Max Garrard

Little evidence exists with regard to changes in cardiac strain that occur during submaximal exercise in young males. The aims of the study were to evaluate the changes that occur in longitudinal (L), radial (R), and endocardial circumferential (EC) strain during submaximal upright cycle ergometry and to examine the test–retest reproducibility of these measurements. Fourteen recreationally active, adolescent (age: 17.9 ± 0.7 years) males volunteered for the study. All subjects underwent an incremental (40 W) submaximal cycle ergometer test. L, R, and EC strain values were obtained using speckle tracking, from two‐dimensional B‐mode images of the left ventricle (LV) during rest and the initial stages of submaximal exercise (40 and 80 W). The average of 6 LV segments was used to determine both peak wall deformation (%) and the time to peak deformation (ms). There was a statistically (P < 0.05) significant increase from rest to submaximal exercise for peak deformation for L, R, and EC strain. There was a statistically significant (P < 0.05) decrease from rest to submaximal exercise for time to peak for L and R and EC strain and between submaximal workloads for time to peak for L strain and EC strain. Coefficients of variation demonstrated reproducibility for upright strain and strain rate measurements similar to published supine measurements. This study has demonstrated that changes in left ventricular wall deformation (L, R and EC strain) that occur during the transition from rest to submaximal exercise can be reliably measured and confirm that a healthy LV has a hyperdynamic response to exercise.

Abstract: Little evidence exists with regard to the effect that exercise training has upon oxygen uptake kinetics in adolescent females. Purpose: The aim of the study was to compare $$\dot{V}{\text{O}}_{2}$$V˙O2 and muscle deoxygenation kinetics in a group of trained (Tr) and untrained (Utr) female adolescents. Method: Twelve trained (6.4 ± 0.9 years training, 10.3 ± 1.4 months per year training, 5.2 ± 2.0 h per week) adolescent female soccer players (age 14.6 ± 0.7 years) were compared to a group (n = 8) of recreationally active adolescent girls (age 15.1 ± 0.6 years) of similar maturity status. Subjects underwent two, 6-min exercise transitions at a workload equivalent to 80 % of lactate threshold from a 3-min baseline of 10 W. All subjects had a passive rest period of 1 h between each square-wave transition. Breath-by-breath oxygen uptake and muscle deoxygenation were measured throughout and were modelled via a mono-exponential decay with a delay relative to the start of exercise. Result: Peak $$\dot{V}{\text{O}}_{2}$$V˙O2 was significantly (p < 0.05) greater in the Tr compared to the Utr (Tr: 43.2 ± 3.2 mL kg

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PURPOSE: The extent that enhanced ventricular function contributes to superior aerobic fitness of trained athletes is unclear. This study compared cardiovascular responses to progressive cycle exercise in 12 adolescent soccer players and 10 untrained boys with assessment of ventricular inotropic and relaxation properties by Doppler ultrasound techniques. METHODS: Resting cardiac dimensions were measured by M-mode echocardiography. Stroke volume was estimated by the Doppler technique, and systolic function by peak aortic flow velocity and ejection flow rate. Diastolic transmitral pressure gradient was assessed by pulse wave peak E-wave velocity, ventricular relaxation properties by tissue Doppler imaging (E' velocity, adjusted for ventricular size), and ventricular filling pressure by E/E' ratio. RESULTS: Size-adjusted cardiac dimensions were significantly greater in the athletes. Peak V O2 values for the athletes and nonathletes were 57.4 +/- 4.8 and 44.4 +/- 6.6 mL.kg.min, respectively. Maximal cardiac index and stroke index were greater in the athletes (11.10+/- 1.52 vs 9.02 +/- 2.05 L.min.m; 59 +/- 8 vs 46 +/- 10 mL.m). Athletes and nonathletes demonstrated similar maximal peak aortic velocity (231 +/- 20 and 208 +/- 45 cm.s, respectively) and ejection rate (13.3 +/- 1.0 and 12.5 +/- 2.8 mL.s.cm x 10, respectively). No significant group differences were observed in Emax (155 +/- 17 and 149 +/- 23 cm.s for athletes and nonathletes, respectively), adjusted E'max (5.9 +/- 1.2 and 5.8 +/- 1.2 cm.s.mm for athletes and nonathletes, respectively), and E/E'max (265 +/- 40 and 262 +/- 56 for athletes and nonathletes, respectively). CONCLUSIONS: This study revealed no differences between young trained athletes and nonathletes in myocardial functional responses to progressive exercise, implying that greater aerobic fitness in these athletes reflected volume expansion of the cardiovascular system without contribution of enhanced systolic or diastolic ventricular function. Such findings should be considered limited to the context of young athletes with limited duration of athletic training.

