Effect of an 11-Week Resistance Training Program on Arterial Stiffness in Young Women.

ABSTRACT: Morgan, B, Mirza, AM, Gimblet, CJ, Ortlip, AT, Ancalmo, J, Kalita, D, Pellinger, TK, Walter, JM, and Werner, TJ. Effect of an 11-week resistance training program on arterial stiffness in young women. J Strength Cond Res 37(2): 315-321, 2023-The current investigation was conducted to determine the effect of 2 resistance training models on indices of arterial stiffness in young, healthy women. Twenty-four women, untrained college students, aged 18-22 years were randomized into 1 of 3 groups: control (CON) group ( n = 8), high-intensity (HI) resistance exercise group ( n = 8), and high-volume (HV) resistance exercise group ( n = 8). Subjects randomized to resistance training groups were required to perform strength training exercises 3-5 days a week for 11 weeks. The exercise regimen consisted of 2-3 sets of 3-8 repetitions (80-90% of 1 repetition maximum [1RM]) for the HI group and 3-4 sets of 10-15 repetitions (50-70% of 1RM) for the HV group. All subjects were instructed to continue their normal diet and avoid cardiovascular exercise during the study. After the intervention, there was a significant increase in carotid femoral pulse wave velocity (PWV) (6.39 ± 0.73 to 8.40 ± 2.31 m·s -1 ; p < 0.05) and carotid radial PWV (9.77 ± 1.74 to 12.58 ± 2.09 m·s -1 ; p < 0.05) in the CON group alone. Both the HI and HV groups increased their maximum squat (36.6 ± 7.9 vs. 41.3 ± 31.8 percent change; p < 0.05), bench press (34.4 ± 12.6 vs. 23.4 ± 11.1 percent change; p < 0.05), and seated row (22.0 ± 12.6 vs. 21.9 ± 12.5 percent change; p < 0.05), respectively. Our findings support the use of resistance training exercise without undue impact on vascular compliance in otherwise healthy women.

Effects of a 12-Week Resistance Training Program on Arterial Stiffness: A Randomized Controlled Trial.

ABSTRACT: Werner, TJ, Pellinger, TK, Rosette, VD, and Ortlip, AT. Effects of a 12-week resistance training program on arterial stiffness: a randomized controlled trial. J Strength Cond Res 35(12): 3281-3287, 2021-Arterial stiffness is an indicator of disease and is an independent predictor of cardiovascular events. Some reports indicate that resistance training increases indices of arterial stiffness, whereas others report no association. This study sought to determine the association between 2 common resistance training models and indices of arterial stiffness. We recruited 30 male, untrained subjects (18-30 years) and randomized them into 1 of 3 groups: control (CON, n = 10), high-intensity resistance exercise (HI, n = 10), and high-volume resistance exercise (HV, n = 10). Subjects randomized to the resistance training groups were required to perform whole-body strength training exercises 3-5 days a week for 12 weeks. The exercise regimen consisted of 2-3 sets of 3-8 repetitions (80-90% of 1 repetition maximum [1RM]) for the HI group and 3-4 sets of 10-15 repetitions (50-70% of 1RM) for the HV group. Anthropometry, carotid artery diameters, peripheral and central blood pressure, and maximal dynamic strength were measured before and after the 12-week study period. Subjects were instructed to maintain their normal diet and avoid aerobic exercise during the study. After the intervention, both the HI and HV groups increased their maximal strength on the back squat, bench press, and seated row (all p < 0.05). However, there were no changes in arterial stiffness indices between the groups. Using a randomized controlled trial with validated measurements of arterial stiffness, chronic resistance training does not appear to influence central arterial stiffness, regardless of training volume and load.

Skeletal Muscle Hyperemia: A Potential Bridge Between Post-exercise Hypotension and Glucose Regulation.

For both healthy individuals and patients with type 2 diabetes (T2D), the hemodynamic response to regular physical activity is important for regulating blood glucose, protecting vascular function, and reducing the risk of cardiovascular disease. In addition to these benefits of regular physical activity, evidence suggests even a single bout of dynamic exercise promotes increased insulin-mediated glucose uptake and insulin sensitivity during the acute recovery period. Importantly, post-exercise hypotension (PEH), which is defined as a sustained reduction in arterial pressure following a single bout of exercise, appears to be blunted in those with T2D compared to their non-diabetic counterparts. In this short review, we describe research that suggests the sustained post-exercise vasodilation often observed in PEH may sub-serve glycemic regulation following exercise in both healthy individuals and those with T2D. Furthermore, we discuss the interplay of enhanced perfusion, both macrovascular and microvascular, and glucose flux following exercise. Finally, we propose future research directions to enhance our understanding of the relationship between post-exercise hemodynamics and glucose regulation in healthy individuals and in those with T2D.

