Clenbuterol diminishes aerobic performance in horses

Kearns, Charles F.; McKeever, Kenneth H.

doi:10.1097/00005768-200212000-00018

Cited by 43 publications

(50 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This led us to examine the deleterious effects of clenbuterol on the mitochondrial subpopulation from different fiber types. The results of this study are consistent with the previous reports, which suggest the detrimental effects of clenbuterol on the aerobic capacity of skeletal muscle [25,26,35].…”

Section: Ultrastructure and Morphometric Analysis Of Isolated Mitochosupporting

confidence: 93%

Ultrastructural Findings for the Mitochondrial Subpopulation of Mice Skeletal Muscle after Adrenergic Stimulation by Clenbuterol

Sundal

Sharma

2007

J. Physiol. Sci

View full text Add to dashboard Cite

Clenbuterol, a β-adrenoceptor agonist, has been reported to induce skeletal muscle hypertrophy. However, it has also been known to reduce aerobic exercise performance and to deleteriously affect endurance and sprint exercise performance in rats. In the present study, the chronic administration of clenbuterol (2 mg/kg body weight; 30 days) resulted in various ultrastructural changes in three different types of muscles, gastrocnemius, a mixed-fiber type; anterior latissimus dorsi (ALD), a predominantly fast-twitch type; and diaphragm, a largely oxidative-type. The most prominent changes included mitochondrial swelling, matricular vesiculation in mitochondria, mitochondrial hyperplasia, sarcoplasmic vesiculation, and intermyofibrillar dilations. An increase in the cross-sectional area of both the subsarcolemmal (170, 167, and 79%) and the intermyofibrillar (129, 134, and 84%) mitochondria is noticed in the gastrocnemius, ALD, and diaphragm, respectively. The ultramicroscopic and morphometric results suggest drug-induced defects in contractile and oxidative activities.

show abstract

Section: Ultrastructure and Morphometric Analysis Of Isolated Mitochosupporting

confidence: 93%

Ultrastructural Findings for the Mitochondrial Subpopulation of Mice Skeletal Muscle after Adrenergic Stimulation by Clenbuterol

Sundal

Sharma

2007

J. Physiol. Sci

View full text Add to dashboard Cite

show abstract

“…The illicit use of this agent persists to the present day (11). However, administration of clenbuterol does not necessarily lead to improved muscle performance (5,13,24,26,28,35). Case reports include body builders who present with tachycardia (6), myocardial infarction (19), and end-stage renal disease (21).…”

mentioning

confidence: 99%

“…Apoptotic cell death can often be induced by lesser stimuli than required to induce necrosis (23). Whether the doses of clenbuterol administered differentiate between its well-known anabolic effects (34) and the more recently reported injurious effects (4,13,26,39) is unknown. But if it does, a rigorously investigated dose dependency is required to find the highest dose of clenbuterol that does not induce myocyte death and could therefore potentially be used as a therapeutic intervention for muscle wasting.…”

mentioning

confidence: 99%

β₂-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle

Burniston¹,

Tan²,

Goldspink³

2005

Journal of Applied Physiology

View full text Add to dashboard Cite

High doses of the β2-adrenergic receptor (AR) agonist clenbuterol can induce necrotic myocyte death in the heart and slow-twitch skeletal muscle of the rat. However, it is not known whether this agent can also induce myocyte apoptosis and whether this would occur at a lower dose than previously reported for myocyte necrosis. Male Wistar rats were given single subcutaneous injections of clenbuterol. Immunohistochemistry was used to detect myocyte-specific apoptosis (detected on cryosections via a caspase 3 antibody and confirmed with annexin V, single-strand DNA labeling, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling). Myocyte apoptosis was first detected at 2 h and peaked 4 h after clenbuterol administration. The lowest dose of clenbuterol to induce cardiomyocyte apoptosis was 1 μg/kg, with peak apoptosis (0.35 ± 0.05%; P < 0.05) occurring in response to 5 mg/kg. In the soleus, peak apoptosis (5.8 ± 2%; P < 0.05) was induced by the lower dose of 10 μg/kg. Cardiomyocyte apoptosis was detected throughout the ventricles, atria, and papillary muscles. However, this damage was most abundant in the left ventricular subendocardium at a point 1.6 mm, that is, approximately one-quarter of the way, from the apex toward the base. β-AR antagonism (involving propranolol, bisoprolol, or ICI 118551) or reserpine was used to show that clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte β1-AR, whereas in the soleus direct stimulation of the myocyte β2-AR was involved. These data show that, when administered in vivo, β2-AR stimulation by clenbuterol is detrimental to cardiac and skeletal muscles even at low doses, by inducing apoptosis through β1- and β2-AR, respectively.

