T. Dylan Olver

Run Sprint Interval Training Improves Aerobic Performance but Not Maximal Cardiac Output

UNLABELLED Repeated maximal-intensity short-duration exercise (sprint interval training, SIT) can produce muscle adaptations similar to endurance training (ET) despite a much reduced training volume. However, most SIT data use cycling, and little is known about its effects on body composition or maximal cardiac output (Qmax). PURPOSE The purpose of this study was to assess body composition, 2000-m run time trial, VO(2max), and Q(max) effects of run SIT versus ET. METHODS Men and women (n = 10 per group; mean ± SD: age = 24 ± 3 yr) trained three times per week for 6 wk with SIT, 30-s all-out run sprints (manually driven treadmill), four to six bouts per session, 4-min recovery per bout, versus ET, 65% VO(2max) for 30 to 60 min·d(-1). RESULTS Training improved (P < 0.05) body composition, 2000-m run time trial performance, and VO(2max) in both groups. Fat mass decreased 12.4% with SIT (mean ± SEM; 13.7 ± 1.6 to 12.0 ± 1.6 kg) and 5.8% with ET (13.9 ± 1.7 to 13.1 ± 1.6 kg). Lean mass increased 1% in both groups. Time trial performance improved 4.6% with SIT (-25.6 ± 8.1 s) and 5.9% with ET (-31.9 ± 6.3 s). VO(2max) increased 11.5% with SIT (46.8 ± 1.6 to 52.2 ± 2.0 mL·kg·(-1)·min(-1)) and 12.5% with ET (44.0 ± 2.0 to 49.5 ± 2.6 mL·kg·(-1)·min(-1)). None of these improvements differed between groups. In contrast, Q(max) increased by 9.5% with ET only (22.2 ± 2.0 to 24.3 ± 1.6 L·min(-1)). CONCLUSIONS Despite a fraction of the time commitment, run SIT induces similar body composition, VO(2max), and performance adaptations as ET, but with no effect on Q(max). These data suggest that adaptations with ET are of central origin primarily, whereas those with SIT are more peripheral

The microcirculation: a key player in obesity-associated cardiovascular disease

It is increasingly recognized that obesity is a risk factor for microvascular disease, involving both structural and functional changes in the microvasculature. This review aims to describe how obesity impacts the microvasculature of a variety of tissues, including visceral adipose tissue, skeletal muscle, heart, brain, kidneys, and lungs. These changes involve endothelial dysfunction, which in turn (i) impacts control of vascular tone, (ii) contributes to development of microvascular insulin resistance, (iii) alters secretion of paracrine factors like nitric oxide and endothelin, but (iv) also influences vascular structure and perivascular inflammation. In concert, these changes impair organ perfusion and organ function thereby contributing to altered release and clearance of neurohumoral factors, such as adipokines and inflammatory cytokines. Global microvascular dysfunction in obese subjects is therefore a common pathway that not only explains exercise-intolerance but also predisposes to development of chronic kidney disease, microvascular dementia, coronary microvascular angina, heart failure with preserved ejection fraction, chronic obstructive pulmonary disease, and pulmonary hypertension.

Exercise training enhances insulin-stimulated nerve arterial vasodilation in rats with insulin-treated experimental diabetes

Insulin stimulates nerve arterial vasodilation through a nitric oxide (NO) synthase (NOS) mechanism. Experimental diabetes reduces vasa nervorum NO reactivity. Studies investigating hyperglycemia and nerve arterial vasodilation typically omit insulin treatment and use sedentary rats resulting in severe hyperglycemia. We tested the hypotheses that 1) insulin-treated experimental diabetes and inactivity (DS rats) will attenuate insulin-mediated nerve arterial vasodilation, and 2) deficits in vasodilation in DS rats will be overcome by concurrent exercise training (DX rats; 75-85% VO2 max, 1 h/day, 5 days/wk, for 10 wk). The baseline index of vascular conductance values (VCi = nerve blood flow velocity/mean arterial blood pressure) were similar (P ≥ 0.68), but peak VCi and the area under the curve (AUCi) for the VCi during a euglycemic hyperinsulinemic clamp (EHC; 10 mU·kg(-1)·min(-1)) were lower in DS rats versus control sedentary (CS) rats and DX rats (P ≤ 0.01). Motor nerve conduction velocity (MNCV) was lower in DS rats versus CS rats and DX rats (P ≤ 0.01). When compared with DS rats, DX rats expressed greater nerve endothelial NOS (eNOS) protein content (P = 0.04). In a separate analysis, we examined the impact of diabetes in exercise-trained rats alone. When compared with exercise-trained control rats (CX), DX rats had a lower AUCi during the EHC, lower MNCV values, and lower sciatic nerve eNOS protein content (P ≤ 0.03). Therefore, vasa nervorum and motor nerve function are impaired in DS rats. Such deficits in rats with diabetes can be overcome by concurrent exercise training. However, in exercise-trained rats (CX and DX groups), moderate hyperglycemia lowers vasa nervorum and nerve function.

Metabolomic Response of Skeletal Muscle to Aerobic Exercise Training in Insulin Resistant Type 1 Diabetic Rats

The etiology of insulin resistance in Type 1 Diabetes (T1D) is unknown, however it affects approximately 20% of T1D patients. Intramyocellular lipids (IMCL) have been identified as a mechanism of insulin resistance. We examined skeletal muscle of T1D rats to determine if alterations in lipid metabolism were evident and whether aerobic exercise training improves IMCL and insulin resistance. To do so, 48 male Sprague-Dawley rats were divided into control (C), sedentary diabetes (D) and diabetes exercise (DX) groups. Following multiple low-dose Streptozotocin (STZ) injections (20 mg/kg), glycemia (9–15 mM) was maintained using insulin treatment. DX were treadmill trained at high intensity (~75% V02max; 5days/week) for 10 weeks. The results demonstrate that D exhibited insulin resistance compared with C and DX, indicated by decreased glucose infusion rate during a hyperinsulinemic-euglycemic clamp (p < 0.05). There were no differences between C and DX, suggesting that exercise improved insulin resistance (p < 0.05). Metabolomics analysis revealed a significant shift in lipid metabolism whereby notable fatty acid metabolites (arachidonic acid, palmitic acid and several polyunsaturated fatty acids) were significantly elevated in D compared to C and DX. Based on the intermediates observed, insulin resistance in T1D is characterized by an insulin-desensitizing intramyocellular fatty acid metabolite profile that is ameliorated with exercise training.

Central vs. peripheral determinants of sympathetic neural recruitment: insights from static handgrip exercise and postexercise circulatory occlusion

Sympathetic outflow is modified during acute homeostatic stress through increased firing of low-threshold axons, recruitment of latent axons, and synaptic delay modifications. However, the role of central mechanisms versus peripheral reflex control over sympathetic recruitment remains unknown. Here, we examined sympathetic discharge patterns during fatiguing static handgrip (SHG) exercise and postexercise circulatory occlusion (PECO) to study the central vs. peripheral reflex elements of sympathetic neural coding. Muscle sympathetic nerve activity (MSNA; microneurography) was measured in six males (25 ± 3 yr) at baseline (3 min) and during 5 min of SHG exercise completed at 20% maximal voluntary contraction. Isolation of the peripheral metaboreflex component was achieved by PECO for 3 min. Action potential (AP) patterns were studied using wavelet-based methodology. Compared with baseline, total MSNA increased by minute 3 of SHG, remaining elevated throughout the duration of exercise and PECO (all P < 0.05). The AP content per burst increased above baseline by minute 4 of SHG (Δ4 ± 2), remaining elevated at minute 5 (Δ6 ± 4) and PECO (Δ4 ± 4; all P < 0.05). Similarly, total AP clusters increased by minute 4 of SHG (Δ5 ± 5) and remained elevated at minute 5 (Δ6 ± 3) and PECO (Δ7 ± 5; all P < 0.01), indicating recruitment of latent subpopulations. Finally, the AP cluster size-latency profile was shifted downward during minutes 4 (-32 ± 22 ms) and 5 (-49 ± 17 ms; both P < 0.05) of SHG but was not different than baseline during PECO (P > 0.05). Our findings suggest that central perceptual factors play a specific role in the synaptic delay aspect of sympathetic discharge timing, whereas peripheral reflex mechanisms affect recruitment of latent axons.

Glucose-stimulated insulin secretion causes an insulin-dependent nitric oxide–mediated vasodilation in the blood supply of the rat sciatic nerve

This study tested the hypothesis that acute hyperglycemia reduces sciatic nerve blood flow in Sprague-Dawley rats. Anesthetized rats underwent cannulation of their right jugular vein (for anesthetic/nutrient/drug infusion) and right carotid artery (for continuous blood pressure measurement via pressure transducer). The left sciatic nerve was exposed and nerve blood velocity (NBV) was assessed from an arterial segment lying superficially along the sciatic nerve (Doppler ultrasound, 40 MHz). NBV and mean arterial pressure (MAP) values were collected, and an index of nerve vascular conductance (NVC) was established (NBV/MAP) at baseline and at 5, 10, 20, and 30 min (and 80 min for insulin) following 1) low glucose infusion, 1 g/kg (50% solution); 2) high glucose infusion, 3 g/kg; 3) high glucose infusion in the absence of a functioning pancreas; 4) euglycemic hyperinsulinemic clamp-insulin infusion (10 mU·kg⁻¹·min⁻¹; 0.4 IU/ml); 5) high glucose infusion + NG-nitro-L-arginine methyl ester (L-NAME) infusion (30 mg/kg); and 6) L-NAME alone followed 20 min later by high glucose infusion. High glucose infusion increased NVC by ~120% relative to baseline (P < 0.001), and this dilation was attenuated in rats without a functioning pancreas (i.e., without insulin secretion) (P = 0.004) and following L-NAME infusion (P = 0.011). Therefore, the vasodilation in rat sciatic nerve during glucose infusion was dependent upon the insulin response and acted through a nitric oxide synthase pathway.

Role of habitual physical activity in modulating vascular actions of insulin.

What is the topic of this review? This review highlights the importance of increased vascular insulin sensitivity for maintaining glycaemic control and cardiovascular health. What advances does it highlight? We discuss the role of habitual physical activity in modulating vascular actions of insulin.

Addition of Synchronous Whole-Body Vibration to Body Mass Resistive Exercise Causes Little or No Effects on Muscle Damage and Inflammation

Abstract Hazell, TJ, Olver, TD, Hamilton, CD, and Lemon, PWR. Addition of synchronous whole-body vibration to body mass resistive exercise causes little or no effects on muscle damage and inflammation. J Strength Cond Res 28(1): 53–60, 2014—The purpose of this study was to determine if a moderate intensity whole-body vibration (WBV) body mass resistive exercise session causes additional muscle damage, soreness, and inflammation compared with the same exercise session without vibration (NoV). Ten recreationally active male university students completed 2 separate 24-hour study periods incorporating an exercise session with WBV or NoV. Muscle torque was measured (at 0, 60, and 240°·s−1 angular velocities), soreness (10-point scale) in the upper (UE [triceps]) and lower (LE [quadriceps]) extremities, and muscle inflammation markers (interleukin [IL]-1&bgr;, IL-6, IL-10) were measured at 4 time points (preexercise, immediately postexercise, 4 hours post, and 24 hours post). Diet was controlled. Compared with NoV, WBV increased (p < 0.01) muscle soreness at 24 hours postexercise in both the UE (2.2 ± 1.7 vs. 0.6 ± 0.9) and LE (2.0 ± 1.5 vs. 0.7 ± 0.7). Muscle torque was decreased immediately postexercise (p < 0.05) in the UE and LE at 0°·s−1 and in the UE at 240°·s−1, but there was no difference between exercise treatments. The exercise session caused significant but small increases in IL-1&bgr; and IL-6 but with no differences between exercise treatments. Interleukin-10 was increased with WBV (2.9 ± 2.0 to 3.6 ± 1.9 pg·ml−1; p < 0.03). These data suggest that the addition of WBV to exercise has little effect on muscle function and damage, soreness, or inflammation.