Acute Lower Leg Heating Increases Exercise Capacity in Patients With Peripheral Artery Disease.

BACKGROUND/OBJECTIVE: In this pilot study, we tested the hypothesis that acute lower leg heating (LLH) increases postheating popliteal artery blood flow and 6-minute walk distance in patients with peripheral artery disease (PAD). METHODS: Six patients (5 male, 1 female) with PAD (69 ± 6.9 years; claudication: ankle-brachial index < 0.90) participated in 3 randomized treatment sessions (2-7 days apart): control or bilateral LLH conducted via water bath immersion (42°C; ~40-cm depth) for either 15 or 45 minutes. Popliteal artery blood flow (Doppler ultrasound) and arterial pressure were measured before and after LLH. Six-minute walk distance was measured on the control day and each experimental day 35 minutes post-LLH. RESULTS: Popliteal artery blood flow increased after heating in a duration-dependent manner (P < .05, postheating vs control for both heating conditions and between them). Six-minute walk distance increased by 10% and 12% after 15- and 45-minute heating treatments, respectively (P < .05 vs control session). CONCLUSIONS: Lower leg heating, for as short as 15 minutes, increases postheating leg perfusion and exercise capacity in patients with PAD.

Effect of H1- and H2-histamine receptor blockade on postexercise insulin sensitivity.

Following a bout of dynamic exercise, humans experience sustained postexercise vasodilatation in the previously exercised skeletal muscle which is mediated by activation of histamine (H1 and H2) receptors. Skeletal muscle glucose uptake is also enhanced following dynamic exercise. Our aim was to determine if blunting the vasodilatation during recovery from exercise would have an adverse effect on blood glucose regulation. Thus, we tested the hypothesis that insulin sensitivity following exercise would be reduced with H1- and H2-receptor blockade versus control (no blockade). We studied 20 healthy young subjects (12 exercise; eight nonexercise sham) on randomized control and H1- and H2-receptor blockade (fexofenadine and ranitidine) days. Following 60 min of upright cycling at 60% VO2 peak or nonexercise sham, subjects consumed an oral glucose tolerance beverage (1.0 g/kg). Blood glucose was determined from "arterialized" blood samples (heated hand vein). Postexercise whole-body insulin sensitivity (Matsuda insulin sensitivity index) was reduced 25% with H1- and H2-receptor blockade (P < 0.05), whereas insulin sensitivity was not affected by histamine receptor blockade in the sham trials. These results indicate that insulin sensitivity following exercise is blunted by H1- and H2-receptor blockade and suggest that postexercise H1- and H2-receptor-mediated skeletal muscle vasodilatation benefits glucose regulation in healthy humans.

Local histamine H(1-) and H(2)-receptor blockade reduces postexercise skeletal muscle interstitial glucose concentrations in humans.

Elevated blood flow can potentially influence skeletal muscle glucose uptake, but the impact of postexercise hyperemia on glucose availability to skeletal muscle remains unknown. Because postexercise hyperemia is mediated by histamine H(1)- and H(2)-receptors, we tested the hypothesis that postexercise interstitial glucose concentrations would be lower in the presence of combined H1- and H2-receptor blockade. To this end, 4 microdialysis probes were inserted into the vastus lateralis muscle of 14 healthy subjects (21-27 years old) immediately after 60 min of either upright cycling at 60% peak oxygen uptake (exercise, n = 7) or quiet rest (sham, n = 7). Microdialysis probes were perfused with a modified Ringer's solution containing 3 mmol L(-1) glucose, 5 mmol L(-1) ethanol, and [6-3H] glucose (200 disintegrations·min-1 microL(-1)). Two sites (blockade) received both H1- and H2-receptor antagonists (1 mmol L(-1) pyrilamine and 3 mmol L-1 cimetidine) and 2 sites (control) did not receive antagonists. Ethanol outflow/inflow ratios (an inverse surrogate of local blood flow) were higher in blockade sites than in control sites following exercise (p < 0.05), whereas blockade had no effect on ethanol outflow/inflow ratios following sham (p = 0.80). Consistent with our hypothesis, during 3 of the 5 dialysate collection periods, interstitial glucose concentrations were lower in blockade sites vs. control sites following exercise (p < 0.05), whereas blockade had no effect on interstitial glucose concentrations following sham (p = 0.79). These findings indicate that local H1- and H2-receptor activation modulates skeletal muscle interstitial glucose levels during recovery from exercise in humans and suggest that the availability of glucose to skeletal muscle is enhanced by postexercise hyperemia.

