The effects of short work vs. longer work periods within intermittent exercise on V̇o_2p kinetics, muscle deoxygenation, and energy system contribution

We report novel observations on the effects of differing heavy-intensity work durations between 3-s recovery periods on pulmonary oxygen uptake (V̇o_2p) kinetics, muscle deoxygenation, and energy system contributions. Relative to continuous exercise, V̇o_2p kinetics are faster in intermittent exercise, and increased frequency of 3-s recovery periods improves microvascular O₂ delivery and reduces V̇o_2p and arterialized-capillary lactate concentration. The metabolic burden of identical intensity work is altered when performed intermittently vs. continuously.

Abstract

We examined the effects of inserting 3-s recovery periods during high-intensity cycling exercise at 25-s and 10-s intervals on pulmonary oxygen uptake (V̇o_2p), muscle deoxygenation [deoxyhemoglobin (HHb)], their associated kinetics (τ), and energy system contributions. Eleven men (24 ± 3 yr) completed two trials of three cycling protocols: an 8-min continuous protocol (CONT) and two 8-min intermittent exercise protocols with work-to-rest periods of 25 s to 3 s (25INT) and 10 s to 3 s (10INT). Each protocol began with a step-transition from a 20-W baseline to a power output (PO) of 60% between lactate threshold and maximal V̇o_2p (Δ60). This PO was maintained for 8 min in CONT, whereas 3-s periods of 20-W cycling were inserted every 10 s and 25 s after the transition to Δ60 in 10INT and 25INT, respectively. Breath-by-breath gas exchange measured by mass spectrometry and turbine and vastus lateralis [HHb] measured by near-infrared spectroscopy were recorded throughout. Arterialized-capillary lactate concentration ([Lac⁻]) was obtained before and 2 min postexercise. The τV̇o_2p was lowest (P < 0.05) for 10INT (24 ± 4 s) and 25INT (23 ± 5 s) compared with CONT (28 ± 4 s), whereas HHb kinetics did not differ (P > 0.05) between conditions. Postexercise [Lac⁻] was lowest (P < 0.05) for 10INT (7.0 ± 1.7 mM), was higher for 25INT (10.3 ± 1.9 mM), and was greatest in CONT (14.3 ± 3.1 mM). Inserting 3-s recovery periods during heavy-intensity exercise speeded V̇o_2p kinetics and reduced overall V̇o_2p, suggesting an increased reliance on PCr-derived phosphorylation during the work period of INT compared with an identical PO performed continuously.

NEW & NOTEWORTHY We report novel observations on the effects of differing heavy-intensity work durations between 3-s recovery periods on pulmonary oxygen uptake (V̇o_2p) kinetics, muscle deoxygenation, and energy system contributions. Relative to continuous exercise, V̇o_2p kinetics are faster in intermittent exercise, and increased frequency of 3-s recovery periods improves microvascular O₂ delivery and reduces V̇o_2p and arterialized-capillary lactate concentration. The metabolic burden of identical intensity work is altered when performed intermittently vs. continuously.

most forms of physical activity require intermittent periods of work and recovery. However, relative to continuous exercise (CONT), the acute physiological responses to intermittent exercise (INT) have received less attention. For example, how might physiological adjustments to open-water, front-crawl swimming differ from swimming in pools where “work periods” of ~10 s (25-yd pool) and 25 s (50-m pool) are interspersed with brief (~2–3 s) “recovery periods” during the push off the wall after a turn?

