Maximum exercise heart rate reduction with maturation in the rat

Maximum exercise heart rate decreases with maturation in the rat as well as in man. The present study was undertaken to investigate the mechanism(s) which might be responsible for this reduction in max exercise heart rate in the rat. Maximum exercise heart rates were 618 +/- 7 vs. 580 +/- 9 beats/min for the young (5 wk) and mature (19 wk) rats, respectively. Atropine had no effect on max exercise heart rate. Propranolol reduced max heart rate in both groups with the older rats having the lowest value. Resting heart rates were recorded following injections of atropine propranolol, and propranolol plus atropine. Under all conditions, including control, heart rates were lower in the mature rats. Electrical stimulation in situ showed a significant difference in the threshold voltage for stimulation at 600 beats/min: 1.1 +/- 0.2 vs. 1.6 +/- 0.1 V for the young and mature rats, respectively. These data suggest that intrinsic changes occur in the myocardium with maturation and the reduction in max exercise heart rate is due to these intrinsic changes as opposed to changes in neural influences.

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Maximum heart rate responses to exercise and isoproterenol in the trained rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1988.254.5.r834 ◽

1988 ◽

Vol 254 (5) ◽

pp. R834-R839 ◽

Cited By ~ 8

Author(s):

C. P. Bolter ◽

K. J. Atkinson

Keyword(s):

Heart Rate ◽

Male Rats ◽

Exercise Heart Rate ◽

Maximum Heart Rate ◽

Heart Rates ◽

Maximum Exercise ◽

Chronotropic Response ◽

The Difference

Male rats were assigned to light (C) or strenuous (T) running programs. Both groups ran at 30 m/min, 8% elevation. Over 16 wk, T and C completed 2,939 +/- 72 and 507 +/- 7 min (mean +/- SE). In a graded running test, maximum exercise heart rates for T and C were 542 +/- 7 and 554 +/- 6 beats/min (P greater than 0.05). Heart rates elicited by maximum effective concentrations of isoproterenol (ISO) in vivo and in vitro were 483 +/- 8 and 489 +/- 11 beats/min for T and 499 +/- 5 and 502 +/- 5 beats/min for C (no difference between groups or treatments). A lower heart rate was recorded in T for both resting (353 +/- 7 vs. 373 +/- 4 beats/min) and in vitro intrinsic states (231 +/- 22 vs. 299 +/- 22 beats/min) (P less than 0.05 for both conditions). The difference between maximum ISO-stimulated and maximum exercise heart rates was attributed to a temperature difference. In a separate group of lightly trained rats, ISO was administered intravenously during hard exercise when heart rate approached exercise maximum. Heart rate after ISO did not increase beyond the maximum heart rate observed in a control run. It was concluded that the maximum chronotropic response to sympathetic stimulation can be elicited during hard exercise and that maximum exercise heart rate reflects this limit rather than a saturation of cardiac sympathetic activity.

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Role of Heart Rate Reduction in the Management of Myocarditis

Current Pharmaceutical Design ◽

10.2174/1381612824666180111105923 ◽

2018 ◽

Vol 24 (3) ◽

pp. 365-378 ◽

Cited By ~ 2

Author(s):

Chen Guang-Yi ◽

Ge Li-Sha ◽

Li Yue-Chun

Keyword(s):

Heart Rate ◽

Nitrosative Stress ◽

Ventricular Remodeling ◽

Animal Experiments ◽

Viral Myocarditis ◽

Protective Effects ◽

Heart Rate Reduction ◽

Rate Reduction ◽

Beneficial Effects ◽

Biological Technique

The morbidity of myocarditis demonstrates an upward tendency by years, is commonly defined as the inflammation of myocytes and is caused by multiple factors. With the development of the molecular biological technique, great breakthroughs in the diagnosis and understanding of pathophysiological mechanisms of myocarditis have recently been achieved. Several questions remain unresolved, however, including standard treatment approaches to myocarditis, which remain controversial and ambiguous. Heart rate, as an independent risk factor, has been shown to be related to cardiac disease. Recent studies also show that the autonomic nervous system is involved in immunomodulatory myocarditis processes. Heart rate reduction treatment is recommended in myocarditis based on a number of animal experiments and clinical trials. It is possible that heart rate-lowering treatments can help to attenuate the inflammatory response and myocyte injury and reverse ventricular remodeling. However, how to execute the protective effects of heart rate reduction on myocarditis is still not clear. In this review, we discuss the pathogenesis and pathophysiological process of viral myocarditis and propose heart rate lowering as a therapeutic target for myocarditis, especially in light of the third-generation β-blockade carvedilol and funny channel blocker ivabradine. We also highlight some additional beneficial effects of such heart rate reduction agents, including anti-inflammatory, antioxidation, anti-nitrosative stress, anti-fibrosis and antiapoptosis properties.

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