Adrenergic control of skeletal muscle blood flow during chronic hypoxia in healthy males.

Sympathetic transduction is reduced following chronic high-altitude (HA) exposure; however, vascular α-adrenergic signaling, the primary mechanism mediating sympathetic vasoconstriction at sea level (SL), has not been examined at HA. In nine male lowlanders, we measured forearm blood flow (Doppler ultrasound) and calculated changes in vascular conductance (ΔFVC) during 1) incremental intra-arterial infusion of phenylephrine to assess α1-adrenergic receptor responsiveness and 2) combined intra-arterial infusion of ß-adrenergic and α-adrenergic antagonists propranolol and phentolamine (α-ß-blockade) to assess adrenergic vascular restraint at rest and during exercise-induced sympathoexcitation (cycling; 60% peak power). Experiments were performed near SL (344 m) and after 3 wk at HA (4,383 m). HA abolished the vasoconstrictor response to low-dose phenylephrine (ΔFVC: SL: -34 ± 15%, vs. HA; +3 ± 18%; P < 0.0001) and markedly attenuated the response to medium (ΔFVC: SL: -45 ± 18% vs. HA: -28 ± 11%; P = 0.009) and high (ΔFVC: SL: -47 ± 20%, vs. HA: -35 ± 20%; P = 0.041) doses. Blockade of ß-adrenergic receptors alone had no effect on resting FVC (P = 0.500) and combined α-ß-blockade induced a similar vasodilatory response at SL and HA (P = 0.580). Forearm vasoconstriction during cycling was not different at SL and HA (P = 0.999). Interestingly, cycling-induced forearm vasoconstriction was attenuated by α-ß-blockade at SL (ΔFVC: Control: -27 ± 128 vs. α-ß-blockade: +19 ± 23%; P = 0.0004), but unaffected at HA (ΔFVC: Control: -20 ± 22 vs. α-ß-blockade: -23 ± 11%; P = 0.999). Our results indicate that in healthy males, altitude acclimatization attenuates α1-adrenergic receptor responsiveness; however, resting α-adrenergic restraint remains intact, due to concurrent resting sympathoexcitation. Furthermore, forearm vasoconstrictor responses to cycling are preserved, although the contribution of adrenergic receptors is diminished, indicating a reliance on alternative vasoconstrictor mechanisms.

The impact of leg position on muscle blood flow and oxygenation during low-intensity rhythmic plantarflexion exercise.

PURPOSE: Resistance training (RT) is an effective countermeasure to combat physical deconditioning whereby localized hypoxia within the limb increases metabolic stress eliciting muscle adaptation. The current study sought to examine the influence of gravity on muscle oxygenation (SmO2) alongside vascular hemodynamic responses. METHODS: In twelve young healthy adults, an ischemic occlusion test and seven minutes of low-intensity rhythmic plantarflexion exercise were used alongside superficial femoral blood flow and calf near-infrared spectroscopy to assess the microvascular vasodilator response, conduit artery flow-mediated dilation, exercise-induced hyperemia, and SmO2 with the leg positioned above or below the heart in a randomized order. RESULTS: The microvascular vasodilator response, assessed by peak blood flow (798 ± 231 mL/min vs. 1348 ± 290 mL/min; p < 0.001) and reperfusion slope 10 s of SmO2 after cuff deflation (0.75 ± 0.45%.s-1 vs.2.40 ± 0.94%.s-1; p < 0.001), was attenuated with the leg above the heart. This caused a blunted dilatation of the superficial femoral artery (3.0 ± 2.4% vs. 5.2 ± 2.1%; p = 0.008). Meanwhile, blood flow area under the curve was comparable (above the heart: 445 ± 147 mL vs. below the heart: 474 ± 118 mL; p = 0.55) in both leg positions. During rhythmic exercise, the increase in femoral blood flow was lower in the leg up position (above the heart: 201 ± 94% vs. below the heart: 292 ± 114%; p = 0.001) and contributed to a lower SmO2 (above the heart: 41 ± 18% vs. below the heart 67 ± 5%; p < 0.001). CONCLUSION: Positioning the leg above the heart results in attenuated peak vascular dilator response and exercise-induced hyperemia that coincided with a lower SmO2 during low-intensity plantarflexion exercise.