At the onset of constant-intensity exercise above the lactate threshold (LT), the adjustment of pulmonary oxygen uptake (V̇o_2p) exhibits an initial exponential profile (phase II) that is followed by a slowly evolving and progressive increase in V̇o_2p (phase III or V̇o_2p slow component) (2, 3, 42). The rate of adjustment of the phase II response is quantitatively described by the V̇o_2p time constant (τ), which represents the time it takes for V̇o_2p to reach ~63% of the phase II amplitude. With larger step-transitions above the LT [heavy intensity (HVY)], the amplitude of the phase III response increases (13, 41, 58). In contrast to constant-intensity cycling exercise, INT with longer duration work-to-recovery cycles (e.g., 60:120 s and 90:180 s) exhibits large oscillations in V̇o_2p, which makes it problematic to justify the use of traditional V̇o_2p kinetic analyses (52). However, INT coupling short work to shorter recovery periods (10:5 s) performed at an identical HVY power output (PO) as CONT elicits only small changes in V̇o_2p over the work recovery phases, yet still yields a V̇o_2p profile resembling that of CONT (6, 52). It is proposed that, if the recovery period during this INT is reduced further, from 5 to 3 s, any oscillations in V̇o_2p over the work and recovery periods would be indistinguishable, and V̇o_2p kinetic analyses would be legitimate (6). Accordingly, the effects of increasing the frequency of these 3-s recovery periods, by inserting them after 25 and 10 s of work (25INT and 10INT), which also changes the mean PO, could facilitate a range of V̇o_2p response profiles to which V̇o_2p kinetics may be evaluated and compared within the INT paradigm.

Based on previous studies, we would expect that, with increased frequency of brief (3 s) recovery periods during HVY cycling exercise, the overall amplitude of the V̇o_2p response would be reduced [e.g., see Fig. 1 in Belfry et al. (6)], resembling transitions from 20 W to lower POs. The effect of altering delta PO for transitions from common low baselines on V̇o_2p kinetics is equivocal. A common feature of these studies (3, 42, 45, 54, 57) is that, with greater step-changes in PO, the phase II V̇o_2p amplitude increases. While some (41, 42) have reported no changes in V̇o_2p kinetics over the spectrum of moderate-to-severe intensity exercise, others reported a speeding (3, 45, 54, 57) or slowing (20, 31) of V̇o_2p kinetics. In the context of the INT paradigm, the forcing stimulus for active muscle V̇o₂ (increased ATP demand), in contrast to the CONT condition, may be periodically “switched off.” Indeed, our laboratory and others have previously observed abrupt increases in PCr concentration after 4 s (7) and 3 s (40) of recovery during HVY exercise and immediate increases in PCr breakdown during the work period relative to time- and PO-matched CONT. This period of increased PCr breakdown for the same PO during the work period of INT relative to CONT acts as a “homeostatic energy buffer to oxidative phosphorylation” (7, 20, 32). Thus, by these mechanisms, brief recovery periods (e.g., 3 s) frequently inserted into HVY exercise may slow V̇o_2p kinetics and reduce phase II V̇o_2p amplitude compared with HVY exercise performed without any recovery periods (i.e., CONT).

Given the strong association between PCr breakdown and V̇o_2p during HVY exercise (46) and our previous observation of a reduced PCr concentration slow-component amplitude with the insertion of the 5-s recovery periods every 10 s during HVY exercise, it might also be expected that, with increased recovery period frequency, the V̇o_2p slow-component amplitude would be reduced compared with CONT. Our previous observation of a progressive decrease in mean H⁺ concentration ([H⁺]) during INT (10:5 s), relative to CONT (7), coupled with an increased reliance on PCr-derived phosphorylation to the energy requirements of the work periods during INT (7), also suggests a reduced glycolytic component to total energy contribution. Recognizing the limitations of inferring glycolytic flux and muscle lactate concentration ([Lac⁻]) from arterialized capillary [Lac⁻] (22), differences between INT and CONT could be inferred. If [Lac⁻] is reduced in INT, relative to a time-matched bout of CONT, concomitant with a lower carbon dioxide output (V̇co_2p), respiratory exchange ratio (RER), and ventilation (V̇e), it is suggested that the burden to buffer lactate-associated increases in arterial [H⁺] has been reduced (4).

