Physiological Responses to Supramaximal Running Exercise with End-Expiratory Breath Holding up to the Breaking Point.

This study aimed to assess the physiological responses to repeated running exercise performed at supramaximal intensity and with end-expiratory breath holding (EEBH) up to the breaking point. Eight male runners participated in two running testing sessions on a motorized treadmill. In the first session, participants performed two sets of 8 repetitions at 125% of maximal aerobic velocity and with maximum EEBH. Each repetition started at the onset of EEBH and ended at its release. In the second session, participants replicated the same procedure, but with unrestricted breathing (URB). The change in cerebral and muscle oxygenation (Δ[Hbdiff]), total haemoglobin concentration (Δ[THb]) and muscle reoxygenation were continuously assessed. End-tidal oxygen (PETO2) and carbon dioxide pressure (PETCO2), arterial oxygen saturation (SpO2) and heart rate (HR) were also measured throughout exercise.On average, EEBH was maintained for 10.1 ± 1 s. At the breaking point of EEBH, PETO2 decreased to 54.1 ± 8 mmHg, whereas PETCO2 increased to 74.8 ± 3.1 mmHg. At the end of repetitions, SpO2 (nadir values 74.9 ± 5.0 vs. 95.7 ± 0.8%) and HR were lower with EEBH than with URB. Cerebral and muscle Δ[Hbdiff] were also lower with EEBH, whereas this condition induced higher cerebral and muscle Δ[THb] and greater muscle reoxygenation. This study showed that performing repeated bouts of supramaximal running exercises with EEBH up to the breaking point induced a fall in arterial, cerebral and muscle oxygenation compared with the URB condition. These phenomena were accompanied by increases in regional blood volume likely resulting from compensatory vasodilation to preserve oxygen delivery to the brain and muscles.

Power Is More Relevant Than Ascensional Speed to Determine Metabolic Demand at Different Gradient Slopes During Running.

ABSTRACT: Hingrand, C, Olivier, N, Combes, A, Bensaid, S, and Daussin, FN. Power is more relevant than ascensional speed to determine metabolic demand at different gradient slopes during running. J Strength Cond Res 37(11): 2298-2301, 2023-Trail running is characterized by successive uphill and downhill running sessions. To prescribe training intensity, an assessment of maximal running capacity is required. This study compared 2 uphill incremental tests using the same ascensional speed increment to identify the influence of the slope gradient on performance. Ten subjects (8 men and 2 women) performed 3 incremental exercises on various slope (1%: IT01, 10%: IT10, and 25%: IT25), and the ascensional speed increment was similar between IT10 and IT25 (100 m·h-1 every minute). Gas exchanges, heart rate, and power were monitored continuously during the tests. Similar V̇o2max levels were observed in the 3 conditions: 68.7 ± 6.2 for IT01, 70.1 ± 7.3 for IT10, and 67.6 ± 7.0 for IT25. A greater maximal ascensional speed was reached in the IT25 (1760 ± 190 vs. 1,330 ± 106 for IT25 and IT10, respectively, p < 0.01). A significant relationship was observed between relative V̇o2 levels and relative power without any effect of slope. Power should be the parameter used for prescribing training intensity compared with ascensional speed in trail.

Muscle Oxygen Supply and Use in Type 1 Diabetes, From Ambient Air to the Mitochondrial Respiratory Chain: Is There a Limiting Step?

