Abstract

The cardiovascular adjustments during exercise are regulated by several neural mechanisms working in concert, including the muscle metaboreflex. The response to this reflex could be involved in the reduced diastolic blood pressure observed in HIV patients during exercise. However, this hypothesis has not been tested yet. Thus, 18 patients living with HIV (46±10 yr, mean ±SD; 16 men; HIV group) and 13 control subjects (41±8 yr; 10 men; Control group) were evaluated. Systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), cardiac output and total vascular resistance were calculated using photoplethysmography and Model flow method. Cardiac index (CI) and total vascular resistance index (TVRI) were corrected by body surface area. SBP and DBP was recorded during 3 minutes of rest, followed by 3 minutes of isometric handgrip exercise at 30% of their maximal voluntary force and 2 minutes of post exercise ischemia to isolate muscle metaboreflex activation. Data were subject to two‐way ANOVA followed by multiple comparisons with Bonferroni correction. SBP increased during exercise (Control: Δ22±6 mmHg vs. HIV: Δ17±8 mmHg) and during metaboreflex activation in both groups (1st min: Control: Δ12±6 mmHg vs. HIV: Δ8±5 mmHg; 2nd min: Control: Δ15±8 mmHg vs. HIV: Δ12±9 mmHg). However, DBP response to exercise was attenuated in HIV patients (Control: Δ16±5 mmHg vs. HIV: Δ10±4 mmHg). This difference remained during metaboreflex activation (1st min: Control: Δ9±5 mmHg vs. HIV: Δ3±2 mmHg; 2nd min: Control: Δ11±6 mmHg vs. HIV: Δ6±4 mmHg). TVRI increased during exercise only in the control group (Control: Δ1.31±0.79 mmHg.min/l vs. HIV: Δ0.28±1.60 mmHg.min/l) and remained elevated during metaboreflex activation. In contrast, a decrease of the TVRI during the 1st minute of the metaboreflex activation (Control: Δ1.43±0.69 mmHg.min/l vs. HIV: Δ0.22±1.22 mmHg.min/l) and a blunted increase at the 2nd minute was observed in HIV patients (Control: Δ1.56±1.04 mmHg.min/l vs. HIV: Δ0.84±1.25 mmHg.min/l). CI increased during exercise (Control: Δ0.43±0.57 l/min vs. HIV: Δ0.42±0.32 l/min) and decreased during metaboreflex activation in both groups (1st min: Control: Δ0.07±0.32 l/min vs. HIV: Δ0.15±0.25 l/min; 2nd min: Control: Δ0.16±0.42 l/min vs. HIV: Δ 0.13±0.25 l/min). HR increased during exercise (Control: Δ9±6 bpm vs. HIV: Δ8±4 bpm) and returned to resting values during metaboreflex activation in both groups (1st min: Control: Δ‐1±2 bpm vs. HIV: Δ0±3 bpm; 2nd min: Control: Δ0±3 bpm vs. HIV: Δ0±4 bpm). In conclusion, seems that patients living with HIV present blunted peripheral vasoconstriction response to metaboreflex activation, which explain the reduced diastolic blood pressure response to exercise, already observed in these patients. We believe that a lower sympathetic activation and/or deficient sympathetic vascular transduction are the two possible mechanisms driving the response.Support or Funding InformationFAPERJ, CAPES and CNPqThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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