Control of blood pressure in the cold: differentiation of skin and skeletal muscle vascular resistance.

NEW FINDINGS: What is the central question of this study? Why does blood pressure increases during cold air exposure? Specifically, what is the contribution of skin and skeletal muscle vascular resistance during whole body versus isolated face cooling? What is the main finding and its importance? Whole-body cooling caused an increase in blood pressure through an increase in skeletal muscle and cutaneous vascular resistance. However, isolated mild face cooling caused an increase in blood pressure predominately via an increase in cutaneous vasoconstriction. ABSTRACT: The primary aim of this investigation was to determine the individual contribution of the cutaneous and skeletal muscle circulations to the cold-induced pressor response. To address this, we examined local vascular resistances in the cutaneous and skeletal muscle of the arm and leg. Thirty-four healthy individuals underwent three different protocols, whereby cold air to clamp skin temperature (27°C) was passed over (1) the whole-body, (2) the whole-body, but with the forearm pre-cooled to clamp cutaneous vascular resistance, and (3) the face. Cold exposure applied to the whole body or isolated to the face increased mean arterial pressure (all, P < 0.001) and total peripheral resistance (all, P < 0.047) compared to thermal neutral baseline. Whole-body cooling increased femoral (P < 0.005) and brachial artery resistance (P < 0.003) compared to thermoneutral baseline. Moreover, when the forearm was pre-cooled to remove the contribution of cutaneous resistance (P = 0.991), there was a further increase in lower arm vasoconstriction (P = 0.036) when whole-body cooling was superimposed. Face cooling also caused a reflex increase in lower arm cutaneous (P = 0.009) and brachial resistance (P = 0.050), yet there was no change in femoral resistance (P = 0.815) despite a reflex increase in leg cutaneous resistance (P = 0.010). Cold stress causes an increase in blood pressure through a change in total peripheral resistance that is largely due to cutaneous vasoconstriction with face cooling, but there is additional vasoconstriction in the skeletal muscle vasculature with whole-body cooling.

High-intensity exercise and passive hot water immersion cause similar postintervention changes in peripheral and cerebral shear.

Passive hot water immersion (PHWI) provides a peripheral vasculature shear stimulus comparable to low-intensity exercise within the active skeletal muscle, whereas moderate- and high-intensity exercise elicit substantially greater shear rates in the peripheral vasculature, likely conferring greater vascular benefits. Notably, few studies have compared postintervention shear rates in the peripheral and cerebral vasculature after high-intensity exercise and PHWI, especially considering that the postintervention recovery period represents a key window in which adaptation occurs. Therefore, we aimed to compare shear rates in the internal carotid artery (ICA), vertebral artery (VA), and common femoral artery (CFA) between high-intensity exercise and whole body PHWI for up to 80 min after intervention. Fifteen healthy (27 ± 4 yr), moderately trained individuals underwent three time-matched interventions in a randomized order that included 30 min of whole body immersion in a 42°C hot bath, 30 min of treadmill running and 5 × 4-min high-intensity intervals (HIIE). There were no differences in ICA (P = 0.4643) and VA (P = 0.1940) shear rates between PHWI and exercise (both continuous and HIIE) after intervention. All three interventions elicited comparable increases in CFA shear rate after intervention (P = 0.0671); however, CFA shear rate was slightly higher 40 min after threshold running (P = 0.0464) and slightly higher, although not statistically, for HIIE (P = 0.0565) compared with PHWI. Our results suggest that time- and core temperature-matched high-intensity exercise and PHWI elicit limited changes in cerebral shear and comparable increases in peripheral vasculature shear rates when measured for up to 80 min after intervention.NEW & NOTEWORTHY The study aimed to compare shear rates in lower limb and extracranial cerebral blood vessels for up to 80 min after high-intensity exercise and whole body passive hot water immersion (PHWI). Time- and core temperature-matched high-intensity exercise and whole body PHWI both elicited minimal, but comparable, postintervention changes in cerebral artery shear rate. Furthermore, 30 min of PHWI caused a postintervention increase in femoral shear rate similar to high-intensity exercise; however, femoral shear remained slightly elevated for a longer period after high-intensity exercise. These results suggest that PHWI provides postintervention changes in lower limb peripheral shear rates comparable to intense exercise and is likely a therapeutic alternative in individuals unable to perform exercise.

