Blood shifts between body compartments during submaximal exercise with induced expiratory flow limitation in healthy humans.

External expiratory flow limitation (EFLe) can be applied in healthy subjects to mimic the effects of chronic obstructive pulmonary disease during exercise. At maximal exercise intensity, EFLe leads to exercise intolerance owing to respiratory pump dysfunction limiting venous return. We quantified blood shifts between body compartments to determine whether such effects can be observed during submaximal exercise, when the load on the respiratory system is milder. Ten healthy men (25.2 ± 3.2 years of age, 177.3 ± 5.4 cm in height and weighing 67.4 ± 5.8 kg) exercised at 100 W (∼40% of maximal oxygen uptake) while breathing spontaneously (CTRL) or with EFLe. We measured respiratory dynamics with optoelectronic plethysmography, oesophageal (Pes ) and gastric (Pga ) pressures with balloon catheters, and blood shifting between body compartments with double body plethysmography. During exercise, EFLe resulted in the following changes: (i) greater intrabreath blood shifts between the trunk and the extremities [518 ± 221 (EFLe) vs. 224 ± 60 ml (CTRL); P < 0.001] associated with lower Pes during inspiration (r = 0.53, P < 0.001) and higher Pga during expiration (r = 0.29, P < 0.024); and (ii) a progressive pooling of blood in the trunk over time (∼700 ml after 3 min of exercise; P < 0.05), explained by a predominant effect of lower inspiratory Pes (r = 0.54, P < 0.001) over that of increased Pga . It follows that during submaximal exercise, EFLe amplifies the respiratory pump mechanism, with a prevailing contribution from lower inspiratory Pes over increased expiratory Pga , drawing blood into the trunk. Whether these results can be replicated in chronic obstructive pulmonary disease patients remains to be determined. KEY POINTS: External expiratory flow limitation (EFLe) can be applied in healthy subjects to mimic the effects of chronic obstructive pulmonary disease and safely study the mechanisms of exercise intolerance associated with the disease. At maximal exercise intensity with EFLe, exercise intolerance results from high expiratory pressures altering the respiratory pump mechanism and limiting venous return. We used double body plethysmography to quantify blood shifting between the trunk and the extremities and to examine whether the same effects occur with EFLe at submaximal exercise intensity, where the increase in expiratory pressures is milder. Our data show that during submaximal exercise, EFLe amplifies the respiratory pump mechanism, each breath producing greater blood displacements between the trunk and the extremities, with a prevailing effect from lower inspiratory intrathoracic pressure progressively drawing blood into the trunk. These results help us to understand the haemodynamic effects of respiratory pressures during submaximal exercise with expiratory flow restriction.

Priming cardiac function with voluntary respiratory maneuvers and effect on early exercise oxygen uptake.

Oxygen uptake (V̇o2) at exercise onset is determined in part by acceleration of pulmonary blood flow ([Formula: see text]). Impairments in the [Formula: see text] response can decrease exercise tolerance. Prior research has shown that voluntary respiratory maneuvers can augment venous return, but the corollary impacts on cardiac function, [Formula: see text] and early-exercise V̇o2 remain uncertain. We examined 1) the cardiovascular effects of three distinct respiratory maneuvers (abdominal, AB; rib cage, RC; and deep breathing, DB) under resting conditions in healthy subjects (Protocol 1, n = 13), and 2) the impact of pre-exercise DB on pulmonary O2 transfer during initiation of moderate-intensity exercise (Protocol 2, n = 8). In Protocol 1, echocardiographic analysis showed increased right ventricular (RV) cardiac output and left ventricular (LV) cardiac output (RVCO and LVCO, respectively), following AB (by +23 ± 13 and +18 ± 15%, respectively, P < 0.05), RC (+23 ± 16; +14 ± 15%, P < 0.05), and DB (+27 ± 21; +23 ± 14%, P < 0.05). In Protocol 2, DB performed for 12 breaths produced a pre-exercise increase in V̇o2 (+801 ± 254 mL·min-1 over ∼6 s), presumably from increased [Formula: see text], followed by a reduction in pulmonary O2 transfer during early phase exercise (first 20 s) compared with the control condition (149 ± 51 vs. 233 ± 65 mL, P < 0.05). We conclude that 1) respiratory maneuvers enhance RVCO and LVCO in healthy subjects under resting conditions, 2) AB, RC, and DB have similar effects on RVCO and LVCO, and 3) DB can increase [Formula: see text] before exercise onset. These findings suggest that pre-exercise respiratory maneuvers may represent a promising strategy to prime V̇o2 kinetics and thereby to potentially improve exercise tolerance in patients with impaired cardiac function.NEW & NOTEWORTHY We demonstrate that different breathing maneuvers can augment both right and left-sided cardiac output in healthy subjects. These maneuvers, when performed immediately before exercise, result in a pre-exercise "cardiodynamic" increase in oxygen uptake (V̇o2) associated with a subsequent reduction in the "cardiodynamic" V̇o2 normally seen during early exercise. We conclude that pre-exercise breathing maneuvers are a plausible tool worthy of additional study to prime V̇o2 kinetics and improve exercise tolerance in patients with cardiovascular disease.

