Weberruss H; Maucher J; Oberhoffer R; Müller J,
European Journal Of Applied Physiology [Eur J Appl Physiol], ISSN: 1439-6327, 2017 Nov 15;
Objective: The body’s adaptation to physical exercise is modulated by sympathetic and parasympathetic (vagal) branches of the autonomic nervous system (ANS). Heart rate variability (HRV), the beat-to-beat variation of the heart, is a proxy measure for ANS activity, whereas blood pressure (BP) is an indicator for cardiovascular function. Impaired vagal activity and lower BP is already described after exercise. However, inconsistent results exist about how long vagal recovery takes and how long post-exercise hypotension persists. Therefore, the aim of this study was to assess HRV and BP 1 h after maximal cardiopulmonary exercise testing (CPET).
Patients and Methods: HRV (Polar RS800CX), peripheral and central BP (Mobil-O-Graph®) were prospectively studied in 107 healthy volunteers (47 female, median age 29.0 years) in supine position, before and 60 min after maximal CPET.
Results: One hour after terminating CPET measures of HRV were still impaired and post-exercise BP was significantly reduced suggesting an improved vascular function compared to pre levels. HRV parameters post-exercise were 34.7% (RMSSD), 67.2% (pNN50), 57.2% (HF), and 42.7% (LF) lower compared to pre-exercise levels (for all p < 0.001). Median reduction in BP was 5 mmHg for systolic BP (p < 0.001), and 4 mmHg for diastolic BP (p = 0.016) and central systolic post-exercise (p = 0.005).
Conclusions: One hour after terminating strenuous exercise, autonomic nervous regulation seems to be postponed which is reflected in reduced HRV, whereas the early recovery of the vasculature, post-exercise hypotension, is still preserved over the recovery period of 1 h.
Palau P; Domínguez E; Núñez J,
European Journal Of Heart Failure [Eur J Heart Fail], ISSN: 1879-0844, 2017 Nov 16;
Purpose: Diaphragm paresis (DP) is characterized by abnormalities of respiratory muscle function. However, the impact of DP on exercise capacity is not well known. This study was performed to assess exercise tolerance in patients with DP and to determine whether inspiratory muscle function was related to exercise capacity, ventilatory pattern and cardiovascular function during exercise.
Methods: This retrospective study included patients with DP who underwent both diaphragmatic force measurements, and cardiopulmonary exercise testing (CPET).
Results: Fourteen patients were included. Dyspnea was the main symptom limiting exertion (86%). Exercise capacity was slightly reduced (median VO2peak: 80% [74.5%-90.5%]), mostly due to ventilatory limitation. Diaphragm and overall inspiratory muscle function were correlated with exercise ventilation. Moreover, overall inspiratory muscle function was related with oxygen consumption (r=0.61) and maximal workload (r=0.68).
Conclusions: DP decreases aerobic capacity due to ventilatory limitation. Diaphragm function is correlated with exercise ventilation whereas overall inspiratory muscle function is correlated with both exercise capacity and ventilation suggesting the importance of the accessory inspiratory muscles during exercise for patients with DP. Further larger prospective studies are needed to confirm these results.
The Practicum at Brockenhurst, from November 7th to November 9th, was a great sucess with a record number of attendees – 120!! The meeting was run by Professor Mike Grocott with Siobhan Mythen doing a lot of the organization. This photo was taken by Glen Jevon using my camera. He is a professional photographer, who took a video of all the talks. Hopefully they will be become available in time.The meeting was in fact a meeting of POETTS, EBPOM as well as CPX International Inc. It was held at a hotel in the New Forest called the Balmer Lawn Hotel. It was a lovely old hotel with old fashioned excellent service. I visited the village of Brockenhurst and saw an amazing butcher with the following sign outside.
Haven’t seen one like that where I come from.
We went out for dinner at restaurants around where we were staying. The food was outstanding and the evenings were memorable.
The lectures were excellent and altogether it was an outstanding Practicum. Our major sponsors were Schiller, Cosmed, Cortex and Geratherm; I really do hope that they felt it was a sucessful meeting.
There was a long Board Meeting on the Monday before the Practicum. Two things to come out of this were that Professor Grocott was elected as Vice President of our Society and the AGM agreed to increase the size of the Board from seven to nine.
The 2018 Practicum will be held in Cologne in October under the auspices of Dr Daniel Dumitrescu
Dr Paul Older
Executive Director CPX International.