Global REACH 2018: increased adrenergic restraint of blood flow preserves coupling of oxygen delivery and demand during exercise at high-altitude.

Chronic exposure to hypoxia (high-altitude, HA; >4000 m) attenuates the vasodilatory response to exercise and is associated with a persistent increase in basal sympathetic nerve activity (SNA). The mechanism(s) responsible for the reduced vasodilatation and exercise hyperaemia at HA remains unknown. We hypothesized that heightened adrenergic signalling restrains skeletal muscle blood flow during handgrip exercise in lowlanders acclimatizing to HA. We tested nine adult males (n = 9) at sea-level (SL; 344 m) and following 21-28 days at HA (∼4300 m). Forearm blood flow (FBF; duplex ultrasonography), mean arterial pressure (MAP; brachial artery catheter), forearm vascular conductance (FVC; FBF/MAP), and arterial and venous blood sampling (O2 delivery ( DO2${D}_{{{\rm{O}}}_{\rm{2}}}$ ) and uptake ( V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ )) were measured at rest and during graded rhythmic handgrip exercise (5%, 15% and 25% of maximum voluntary isometric contraction; MVC) before and after local α- and ß-adrenergic blockade (intra-arterial phentolamine and propranolol). HA reduced ΔFBF (25% MVC: SL: 138.3 ± 47.6 vs. HA: 113.4 ± 37.1 ml min-1 ; P = 0.022) and Δ V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ (25% MVC: SL: 20.3 ± 7.5 vs. HA: 14.3 ± 6.2 ml min-1 ; P = 0.014) during exercise. Local adrenoreceptor blockade at HA restored FBF during exercise (25% MVC: SLα-ß blockade : 164.1 ± 71.7 vs. HAα-ß blockade : 185.4 ± 66.6 ml min-1 ; P = 0.947) but resulted in an exaggerated relationship between DO2${D}_{{{\rm{O}}}_{\rm{2}}}$ and V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ ( DO2${D}_{{{\rm{O}}}_{\rm{2}}}$ / V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ slope: SL: 1.32; HA: slope: 1.86; P = 0.037). These results indicate that tonic adrenergic signalling restrains exercise hyperaemia in lowlanders acclimatizing to HA. The increase in adrenergic restraint is necessary to match oxygen delivery to demand and prevent over perfusion of contracting muscle at HA. KEY POINTS: In exercising skeletal muscle, local vasodilatory signalling and sympathetic vasoconstriction integrate to match oxygen delivery to demand and maintain arterial blood pressure. Exposure to chronic hypoxia (altitude, >4000 m) causes a persistent increase in sympathetic nervous system activity that is associated with impaired functional capacity and diminished vasodilatation during exercise. In healthy male lowlanders exposed to chronic hypoxia (21-28 days; ∼4300 m), local adrenoreceptor blockade (combined α- and ß-adrenergic blockade) restored skeletal muscle blood flow during handgrip exercise. However, removal of tonic adrenergic restraint at high altitude caused an excessive rise in blood flow and subsequently oxygen delivery for any given metabolic demand. This investigation is the first to identify greater adrenergic restraint of blood flow during acclimatization to high altitude and provides evidence of a functional role for this adaptive response in regulating oxygen delivery and demand.

Global Reach 2018: sympathetic neural and hemodynamic responses to submaximal exercise in Andeans with and without chronic mountain sickness.