UNLABELLED: Exercise training results in a speeding of pulmonary oxygen uptake (VO2) kinetics at the onset of exercise in adults; however, only limited research has been conducted with children and adolescents. PURPOSE: The aim of the present study was to examine VO2 and muscle deoxygenation kinetics in trained and untrained male adolescents. METHODS: Sixteen trained (15 +/- 0.8 yr, VO2peak = 54.7 +/- 6.2 mL x kg-1 x min-1, self-assessed Tanner stage range 2-4) and nine untrained (15 +/- 0.6 yr, VO2peak = 43.1 +/- 5.2 mL x kg-1 x min-1, Tanner stage range 2-4) male adolescents performed two 6-min exercise transitions from a 3-min baseline of 10 W to a workload equivalent to 80% lactate threshold separated by a minimum of 1 h of passive rest. Oxygen uptake (breath-by-breath) and muscle deoxygenation (deoxyhemoglobin signal from near-infrared spectroscopy) were measured continuously throughout baseline and exercise transition. RESULTS: The time constant of the fundamental phase of VO2 kinetics was significantly faster in trained versus untrained subjects (trained: 22.3 +/- 7.2 s vs untrained: 29.8 +/- 8.4 s, P = 0.03). In contrast, neither the time constant (trained: 9.7 +/- 2.9 s vs untrained: 10.1 +/- 3.4 s, P = 0.78) nor the mean response time (trained: 17.4 +/- 2.5 s vs untrained: 18.3 +/- 2.3 s, P = 0.39) of muscle deoxygenation kinetics differed with training status. CONCLUSIONS: The present data suggest that exercise training results in faster VO2 kinetics in male adolescents, although inherent capabilities cannot be ruled out. Because muscle deoxygenation kinetics were unchanged, it is likely that faster VO2 kinetics were due to adaptations to both the cardiovascular system and the peripheral musculature.

Objectives: Ventricular systolic functional response to exercise has been reported to be superior in adult men compared to women. This study explored myocardial responses to maximal upright progressive exercise in late pubertal males and females. Methods: Doppler echocardiographic techniques were utilized to estimate myocardial function response to a bout of progressive cycle exercise. Results: Systolic functional capacity, as indicated by ejection rate (12.5 ± 2.8 and 13.1 ± 1.0 [×10−2] ml s−1 cm−2 for boys and girls, respectively) and peak aortic velocity (208 ± 45 and 196 ± 12 cm s−1, respectively) at maximal exercise, did not differ between the two groups. Similarly, peak values as well as increases in transmitral pressure gradient (mitral E flow velocity), ventricular relaxation (tissue Doppler imaging E′), and left ventricular filling pressure (E/E′ ratio) as estimates of diastolic function were similar in males and females. Conclusions: This study failed to reveal qualitative or quantitative differences between adolescent boys and girls in ventricular systolic or diastolic functional responses to maximal cycle exercise.

his study was designed to examine time-of-day effects on markers of cardiac functional capacity during a standard progressive cycle exercise test. Fourteen healthy, untrained young males (mean ± SD: 17.9 ± 0.7 yrs of age) performed identical maximal cycle tests in the morning (08:00–11:00 h) and late afternoon (16:00–19:00 h) in random order. Cardiac variables were measured at rest, submaximal exercise, and maximal exercise by standard echocardiographic techniques. No differences in morning and afternoon testing values at rest or during exercise were observed for oxygen uptake, heart rate, cardiac output, or markers of systolic and diastolic myocardial function. Values at peak exercise for Vo2 at morning and afternoon testing were 3.20 ± 0.49 and 3.24 ± 0.55 L min−1, respectively, for heart rate 190 ± 11 and 188 ± 15 bpm, and for cardiac output 19.5 ± 2.8 and 19.8 ± 3.5 L min−1. Coefficients of variation for morning and afternoon values for these variables were similar to those previously published for test-retest reproducibility. This study failed to demonstrate evidence for significant time-of-day variation in Vo2max or cardiac function during standard progressive exercise testing in adolescent males.