Priming the cardiodynamic phase of pulmonary oxygen uptake through voluntary modulations of the respiratory pump at the onset of exercise.

NEW FINDINGS: What is the central question of this study? The initial increase in oxygen uptake ( V̇O2 ) at exercise onset results from pulmonary perfusion changes secondary to an increased venous return. Breathing mechanics contribute to venous return through abdominal and intrathoracic pressures variation. Can voluntary breathing techniques (abdominal or rib cage breathing) increase venous return and improve V̇O2 at exercise onset? What is the main finding and its importance? Abdominal and rib cage breathing increase venous return and V̇O2 at exercise onset. This mechanism could be clinically relevant in patients with impaired cardiac function limiting oxygen transport. ABSTRACT: We examined how different breathing patterns can modulate venous return and alveolar gas transfer during exercise transients in humans. Ten healthy men transitioned from rest to moderate cycling while breathing spontaneously (SP) or with voluntary increases in abdominal (AB) or intrathoracic (RC) pressure swings. We used double body plethysmography to determine blood displacements between the trunk and the extremities (Vbs ). From continuous signals of airflow and O2 fraction, we calculated breath-by-breath oxygen uptake at the mouth and used optoelectronic plethysmography to correct for lung O2 store changes and calculate alveolar O2 transfer ( V̇O2A ). Oesophageal (Poes ) and gastric (Pga ) pressures were monitored using balloon-tipped catheters. Cardiac stroke volume was measured using impedance cardiography. During the cardiodynamic phase (Φ1) of V̇O2A -on kinetics (20 s following exercise onset), AB and RC increased total alveolar oxygen transfer compared to SP (227 ± 32, P = 0.019 vs. 235 ± 27, P = 0.001 vs. 206 ± 20 ml, mean ± SD). Pga and Poes swings increased with AB (by 24.4 ± 9.6 cmH2 O, P < 0.001) and RC (by 14.5 ± 5.7 cmH2 O, P < 0.001), respectively. AB yielded a greater increase in intra-breath Vbs swings compared with RC and SP (+0.30 ± 0.14 vs. +0.16 ± 0.11, P < 0.001 vs. +0.10 ± 0.05 ml, P = 0.006) and increased the sum of stroke volumes compared to SP (4.47 ± 1.28 vs. 3.89 ± 0.96 litres, P = 0.053), while RC produced significant central blood translocation from the extremities compared with SP (by 493 ± 311 ml, P < 0.001). Our findings indicate that combining exercise onset with AB or RC increases venous return, thus increasing mass oxygen transport above metabolic consumption during Φ1 and limiting the oxygen deficit incurred.

Automating the correction of flow integration drift during whole-body plethysmography.

Prolonged measurement of total body volume variations (deltaVb) with whole-body, flow-based plethysmography (WBP) results in a drift of the signal due to changes in temperature and humidity inside the plethysmograph and to numerical integration of the flow to obtain deltaVb. This drift has been previously corrected with the application of a wavelet- based filter using visual inspection of the signal to select the optimal filter level (Uva et al. Front. Physiol. 6:411, 2016), thus introducing potential operator bias. To exclude the latter we compared this approach with a newly developed automatic method based on (1) correction for actual changes in temperature and humidity inside the plethysmograph (algorithm TH) and (2) automatic selection of the wavelet filter level based on comparison between deltaVb and intra-thoracic and abdominal pressure variations measured simultaneously (algorithm WAV). The Pearson's correlation coefficient between deltaVb and the changes in volume of the chest wall (deltaVcw) simultaneously obtained by optoelectronic plethysmography (OEP) was calculated after correction of deltaVb with TH and WAV applied separately, TH and WAV applied consecutively (TH+WAV), manual selection of a wavelet filter based on visual inspection (MAN) or no correction (CTRL). The correlation between deltaVb and deltaVcw increased marginally with WAV, TH+WAV and MAN compared to CTRL (P <; 0.01). Conversely, TH alone yielded a lower correlation (P <; 0.01). It follows that while the automated wavelet filter level selection method (WAV) represents an effective, operator-independent method for the correction of deltaVb, whether or not it is combined with specific correction for changes in thermodynamic conditions inside the plethysmograph, the manual method (MAN) yields satisfactory results without the constraints of intra-thoracic and abdominal pressure measurement.