Andeans with chronic mountain sickness (CMS) and polycythemia have similar maximal oxygen uptakes to healthy Andeans. Therefore, this study aimed to explore potential adaptations in convective oxygen transport, with a specific focus on sympathetically mediated vasoconstriction of nonactive skeletal muscle. In Andeans with (CMS+, n = 7) and without (CMS-, n = 9) CMS, we measured components of convective oxygen delivery, hemodynamic (arterial blood pressure via intra-arterial catheter), and autonomic responses [muscle sympathetic nerve activity (MSNA)] at rest and during steady-state submaximal cycling exercise [30% and 60% peak power output (PPO) for 5 min each]. Cycling caused similar increases in heart rate, cardiac output, and oxygen delivery at both workloads between both Andean groups. However, at 60% PPO, CMS+ had a blunted reduction in Δtotal peripheral resistance (CMS-, -10.7 ± 3.8 vs. CMS+, -4.9 ± 4.1 mmHg·L-1·min-1; P = 0.012; d = 1.5) that coincided with a greater Δforearm vasoconstriction (CMS-, -0.2 ± 0.6 vs. CMS+, 1.5 ± 1.3 mmHg·mL-1·min-1; P = 0.008; d = 1.7) and a rise in Δdiastolic blood pressure (CMS-, 14.2 ± 7.2 vs. CMS+, 21.6 ± 4.2 mmHg; P = 0.023; d = 1.2) compared with CMS-. Interestingly, although MSNA burst frequency did not change at 30% or 60% of PPO in either group, at 60% Δburst incidence was attenuated in CMS+ (P = 0.028; d = 1.4). These findings indicate that in Andeans with polycythemia, light intensity exercise elicited similar cardiovascular and autonomic responses compared with CMS-. Furthermore, convective oxygen delivery is maintained during moderate-intensity exercise despite higher peripheral resistance. In addition, the elevated peripheral resistance during exercise was not mediated by greater sympathetic neural outflow, thus other neural and/or nonneural factors are perhaps involved.NEW & NOTEWORTHY During submaximal exercise, convective oxygen transport is maintained in Andeans suffering from polycythemia. Light intensity exercise elicited similar cardiovascular and autonomic responses compared with healthy Andeans. However, during moderate-intensity exercise, we observed a blunted reduction in total peripheral resistance, which cannot be ascribed to an exaggerated increase in muscle sympathetic nerve activity, indicating possible contributions from other neural and/or nonneural mechanisms.

Effects of Regular Long-Term Circuit Training (Once per Week) on Cardiorespiratory Fitness in Previously Sedentary Adults.

The purpose of the study was (1) to investigate the effects of regular long-term circuit training (once per week) on cardiorespiratory fitness (CRF) in sedentary adults and (2) to compare training progress with the effects of continued exercise participation by regularly active age-matched individuals. Ten sedentary, middle-aged (51 ± 6 years) individuals (sedentary group, SG) of both sexes performed 32 weeks (1 training session/week) of supervised circuit training and 10 weeks of self-managed training. Effects were compared to an age-matched group (51 ± 8 years; n = 10) of regularly active individuals (active group, AG). CRF (expressed as peak oxygen uptake: VO2peak; peak power output: PPO) and systemic blood pressure (BP) during the incremental test were measured at the start and after the training intervention. CRF decreased significantly within the AG (VO2peak: 43.1 ± 7.3 vs. 40.3 ± 6.5 mL/min/kg, p < 0.05; PPO: 3.3 ± 0.6 vs. 3.1 ± 0.6; p < 0.05) but was maintained in the SG. In addition, significant improvements in restoration of the oxygen level in leg muscles after exercise and reduced systolic BP (180 ± 14 vs. 170 ± 17 mmHg, p = 0.01) at submaximal exercise were found within the SG. However, differences in changes from pre to post did not reach significance between groups. In contrast to the regularly active individuals, circuit training once per week over 32 weeks prevented the aging-related decline of CRF in previously sedentary subjects and reduced systolic BP during submaximal exercise, indicating improved exercise tolerance.

Intra-rater reliability of leg blood flow during dynamic exercise using Doppler ultrasound.

Developing an exercise model that resembles a traditional form of aerobic exercise and facilitates a complete simultaneous assessment of multiple parameters within the oxygen cascade is critically for understanding exercise intolerances in diseased populations. Measurement of muscle blood flow is a crucial component of such a model and previous studies have used invasive procedures to determine blood flow kinetics; however, this may not be appropriate in certain populations. Furthermore, current models utilizing Doppler ultrasound use isolated limb exercise and while these studies have provided useful data, the exercise model does not mimic the whole-body physiological response to continuous dynamic exercise. Therefore, we aimed to measure common femoral artery blood flow using Doppler ultrasound during continuous dynamic stepping exercise performed at three independent workloads to assess the within day and between-day reliability for such an exercise modality. We report a within-session coefficient of variation of 5.8% from three combined workloads and a between-day coefficient of variation of 12.7%. These values demonstrate acceptable measurement accuracy and support our intention of utilizing this noninvasive exercise model for an integrative assessment of the whole-body physiological response to exercise in a range of populations.

