The search for more effective training interventions for both competitive swimmers and recreational swimmers has expanded to include several external aids that can enhance CRF variables including oxygen uptake (VO 2), respiratory minute ventilation (VE), tidal volume (VT), respiratory frequency (RF), heart rate (HR), and associated metabolic measures such as lipid oxidation (Heinicke et al., 2005 Koppers et al., 2006 Millet et al., 2010).
Several effective and time-efficient exercise strategies have been identified that improve CRF and induce positive metabolic changes (Latt et al., 2009). Improving cardiorespiratory fitness (CRF) concomitant with metabolic function is an important component of swimming training (Jorgić et al., 2011) and serves as a key predictor of swimming performance and fitness (Lahart and Metsios, 2018). No change in ΔGLY is evident of a lack of enhanced triglyceride hydrolyzation that was also confirmed by similar pre- and post-intervention BMI, FM, and FMM. The RER increase in group E is not indicative of a substrate shift towards increased lipid utilization. A 6-week swimming intervention with ARDS did not enhance CRF. No within-group differences were observed at post-intervention except for RER which increased in group E at maximal workload. No significant between-group differences were observed at post-intervention. The mean difference in glycerol concentration (ΔGLY) was assessed after the first and last swimming session.
Body mass index (BMI), fat mass (FM), and fat-free mass (FFM) were also measured. An incremental exercise test was administered pre- and post-intervention to assess cardiorespiratory fitness (CRF) by measuring VO 2max, carbon dioxide volume, respiratory minute ventilation, respiratory exchange ratio (RER), and heart rate at 50, 100, 150, 200 W and at maximal workload. ARDS was induced via tube breathing (1000 ml) in group E. The intervention involved 50 min of front crawl swimming performed at 60% VO 2max twice weekly for 6 consecutive weeks.
A mixed-sex sample of 22 individuals was divided into homogeneous experimental (E) and control (C) groups controlled for maximal oxygen uptake (VO 2max). The aim of this study was to investigate the circulatory, respiratory, and metabolic effects of induced hypercapnia via added respiratory dead space (ARDS) during moderate-intensity swimming in recreational swimmers.
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