Mike Stembridge

Predominance of normal left ventricular geometry in the male ‘athlete's heart’

Aims This study evaluated (a) global LV adaption to endurance versus resistance training in male athletes, (b) LV assessment using by modern imaging technologies and (c) the impact of scaling for body size on LV structural data. Methods A prospective cross-sectional design assessed the LV in 18 elite endurance-trained (ET), 19 elite resistance-trained (RT) and 17 sedentary control (CT) participants. Standard 2D, tissue Doppler and speckle tracking echocardiography assessed LV structure and function. Indexing of LV structures to body surface area (BSA) was undertaken using ratio and allometric scaling. Results Absolute and scaled LV end-diastolic volume (ET: 43.7±6.8; RT: 34.2±7.4; CT 32.5±8.9 mL/m1.5; p<0.05) and LV mass (ET: 29.8±6.6; RT: 25.4±8.7; CT 25.9±6.4 g/m2.7; p < 0.05) were significantly higher in ET compared with RT and CT. LV wall thickness were not different between ET and RT. 65% of ET and 95% of RT had normal geometry. Stroke volume was higher in ET compared with both RT and CT (p<0.05). Whilst regional tissue velocity data were not different between groups, longitudinal and basal circumferential strain (ε) was reduced in RT compared with ET. Conclusions In this comprehensive evaluation of the male athletes heart (AH), normal LV geometry was predominant in both athlete groups. In the ET, 30% demonstrated an eccentric hypertrophy with no concentric hypertrophy in RT. Cardiac ε data in RT require further evaluation, and any interpretation of LV size should appropriately index for differences in body size.

Conduit artery structure and function in lowlanders and native highlanders: relationships with oxidative stress and role of sympathoexcitation

Information describing alterations in vascular function during either acute or prolonged normobaric or hypobaric hypoxia is sparse and often confounded by pathology and methodological limitations. We show that high altitude exposure in lowlanders is associated with impairments in both endothelial and smooth muscle function, and with increased central arterial stiffness; furthermore, in all of these respects, lowlanders’ vasculature becomes comparable to that of natives born and raised at altitude. Changes in endothelial function occur very rapidly in normobaric hypoxia, and partly under the influence of sympathetic nerve activity. Thus, a lifetime of high‐altitude exposure neither attenuates nor intensifies the impairments in vascular function observed with short‐term exposure in lowlanders; such impairment and altered structure likely translate into an elevated cardiovascular risk.

Ventricular structure, function, and mechanics at high altitude: chronic remodeling in Sherpa vs. short-term lowlander adaptation.

Short-term, high-altitude (HA) exposure raises pulmonary artery systolic pressure (PASP) and decreases left-ventricular (LV) volumes. However, relatively little is known of the long-term cardiac consequences of prolonged exposure in Sherpa, a highly adapted HA population. To investigate short-term adaptation and potential long-term cardiac remodeling, we studied ventricular structure and function in Sherpa at 5,050 m (n = 11; 31 ± 13 yr; mass 68 ± 10 kg; height 169 ± 6 cm) and lowlanders at sea level (SL) and following 10 ± 3 days at 5,050 m (n = 9; 34 ± 7 yr; mass 82 ± 10 kg; height 177 ± 6 cm) using conventional and speckle-tracking echocardiography. At HA, PASP was higher in Sherpa and lowlanders compared with lowlanders at SL (both P < 0.05). Sherpa had smaller right-ventricular (RV) and LV stroke volumes than lowlanders at SL with lower RV systolic strain (P < 0.05) but similar LV systolic mechanics. In contrast to LV systolic mechanics, LV diastolic, untwisting velocity was significantly lower in Sherpa compared with lowlanders at both SL and HA. After partial acclimatization, lowlanders demonstrated no change in the RV end-diastolic area; however, both RV strain and LV end-diastolic volume were reduced. In conclusion, short-term hypoxia induced a reduction in RV systolic function that was also evident in Sherpa following chronic exposure. We propose that this was consequent to a persistently higher PASP. In contrast to the RV, remodeling of LV volumes and normalization of systolic mechanics indicate structural and functional adaptation to HA. However, altered LV diastolic relaxation after chronic hypoxic exposure may reflect differential remodeling of systolic and diastolic LV function.

Resting pulmonary haemodynamics and shunting: a comparison of sea‐level inhabitants to high altitude Sherpas

Evolutionary pressure to improve gas exchange and/or resting pulmonary haemodynamics in hypoxic environments may have led to differences in the amount of blood that flows through right‐to‐left shunt pathways between Sherpas and sea‐level inhabitants. We studied sea‐level inhabitants during rest at sea level and acute isocapnic hypoxia and during rest at high altitude following 3 weeks of acclimatization and compared their responses to those of Sherpas during rest at high altitude. Contrary to some previous literature, we found similar resting pulmonary pressure and total pulmonary resistance between acclimatized sea‐level inhabitants and Sherpas at high altitude. We also found a similar number of subjects from each group with intracardiac shunt and intrapulmonary shunt at high altitude. These results help us better understand resting cardiopulmonary adaptations to high altitude by comparing life‐long high altitude residents with sea‐level inhabitants acclimatized to high altitude.