show abstract

“…The effects and long-term effects of these medications on the skeletal musculature in the horse are not completely understood. Clenbuterol is known to induce different structural changes in skeletal muscle (Kearns et al 2002, Kearns et al 2001). An increased blood supply, an improved oxygen metabolism muscle and a direct anabolic effect of b2-mimetic agents has been found in human muscle and with a high probability also in equine muscle.…”

Section: Effect Of Therapymentioning

confidence: 99%

“…In contrast, glucocorticoids exert a catabolic effect. Although clenbuterol has been shown to increase lung function in several studies (Kearns et al 2002, Kearns et al 2001), a direct effect on the mitochondria can be suspected. According to our results, mitochondrial hyperplasia/acitivity was obviously reduced by clenbuterol, although respiratory function did not increase in most horses.…”

Section: Effect Of Therapymentioning

confidence: 99%

Effects of clenbuterol therapy on mitochondrial activity in skeletal musculature of RAO affected horses

Gehlen¹,

Stave²,

Bilzer³

et al. 2015

PHK

View full text Add to dashboard Cite

Summary: Chronic pulmonary disease alters skeletal muscle in humans and horses. The purpose of this study was to evaluate a possible effect of the ß2-sympathomimetic agent clenbuterol, known for its bronchodilatory and anabolic effects on skeletal musculature, on mitochondrial activity and histopathologic changes of skeletal musculature horses suffering from recurrent airway obstruction (RAO). We hypothesized that clenbuterol treatment has an effect on mitochondrial activity and histopathologic changes of RAO patients. Therefore 14 healthy horses (control) and 18 RAO patients without primary muscle disease were examined in a prospective clinical trial. In all horses a complete lung examination was performed. All horses received clenbuterol at a dosage of 0.8 µg/kg BDW bid for 2 intervals of 12 days and a 4-day-break. Muscle enzymes and muscle biopsies (M. gluteus medius) were examined histologically and histochemically at rest and 24 h after exercise before and after clenbuterol treatment. Clinical, laboratory and histopathologic examination of skeletal muscle samples excluded primary myopathies in all horses. A significant increase of mitochondrial activity was found in RAO patients compared to healthy controls. A significant reduction in mitochondrial activity was obvious after clenbuterol application in RAO patients. An effect of standardized exercise on mitochondrial activity in skeletal musculature could not be found. In conclusion clenbuterol therapy reduces skeletal muscle changes in RAO patients.

show abstract

Clenbuterol diminishes aerobic performance in horses

Abstract: These data suggest that the combined effect of therapeutic levels of clenbuterol and training decrease aerobic performance and that the resultant reduction in plasma volume may affect improvements in cardiovascular function during recovery normally seen with exercise training.

Cited by 43 publications

References 38 publications

Ultrastructural Findings for the Mitochondrial Subpopulation of Mice Skeletal Muscle after Adrenergic Stimulation by Clenbuterol

Ultrastructural Findings for the Mitochondrial Subpopulation of Mice Skeletal Muscle after Adrenergic Stimulation by Clenbuterol

β₂-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle

Effects of clenbuterol therapy on mitochondrial activity in skeletal musculature of RAO affected horses

Contact Info

Product

Resources

About

Clenbuterol diminishes aerobic performance in horses

Abstract: These data suggest that the combined effect of therapeutic levels of clenbuterol and training decrease aerobic performance and that the resultant reduction in plasma volume may affect improvements in cardiovascular function during recovery normally seen with exercise training.

Cited by 43 publications

References 38 publications

Ultrastructural Findings for the Mitochondrial Subpopulation of Mice Skeletal Muscle after Adrenergic Stimulation by Clenbuterol

Ultrastructural Findings for the Mitochondrial Subpopulation of Mice Skeletal Muscle after Adrenergic Stimulation by Clenbuterol

β2-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle

Effects of clenbuterol therapy on mitochondrial activity in skeletal musculature of RAO affected horses

Contact Info

Product

Resources

About

β₂-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle