Richard A. Ferguson’s research while affiliated with Loughborough University and other places

The ‘cycling hour‐record’ is one of the most prestigious events in cycling. However, little detailed analysis of such attempts is available. In preparation for a successful cycling hour‐record attempt, an elite cyclist performed a full‐hour simulation to provide insights into performance, physiological, aerodynamic and biomechanical limitations that could be identified in the preparation for a subsequent official attempt. Performance (speed, lap time, power and cadence), physiological (heart rate and estimated body temperature), aerodynamic (CDA, helmet angle, rotation and rock) and biomechanical (helmet, thigh and foot position changes) measurements were made throughout the attempt, in which an even‐pacing strategy was employed where the point of task failure was defined as the lap which the rider could no longer perform at the targeted lap split (16.6 s) or quicker. The cyclist did not achieve the target distance (54,000 m) during the simulation. The final distance achieved for the hour was 53,250 m. Task failure occurred at 38 min and 33 s (lap 139/34,750 m) into the simulation. Notably, there was a decrease in power output, accompanied with an increase in the estimated body temperature, changes in pedalling kinematics and an increase in aerodynamic drag. The reduction in performance (leading to task failure) during a cycling hour record simulation is underpinned by a decrease in power output as well as an increase in aerodynamic drag due to biomechanical changes in the cycling technique.

Purpose This study investigated the effect of sprint-interval training combined with post-exercise blood flow restriction (i.e., SIT + BFR) on pulmonary gas exchange and microvascular deoxygenation responses during ramp incremental (RI) cycling. Methods Nineteen healthy, untrained males (mean ± SD age: 24 ± 5 years; height: 178 ± 6 cm; body mass: 77.0 ± 10.7 kg) were assigned to receive 4 weeks of SIT or SIT + BFR. Before and after the intervention period, each participant completed a RI cycling test for determination of peak oxygen uptake ($\dot {\text{V}}\text{O}_{\text{2peak}}$) and the gas exchange threshold (GET) with deoxygenated heme (Δdeoxy[heme]) and tissue oxygenation index (TOI) measured by near–infrared spectroscopy (NIRS) in vastus lateralis (VL) muscle. Results Relative $\dot {\text{V}}\text{O}_{\text{2peak}}$ increased by 7% following both interventions (P ≤ 0.03). SIT + BFR increased peak Δdeoxy[heme] when normalized relative to leg arterial occlusion (PRE: 57.3 ± 13.0 vs. POST: 62.0 ± 13.2%; P = 0.009) whereas there was no significant difference following SIT (PRE: 64.9 ± 14.3 vs. POST: 71.4 ± 11.7%; P = 0.17). Likewise, TOI nadir decreased at exhaustion following SIT + BFR (PRE: 56.9 ± 9.1 vs. POST: 51.4 ± 9.2%; P = 0.002) but not after SIT (PRE: 58.5 ± 7.1 vs. POST: 56.3 ± 8.2%; P = 0.29). The absolute cycling power at the GET increased following SIT + BFR (PRE: 108 ± 13 vs. POST: 125 ± 17 W, P = 0.001) but was not significantly different following SIT (PRE: 112 ± 7 VS. POST: 116 ± 11 W, P = 0.54). Conclusion The addition of post-exercise BFR to SIT alters the mechanism underlying the enhancement in $\dot {\text{V}}\text{O}_{\text{2peak}}$ by increasing the peak rate of muscle fractional O2 extraction in previously untrained males.

Blood flow restriction (BFR) is increasingly being used to enhance aerobic performance in endurance athletes. This study examined physiological responses to BFR applied in recovery phases within a high‐intensity interval training (HIIT) session in trained cyclists. Eleven competitive road cyclists (mean ± SD, age: 28 ± 7 years, body mass: 69 ± 6 kg, peak oxygen uptake: 65 ± 9 mL · kg⁻¹ · min⁻¹) completed two randomised crossover conditions: HIIT with (BFR) and without (CON) BFR applied during recovery phases. HIIT consisted of six 30‐s cycling bouts at an intensity equivalent to 85% of maximal 30‐s power (523 ± 93 W), interspersed with 4.5‐min recovery. BFR (200 mmHg, 12 cm cuff width) was applied for 2‐min in the early recovery phase between each interval. Pulmonary gas exchange (V̇O2, V̇CO2, and V̇E), tissue oxygen saturation index (TSI), heart rate (HR), and serum vascular endothelial growth factor concentration (VEGF) were measured. Compared to CON, BFR increased V̇CO2 and V̇E during work bouts (both p < 0.05, dz < 0.5), but there was no effect on V̇O2, TSI, or HR (p > 0.05). In early recovery, BFR decreased TSI, V̇O2, V̇CO2, and V̇E (all p < 0.05, dz > 0.8) versus CON, with no change in HR (p > 0.05). In late recovery, when BFR was released, V̇O2, V̇CO2, V̇E, and HR increased, but TSI decreased versus CON (all p < 0.05, dz > 0.8). There was a greater increase in VEGF at 3‐h post‐exercise in BFR compared to CON (p < 0.05, dz > 0.8). Incorporating BFR into HIIT recovery phases altered physiological responses compared to exercise alone.