A recent report indicated that variations in myocardial functional (systolic and diastolic) responses to exercise do not contribute to inter-individual differences in aerobic fitness (peak VO(2)) among young males. This study was designed to investigate the same question among adolescent females. Thirteen highly fit adolescent football (soccer) players (peak VO(2) 43.5 ± 3.4 ml kg(-1) min(-1)) and nine untrained girls (peak VO(2) 36.0 ± 5.1 ml kg(-1) min(-1)) matched for age underwent a progressive cycle exercise test to exhaustion. Cardiac variables were measured by standard echocardiographic techniques. Maximal stroke index was greater in the high-fit group (50 ± 5 vs. 41 ± 4 ml m(-2)), but no significant group differences were observed in maximal heart rate or arterial venous oxygen difference. Increases in markers of both systolic (ejection rate, tissue Doppler S') and diastolic (tissue Doppler E', mitral E velocity) myocardial functions at rest and during the acute bout of exercise were similar in the two groups. This study suggests that among healthy adolescent females, like young males, myocardial systolic and diastolic functional capacities do not contribute to inter-individual variability in physiologic aerobic fitness.

Previous studies have demonstrated faster pulmonary oxygen uptake (VO2) kinetics in the trained state during the transition to and from moderate-intensity exercise in adults. Whilst a similar effect of training status has previously been observed during the on-transition in adolescents, whether this is also observed during recovery from exercise is presently unknown. The aim of the present study was therefore to examine VO2 kinetics in trained and untrained male adolescents during recovery from moderate-intensity exercise. 15 trained (15 ± 0.8 years, VO2max 54.9 ± 6.4 mL kg(-1) min(-1)) and 8 untrained (15 ± 0.5 years, VO2max 44.0 ± 4.6 mL kg(-1) min(-1)) male adolescents performed two 6-min exercise off-transitions to 10 W from a preceding "baseline" of exercise at a workload equivalent to 80% lactate threshold; VO2 (breath-by-breath) and muscle deoxyhaemoglobin (near-infrared spectroscopy) were measured continuously. The time constant of the fundamental phase of VO2 off-kinetics was not different between trained and untrained (trained 27.8 ± 5.9 s vs. untrained 28.9 ± 7.6 s, P = 0.71). However, the time constant (trained 17.0 ± 7.5 s vs. untrained 32 ± 11 s, P < 0.01) and mean response time (trained 24.2 ± 9.2 s vs. untrained 34 ± 13 s, P = 0.05) of muscle deoxyhaemoglobin off-kinetics was faster in the trained subjects compared to the untrained subjects. VO2 kinetics was unaffected by training status; the faster muscle deoxyhaemoglobin kinetics in the trained subjects thus indicates slower blood flow kinetics during recovery from exercise compared to the untrained subjects.

Whilst endothelial dysfunction is associated with a sedentary lifestyle, enhanced endothelial function has been documented in the skin of trained individuals. The purpose of this study was to investigate whether highly trained adolescent males possess enhanced skin microvascular endothelial function compared to their untrained peers. Seventeen highly and predominantly soccer trained boys (V(O)(2)(peak): 55 +/- 6 mL kg(-1) min(-1)) and nine age- and maturation-matched untrained controls (V(O)(2)(peak): 43 +/- 5 mL kg(-1) min(-1)) aged 13-15 years had skin microvascular endothelial function assessed using laser Doppler flowmetry. Baseline and maximal thermally stimulated skin blood flow (SkBF) responses were higher in forearms of trained subjects compared to untrained participants [baseline SkBF: 11 +/- 4 vs. 9 +/- 3 perfusion units (PU), p < 0.05; SkBF(max): 282 +/- 120 vs. 204 +/- 68 PU, p < 0.05]. Similarly, cutaneous vascular conductance (CVC) during local heating was superior in the forearm skin of trained versus untrained individuals (CVC(max): 3 +/- 1 vs. 2 +/- 1 PU mmHg(-1), p < 0.05). Peak hyperaemia following arterial occlusion and area under the reactive hyperaemia curve were also greater in forearm skin of the trained group (peak hyperaemia: 51 +/- 21 vs. 35 +/- 15 PU, p < 0.05; area under curve: 1596 +/- 739 vs. 962 +/- 796 PUs, p < 0.05). These results suggest that chronic exercise training in adolescents is associated with enhanced microvascular endothelial vasodilation in non-glabrous skin.