Effects of playing surface on physiological responses and performance variables in a controlled football simulation

Abstract In spite of the increased acceptance of artificial turf in football, few studies have investigated if matches are altered by the type of surface used and no research has compared physiological responses to football activity on artificial and natural surfaces. In the present study, participants performed a football match simulation on high-quality artificial and natural surfaces. Neither mean heart rate (171 ± 9 beats · min−1 vs. 171 ± 9 beats · min−1; P > 0.05) nor blood lactate (4.8 ± 1.6 mM vs. 5.3 ± 1.8 mM; P > 0.05) differed between the artificial and natural surface, respectively. Measures of sprint, jumping and agility performance declined through the match simulation but surface type did not affect the decrease in performance. For example, the fatigue index of repeated sprints did not differ (P > 0.05) between the artificial, (6.9 ± 2.1%) and natural surface (7.4 ± 2.4%). The ability to turn after sprinting was affected by surface type but this difference was dependent on the type of turn. Although there were small differences in the ability to perform certain movements between artificial and natural surfaces, the results suggest that fatigue and physiological responses to football activity do not differ markedly between surface-type using the high-quality pitches of the present study.

Impaired myocardial function does not explain reduced left ventricular filling and stroke volume at rest or during exercise at high altitude

Impaired myocardial systolic contraction and diastolic relaxation have been suggested as possible mechanisms contributing to the decreased stroke volume (SV) observed at high altitude (HA). To determine whether intrinsic myocardial performance is a limiting factor in the generation of SV at HA, we assessed left ventricular (LV) systolic and diastolic mechanics and volumes in 10 healthy participants (aged 32 ± 7; mean ± SD) at rest and during exercise at sea level (SL; 344 m) and after 10 days at 5,050 m. In contrast to SL, LV end-diastolic volume was ∼19% lower at rest (P = 0.004) and did not increase during exercise despite a greater untwisting velocity. Furthermore, resting SV was lower at HA (∼17%; 60 ± 10 vs. 70 ± 8 ml) despite higher LV twist (43%), apical rotation (115%), and circumferential strain (17%). With exercise at HA, the increase in SV was limited (12 vs. 22 ml at SL), and LV apical rotation failed to augment. For the first time, we have demonstrated that EDV does not increase upon exercise at high altitude despite enhanced in vivo diastolic relaxation. The increase in LV mechanics at rest may represent a mechanism by which SV is defended in the presence of a reduced EDV. However, likely because of the higher LV mechanics at rest, no further increase was observed up to 50% peak power. Consequently, although hypoxia does not suppress systolic function per se, the capacity to increase SV through greater deformation during submaximal exercise at HA is restricted.

Hypoxia, not pulmonary vascular pressure, induces blood flow through intrapulmonary arteriovenous anastomoses

Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased by acute hypoxia during rest by unknown mechanisms. Oral administration of acetazolamide blunts the pulmonary vascular pressure response to acute hypoxia, thus permitting the observation of IPAVA blood flow with minimal pulmonary pressure change. Hypoxic pulmonary vasoconstriction was attenuated in humans following acetazolamide administration and partially restored with bicarbonate infusion, indicating that the effects of acetazolamide on hypoxic pulmonary vasoconstriction may involve an interaction between arterial pH and PCO2 . We observed that IPAVA blood flow during hypoxia was similar before and after acetazolamide administration, even after acid–base status correction, indicating that pulmonary pressure, pH and PCO2 are unlikely regulators of IPAVA blood flow.

In vivo human cardiac shortening and lengthening velocity is region-dependent and not coupled with heart rate

What is the central question of this study? Regulation of cardiac function is typically achieved by changes in heart rate (HR) and cardiac shortening velocity (strain rate; SR), but their interdependence in vivo remains poorly understood. What is the main finding and its importance? Using resistance exercise to increase heart rate and arterial resistance physiologically in humans and measuring regional cardiac SR (at the base and apex), we found that HR and SR were not strictly coupled because SR at the base and apex responded differently, despite the same HR. Importantly, our data show that the region‐averaged ‘longitudinal’ SR, which is currently popular in the clinical setting, markedly underestimates the contribution of the apex.

In vivo human cardiac shortening and lengthening velocity is region dependent and not coupled with heart rate: ‘longitudinal’ strain rate markedly underestimates apical contribution

What is the central question of this study? Regulation of cardiac function is typically achieved by changes in heart rate (HR) and cardiac shortening velocity (strain rate; SR), but their interdependence in vivo remains poorly understood. What is the main finding and its importance? Using resistance exercise to increase heart rate and arterial resistance physiologically in humans and measuring regional cardiac SR (at the base and apex), we found that HR and SR were not strictly coupled because SR at the base and apex responded differently, despite the same HR. Importantly, our data show that the region‐averaged ‘longitudinal’ SR, which is currently popular in the clinical setting, markedly underestimates the contribution of the apex.

A Testing Battery for the Assessment of Fitness in Soccer Players

STRENGTH AND CONDITIONING PROFESSIONALS WORKING WITH SOCCER TEAMS MUST BE ABLE TO ADMINISTER A TIME-EFFICIENT, VALID, AND RELIABLE FITNESS TEST, WITH HIGH CONTENT VALIDITY. BASED ON THESE CRITERIA AND THE RESEARCH HEREIN, THE FOLLOWING BATTERY IS ADVISED: ANTHROPOMETRY, SQUAT JUMP, COUNTER MOVEMENT JUMP, REACTIVE STRENGTH, 1 REPETITION MAXIMUM (1RM) POWER CLEAN, 1RM SQUAT, PRO-AGILITY, LINEAR SPEED, AND YO-YO INTERMITTENT RECOVERY TEST. THE RESULTS CAN GUIDE THE STRENGTH AND CONDITIONING PROFESSIONALS AND TECHNICAL COACHES IN PROGRAM DESIGN, LEADING TO MORE EFFECTIVE AND EFFICIENT GOAL ACHIEVEMENT.