The asymptote (critical power; CP) and curvature constant ( W' ) of the hyperbolic power–duration relationship can predict performance within the severe‐intensity exercise domain. However, the extent to which these parameters relate to skeletal muscle mitochondrial content and respiratory function is not known. Fifteen males (peak O 2 uptake, 52.2 ± 8.7 mL kg ⁻¹ min ⁻¹ ; peak work rate, 366 ± 40 W; and gas exchange threshold, 162 ± 41 W) performed three to five constant‐load tests to task failure for the determination of CP (246 ± 44 W) and W' (18.6 ± 4.1 kJ). Skeletal muscle biopsies were obtained from the vastus lateralis to determine citrate synthase (CS) activity, as a marker of mitochondrial content, and the ADP‐stimulated respiration ( P ) and maximal electron transfer ( E ) through mitochondrial complexes (C) I–IV. The CP was positively correlated with CS activity (absolute CP, r = 0.881, P < 0.001; relative CP, r = 0.751, P = 0.001). The W' was not correlated with CS activity ( P > 0.05). Relative CP was positively correlated with mass‐corrected CI + II E ( r = 0.659, P = 0.038), with absolute CP being inversely correlated with CS activity‐corrected CIV E ( r = −0.701, P = 0.024). Relative W' was positively correlated with CS activity‐corrected CI + II P ( r = 0.713, P = 0.021) and the phosphorylation control ratio ( r = 0.661, P = 0.038). There were no further correlations between CP or W' and mitochondrial respiratory variables. These findings support the assertion that skeletal muscle mitochondrial oxidative capacity is positively associated with CP and that this relationship is strongly determined by mitochondrial content.

SESNZ 2023 Conference presentation slides

Introduction. High-intensity interval training (HIIT) is a key component in preparing for competitive cycling by enhancing aerobic and anaerobic capacities. However, the muscle’s adaptive capacity can be attenuated with increased training status, indicating the need for varied and progressive training strategies. Blood flow restriction (BFR) is increasingly used as a supplementary training methodology to enhance sports performance. This study examines the physiological responses to BFR applied in recovery phases within a HIIT session in trained cyclists. Methods. Eleven highly-trained road cyclists (mean±SD age: 28±7 y, height: 175±7 cm, body mass: 69±6 kg, V̇O2peak 65±9 mL·kg-1·min-1) completed two conditions in a randomised crossover design: HIIT with BFR (BFR) and without (CON). HIIT consisted of 6x 30-second cycling work bouts at 85% maximal 30-second power output interspersed with 4.5-minutes of recovery. In the BFR condition, 2-minutes of quadricep occlusion was applied during the early recovery phase and removed thereafter (late recovery phase). Respiratory responses (V̇O2, V̇CO2, and V̇E), muscle oxygen saturation (TSI), heart rate (HR), and serum vascular endothelial growth factor (VEGF) were assessed. Results. During work bouts, BFR led to a small but significant increase in V̇CO2 and V̇E (both p<0.05, d<0.5), compared to CON, with no differences in V̇O2, TSI, or HR (all p>0.05). In the early recovery phase, BFR resulted in large and significant decreases in TSI, V̇O2, V̇CO2, and V̇E (all p<0.01, d>0.8) compared to CON, with no change in HR (p>0.05). During the late recovery phase, BFR was associated with large and significant increases in V̇O2, V̇CO2, and V̇E (all p<0.05, d>0.8), small but significant increases in HR (p<0.05, d<0.5), and a large and significant decrease in TSI (p<0.01, d>0.8). A significant condition x time interaction for VEGF revealed that VEGF increased by a greater magnitude following the BFR condition with a large effect size (d>0.8), compared to the CON condition. Conclusions. The results suggest that applying quadricep BFR during recovery from high-intensity cycling augmented metabolic and oxidative stress and angiogenic signalling in trained cyclists compared to exercise alone. The greater physiological perturbations suggest incorporating BFR into HIIT may enhance the training stimulus and adaptations over time.