Anabolic steroids alter the haemodynamic effects of endurance training and deconditioning in rats

Karhunen, M. K.; Rämö, M.Pauliina; Kettunen, Raimo

doi:10.1111/j.1748-1716.1988.tb08411.x

Cited by 24 publications

(11 citation statements)

References 17 publications

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“…Similar findings were obtained in humans by Karhunen et al (1988), who observed that supra-physiological doses of nandrolone induced cardiac hypertrophy and depressed myocardial contractility. Urhausen et al (1989) reported that AAS in highly trained bodybuilders induced an increase in left ventricular isovolumic relaxation time, and De Piccoli et al (1991) showed that AAS abuse is associated with pathological left ventricle hypertrophy and altered diastolic filling.…”

Section: Discussionsupporting

confidence: 88%

Nandrolone and resistance training induce heart remodeling: Role of fetal genes and implications for cardiac pathophysiology

et al. 2011

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Section: Discussionsupporting

confidence: 88%

Nandrolone and resistance training induce heart remodeling: Role of fetal genes and implications for cardiac pathophysiology

et al. 2011

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“…However, Liang et al (1993) have found no dierences in heart masses subsequent to steroid administration in either control or exercise-trained rats. The lack of eect of nandrolone decanoate on cardiac mass noted by Liang et al (1993) in comparison to those ®ndings of Karhunen et al (1988) and us (this study) is likely to have been due to the lower frequency of steroid administration (a once weekly instead o a twice weekly dose) used by Liang et al (1993).…”

Section: Discussioncontrasting

confidence: 72%

“…However, the discrepancy between the somatic and the cardiac growth eect of androgenic steroids has not been explored. The data showing a potential positive action on cardiac growth are congruous with eects described by Karhunen et al (1988), who have shown an increase in heart mass associated with an exercise programme in rats receiving an androgenic steroid but not in those exercise-trained rats not receiving an androgenic steroid. However, Liang et al (1993) have found no dierences in heart masses subsequent to steroid administration in either control or exercise-trained rats.…”

Section: Discussionsupporting

confidence: 57%

Attenuated β-adrenoceptor-mediated cardiac contractile responses following androgenic steroid administration to sedentary rats

Norton¹,

Trifunovic²,

Woodiwiss³

2000

European Journal of Applied Physiology

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Androgenic steroids administered in doses at pharmacological levels to sedentary animals have been shown to result in a reduced beta-adrenoceptor-mediated increase in systolic cardiac performance when assessed in vivo. Whether the attenuated adrenergic response occurs as a consequence of alterations in either cardiac loads, heart rate, modifications in left ventricular (LV) geometry, or a decrease in myocardial contractile performance has not been determined. In this study the effect of chronic administration (over 3 months) of an androgenic steroid (nandrolone decanoate, 5 mg. kg(-1) biweekly) on the response of load-insensitive indices of myocardial contractile function [the slope of the LV systolic stress-strain relationship (LV-E(n)(max), where E(n)(max) is systolic myocardial elastance)] to an adrenergic-inotropic stimulus was examined ex vivo in paced rat hearts. Systolic cardiac performance was assessed at 300 beats. min(-1) in isolated constant flow perfused heart preparations both before and during 10(-8.5) mol. l(-1) isoproterenol (ISO) infusion (approximate concentration of ISO eliciting 50% maximal inotropic response to ISO). Steroid administration resulted in left-shifted LV systolic and diastolic pressure-volume (P-V ) relationships. The leftshifted P-V relationships were attributed, in part, to increased slopes of these relationships. However, the steroid-mediated increment in the slope of the systolic P-V relationship (systolic chamber elastance, E(max)) was not associated with a similar change in LV E(n)(max) [control 19.2 (SEM 2.1) g. cm(-2), steroid 18.3 (SEM 2.4) g. cm(-2)] as determined in the absence of ISO. Isoproterenol infusion resulted in an increase in both E(max) and E(n)(max) in the control rats, without altering systolic performance in the steroid treated rats. Consequently, in the presence of ISO, the steroid treated rats exhibited a similar E(max), but a reduction in E(n)(max) compared to the control rats [control 25.6 (SEM 1.9) g. cm(-2), steroid 18.5 (SEM 1.5) g. cm(-2); P < 0.05]. In conclusion, these results would suggest that chronic high dose androgenic steroid administration produces a decrease in myocardial contractile reserve to beta-adrenoceptor stimulation.

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“…7,8 Regression of LVH may occur in patients after discontinuation of steroid use, but the loss of compliance and reduced inotropism of the ventricle may not recover. 9 The degree of hypertrophy of the myocardium in this man's case was considerably larger than that reported in similar cases, and the absence of asymetrical septal hypertrophy or abnormal mitral valve function renders unlikely coincidental hypertrophic obstructive cardiomyopathy.…”

Section: Discussionmentioning

confidence: 46%

Body beautiful?

Owens¹,

Lyons²,

O’Brien³

1998

J Hum Hypertens

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Case reportMr LD, a 38-year-old male from Dublin was admitted with cellulitis of the right arm. On admission he was noted to be hypertensive, with a clinic reading of 200/115 mm Hg, and was referred for assessment by the cardiology department.The patient was a body builder ( Figure 1) and had been actively training for the past 10 years. He admitted to taking anabolic steroids over this time period (see Table 1). He had a positive family history of hypertension. Ambulatory blood pressure monitoring ( Figure 2) revealed severe systolic and diastolic hypertension, with preservation of the normal nocturnal dipping pattern. A work-up for target organ damage showed severe concentric left ventricular hypertrophy (Figure 3) on echocardiography, with a calculated left ventricular mass of 661 grams. He also had mild left atrial enlargement. The serum HDL cholesterol was 0.66 mmol/l, and the LDL fraction was 4.97 mmol/l. In view of the severity of the pressure elevation he underwent evaluation for an underlying primary cause for his hyper-

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Anabolic steroids alter the haemodynamic effects of endurance training and deconditioning in rats

Cited by 24 publications

References 17 publications

Nandrolone and resistance training induce heart remodeling: Role of fetal genes and implications for cardiac pathophysiology

Nandrolone and resistance training induce heart remodeling: Role of fetal genes and implications for cardiac pathophysiology

Attenuated β-adrenoceptor-mediated cardiac contractile responses following androgenic steroid administration to sedentary rats

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