PURPOSE: Evidence suggests acute mountain sickness (AMS) aligns to heart rate variability (HRV) suppression at high altitude. This study explored associations between measures of autonomic cardiac function and AMS scores in normobaric hypoxia (NH) and during ascent to very high altitude in the natural environment. METHODS: Thirty participants (17 male and 13 female, aged 20-62 years) trekked from 2800m to 5350m (Himalaya, Nepal) over 14 days. Short term temporal and spectral measures of HRV were recorded at rest (paced breathing, 12 breaths per minute), in NH (FIO2=0.124, ~4100m) and in hypobaric hypoxia (HH) at 4356m and 5350m, during ascent. RMSSD and 60 second heart rate recovery (HRR60) following stepping exercise (3 min at 50-60% maximal aerobic capacity) were accepted measures of parasympathetic neural activity. The heart rate response (∆HR) to an orthostatic postural challenge (two minutes supine followed by two minutes standing), reflective of sympathetic neural activity, was measured at the same time points (∆HR = HR [peak stand] - HR [mean supine]). AMS diagnosis was confirmed for scores ≥ 5.0 (Lake Louise Survey, LLS) or ≥ 0.70 (Environmental Symptoms Questionnaire, ESQ-c) at least once during the ascent. Institutional ethical approval was gained. RESULTS: Data analysis reflects 24 participants. Eleven (46%) developed AMS. Peak LLS AMS scores ranged between 1-5, 0-10 and 2-11 units in the AMS group at 2800m, 4356m and 5350m respectively, and 0-4 for the non-AMS group. No significant interaction (P=0.161) nor a main effect for altitude (P=0.093) was observed, however a significantly greater LLS score was observed in the AMS group at 5300m (P<0.001). Peak LLS scores at 2800m correlated with RMSSD (NH) (r=.483, P=.020) and at 4300m correlated with RMSSD at 4300m (-.487, P=.025). Postural ∆HR at 2800m correlated significantly with the ESQ-c and peak LLS scores at 4300m (r=-.601, P=.002 and r=-.579, P=.004), and the ∆HR at 4300m correlated with ESQ-c and LLS scores at 4300m (r=.-570, P=.005 and r=-.471, P=.023). HRR60 (NH) correlated with LLS score at 4300 m and peak LLS score at this altitude (r=-.495, P=.026 and r=-.450, P=.047 respectively), CONCLUSION: AMS-susceptible individuals show vagal suppression at high altitude. Vagal measures may be useful indicators for AMS susceptibility at very high altitude.

Introduction: Intermittent hypoxic exposure (IHE) prior to ascent to high altitude is postulated as a beneficial pre-conditioning strategy in the prevention of high altitude illness. Variations in arterial stiffness and endothelial function (vascular tone) may also be important in the pathogenesis of altitude related illness. The influence of IHE pre-conditioning on cardiovascular adaptations (notably arterial stiffness and vascular tone) to altitude is less clear. This study explored the impact of normobaric IHE pre-conditioning on acute cardiovascular adaptations to high altitude. Method: Participants were assigned to one of three intervention groups: control (no IHE), IHE at rest (IHE-rest) or IHE with training (IHE-training) matched for fitness, age and sex. In the 14- day period prior to a high altitude expedition IHE groups completed 10×2 hour hypoxic exposures in an environmental chamber (12.2% O2 equivalent to 4300 m), at rest (IHE-rest) or rest plus 20 minutes running at 80% heart rate reserve (calculated from individual predetermined VO2max at altitude). Arterial stiffness (SI) and vascular tone (RI) responses were recorded using a non-invasive finger photoplethysmography technique at sea-level (baseline), pre and post IHE intervention period, 12 and 72 hours post arrival at altitude (Lukla, Nepal, 2800 m). Results: Thirty apparently healthy participants (18 male, 12 female, age range 20-62 years) free from cardiovascular disease were recruited (n = 10 per condition). Two-way repeated measures (intervention x time) ANOVA revealed no main effect for intervention for SI (control_1.07±1.41 m.s-1, IHE-rest _0.50±0.65 m.s-1, IHE-training_1.07±0.81 m.s-1; P = 0.083) or RI (control_3.3±4.4%, IHE-rest_7.6±25.6%, IHE-training 7.2±18.1%; P = 0.174). There were no between-group interaction effects for any cardiovascular measurements (P = 0.059 for RI; P = 0.112 for SI) Conclusion: Intermittent hypoxic exposure prior to ascent to high altitude does not significantly alter vascular tone or arterial stiffness in apparently healthy adults. The impact of IHE preconditioning on endothelial function at higher altitudes and in the prevention of altitude related illness remains to be elucidated.

