Improving cardiorespiratory fitness (CRF) concomitant with metabolic function is an important component of swimming training (Jorgic et al., 2011) and serves as a key predictor of swimming performance and fitness (Lahart and Metsios, 2018). Several effective and time-efficient exercise strategies have been identified that improve CRF and induce positive metabolic changes (Latt et al., 2009). 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 (V[O.sub.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).
One method that has shown promise is inducing a condition known as hypercapnia or the abnormal elevation of the partial pressure of carbon dioxide in arterial blood (pC[O.sub.2]) above 45 mmHg (Kato et al., 2005; Schneider et al., 2013). A low-cost strategy that can safely induce hypercapnia is by increasing the volume of external respiratory dead space such as by breathing through a tube (Hebisz et al., 2013; Khayat et al., 2003; Zaton et al., 2010). According to numerous studies (Cathcart et al., 2005; Toklu et al., 2003), the added respiratory dead space (ARDS) supplemented by tube breathing increases the amount of C[O.sub.2] that is inspired in subsequent breaths proportional to the added volume. The retention of C[O.sub.2] induces a condition known as acute respiratory acidosis (Jones, 2008; Kraut and Madias, 2014). In response to increased C[O.sub.2] levels, chemoreceptors provide respiratory feedback (Kumar and Bin-Jaliach, 2007) increasing VE, VT, and RF (Mercier et al., 1992) to levels observed at higher training intensities (Zaton and Smolka, 2011). Several studies suggested that regular training with induced hypercapnia can condition muscle cells to utilize lipids at a greater rate than other substrates and enhance the reduction of body fat content (Hollidge-Horvat et al., 1999; McLellan, 1991; Ostergaard et al., 2012).
Original research on exercise with ARDS dates back to the 1970s in which participants breathed through a 1200 ml tube during 6 min of ergometer cycling corresponding to 30%, 50%, and 70% of predicted maximal oxygen uptake (VO.sub.2max) (Kelman and Watson, 1973). This protocol resulted in an increase in RF and VE with the latter attributed to increased VT. In the previous study Zaton et al. (2010) have found that a 5-week endurance cycling intervention with 1000-ml ARDS improved performance (total work) in the incremental exercise test with simultaneous decreases in hematocrit, hemoglobin, and red blood cell concentrations. In another study by the same research group, the respiratory response to cycle ergometry at 100 W with increasing ARDS volume (up to 1600 ml) was investigated (Zaton and Smolka, 2011). In this study, VE increased proportional to the volume of ARDS and both pCO.sub.2 and blood pH decreased. A study on incorporating 1000 ml ARDS in a 10-week training macrocycle in trained cyclists showed increases in V[O.sub.2]max, VC[O.sub.2]max, and VE-max during exercise testing although a decrease was observed in mechanical efficiency (Hebisz et al., 2013). Another investigation on cycling training with 1200 ml ARDS at submaximal intensities found no reduction in RER and VC[O.sub.2] but an increase in endurance capacity (Smolka et al., 2014). A recent study involving triathlon athletes included ARDS in an 8-week interval training intervention and found greater increases in VC[O.sub.2]max, VE, maximal power, and post-exercise lactate concentrations when compared with a non-ARDS cohort (Michalik et al., 2018).
In the swimming domain, Adam et al. (2015) introduced ARDS in an 8-week training intervention targeting glycolytic power in a sample of competitive swimmers. Two sessions were held per week in which repeated 50-m swims were performed at maximal intensity until volitional exhaustion. This protocol enhanced 100-m freestyle swim speed as well as V[O.sub.2]max and VE ascertained in an incremental exercise test. Another study examined the effects of a 5-week swimming intervention (two session per week) with ARDS in competitive swimmers and observed reduced HR and a lowered physiological cost of swimming (Zaton and Ziebura, 2012). Additionally, Zoretic et al. (2014) investigated an 8-week hypercapnic-hypoxic training program in elite swimmers. At the end of the program they observed a 5.35% increase in hemoglobin concentration and a 10.79% increase inV[O.sub.2]max. Karaula et al. (2016) examined the effects of 8 weeks of hypercapnic--hypoxic training in elite swimmers and reported improved swimming efficacy and increased maximal inspiratory and expiratory muscle strength.
The aforementioned studies (Zaton and Ziebura, 2012, Adam et al., 2015) involving elite swimmers suggests that swimming with ARDS may enhance swimming performance and CRF and maintain CRF among athletes during the off-season mesocycle when exercise intensity is reduced. However, less is known about the effects of ARDS in recreational swimmers as previous studies recruited elite or trained cohorts. Furthermore, as a reduction in fat tissue is a common goal of recreational swimmers, there is a lack of data on changes in substrate metabolism after several weeks of swimming with ARDS. Hence, investigating the effects of swimming with ARDS on CRF and lipid metabolism in recreational swimmers can provide new insights on the use of this exercise enhancement. Therefore, the aim of this study was to assess the circulatory, respiratory, and metabolic effects of a moderate-intensity swimming intervention with ARDS in recreational swimmers. Moderate intensity exercise was selected as the literature recommends prescribing this intensity level to promote lipid utilization and cardiovascular adaptations (Alkahtani, 2014). It was hypothesized that ARDS would show large improvements in CRF with beneficial metabolic changes towards increased exercise-induced lipid oxidation.
Twenty-two healthy male and female physical education students were recruited. All swam regularly for recreational purposes averaging 2 km twice a week. Subjects were assigned to a control (C) and experimental (E) group based on V[O.sub.2]max to ascertain similar CRF between the two groups. V[O.sub.2]max was obtained for each participant in an incremental exercise test (detailed below). The V[O.sub.2]max scores were ranked from highest to lowest and participants were then alternately assigned to group E (n = 11, age 24.27 [+ or -] 2.69 years, body height 1.73 [+ or -] 0.09 m, body mass 70.03 [+ or -] 13.14 kg, V[O.sub.2]max 45.55 [+ or -] 7.47 mL*[kg.sup.-1]*[min.sup.-1]) and group C (n = 11; age 24.00 [+ or -] 3.35 years, body height 1.68 [+ or -] 0.03 m, body mass 72.32 [+ or -] 10.13 kg, VO.sub.2max 47.09 [+ or -] 8.85 mL*[kg.sup.-1]*[min.sup.-1]). The groups were compared at this stage with the non-parametric Wilcoxon test ([alpha] = 0.05) and no between-group differences were observed for age (p = 0.72), body height (p = 0.50), body mass (p = 0.65), and V[O.sub.2]max (p = 0.65). This generated comparable intervention groups with an objective baseline measurement of CRF.
All participants provided their written consent to participate in the study and were informed they could withdraw at any time. They were instructed to maintain their normal lifestyle and diet and refrain from any additional exercise external to the training prescribed in the study. The design was approved by the local ethics committee (No. 14/2017) and all procedures adhered to the prerogatives set out in the Declaration of Helsinki.
Incremental exercise test
An incremental exercise test (IET) on a cycle ergometer was administered 3 days...