OBJECTIVE: Long before clinical complications of type 1 diabetes (T1D) develop, oxygen supply and use can be altered during activities of daily life. We examined in patients with uncomplicated T1D all steps of the oxygen pathway, from the lungs to the mitochondria, using an integrative ex vivo (muscle biopsies) and in vivo (during exercise) approach. RESEARCH DESIGN AND METHODS: We compared 16 adults with T1D with 16 strictly matched healthy control subjects. We assessed lung diffusion capacity for carbon monoxide and nitric oxide, exercise-induced changes in arterial O2 content (SaO2, PaO2, hemoglobin), muscle blood volume, and O2 extraction (via near-infrared spectroscopy). We analyzed blood samples for metabolic and hormonal vasoactive moieties and factors that are able to shift the O2-hemoglobin dissociation curve. Mitochondrial oxidative capacities were assessed in permeabilized vastus lateralis muscle fibers. RESULTS: Lung diffusion capacity and arterial O2 transport were normal in patients with T1D. However, those patients displayed blunted exercise-induced increases in muscle blood volume, despite higher serum insulin, and in O2 extraction, despite higher erythrocyte 2,3-diphosphoglycerate. Although complex I- and complex II-supported mitochondrial respirations were unaltered, complex IV capacity (relative to complex I capacity) was impaired in patients with T1D, and this was even more apparent in those with long-standing diabetes and high HbA1c. [Formula: see text]O2max was lower in patients with T1D than in the control subjects. CONCLUSIONS: Early defects in microvascular delivery of blood to skeletal muscle and in complex IV capacity in the mitochondrial respiratory chain may negatively impact aerobic fitness. These findings are clinically relevant considering the main role of skeletal muscle oxidation in whole-body glucose disposal.

Continuous exercise induces airway epithelium damage while a matched-intensity and volume intermittent exercise does not.

BACKGROUND: While continuous exercise (CE) induces greater ventilation ([Formula: see text]E) when compared to intermittent exercise (IE), little is known of the consequences on airway damage. Our aim was to investigate markers of epithelial cell damage - i.e. serum levels of CC16 and of the CC16/SP-D ratio - during and following a bout of CE and IE of matched work. METHODS: Sixteen healthy young adults performed a 30-min continuous (CE) and a 60-min intermittent exercise (IE; 1-min work: 1-min rest) on separate occasions in a random order. Intensity was set at 70% of their maximum work rate (WRmax). Heart rate (HR) and [Formula: see text]E were measured throughout both tests. Blood samples were taken at rest, after the 10th min of the warm-up, at the end of both exercises, half way through IE (matched time but 50% work done for IE) as well as 30- and 60-min post-exercise. Lactate and CC16 and SP-D were determined. RESULTS: Mean [Formula: see text]E was higher for CE compared to IE (85 ± 17 l.min- 1 vs 50 ± 8 l.min- 1, respectively; P < 0.001). Serum-based markers of epithelial cell damage remained unchanged during IE. Interaction of test × time was observed for SP-D (P = 0.02), CC16 (µg.l- 1) (P = 0.006) and CC16/SP-D ratio (P = 0.03). Maximum delta CC16/SP-D was significantly correlated with mean [Formula: see text]E sustained (r = 0.83, P < 0.001) during CE but not during IE. CONCLUSION: The 30-min CE performed at 70% WRmax induced mild airway damage, while a time- or work-matched IE did not. The extent of the damage during CE was associated with the higher ventilation rate.

Physiological comparison of intensity-controlled, isocaloric intermittent and continuous exercise.

VO2 fluctuations are argued to be an important mechanism underpinning chronic adaptations following interval training. We compared the effect of exercise modality, continuous vs. intermittent realized at a same intensity, on electrical muscular activity, muscular oxygenation and on whole body oxygen uptake. Twelve participants (24 ± 5 years; VO2peak: 43 ± 6 mL·â€…min-1·kg-1) performed (i) an incremental test to exhaustion to determine peak work rate (WRpeak); two randomized isocaloric exercises at 70%WRpeak; (ii) 1 bout of 30 min; (iii) 30 bouts of 1 min work intercepted with 1 min passive recovery. For electromyography, only the CON exercise showed change for the vastus lateralis root-mean-square (+6.4 ± 5.1%, P < .01, 95%CI 3.2, 8.3) and mean power frequency (-5.2 ± 4.8, P < .01, 95%CI -8.2, -3.5). Metabolic fluctuations (i.e. Oxygen Fluctuation Index and HHb Fluctuation Index) were higher in the intermittent modality, while post-exercise blood lactate concentrations (4.80 ± 1.50 vs. 2.32 ± 1.21 mM, respectively, for the CON and INT, P < .01, 95%CI 1.72, 3.12) and the time spent over 90% of VO2 target (1644 ± 152 vs. 356 ± 301 sec, respectively, for the CON and INT, P < .01, 95%CI 1130, 1446) were higher in the continuous modality. In conclusion, despite a similar energy expenditure and intensity, intermittent and continuous exercises showed two very different physiological responses. The intermittent modality would lead to a larger recruitment of fast twitch fibres that are less mitochondria-equipped and therefore may be more likely respondent to mitochondrial adaptations. In addition, this modality induces greater metabolic variations, a stimulus who could lead to mitochondrial development.