PURPOSE: This study evaluated the impact of passive and active intermittent hypoxic (IH) exposure pre-acclimatization strategies on temporal and spectral power measures of heart rate variability (HRV) in normobaric hypoxia (NH), and natural altitude. METHODS: Thirty participants (17 male and 13 female, aged 20-62 years), matched by sex, age and maximal aerobic capacity (VO2peak), were randomly allocated to either a control, passive IH or active IH group. Experimental groups completed 10 x 2-h, passive (PIH) or active (AIH), normobaric IH exposures (FIO2 = 0.124, ~4,011 m) over the 14-day intervention period (weekends excluded). The control group received no IH exposure. During the intervention period, participants completed 20 minutes daily running training, at an individualised intensity equivalent to 80% heart rate reserve (HRR). Training workload was determined by regressing HR and running speed data from individual VO2peak tests in normal ambient conditions (control and PIH groups) or NH (AIH group, FIO2 = 0.124). AIH participants completed the exercise training sessions under supervision, during scheduled IH exposure sessions, while control and PIH groups completed training unsupervised in normal ambient conditions. Within 48 hours of completing pre-acclimatization, participants travelled by air from the UK to Nepal, a journey time of approximately 36 hours. Participants then trekked from 2800 m to 5300 m over 14 days. Temporal (RR, SDNN, RMSSD) and spectral power measures (LFnu, HFnu and LFHF ratio) of HRV were recorded, at rest with spontaneous breathing, in normal ambient conditions (FIO2 = 0.209), NH (FIO2 =0.124, ~4011 m) and in hypobaric hypoxia (HH) at 4356 m and 5350 m, during ascent. RESULTS: Two-way ANOVA (group x condition) with repeated measures revealed neither significant interactions (P>0.05), nor between-group (P>0.05) nor within-group (P>0.05) differences for temporal or power spectral HRV measures between baseline, pre-IH and post-IH. No significant interactions, between-group or within-group changes were noted between post-IH, 4300 m and 5300 m (P>0.05) natural altitude. CONCLUSION: Pre-acclimatization using active and passive intermittent hypoxic exposure did not significantly alter heart rate variability responses during ascent to very high altitude.

PURPOSE: This study evaluated the impact of passive and active intermittent hypoxic (IH) exposure pre-acclimatization strategies on temporal and spectral power measures of heart rate variability (HRV) in normobaric hypoxia (NH), and natural altitude. METHODS: Thirty participants (17 male and 13 female, aged 20-62 years), matched by sex, age and maximal aerobic capacity (VO2peak), were randomly allocated to either a control, passive IH or active IH group. Experimental groups completed 10 x 2-h, passive (PIH) or active (AIH), normobaric IH exposures (FIO2 = 0.124, ~4,011 m) over the 14-day intervention period (weekends excluded). The control group received no IH exposure. During the intervention period, participants completed 20 minutes daily running training, at an individualised intensity equivalent to 80% heart rate reserve (HRR). Training workload was determined by regressing HR and running speed data from individual VO2peak tests in normal ambient conditions (control and PIH groups) or NH (AIH group, FIO2 = 0.124). AIH participants completed the exercise training sessions under supervision, during scheduled IH exposure sessions, while control and PIH groups completed training unsupervised in normal ambient conditions. Within 48 hours of completing pre-acclimatization, participants travelled by air from the UK to Nepal, a journey time of approximately 36 hours. Participants then trekked from 2800 m to 5300 m over 14 days. Temporal (RR, SDNN, RMSSD) and spectral power measures (LFnu, HFnu and LFHF ratio) of HRV were recorded, at rest with spontaneous breathing, in normal ambient conditions (FIO2 = 0.209), NH (FIO2 = 0.124, ~4011 m) and in hypobaric hypoxia (HH) at 4356 m and 5350 m, during ascent. RESULTS: Two-way ANOVA (group x condition) with repeated measures revealed neither significant interactions (P>0.05), nor between-group (P>0.05) nor within-group (P>0.05) differences for temporal or power spectral HRV measures between baseline, pre-IH and post-IH. No significant interactions, between-group or within-group changes were noted between post-IH, 4300 m and 5300 m (P>0.05) natural altitude. CONCLUSION: Pre-acclimatization using active and passive intermittent hypoxic exposure did not significantly alter heart rate variability responses during ascent to very high altitude.