Global REACH 2018: the adaptive phenotype to life with chronic mountain sickness and polycythaemia.

KEY POINTS: Humans suffering from polycythaemia undergo multiple circulatory adaptations including changes in blood rheology and structural and functional vascular adaptations to maintain normal blood pressure and vascular shear stresses, despite high blood viscosity. During exercise, several circulatory adaptations are observed, especially involving adrenergic and non-adrenergic mechanisms within non-active and active skeletal muscle to maintain exercise capacity, which is not observed in animal models. Despite profound circulatory stress, i.e. polycythaemia, several adaptations can occur to maintain exercise capacity, therefore making early identification of the disease difficult without overt symptomology. Pharmacological treatment of the background heightened sympathetic activity may impair the adaptive sympathetic response needed to match local oxygen delivery to active skeletal muscle oxygen demand and therefore inadvertently impair exercise capacity. ABSTRACT: Excessive haematocrit and blood viscosity can increase blood pressure, cardiac work and reduce aerobic capacity. However, past clinical investigations have demonstrated that certain human high-altitude populations suffering from excessive erythrocytosis, Andeans with chronic mountain sickness, appear to have phenotypically adapted to life with polycythaemia, as their exercise capacity is comparable to healthy Andeans and even with sea-level inhabitants residing at high altitude. By studying this unique population, which has adapted through natural selection, this study aimed to describe how humans can adapt to life with polycythaemia. Experimental studies included Andeans with (n = 19) and without (n = 17) chronic mountain sickness, documenting exercise capacity and characterizing the transport of oxygen through blood rheology, including haemoglobin mass, blood and plasma volume and blood viscosity, cardiac output, blood pressure and changes in total and local vascular resistances through pharmacological dissection of α-adrenergic signalling pathways within non-active and active skeletal muscle. At rest, Andeans with chronic mountain sickness had a substantial plasma volume contraction, which alongside a higher red blood cell volume, caused an increase in blood viscosity yet similar total blood volume. Moreover, both morphological and functional alterations in the periphery normalized vascular shear stress and blood pressure despite high sympathetic nerve activity. During exercise, blood pressure, cardiac work and global oxygen delivery increased similar to healthy Andeans but were sustained by modifications in both non-active and active skeletal muscle vascular function. These findings highlight widespread physiological adaptations that can occur in response to polycythaemia, which allow the maintenance of exercise capacity.

Reducing intracranial pressure by reducing central venous pressure: assessment of potential countermeasures to spaceflight-associated neuro-ocular syndrome.

Spaceflight-associated neuro-ocular syndrome (SANS) involves unilateral or bilateral optic disc edema, widening of the optic nerve sheath, and posterior globe flattening. Owing to posterior globe flattening, it is hypothesized that microgravity causes a disproportionate change in intracranial pressure (ICP) relative to intraocular pressure. Countermeasures capable of reducing ICP include thigh cuffs and breathing against inspiratory resistance. Owing to the coupling of central venous pressure (CVP) and intracranial pressure, we hypothesized that both ICP and CVP will be reduced during both countermeasures. In four male participants (32 ± 13 yr) who were previously implanted with Ommaya reservoirs for treatment of unrelated clinical conditions, ICP was measured invasively through these ports. Subjects were healthy at the time of testing. CVP was measured invasively by a peripherally inserted central catheter. Participants breathed through an impedance threshold device (ITD, -7 cmH2O) to generate negative intrathoracic pressure for 5 min, and subsequently, wore bilateral thigh cuffs inflated to 30 mmHg for 2 min. Breathing through an ITD reduced both CVP (6 ± 2 vs. 3 ± 1 mmHg; P = 0.02) and ICP (16 ± 3 vs. 12 ± 1 mmHg; P = 0.04) compared to baseline, a result that was not observed during the free breathing condition (CVP, 6 ± 2 vs. 6 ± 2 mmHg, P = 0.87; ICP, 15 ± 3 vs. 15 ± 4 mmHg, P = 0.68). Inflation of the thigh cuffs to 30 mmHg caused no meaningful reduction in CVP in all four individuals (5 ± 4 vs. 5 ± 4 mmHg; P = 0.1), coincident with minimal reduction in ICP (15 ± 3 vs. 14 ± 4 mmHg; P = 0.13). The application of inspiratory resistance breathing resulted in reductions in both ICP and CVP, likely due to intrathoracic unloading.NEW & NOTEWORTHY Spaceflight causes pathological changes in the eye that may be due to the absence of gravitational unloading of intracranial pressure (ICP) under microgravity conditions commonly referred to as spaceflight-associated neuro-ocular syndrome (SANS), whereby countermeasures aimed at lowering ICP are necessary. These data show that impedance threshold breathing acutely reduces ICP via a reduction in central venous pressure (CVP). Whereas, acute thigh cuff inflation, a popular known spaceflight-associated countermeasure, had little effect on ICP and CVP.

