Approximately 45% to 50% of line-of-duty deaths in the fire service are caused by sudden cardiac deaths, which most often occur during or shortly after firefighting duties. We present a theoretical model linking the cardiac, vascular, and hematological responses of firefighting to the triggering of sudden cardiac death in susceptible individuals.
Cerebral pulsatility reflects a balance between the transmission and damping of pulsatility in the cerebrovasculature. Females experience greater cerebral pulsatility with aging which may have implications for sex differences in stroke risk and cognitive decline. This study sought to explore vascular contributors to cerebral pulsatility and pulsatile damping in men and women. 282 adults (53% female) underwent measurements of cerebral (middle cerebral artery) pulsatility, pulsatile damping (ratio of cerebral to carotid pulsatility), large artery stiffening (ratio of aortic to carotid pulse wave velocity), and carotid wave transmission/reflection dynamics using wave-intensity analysis. Multiple regression revealed older age, female sex, greater large artery stiffening, higher carotid pulse pressure, and greater forward wave energy was associated with increased cerebral pulsatility (adjusted R2=0.44, p<0.05). Contributors to decreased cerebral pulsatile damping included older age, female sex, and lower wave reflection index (adjusted R2=0.51, p<0.05). Our data link greater large artery stiffening, carotid pulse pressure, and forward wave energy to greater cerebral pulsatility, while greater carotid wave reflection may enhance cerebral pulsatile damping. Lower cerebral pulsatile damping among females may contribute to greater age-associated cerebral pulsatile burden compared to males.
Firefighters arriving in a dehydrated state are at risk for heat injuries and may be in a physically and/or psychologically compromised state at the outset of firefighter training. Even during cool autumn days with ample fluids available, firefighters experience dehydration during typical firefighting activities, so the ability to measure hydration status throughout such activities may be important. Our data suggest that quantification of changes in hydration status through salivary osmolality measurements may provide a viable field measurement tool for such activities.
Christie AD, Tonson A, Larsen RG, DeBlois JP, Kent JA. Human skeletal muscle metabolic economy in vivo: effects of contraction intensity, age, and mobility impairment. Am J Physiol Regul Integr Comp Physiol 307: R1124 -R1135, 2014. First published August, 27, 2014; doi:10.1152/ajpregu.00083.2014.-We tested the hypothesis that older muscle has greater metabolic economy (ME) in vivo than young, in a manner dependent, in part, on contraction intensity. Twenty young (Y; 24 Ϯ 1 yr, 10 women), 18 older healthy (O; 73 Ϯ 2, 9 women) and 9 older individuals with mild-to-moderate mobility impairment (OI; 74 Ϯ 1, 7 women) received stimulated twitches (2 Hz, 3 min) and performed nonfatiguing voluntary (20, 50, and 100% maximal; 12 s each) isometric dorsiflexion contractions. Torque-time integrals (TTI; Nm·s) were calculated and expressed relative to maximal fat-free muscle cross-sectional area (cm 2 ), and torque variability during voluntary contractions was calculated as the coefficient of variation. Total ATP cost of contraction (mM) was determined from flux through the creatine kinase reaction, nonoxidative glycolysis and oxidative phosphorylation, and used to calculate ME (Nm·s·cm Ϫ2 ·mM ATP Ϫ1 ). While twitch torque relaxation was slower in O and OI compared with Y (P Յ 0.001), twitch TTI, ATP cost, and economy were similar across groups (P Ն 0.15), indicating comparable intrinsic muscle economy during electrically induced isometric contractions in vivo. During voluntary contractions, normalized TTI and total ATP cost did not differ significantly across groups (P Ն 0.20). However, ME was lower in OI than Y or O at 20% and 50% MVC (P Յ 0.02), and torque variability was greater in OI than Y or O at 20% MVC (P Յ 0.05). These results refute the hypothesis of greater muscle ME in old age, and provide support for lower ME in impaired older adults as a potential mechanism or consequence of age-related reductions in functional mobility. bioenergetics; mitochondria; creatine kinase; glycolysis; oxidative phosphorylation WHILE MANY OF THE CHANGES in neuromuscular properties that occur with advanced age, such as declines in strength and contractile velocity (5, 64), can be detrimental to physical function, some age-related physiological changes may act in a compensatory manner and, thereby, help maintain function to some degree. For instance, it has been suggested that a greater proportion of type I muscle fibers (35,55,56), slowed contractile properties (62, 71), and slower motor unit discharge rates, particularly during maximal contractions (8,12,37,38,68), may place older muscle at an economic advantage (41, 49). While age-related differences in muscle metabolic economy (ME; mass-normalized torque produced per unit ATP consumed) have been shown in rat muscle (13, 32), a systematic analysis of muscle ME in aging humans has only recently begun (41,54). Such a focus on muscle ME is critical to informing studies of age-related changes in the energy cost of whole body activities, such as walking, which generally involve measures of...
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