The influence of age and sex on cerebrovascular reactivity and ventilatory response to hypercapnia in children and adults

This is the author accepted manuscript. The final version is available from Wiley via the DOI in this recordThe purpose of this study was to compare the integrated intracranial cerebrovascular reactivity (CVR) and hypercapnic ventilatory response (HCVR) between children and adults, as well as explore the dynamic response of the middle cerebral artery mean velocity (MCAV). Children (n = 20; 9.9 ± 0.7 years) and adults (n = 21; 24.4 ± 2.0 years) completed assessment of CVR over 240s using a fixed concentration of inspired CO2 (FICO2, 0.06). Baseline MCAV was higher in the adult females compared to the males (p ≤ .05). MCAV was greater in female children compared to male children (p ≤ .05), and in female adults compared to male adults (p ≤ .05) with hypercapnia. Relative CVR was similar in children and adults (3.71 ± 1.06 vs. 4.12 ± 1.32 %/mmHg; p = .098), with absolute CVR higher in adult females than males (3.27 ± .86 vs. 2.53 ± .70 cm/s/mmHg; p ≤ . 001). Likewise, HCVR did not differ between the children and adults (1.89 ± 1.00 vs. 1.77 ± 1.34 L/min/mmHg; p = .597), but was lower in adult females than males (1.815 ± 37 vs. 2.33 ± 1.66 L/min/mmHg; p ≤ .05). The heart rate response to hypercapnia was greater in children than adults (p = 001). A mono‐exponential regression model was used to characterize the dynamic onset, consisting of a delay term, amplitude and time constant (τ). The results revealed that MCAV τ was faster in adults than in children (34 ± 18 vs .74 ± 28 s; p = .001). Our study provides new insight into the impact of age and sex on CVR and the dynamic response of the MCAV to hypercapnia.Natural Sciences and Engineering Research CouncilCanadian Foundation for Innovatio

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage