https://orcid.org/0000-0003-1447-8817
Dear editor,
Human immunodeficiency virus (HIV) is a ribonucleic acid retrovirus that can be spread blood transmission or through sexual activity. Over 34 million people are reportedly affected globally as a result of this pandemic virus [Citation1–3].
Highly active antiretroviral therapy (HAART) is the best clinical management for HIV-infected sufferers. Despite its importance as a first-line treatment for HIV, HAART is the cause of some of the common sexual dysfunctions in HIV men such as erectile dysfunction (ED) (9–74%), ejaculatory disturbances (36–42%), and low sexual desire. Besides HAART, many factors may predispose to the high prevalence of ED [Citation4] (inability to attain or maintain a penile erection sufficient for sexual intercourse) [Citation5,Citation6] in HIV-positive men such as HIV-associated psychological conditions, cardiovascular comorbidities or risk factors, and hypogonadism (testosterone deficiency which is highly prevalent in HIV men) [Citation4].
Poor emotional status is contemplated in the presence of ED in HIV men. States of depression and anxiety together cause a decrease in sexual response, which helps ED start. HIV-positive men’s sexual dysfunction is exacerbated by the impression of body image change caused by lipodystrophy (peripheral fat wasting). Relationship intimacy and erectile function may be negatively impacted by anxiety related to guilt and the worry of spreading the disease through sexual activity [Citation7].
Endocrine factors which are mainly related to the highly frequent testosterone deficiency in HIV-infected men are also involved in the induction of ED in HIV men. Testosterone (T) mediates components of the penile erectile response through men’s sexual desire. It also plays a role in supplying the cavernous smooth muscles of the penis with vasodilating substances such as nitric oxide (NO). This increase in this substance means greater blood supply to the penis and greater penile erection. A deficiency of testosterone in men with HIV negatively impacts penile erection due to the loss of T effects on the physiological process of erection [Citation7].
HAART in HIV infection produces massive metabolic complications that predispose the frequent complaints of ED in HIV men. These HIV-related metabolic complications are hyperlipidemia or dyslipidemia, insulin resistance and/or diabetes mellitus, peripheral fat wasting (lipoatrophy), abdominal or visceral fat accumulation (lipohypertrophy), disturbances in adipokines and circulating proinflammatory molecules. Disturbances of these molecules not only accelerate the paradigm of cardiovascular diseases and mortality but also accelerates the early complaints of ED in HIV-positive men [Citation8].
In the course of treating HIV, it is strongly advised to encourage lifestyle adjustment techniques such as safer sex, greater physical activity, and changes to cardiovascular risk factors [Citation4,Citation9]. Exercise is a complementary therapeutic option to the commonly used pharmaceutical drugs, phosphodiesterase type 5 inhibitors, which are used to treat ED [Citation10–13]. However, the role of exercise in HIV men with ED has not yet been explored.
Exercise may improve cardiovascular and metabolic risk factors (insulin resistance and/or diabetes, high blood pressure, obesity, dyslipidemia, endothelial dysfunction, and hepatopathy), which are highly prevalent in HIV patients. Improvements in cardiometabolic comorbidities may improve the highly prevalent ED complaint in HIV-positive men.
Exercise is a good recommended therapeutic approach to increase T levels, especially in T deficiency. The improvement of insulin resistance, insulin levels, leptin levels, lipid profiles, systemic inflammatory markers, and central obesity may all be associated with increased T synthesis after exercise training [Citation14,Citation15]. Increased T synthesis increases men’s sexual desire and increases the synthesis of components responsible for penile erection such as NO, hence ED in HIV sufferers may improve.
By reducing the release of pro-inflammatory molecules and adipokines from central adipose tissue, long-term exercise training itself creates an anti-inflammatory milieu. Improvements in chronic low-grade systemic inflammation or inflammatory milieu may improve the dysfunction of the hypothalamic-pituitary-adrenal axis or stress axis. Improvement of stress-axis dysfunctions improves negative body image, worry, stress, anxiety, depression, poor self-esteem, and poor emotional status, hence HIV-induced ED may improve.
Prescribing future exercise studies for men with HIV-induced ED are needed to investigate the role/rationale of exercise in the treatment of this complaint. Detecting the most appropriate intensity, type, duration, and frequency of exercise under the supervision of physiotherapists is needed to implement complementary exercise programs in the treatment of HIV-induced ED.
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