±19.2 and 23.0±10.9 mmHg respectively; P < 0.01), but this was not the case during PECO. During electrically evoked contraction, but not during PECO, the CHF group had smaller (P < 0.05) mean increases in both systolic and diastolic blood pressure than controls (13.0±5.3 compared with 25.4±14.0 mmHg and 7.6±3.0 compared with 12.9±7.2 mmHg respectively). Intra-group comparison between responses to voluntary and electrically evoked contractions revealed greater (P < 0.05) mean increases in systolic and diastolic blood pressure during the voluntary contraction in both the patients and the control subjects. These data suggest that muscle afferent drive to the pressor response from the triceps surae is low in this age group, both in control subjects and in CHF patients. Additionally, the patients may have a relatively desensitized muscle mechanoreceptor reflex.

Voltage-Gated Potassium Channel Dysfunction in Dorsal Root Ganglia Contributes to the Exaggerated Exercise Pressor Reflex in Rats with Chronic Heart Failure

2021 ◽  
Author(s):  
Juan Hong ◽  
Shubin Fu ◽  
Lie Gao ◽  
Yanhui Cai ◽  
Eric D. Lazartigues ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Critical Role ◽  
Exercise Intolerance ◽  
Voltage Gated ◽  
Kv Channel ◽  
Exercise Pressor Reflex ◽  
Kv Channels ◽  
Muscle Afferent ◽  
Pressor Reflex

An exaggerated exercise pressor reflex (EPR) causes excessive sympatho-excitation and exercise intolerance during physical activity in the chronic heart failure (CHF) state. Muscle afferent sensitization contributes to the genesis of the exaggerated EPR in CHF. However, the cellular mechanisms underlying muscle afferent sensitization in CHF remain unclear. Considering that voltage-gated potassium (Kv) channels critically regulate afferent neuronal excitability, we examined the potential role of Kv channels in mediating the sensitized EPR in male CHF rats. Real time RT-PCR and western blotting experiments demonstrate that both mRNA and protein expressions of multiple Kv channel isoforms (Kv1.4, Kv3.4, Kv4.2 and Kv4.3) were downregulated in lumbar DRGs of CHF rats compared to sham rats. Immunofluorescence data demonstrates significant decreased Kv channel staining in both NF200-positive and IB4-positive lumbar DRG neurons in CHF rats compared to sham rats. Data from patch clamp experiments demonstrate that the total Kv current, especially IA, was dramatically decreased in medium-sized IB4-negative muscle afferent neurons (a subpopulation containing mostly Aδ neurons) from CHF rats compared to sham rats, indicating a potential functional loss of Kv channels in muscle afferent Aδ neurons. In in vivo experiments, adenoviral overexpression of Kv4.3 in lumbar DRGs for one week attenuated the exaggerated EPR induced by muscle static contraction and the mechanoreflex by passive stretch without affecting the blunted cardiovascular response to hindlimb arterial injection of capsaicin in CHF rats. These data suggest that Kv channel dysfunction in DRGs play a critical role in mediating the exaggerated EPR and muscle afferent sensitization in CHF.

scholarly journals Hemodynamic, ventilatory and metabolic effects of light isometric exercise in patients with chronic heart failure

1988 ◽  
Vol 12 (2) ◽  
pp. 353-358 ◽  
Author(s):  
Hanumanth K. Reddy ◽  
Karl T. Weber ◽  
Joseph S. Janicki ◽  
Patricia A. McElroy
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Isometric Exercise ◽  
Metabolic Effects

Muscle afferent inputs to cardiovascular control during isometric exercise vary with muscle group in patients with chronic heart failure

2004 ◽  
Vol 107 (2) ◽  
pp. 197-204 ◽  
Author(s):  
Charlotte A. CARRINGTON ◽  
James P. FISHER ◽  
Mick K. DAVIES ◽  
Michael J. WHITE
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Muscle Fibre ◽  
Fibre Type ◽  
Isometric Exercise ◽  
Muscle Group ◽  
Muscle Fibre Type ◽  
Training Status ◽  
Muscle Metaboreflex ◽  
And Training

It is not known whether the contribution of the muscle metaboreflex to the cardiovascular response to isometric exercise varies between different muscles in patients with CHF (chronic heart failure) or whether this depends upon muscle fibre type and training status. To resolve these issues BP (blood pressure) and HR (heart rate) responses were recorded in seven stable CHF patients (ejection fraction 30–40%; age 67±3 years) and in six healthy AMA (age-matched active) subjects. The experimental protocol consisted of 2 min of ischaemic isometric exercise at 30% maximum voluntary force, performed in separate trials by the calf plantar flexors (CALF) and handgrip muscles (FOREARM). To isolate the muscle metaboreflex a subsequent period of PECO (post-exercise circulatory occlusion) was performed following exercise. FOREARM and CALF produced similar increases in BP in both the AMA subjects and CHF patients. CHF patients elicited a significantly lower diastolic BP during PECO following CALF in comparison with that following FOREARM (5±5 compared with 12±3 mmHg respectively). A similar result was seen in AMA subjects. It may be that even the limited weight-bearing locomotor role of the calf muscles constitutes a conditioning stimulus in CHF patients, which leads to desensitization of the muscle metaboreflex, thus producing an attenuated BP elevation. We conclude that it would be incorrect to make general statements about muscle chemoreflex inputs to cardiovascular control in CHF patients based upon measurements made on only one muscle group and without reference to muscle fibre type and training status.

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