Nakano Y, Okumura N, Adachi S, Shimokata S, Tajima F, Kamimura
Y, Murohara T, Kondo T
Heart Vessels. 2017 Nov 15
Little is known regarding a correlation of hemodynamics at rest or exercise
capacity with echocardiographic parameters in patients with pulmonary
hypertension (PH). To clarify these potential correlations, we performed
transthoracic echocardiography, right heart catheterization, and cardiopulmonary
exercise testing in 53 patients with pulmonary arterial hypertension (PAH) and
chronic thromboembolic pulmonary hypertension (CTEPH). Left ventricular
end-diastolic dimension (LVDd), early diastolic velocity of the septal mitral
annulus (septal e’), tricuspid regurgitation peak gradient (TRPG), and tricuspid
annular plane systolic excursion (TAPSE) were significantly correlated with
cardiac index (LVDd; r = 0.477, P < 0.001, septal e’; r = 0.463, P = 0.001, TRPG;
r = – 0.455, P = 0.001 and TAPSE; r = 0.406, P = 0.003, respectively). Multiple
regression analysis revealed that LVDd and septal e’ were significantly
associated with cardiac index (CI) and stroke volume index at rest. Among the
exercise capacity markers evaluated, TAPSE, TRPG, and LVDd were significantly
correlated with peak oxygen uptake (TAPSE; r = 0.534, P < 0.001, TRPG;
r = – 0.466, P = 0.001 and LVDd; r = 0.411, P = 0.002, respectively). Multiple
regression analysis showed that TAPSE was significantly associated with peak
oxygen uptake (VO2). In PAH and CTEPH patients, LVDd and septal e’ were
significantly associated with CI at rest, whereas TAPSE was significantly
associated with peak VO2. Echocardiographic parameters may predict the prognostic
factors of PAH and CTEPH patients.
Weberruss H, Maucher J, Oberhoffer R, Müller J
Eur J Appl Physiol. 2017 Nov 15
OBJECTIVE: The body’s adaptation to physical exercise is modulated by sympathetic
and parasympathetic (vagal) branches of the autonomic nervous system (ANS). Heart
rate variability (HRV), the beat-to-beat variation of the heart, is a proxy
measure for ANS activity, whereas blood pressure (BP) is an indicator for
cardiovascular function. Impaired vagal activity and lower BP is already
described after exercise. However, inconsistent results exist about how long
vagal recovery takes and how long post-exercise hypotension persists. Therefore,
the aim of this study was to assess HRV and BP 1 h after maximal cardiopulmonary
exercise testing (CPET).
PATIENTS AND METHODS: HRV (Polar RS800CX), peripheral and central BP
(Mobil-O-Graph(®)) were prospectively studied in 107 healthy volunteers (47
female, median age 29.0 years) in supine position, before and 60 min after
RESULTS: One hour after terminating CPET measures of HRV were still impaired and
post-exercise BP was significantly reduced suggesting an improved vascular
function compared to pre levels. HRV parameters post-exercise were 34.7% (RMSSD),
67.2% (pNN50), 57.2% (HF), and 42.7% (LF) lower compared to pre-exercise levels
(for all p < 0.001). Median reduction in BP was 5 mmHg for systolic BP
(p < 0.001), and 4 mmHg for diastolic BP (p = 0.016) and central systolic
post-exercise (p = 0.005).
CONCLUSIONS: One hour after terminating strenuous exercise, autonomic nervous
regulation seems to be postponed which is reflected in reduced HRV, whereas the
early recovery of the vasculature, post-exercise hypotension, is still preserved
over the recovery period of 1 h
Babu AS, Arena R, Morris NR
Adv Exp Med Biol. 2017;1000:153-172.
Pulmonary hypertension (PH) is a chronic, debilitating condition which gravely
affects exercise tolerance and quality of life. Though most therapies focus
purely on medical intervention, there is a growing body of evidence to suggest
the role and benefits of exercise training. This chapter discusses the various
physiological basis for exercise intolerance observed in PH and highlights the
rationale for exercise training. Recent evidence related to exercise training is
summarized and potential pathways to suggest adaptations to exercise training are
put forward. While keeping the paper applicable to clinicians, details on
evaluating exercise intolerance, prescribing exercise and setting up
rehabilitation centers for PH are discussed
Canada JM; Trankle CR; Buckley LF; Carbone S; Abouzaki NA; Kadariya D; Shah K; Cooke R;
Kontos MC; Patel J; Mankad P; Schatz A; Bhatnagar A; Arena R; Van Tassell BW; Abbate A
The American Journal Of Cardiology [Am J
Cardiol], ISSN: 1879-1913, 2017 Nov 15; Vol. 120 (10), pp. 1854-1857
Hospital admission for
decompensated heart failure marks a critical inflection point in a
patient’s health. Despite the improvement in signs or symptoms during
hospitalization, patients have a high likelihood of readmission,
reflecting a lack of resolution of the underlying condition.