It has also been reported that short-work/short-recovery INT elicits a recovery-dependent effect that improves microvascular blood flow distribution and/or O₂ delivery during the work and recovery periods compared with CONT (6, 34). For example, the near infrared spectroscopy (NIRS)-derived muscle deoxygenation signal (deoxyhemoglobin concentration, [HHb]) has been shown to be lower during high-intensity INT (10:5 s) compared with a continuous high-intensity condition (6). When the change in [HHb] was expressed relative to the change in V̇o_2p, this ratio, which provides insight into the dynamic O₂ delivery-to-utilization relationship within the microvasculature (39), was attenuated in the intermittent condition. This reflects improved muscle perfusion, which could be attributed to recovery-induced reductions in intramuscular pressures and impedance within the contracting muscle group, serving to increase mean blood flow during the subsequent work period (44). Thus it is possible that increasing the frequency of short recovery periods would exacerbate this recovery-dependent effect on O₂ delivery and/or O₂ utilization and manifest a reduction in both active muscle [HHb] and the [HHb]-to-V̇o_2p ratio. Furthermore, given that the V̇o_2p slow-component amplitude may be reduced under conditions of elevated O₂ delivery (18), it might also be expected that INT could have a similar effect.

The purposes of this study were to compare HVY CONT with and without the insertion of 3-s recovery periods at 25-s and 10-s intervals on the following: 1) V̇o_2p and [HHb] kinetics; 2) the [HHb]-to-V̇o_2p ratio; and 3) the energy system contributions reflected by V̇o_2p, V̇co_2p, arterialized-capillary [Lac⁻], and [HHb]. It was hypothesized that 1) increasing the frequency of 3-s recovery periods during HVY exercise would slow phase II V̇o_2p kinetics; 2) the [HHb]-to-V̇o_2p ratio would be mitigated with the inclusion of more frequent recovery periods; 3) V̇o_2p would be lowest during the work phase of 10INT relative to 25INT and CONT, respectively; and 4) [HHb] and arterialized-capillary [Lac⁻] would be lower with the more frequent inclusion of 3-s recovery periods.

METHODS

Subjects.

Ten healthy young men (age 24 ± 3 yr; height 180 ± 6 cm; weight 79 ± 7 kg) volunteered and gave written, informed consent to participate in this study. All procedures were approved by The University of Western Ontario Ethics Board for Health Sciences Research Involving Human Subjects. Subjects were recreationally active and nonsmokers and had no known cardiovascular, respiratory, metabolic, or musculoskeletal diseases. No participants were taking any medications that might affect the cardiorespiratory and hemodynamic responses to exercise. Subjects were instructed not to perform any strenuous exercise for up to 24 h before visits to the laboratory, nor were they to consume any food or caffeine 2 h prior.

Preexperimental protocol.

Each subject reported to the laboratory to perform a ramp incremental exercise test (20 W baseline for 4 min followed by a 25 W/min ramp) on an electronically braked cycle ergometer (H-300-R Lode; Lode B. V., Groningen, the Netherlands) for determination of peak V̇o_2p (V̇o_2peak), peak PO (PPO), and estimated LT. Subjects were asked to maintain a cadence between 60 and 70 rpm during the test. V̇o_2peak was defined as the highest 20-s V̇o_2p computed from a rolling average. The test was terminated when the subjects were unable to maintain 50 rpm. PPO was defined as the work rate achieved at the termination of the ramp-incremental test.

The LT was estimated by visual inspection using standard gas exchange and ventilatory parameters, as previously described (5). Briefly, LT was determined as the V̇o_2p at which V̇co_2p and V̇e began to increase out of proportion to V̇o_2p. This point was corroborated with the observation of an increase in end-tidal Po₂, while the V̇e-to-V̇co₂ ratio and end-tidal Pco₂ were unchanged. Two exercise physiologists with experience in identifying LT evaluated each data set. If a discrepancy arose between the two investigators, a mean of the identified points was utilized.

Experimental protocol.

Subjects returned to the laboratory on six separate occasions to perform one of three cycling-based exercise protocols on each visit. The three exercise protocols consisted of the following: 1) an 8-min continuous protocol (CONT) at a work rate corresponding to 60% of the difference between the work rate associated with LT and V̇o_2peak (Δ60); 2) an 8-min, 25-s work to 3-s recovery intermittent protocol (25INT), where the “work period” was performed at Δ60 and the “recovery period” at 20 W; and 3) an 8-min 10-s work to 3-s recovery protocol (10INT) with exercise intensities identical to 25INT. Each exercise protocol was preceded by a 4-min baseline of 20-W cycling. Thus each exercise protocol lasted 12 min. Subjects performed two trials of each protocol in a randomized order and were asked to maintain a cadence of 60–70 rpm.