Cardiac Baroreflex Variability and Resetting during Sustained Mild Effort

This exploratory study assessed the pattern of closed-loop baroreflex resetting using multi-logistic-curve analysis. Operating point gain and ranges of RR-interval (RRI) and systolic blood pressure (SBP) are derived to examine how these relate to sympathetic activation. Sustained low-intensity isometric handgrip exercise, with a period of post-exercise circulatory occlusion (PECO), provided a model to study baroreflex resetting because the progression toward fatigue at constant tension induces a continuous increase in volitional contribution to neuro-cardiovascular control. Continuous measurements of muscle sympathetic nerve activity (MSNA), blood pressure, and RRI were made simultaneously throughout the experimental session. Spontaneous sequence analysis was used to detect episodes of baroreflex “engagements”, but the results are examined with a view to the fundamental difference between experimental conditions that isolate the carotid sinus (open-loop) and intact physiological conditions (closed-loop). While baroreflex function under open-loop conditions can be described in terms of a single logistic curve, intact physiologic conditions require a family of logistic curves. The results suggest that the baroreflex is in a “floating” state whereby it is continuously resetting during the timeline of the experiment but with minute-by-minute average values that mimic the less complex step-wise resetting pattern reported under open-loop conditions. Furthermore, the results indicate that baroreflex function and resetting of the operating point gain is reflected not in terms of change in the values of blood pressure or RR-interval but in terms of change in the range of values of these variables prevailing under different experimental conditions.

The protective role of sex hormones in females and exercise prehabilitation in males on sternotomy-induced cranial hypoperfusion in aortic-banded mini-swine

During cardiac surgery, specifically sternotomy, cranial hypoperfusion is linked to cerebral ischemia, increased risk of perioperative watershed stroke, and other neurocognitive complications. The purpose of this study was to retrospectively examine the effect of sex hormones in females and exercise prehabilitation in males on median sternotomy-induced changes in cranial perfusion in a large animal model of heart failure. Cranial blood flow (CBF) before and 10 and 60 min poststernotomy was analyzed in eight groups of Yucatan mini-swine: female control, aortic banded, ovariectomized, and ovariectomized + aortic banded; male control, aortic banded, aortic banded + continuous exercise trained, and aortic banded + interval exercise trained. A median sternotomy decreased cranial perfusion during surgery in all pigs (~24 ± 2% relative to baseline; P ≤ 0.05). CBF was 30 ± 7% lower across all time points in all females vs. all males (P ≤ 0.05) and sternotomy decreased cranial perfusion (P ≤ 0.05) independent of sex (females = 34 ± 3% and males = 14 ± 3%) and aortic banding (intact control = 31 ± 5% and intact aortic banded = 31 ± 4%). CBF recovery at 60 min tended to be better in females vs. males (relative to 10 min poststernotomy, females = 23 ± 13% vs. males = -1 ± 5%) and intact aortic banded vs. control pigs (relative to 10 min poststernotomy, aortic banded = 43 ± 20% vs. control = 6 ± 16%; P ≤ 0.05) at 60 min poststernotomy. Ovariectomy impaired CBF recovery during cranial reperfusion 60 min following sternotomy (relative to baseline, all intact females = -1 ± 9% vs. all ovariectomized females = -15 ± 4%; P ≤ 0.05). Chronic exercise training completely prevented significant sternotomy-induced cranial hypoperfusion independent of aortic banding (sternotomy-induced deficit, all sedentary males = -24 ± 6% vs. all exercise-trained males = -7 ± 3%; P ≤ 0.05). Female sex hormones protected against impaired CBF recovery during reperfusion, while chronic exercise training prevented sternotomy-induced cranial hypoperfusion despite cardiac pressure overload.NEW & NOTEWORTHY Our findings suggest a median sternotomy may predispose patients, possibly postmenopausal women and sedentary men, to perioperative cerebral ischemia, an increased risk of cardiac surgery-related stroke, and resulting neurocognitive impairments. Specifically, data from this common surgical procedure show: 1) median sternotomy independently decreases cranial perfusion; 2) female sex hormones improve cranial blood flow recovery following sternotomy; and 3) exercise prehabilitation prevents sternotomy-induced cranial hypoperfusion. Exercise prehabilitation before cardiac surgery may be advantageous for capable patients.