The Effect of Lower-Body Positive Pressure on the Cardiorespiratory Response at Rest and during Submaximal Running Exercise.

Anti-gravity treadmills facilitate locomotion by lower-body positive pressure (LBPP). Effects on cardiorespiratory regulation are unknown. Healthy men (30 ± 8 y, 178.3 ± 5.7 cm, 70.3 ± 8.0 kg; mean ± SD) stood upright (n = 10) or ran (n = 9) at 9, 11, 13, and 15 km.h-1 (5 min stages) with LBPP (0, 15, 40 mmHg). Cardiac output (CO), stroke volume (SV), heart rate (HR), blood pressure (BP), peripheral resistance (PR), and oxygen uptake (VO2) were monitored continuously. During standing, LBPP increased SV [by +29 ± 13 (+41%) and +42 ± 15 (+60%) ml, at 15 and 40 mmHg, respectively (p < 0.05)] and decreased HR [by -15 ± 6 (-20%) and -22 ± 9 (-29%) bpm (p < 0.05)] resulting in a transitory increase in CO [by +1.6 ± 1.0 (+32%) and +2.0 ± 1.0 (+39%) l.min-1 (p < 0.05)] within the first seconds of LBPP. This was accompanied by a transitory decrease in end-tidal PO2 [by -5 ± 3 (-5%) and -10 ± 4 (-10%) mmHg (p < 0.05)] and increase in VO2 [by +66 ± 53 (+26%) and +116 ± 64 (+46%) ml.min-1 (p < 0.05)], suggesting increased venous return and pulmonary blood flow. The application of LBPP increased baroreflex sensitivity (BRS) [by +1.8 ± 1.6 (+18%) and +4.6 ± 3.7 (+47%) at 15 and 40 mmHg LBPP, respectively P < 0.05]. After reaching steady-state exercise CO vs. VO2 relationships remained linear with similar slope and intercept for each participant (mean R2 = 0.84 ± 0.13) while MAP remained unchanged. It follows that (1) LBPP affects cardiorespiratory integration at the onset of exercise; (2) at a given LBPP, once reaching steady-state exercise, the cardiorespiratory load is reduced proportionally to the lower metabolic demand resulting from the body weight support; (3) the balance between cardiovascular response, oxygen delivery to the exercising muscles and blood pressure regulation is maintained at exercise steady-state; and (4) changes in baroreflex sensitivity may be involved in the regulation of cardiovascular parameters during LBPP.

Neuromuscular adaptations to sprint interval training and the effect of mammalian omega-3 fatty acid supplementation.

PURPOSE: Sprint interval training (SIT) stimulates rapid metabolic adaptations within skeletal muscle but the nature of neuromuscular adaptions is unknown. Omega-3 polyunsaturated fatty acids (N-3 PUFA) are suggested to enhance neuromuscular adaptations to exercise. METHODS: We measured the neuromuscular adaptations to SIT (Study-1) and conducted a placebo-controlled randomized double blinded study to determine the effect of N-3 PUFA supplementation on neuromuscular adaptations to SIT (Study-2). In Study-1, seven active men (24.4 ± 2.6 years, VO2 peak 43.8 ± 8.7 ml kg min-1) completed 2-weeks of SIT with pre- and post-training 10 km cycling time trials (TT). In Study-2, 30 active men (24.5 ± 4.2 years, VO2 peak 41.0 ± 5.1 ml kg min-1) were randomly assigned to receive N-3 PUFA (2330 mg day-1) (n = 14) or olive oil (n = 16) during 2-weeks of SIT with pre- and post-training TTs. Four week post-training, a SIT session and TT were also performed. Change in neuromuscular function was assessed from resting twitches, quadriceps maximal voluntary contraction (MVC) force, and potentiated twitch force (Q tw). RESULTS: Study-1 showed that SIT did not elicit significant neuromuscular adaptations. Study-2 showed that N-3 PUFA supplementation had no significant effect on neuromuscular adaptations. Training caused lower MVC force [mean ± SD; N-3 PUFA -9 ± 11%, placebo -9 ± 13% (p < 0.05 time)] and Q tw peripheral fatigue [N-3 PUFA -10 ± 19%, placebo -14 ± 13% (p < 0.05 time)]. TT time was lower after training in all groups [Study-1 -10%, Study-2 N-3 PUFA -8%, placebo -12% (p < 0.05 time)]. CONCLUSION: Two weeks of SIT improved TT performance in the absence of measurable neuromuscular adaptations. N-3 PUFA supplementation had no significant effect on SIT training adaptations.