Healthy aging does not compromise the augmentation of cardiac function during heat stress.
During heat stress, stroke volume is maintained in young adults despite reductions in cardiac filling pressures. This is achieved by a general augmentation of cardiac function, highlighted by a left and upward shift of the Frank-Starling relation. In contrast, healthy aged adults are unable to maintain stroke volume during heat stress. We hypothesized that this would be associated with a lack of shift in the Frank-Starling relation. Frank-Starling relations were examined in 11 aged [69 ± 4 (SD) yr, 4 men/7 women] and 12 young (26 ± 5 yr, 6 men/6 women) adults during normothermic and heat stress (1.5°C increase in core temperature) conditions. During heat stress, increases in cardiac output were attenuated in aged adults (+2.5 ± 0.3 (95% CI) vs. young: +4.5 ± 0.5 l/min, P < 0.01) because of an attenuated chronotropic response (+30 ± 4 vs. young: +42 ± 5 beats/min, P < 0.01). In contrast to our hypothesis, a leftward shift of the Frank-Starling relation maintained stroke volume during heat stress in aged adults (76 ± 8 vs. normothermic: 74 ± 8 ml, P = 0.38) despite reductions in cardiac filling pressure (6.6 ± 1.0 vs. normothermic: 8.9 ± 1.1 mmHg, P < 0.01). In a subset of participants, volume loading was used to return cardiac filling pressure during heat stress to normothermic values, which resulted in a greater stroke volume for a given cardiac filling pressure in both groups. These results demonstrate that the Frank-Starling relation shifts during heat stress in healthy young and aged adults, thereby preserving stroke volume despite reductions in cardiac filling pressures.
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas; Cardiovascular Prevention and Rehabilitation Centre (ÉPIC), Montreal Heart Institute Research Centre, Montreal, Quebec, Canada; and Département de physiologie moléculaire et intégrative, Faculté de Médecine, Université de Montréal, Montreal, Quebec, Canada.
Daniel
D
Gagnon
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas.
Steven A
SA
Romero
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas.
Hai
H
Ngo
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas.
Satyam
S
Sarma
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas.
William K
WK
Cornwell
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas.
Paula Y S
PY
Poh
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas.
Douglas
D
Stoller
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas.
Benjamin D
BD
Levine
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas; craigcrandall@texashealth.org.
Craig G
CG
Crandall
D000328:Adult; D000368:Aged; D000375:Aging / Q000502:physiology*; D003198:Computer Simulation; D005260:Female; D018869:Heat-Shock Response / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D013318:Stroke Volume / Q000502:physiology*; D000071436:Thermotolerance / Q000502:physiology*
age; cardiac output; heart rate; stroke volume