Effect of work:rest cycle duration on [Formula: see text] fluctuations during intermittent exercise.

The succession of on-transient phases that induce a repetition of metabolic changes is a possible mechanism responsible for the greater response to intermittent training (IT). The objective of this study was to quantify [Formula: see text] fluctuations during intermittent exercise characterised by the same work:rest ratio, but different durations and identify which duration leads to the greatest fluctuations. Ten participants (24 ± 5 years; [Formula: see text]: 42 ± 7 mL·min-1·kg-1) performed (1) an incremental test to exhaustion to determine peak work rate (WRpeak) and oxygen uptake ([Formula: see text]), (2), and three 1 h intermittent exercises alternating work period at 70% WRpeak with passive recovery period of different 1:1 work:recovery duty cycles (30 s:30 s, 60 s:60 s, 120 s:120 s). [Formula: see text] response analysis revealed differences in the fluctuations across the intermittent conditions despite an identical total energy expenditure. The sum of the cycle's nadir-to-peak [Formula: see text] differences (ΣΔ[Formula: see text]) and the oxygen fluctuation index (OFI) were both greater in the 60 s:60 s condition (ΣΔ[Formula: see text]: +38% ± 13% and +19% ± 18% vs. 120 s:120 s and 30 s:30 s, P < 0.05; OFI: +41% ± 29% and +67% ± 62% vs. 120 s:120 s and 30:30 s, P < 0.05). [Formula: see text] fluctuation analysis was successful in identifying the intermittent condition associated with the greatest disturbances: the 60 s:60 s duty cycle induces more [Formula: see text] fluctuations. The present findings also demonstrate that the selection of the duty cycle duration for submaximal intermittent exercise (70% of WRpeak) prescription is of interest to produce high [Formula: see text] fluctuations.

Exercise-induced metabolic fluctuations influence AMPK, p38-MAPK and CaMKII phosphorylation in human skeletal muscle.

During transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of this study was to determine whether metabolic fluctuations per se affect the signaling cascades known to regulate peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). On two separate occasions, nine men performed a continuous (30-min) and an intermittent exercise (30 × 1-min intervals separated by 1-min of recovery) at 70% of V˙O2peak. Skeletal muscle biopsies from the vastus lateralis were taken at rest and at +0 h and +3 h after each exercise. Metabolic fluctuations that correspond to exercise-induced variation in metabolic rates were determined by analysis of VO2 responses. During intermittent exercise metabolic fluctuations were 2.8-fold higher despite identical total work done to continuous exercise (317 ± 41 vs. 312 ± 56 kJ after intermittent and continuous exercise, respectively). Increased phosphorylation of AMP-activated protein kinase (AMPK) (~2.9-fold, P < 0.01), calcium/calmodulin-dependent protein kinase II (CaMKII) (~2.7-fold, P < 0.01) and p38-mitogen-activated protein kinase (MAPK) (~4.2-fold, P < 0.01) occurred immediately in both exercises and to a greater extent after the intermittent exercise (condition x time interaction, P < 0.05). A single bout of intermittent exercise induces a greater activation of these signaling pathways regulating PGC-1α when compared to a single bout of continuous exercise of matched work and intensity. Chronic adaptations to exercise on mitochondria biogenesis are yet to be investigated.