Surprisingly, no studies have characterized the cardiorespiratory
fitness of such patients. Fifty-two patients (38 [73%] male, age 57 [52
to 65] years, left ventricular ejection fraction 31% [24 to 38])
underwent cardiopulmonary exercise testing 4 (1 to 10) days after
hospital discharge, when stable and without overt signs of volume
overload. Transthoracic Doppler echocardiography, measurement of
N-terminal pro-B-natriuretic peptide, and quality of life were also
assessed. Aerobic exercise capacity was severely reduced: peak oxygen
consumption (pVO2) was 14.1 (11.2 to 16.3) ml/kg/min. Ventilatory
inefficiency as indicated by the minute ventilation carbon dioxide
production relation (VE/VCO2 slope) >30 and oxygen uptake efficiency
slope <2.0 was noted in 41 (77%) and 39 (75%) patients, respectively.
Forty-five (87%) patients had 1 of 2 high-risk features
(pVO2 < 14 ml/kg/min or VE/VCO2 >30). Perceived functional capacity,
measured by the Duke Activity Status Index, was also severely reduced
and correlated with pVO2. N-terminal pro-B-natriuretic peptide levels
and early transmitral velocity/early mitral annulus velocity (E/e’)
ratio at echocardiography showed a modest correlation with lower pVO2.
In conclusion, patients with recently decompensated systolic heart
failure demonstrate severe impairment in cardiorespiratory fitness,
severely limiting quality of life.
JACC Heart Fail. 2017 Oct;5(10):724-734. doi: 10.1016/j.jchf.2017.07.013
Sharma A, Stevens SR, Lucas J, Fiuzat M, Adams KF, Whellan DJ,
Donahue MP, Kitzman DW, Piña IL, Zannad F, Kraus WE, O’Connor
CM, Felker GM.
OBJECTIVES: This study sought to determine the relationship between growth
differentiation factor (GDF)-15 and clinical outcomes in ambulatory patients with
heart failure and reduced ejection fraction (HFrEF).
BACKGROUND: The prognostic utility of GDF-15, a member of the transforming growth
factor-β cytokine family, among patients with HF is unclear.
METHODS: We assessed GDF-15 levels in 910 patients enrolled in the HF-ACTION
(Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training)
trial, a randomized clinical trial of exercise training in patients with HFrEF.
Median follow-up was 30 months. Cox proportional hazard models assessed the
relationships between GDF-15 and clinical outcomes.
RESULTS: The median GDF-15 concentration was 1,596 pg/ml. Patients in the highest
tertile of GDF-15 were older and had measurements of more severe HF (higher
N-terminal pro-B-type natriuretic peptide [NT-proBNP] concentrations and lower
peak oxygen uptake on cardiopulmonary exercise testing [CPX]). GDF-15 therapy was
a significant predictor of all-cause death (unadjusted hazard ratio [HR]: 2.03
when GDF-15 was doubled; p < 0.0001). This association persisted after adjustment
for demographic and clinical and biomarkers including high sensitivity troponin T
(hs-TnT) and NT-proBNP (HR: 1.30 per doubling of GDF-15; p = 0.029). GDF-15 did
not improve discrimination (as measured by changes in c-statistics and
the integrated discrimination improvement) in addition to baseline variables,
including hs-TnT and NT-proBNP or variables found in CPX testing.
CONCLUSIONS: In demographically diverse, well-managed patients with HFrEF, GDF-15
therapy provided independent prognostic information in addition to established
predictors of outcomes. These data support a possible role for GDF-15 in the risk
stratification of patients with chronic HFrEF. (Heart Failure: A Controlled Trial
Investigating Outcomes of Exercise Training [HF-ACTION]
American College of Cardiology Foundation
Van Iterson EH, Johnson BD, Borlaug BA, Olson TP
Eur J Heart Fail. 2017 Oct 8. doi: 10.1002/ejhf.913. [Epub ahead of print]
AIMS: Patients with heart failure (HF) with reduced (HFrEF) or preserved (HFpEF)
ejection fraction demonstrate an increased ventilatory equivalent for carbon
dioxide (V̇E /V̇CO2 ) slope. The physiological correlates of the V̇E /V̇CO2 slope
remain unclear in the two HF phenotypes. We hypothesized that changes in the
physiological dead space to tidal volume ratio (VD /VT ) and arterial CO2 tension
(PaCO2 ) differentially contribute to the V̇E /V̇CO2 slope in HFrEF vs. HFpEF.
