Exercise modality, but not exercise training, alters the acute effect of exercise on endothelial function in healthy men.

We used a within-subject crossover design to examine the impact of exercise modality, i.e., resistance (RT) and endurance (END), on the acute impact of exercise on endothelial function. Then, we examined whether a 4-wk period of chronic exercise training altered the acute exercise-induced change in endothelial function in healthy individuals. Thirty-four healthy, young men (21 ± 2 yr) reported to our laboratory and completed assessment of endothelial function [using the brachial artery flow-mediated dilation test (FMD)] before and immediately after a single bout of RT (leg-extension) or END (cycling). Subsequently, participants completed a 4-wk period of training (12 sessions), followed by evaluation of the FMD before and after a single bout of exercise. Following a 3-wk washout, participants repeated these experiments with the different exercise modality (in a balanced crossover design). An exercise × modality interaction effect was found (P < 0.001). Post hoc pairwise analyses revealed a decrease in FMD after END (P < 0.001) but not after RT (P = 0.06). Four weeks of exercise training improved resting FMD after END and RT (P = 0.04) but did not alter the acute effect of exercise on FMD (exercise × modality × training effect: P = 0.63), an effect independent of the modality of exercise (exercise × training interaction: P = 0.46 and P = 0.11 in RT and END, respectively). These distinct changes in FMD following acute exercise may relate to the different prolonged physiological responses induced by endurance versus resistance exercise. Specifically, endurance exercise, but not resistance exercise, causes a decrease in brachial artery endothelial function, which was unaffected by 4 wk of chronic exercise training.NEW & NOTEWORTHY We found that resistance and endurance exercise modalities lead to different endothelial function responses after a single bout of exercise. Endothelial function increased after an acute bout of resistance exercise, whereas it decreased after an acute bout of endurance exercise. Four weeks of chronic exercise training did not affect the acute endothelial function response.

Intra-individual differences in the effect of endurance versus resistance training on vascular function: A cross-over study.

We used a within-subject, cross-over design study to compare the impact of 4-weeks' resistance (RT) versus endurance (END) training on vascular function. We subsequently explored the association of intra-individual effects of RT versus END on vascular function with a single nucleotide polymorphism (SNP) of the NOS3 gene. Thirty-five healthy males (21 ± 2 years old) were genotyped for the NOS3 rs2070744 SNP and completed both training modalities. Participants completed 12 sessions over a 4-week period, either RT (leg-extension) or END (cycling) training in a randomized, balanced cross-over design with a 3-week washout period. Participants performed peak oxygen uptake (peak VO2 ) and leg-extension single-repetition maximum (1-RM) testing, and vascular function assessment using flow-mediated dilation (FMD) on 3 separated days pre/post-training. Peak VO2 increased after END (p < 0.001), while 1-RM increased after RT (p < 0.001). FMD improved after 4-weeks' training (time effect: p = 0.006), with no difference between exercise modalities (interaction effect: p = 0.92). No relation was found between individual changes (delta, pre-post) in FMD to both types of training (R2  = 0.06, p = 0.14). Intra-individual changes in FMD following END and RT were associated with the NOS3 SNP, with TT homozygotes significantly favoring only END (p = 0.016) and TC/CC tending to favor RT only (p = 0.056). Although both training modes improved vascular function, significant intra-individual variation in the adaptation of FMD was found. The association with NOS3 genotype suggests a genetic predisposition to FMD adapting to a specific mode of chronic exercise. This study therefore provides novel evidence for personalized exercise training to optimize vascular health.

Cardiac output during exercise is related to plasma atrial natriuretic peptide but not to central venous pressure in humans.

NEW FINDINGS: What is the central question of this study? Is cardiac output during exercise dependent on central venous pressure? What is the main finding and its importance? The increase in cardiac output during both rowing and running is related to preload to the heart, as indicated by plasma atrial natriuretic peptide, but unrelated to central venous pressure. The results indicate that in upright humans, central venous pressure reflects the gravitational influence on central venous blood rather than preload to the heart. ABSTRACT: We evaluated the increase in cardiac output (CO) during exercise in relationship to central venous pressure (CVP) and plasma arterial natriuretic peptide (ANP) as expressions of preload to the heart. Seven healthy subjects (four men; mean ± SD: age 26 ± 3 years, height 181± 8 cm and weight 76 ± 11 kg;) rested in sitting and standing positions (in randomized order) and then rowed and ran at submaximal workloads. The CVP was recorded, CO (Modelflow) calculated and arterial plasma ANP determined by radioimmunoassay. While sitting, (mean ± SD) CO was 6.2 ± 1.6 l min-1 , plasma ANP 70 ± 10 pg ml-1 and CVP 1.8 ± 1.1 mmHg, and when standing decreased to 5.9 ± 1.0 l min-1 , 63 ± 10 pg ml-1 and -3.8 ± 1.2 mmHg, respectively (P < 0.05). Ergometer rowing elicited an increase in CO to 22.5 ± 5.5 l min-1 as plasma ANP increased to 156 ± 11 pg ml-1 and CVP to 3.8 ± 0.9 mmHg (P < 0.05). Likewise, CO increased to 23.5 ± 6.0 l min-1 during running, albeit with a smaller (P < 0.05) increase in plasma ANP, but with little change in CVP (-0.9 ± 0.4 mmHg). The increase in CO in response to exercise is related to preload to the heart, as indicated by plasma ANP, but unrelated to CVP. The results indicate that in upright humans, CVP reflects the gravitational influence on central venous blood rather than preload to the heart.

Conduit diameter and wall remodeling in elite athletes and spinal cord injury.

PURPOSE: This study aimed to investigate localized and systemic effects of chronic exercise and inactivity on conduit artery remodeling in humans. METHODS: We recruited elite athletes engaged in predominantly lower limb (LL runners/cyclists, n = 10) or upper limb (UL canoe paddlers, n = 12) exercise and matched able-bodied, recreationally active, controls (C, n = 16). We also studied wheelchair controls (spinal cord injury, n = 9) and athletes (spinal cord injury, n = 1; spina bifida, n = 4). Carotid, brachial, and superficial femoral (SF) artery diameter and wall thickness were assessed using high-resolution ultrasound. RESULTS: Brachial diameters were significantly larger in UL and wheelchair users (athletes and controls) compared with C (both P < 0.05). SF artery diameter in wheelchair controls was significantly smaller compared with the other groups, with LL athletes having significantly greater lumen diameter than controls (both P < 0.05). In all arteries, a lower wall thickness was found in able-bodied athletes compared with C, including wheelchair athletes compared with wheelchair controls (P < 0.001). In the SF artery, wall-to-lumen-ratio was significantly lower in able-bodied athletes and higher in wheelchair controls compared with able-bodied controls (P < 0.001). In the brachial and carotid arteries, able-bodied and wheelchair athletes demonstrated lower wall-to-lumen-ratio than less active wheelchair controls and able-bodied controls (P < 0.001). CONCLUSIONS: These findings suggest that remodeling of the arterial wall occurs systemically in response to exercise training and is unrelated to exercise type in humans. Conversely, localized effects are evident with respect to the effect of exercise on arterial diameter. These findings have implications for our understanding of the effects of exercise on arterial structure and function in humans.