Essential hypertension is associated with blunted smooth muscle cell vasodilator responsiveness and is reversed by 10-20-30 training in men

Abstract

Essential hypertension is associated with impairments in vascular function and sympathetic nerve hyperactivity; however, the extent to which the lower limbs are affected remains unclear. We examined the leg vascular responsiveness to infusion of acetylcholine (ACh), sodium nitroprusside (SNP), and phenylephrine (PEP) in 10 hypertensive men [HYP: age 59.5 ± 9.7 (means ± SD) yr; clinical and nighttime blood pressure: 142 ± 10/86 ± 10 and 141 ± 11/83 ± 6 mmHg, respectively; and body mass index (BMI): 29.2 ± 4.0 kg/m2] and 8 age-matched normotensive counterparts (NORM: age 57.9 ± 10.8 yr; clinical and nighttime blood pressure: 128 ± 9/78 ± 7 and 116 ± 3/69 ± 3 mmHg, respectively; and BMI: 26.3 ± 3.1 kg/m2). The vascular responsiveness was evaluated before and after 6 wk of 10-20-30 training, consisting of 3 × 5 × 10-s sprint followed by 30 and 20 s of low- to moderate-intensity cycling, respectively, interspersed by 3 min of rest. Before training, the vascular responsiveness to infusion of SNP was lower ( P < 0.05) in HYP compared with NORM, with no difference in the responsiveness to infusion of ACh and PEP. The vascular responsiveness to infusion of SNP and ACh improved ( P < 0.05) with training in HYP, with no change in NORM. With training, intra-arterial systolic blood pressure decreased ( P < 0.05) by 9 mmHg in both HYP and NORM whereas diastolic blood pressure decreased (5 mmHg; P < 0.05) in HYP only. We provide here the first line of evidence in humans that smooth muscle cell vasodilator responsiveness is blunted in the lower limbs of hypertensive men. This impairment can be reversed by 10-20-30 training, which is an effective intervention to improve the responsiveness of smooth muscle cells in men with essential hypertension.

High-Intensity Interval Training Decreases Muscle Sympathetic Nerve Activity in Men With Essential Hypertension and in Normotensive Controls

“…It is notable that the hypertensive group did not improve theirVO 2 -max during the training intervention, which is in contrast to the normotensive group and to previous observations in similar patient groups implementing 10-20-30 cycling training (Fiorenza et al, 2019;Gunnarsson et al, 2020). ThatVO 2 -max did not improve with training in the hypertensive individuals of the present study is not easily explained as 7-8 weeks of 10-20-30 training improved thė VO 2 -max in trained runners (Gunnarsson and Bangsbo, 2012;Gliemann et al, 2015).…”

Reply to “Letter to the editor: In response to Gunnarsson et al. on improving the quality of exercise interventions”

“…A disadvantage to these "simpler" bikes is that the power output during the 10-20-30 training cannot be measured, which is why external load (W) was not measured in our study (9). The 30/50/100% of maximal intensity reported for the 30/20/10 s exercise periods in our study are rough estimates of power output during 10-20-30 cycling training.…”

“…As evident from Fig. 1, heart rate during a 10-20-30 training session (excluding the first and second sprint) is in the range of 85-91% of maximal heart rate (HR max ) in the hypertensive men (9), and drops to $70% of HR max during recovery periods. The high heart rates are indicative of a high aerobic load during the 10-20-30 cycling training and comparable to longer duration high-intensity interval training, e.g., 3-to 4-min exercise intervals (2,8).…”

“…During a 10-20-30 cycling training session, the repeated allout sprints will induce marked muscle ionic perturbations, full recruitment of skeletal muscle fibers, and heavy taxation of both aerobic and anaerobic energy metabolism (5,7), despite that exercise intensity may drop from the first to the last sprint. These combined marked muscular responses and high aerobic load during the 10-20-30 cycling training are believed to be the main driving force for the significant health-related adaptations observed following a period of 10-20-30 training in men with cardiometabolic disease (1,4,9) and in healthy individuals (6).…”

Hypertension is associated with blunted NO-mediated leg vasodilator responsiveness that is reversed by high-intensity training in postmenopausal women

“…In hypertensive postmenopausal women, an impaired endothelial function has been reported when compared to normotensive counterparts (39). In addition, we recently observed a blunted NO-mediated smooth muscle cell vasodilator responsiveness (assessed by femoral-arterial infusion of sodium nitroprusside (SNP)) in the leg of hypertensive men (~60 years) compared to normotensive counterparts (11), suggesting that impaired vascular regulation of the second messenger cyclic guanosine monophosphate (cGMP), may be involved in the pathology of hypertension. Whether the smooth muscle cell NO sensitivity in the leg of hypertensive postmenopausal women is impaired compared to normotensive counterparts, as recently observed in hypertensive men, is unknown.…”