METHODS AND RESULTS: Adults with HFrEF (n = 32) and HFpEF (n = 27)
[mean ± standard deviation (SD) left ventricular ejection fraction: 22 ± 7% and
61 ± 9%, respectively; mean ± SD body mass index: 28 ± 4 kg/m(2) and
33 ± 6 kg/m(2) , respectively; P < 0.01] performed cardiopulmonary exercise
testing with breath-by-breath ventilation and gas exchange measurements. PaCO2
was measured via radial arterial catheterization. We calculated the V̇E /V̇CO2
slope via linear regression, and VD /VT = 1 - [(863 × V̇CO2 )/(V̇E × PaCO2 )].
Resting VD /VT (0.48 ± 0.08 vs. 0.41 ± 0.11; P = 0.04), but not PaCO2
(38 ± 5 mmHg vs. 40 ± 3 mmHg; P = 0.21) differed between HFrEF and HFpEF. Peak
exercise VD /VT (0.39 ± 0.08 vs. 0.32 ± 0.12; P = 0.02) and PaCO2 (33 ± 6 mmHg
vs. 38 ± 4 mmHg; P < 0.01) differed between HFrEF and HFpEF. The V̇E /V̇CO2 slope
was higher in HFrEF compared with HFpEF (44 ± 11 vs. 35 ± 8; P < 0.01). Variance
associated with the V̇E /V̇CO2 slope in HFrEF and HFpEF was explained by peak
exercise VD /VT (R(2) = 0.30 and R(2) = 0.50, respectively) and PaCO2 (R(2)
= 0.64 and R(2) = 0.28, respectively), but the relative contributions of each
differed (all P < 0.01).
CONCLUSIONS: Relationships between the V̇E /V̇CO2 slope and both VD /VT and PaCO2
are robust, but differ between HFpEF and HFrEF. Increasing V̇E /V̇CO2 slope
appears to be strongly explained by mechanisms influential in regulating PaCO2 in
HFrEF, which contrasts with the strong role of increased VD /VT in HFpEF.
Houstis NE, Eisman AS, Pappagianopoulos PP, Wooster L, Bailey CS,
Wagner PD, Lewis GD
Circulation. 2017 Oct 9. pii:
Background -Heart failure with preserved ejection fraction (HFpEF) is a common
syndrome with a pressing shortage of therapies. Exercise intolerance is a
cardinal symptom of HFpEF, yet its pathophysiology remains uncertain.
Methods -We investigated the mechanism of exercise intolerance in each of 134 patients
referred for cardiopulmonary exercise testing (CPET): 79 with HFpEF and 55
controls. We performed CPET with invasive monitoring to measure hemodynamics,
blood gases, and gas exchange during exercise. We used these measurements to
quantify 6 steps of oxygen transport and utilization (the “O2 pathway”) in each
HFpEF patient, identifying the defective steps that impair each one’s exercise
capacity (peak VO2). We then quantified the functional significance of each O2
pathway defect by calculating the improvement in exercise capacity a patient
could expect from correcting the defect.
Results -Peak VO2 was reduced by 34%±2% (mean±SEM, P<0.001) in HFpEF
compared with controls of comparable age, gender,
and body mass index. The vast majority (97%) of HFpEF patients harbored defects
at multiple steps of the O2 pathway, the identity and magnitude of which varied
widely. Two of these steps, cardiac output and skeletal muscle O2 diffusion, were
impaired relative to controls by an average of 27±3% and 36±2%, respectively
(P<0.001 for both). Due to interactions between a given patient’s defects, the
predicted benefit of correcting any single one was often minor; on average,
correcting a patient’s cardiac output led to a 7±0.5% predicted improvement in
exercise intolerance, while correcting a patient’s muscle diffusion capacity led
to a 27±1% improvement. At the individual level, the impact of any given O2
pathway defect on a patient’s exercise capacity was strongly influenced by
Conclusions -Systematic analysis of the O2 pathway in HFpEF
showed that exercise capacity was undermined by multiple defects, including
reductions in cardiac output and skeletal muscle diffusion capacity. An important
source of disease heterogeneity stemmed from variation in each patient’s personal
profile of defects. Personalized O2 pathway analysis could identify patients most
likely to benefit from treating a specific defect; however, the system properties
of O2 transport favor treating multiple defects at once, as with exercise