Whole body passive heating versus dynamic lower body exercise: a comparison of peripheral hemodynamic profiles.

Passive heating has emerged as a therapeutic intervention for the treatment and prevention of cardiovascular disease. Like exercise, heating increases peripheral artery blood flow and shear rate, which is thought to be a primary mechanism underpinning endothelium-mediated vascular adaptation. However, few studies have compared the increase in arterial blood flow and shear rate between dynamic exercise and passive heating. In a fixed crossover design study, 15 moderately trained healthy participants (25.6 ± 3.4 yr) (5 female) underwent 30 min of whole body passive heating (42°C bath), followed on a separate day by 30 min of semi-recumbent stepping exercise performed at two workloads corresponding to the increase in cardiac output (Qc) (Δ3.72 L·min-1) and heart rate (HR) (Δ40 beats/min) recorded at the end of passive heating. At the same Qc (Δ3.72 L·min-1 vs. 3.78 L·min-1), femoral artery blood flow (1,599 mL/min vs. 1,947 mL/min) (P = 0.596) and shear rate (162 s-1 vs. 192 s-1) (P = 0.471) measured by ultrasonography were similar between passive heating and stepping exercise. However, for the same HRMATCHED intensity, femoral blood flow (1,599 mL·min-1 vs. 2,588 mL·min-1) and shear rate (161 s-1 vs. 271 s-1) were significantly greater during exercise, compared with heating (both P = <0.001). The results indicate that, for moderately trained individuals, passive heating increases common femoral artery blood flow and shear rate similar to low-intensity continuous dynamic exercise (29% V̇o2max); however, exercise performed at a higher intensity (53% V̇o2max) results in significantly larger shear rates toward the active skeletal muscle.NEW & NOTEWORTHY Passive heating and exercise increase blood flow through arteries, generating a frictional force, termed shear rate, which is associated with positive vascular health. Few studies have compared the increase in arterial blood flow and shear rate elicited by passive heating with that elicited by dynamic continuous exercise. We found that 30 min of whole body passive hot-water immersion (42°C bath) increased femoral artery blood flow and shear rate equivalent to exercising at a moderate intensity (∼57% HRmax).

Functional Vs. Running Low-Volume High-Intensity Interval Training: Effects on VO2max and Muscular Endurance.

The purpose of the study was to assess if high-intensity interval training (HIIT) using functional exercises is as effective as traditional running HIIT in improving maximum oxygen uptake (VO2max) and muscular endurance. Fifteen healthy, moderately trained female (n = 11) and male (n= 4) participants (age 25.6 ± 2.6 years) were assigned to either running HIIT (HIIT-R; n = 8, 6 females, 2 males) or functional HIIT (HIIT-F; n = 7, 5 females, 2 males). Over a four-week period, both groups performed 14 exercise sessions of either HIIT-R or, HIIT-F consisting of 3-4 sets of low-volume HIIT (8x 20 s, 10 s rest; set rest: 5 min). Training heart rate (HR) data were collected throughout all training sessions. Mean and peak HR during the training sessions were significantly different (p = 0.018 and p = 0.022, respectively) between training groups, with HIIT-F eliciting lower HR responses than the HIIT-R. However, despite these differences in exercise HR, VO2max improved similarly (~13% for the HIIT-R versus ~11% for the HIIT-F, p=0.300). Muscular endurance (burpees and toes to bar) significantly improved (p =0.004 and p = 0.001, respectively) independent of training modality. These findings suggest that classic running HIIT and functional HIIT both improve VO2max and affect muscular endurance to the same extent despite a lower cardiovascular strain in the functional protocol.