Potential benefit from an H1-receptor antagonist on postexercise syncope in the heat.

PURPOSE: H1-receptors mediate the early portion (i.e., first 30 min after exercise) of postexercise hypotension. Immediately after exercise, syncope can occur due to an exaggerated form of postexercise hypotension. Therefore, we hypothesized that orthostatic hypotension occurring immediately after exercise would be attenuated with an H1-receptor antagonist. METHODS: We studied 15 endurance exercise-trained men and women in an environmental chamber set at 35 degrees C and 30.0% humidity. Subjects were studied in the supine position before a 45-min bout of treadmill running at 50% of VO2max. Immediately after exercise, measurements were taken in the supine position before the subjects were moved from a supine to a 60 degrees head-up tilt. Measurements included arterial pressure, heart rate, and brachial and cutaneous blood flow on a control and an H1-receptor antagonist (blockade) day. RESULTS: Mean arterial pressure was reduced 1 min into the tilt compared with preexercise values on the control day (76.2 +/- 0.5 vs 74.2 +/- 0.5 mm Hg; P < 0.05). This reduction was not seen on the blockade day (75.2 +/- 0.3 vs 75.0 +/- 0.5 mm Hg; P > 0.41). There were no differences in brachial vascular conductance (calculated as flow/pressure) in response to the head-up tilt between the study days (P > 0.23). The length of the head-up tilt was compared between study days for each subject. When contrasting this difference, the blockade lengthened the mean tilt time by 94 s (P = 0.098). CONCLUSION: These data suggest that an H1-receptor antagonist could potentially benefit postexercise syncope in a hot environment.

Effect of propranolol on sympathetically mediated leg vasoconstriction in humans.

Sympatho-excitatory manoeuvres are used to study vascular responsiveness in humans, but it is unclear if circulating adrenaline attenuates peripheral vasoconstriction during these manoeuvres. We hypothesized that vasoconstrictor responses to three manoeuvres (neck pressure, unilateral thigh-cuff release and isometric handgrip) would be greater after the administration of the beta-adrenergic blocker propranolol. Seven men and six women underwent these manoeuvres while beat-by-beat arterial pressure (finger photoplethysmography), femoral mean blood velocity (Doppler ultrasound) and femoral artery diameter (edge-detection software) were measured. Femoral vascular conductance was calculated as flow/pressure. Propranolol had no effect on baseline femoral vascular conductance (P > 0.05). As a result of neck pressure, femoral vascular conductance was reduced 23.9 +/- 3.5% before vs. 33.2 +/- 3.2% after infusion of propranolol (P = 0.033). After thigh-cuff release, femoral vascular conductance declined 50.2 +/- 5.8% before vs. 57.4 +/- 9.6% after propranolol infusion (P = 0.496). During handgrip, femoral vascular conductance was reduced 47.2 +/- 9.6% before vs. 55.2 +/- 9.2% after propranolol administration (P = 0.447). After handgrip, women had a greater rise in conductance than men (women: 153 +/- 16.2%; men: 36.4 +/- 10.6%; P < 0.001), which was blunted by 54.8% by propranolol (P < 0.001 vs. control), but unaffected by propranolol in men (P = 0.355 vs. control). The finding that beta-adrenergic receptor-mediated vasodilatation minimally affects vascular responses to these sympatho-excitatory manoeuvres reinforces their utility in the investigation of sympathetic vascular regulation in humans. Interestingly, post-handgrip hyperaemia is greater in women than men and is, in part, beta-adrenergic receptor mediated.

The effect of back squat depth on the EMG activity of 4 superficial hip and thigh muscles.

The purpose of this study was to measure the relative contributions of 4 hip and thigh muscles while performing squats at 3 depths. Ten experienced lifters performed randomized trials of squats at partial, parallel, and full depths, using 100-125% of body weight as resistance. Electromyographic (EMG) surface electrodes were placed on the vastus medialis (VMO), the vastus lateralis, (VL), the biceps femoris (BF), and the gluteus maximus (GM). EMG data were quantified by integration and expressed as a percentage of the total electrical activity of the 4 muscles. Analysis of variance (ANOVA) and Tukey post hoc tests indicated a significant difference (p < 0.001*, p = 0.056**) in the relative contribution of the GM during the concentric phases among the partial- (16.9%*), parallel- (28.0%**), and full-depth (35.4%*) squats. There were no significant differences between the relative contributions of the BF, the VMO, and the VL at different squatting depths during this phase. The results suggest that the GM, rather than the BF, the VMO, or the VL, becomes more active in concentric contraction as squat depth increases.