Data collection.

Breath-by-breath gas exchange measurements were made continuously during each exercise protocol and were similar to those previously described (28). During each trial, subjects breathed through a mouthpiece and wore a nose clip. Inspired and expired flow rates and volumes were measured using a pneumotach (Hans Rudolph, model 4813) and a low dead space (90 ml) bidirectional turbine (Alpha Technologies, VMM 110) positioned in series with the mouthpiece. The pneumotach was adjusted for zero flow, whereas the volume turbine was calibrated before each test using a syringe of known volume (3 liters). Respired gas was sampled continuously at the mouth by mass spectrometry (Perkin Elmer, Medical Gas Analyzer 1100) and analyzed for fractional concentrations of O₂, CO₂, and N₂. Gas concentrations were calibrated with precision-analyzed gas mixtures. The time delay (TD) between an instantaneous, square-wave change in fractional gas concentration at the sampling inlet and its detection by the mass spectrometer was measured electronically. Respiratory volumes, flow, and fractional gas concentrations were recorded in real-time at a sampling frequency of 100 Hz and transferred to a computer. Gas data were aligned with respiratory flow using the measured TD of the mass spectrometer. The computer executed a peak-detection program to determine end-tidal Po₂ and end-tidal Pco₂, as well as inspired and expired volumes and durations to build a profile of each breath. Breath-by-breath gas exchange at the pulmonary capillary was calculated using the algorithms of Swanson (51).

Muscle deoxygenation ([HHb]), which includes contributions from both myoglobin and hemoglobin of the vastus lateralis muscle, was measured using a frequency domain multidistance NIRS system (Oxiplex TS, Model 92505, ISS, Champaign, IL), as described elsewhere (49). Briefly, the system comprised a single channel consisting of eight laser diodes operating at two wavelengths (λ = 690 and 828 nm, four at each wavelength), which were pulsed in a rapid succession down a photomultiplier tube. A rigid plastic NIRS probe (connected to laser diodes and photomultiplier tube by optical fibers) consisted of two parallel rows of light emitter fibers and one detector fiber bundle; the source-detector separations for this probe were 2.0, 2.5, 3.0, and 3.5 cm for both wavelengths. The probe was placed on the greatest circumference of the vastus lateralis muscle. NIRS measurements were collected continuously for the entire duration of each trial. The NIRS unit was calibrated at the beginning of each testing session after the unit had been on for at least 20 min. Continuous measurements of the absolute scattering (u_s) and absorption (u_a) coefficients were determined from the measured intensity and phase shift of the light entering and traversing the tissue (at both wavelengths) from which absolute concentrations of HHb and oxyhemoglobin were determined. Data were collected at a frequency of 25 Hz and then reduced to 1-s bins for subsequent analyses.

Heart rate was collected using a Polar Wearlink Chest Strap, H1 Heart Rate Sensor and SP0180 Polar Transmitter (Polar Electro, Lachine, QC, Canada) linked to a PowerLab Chart data collection system (version 7.3.1 ADInstruments, Colorado, CO).

Arterialized-capillary blood samples (~5 µl) were taken from the index finger 6 min before and 2 min after all trials and immediately analyzed for [Lac⁻] (mM) using a lactate analyzer (Lactate Scout; Sports Resource Group, Hawthorne, NY).

Data analysis.

Breath-by-breath V̇o_2p data were edited on an individual basis by removing aberrant data ≥3 SD from the local mean (33). After each subject’s individual trial was edited, trial repeats were linearly interpolated on a second-by-second basis, time aligned such that time “zero” represented the onset of the transition, and ensemble-averaged into 5-s time bins. The on-transient of each profile was modeled with the following monoexponential function (Eq. 1):

$$y\left(t\right)=y_{BSL}+A_p·\left(1–e^{-\left(t-TD\right)/\tau }\right)$$ (1)

where y(t) is the value of the dependent variable at any time during the transition; y_BSL is the pretransition baseline value, A_p is the steady-state increase in y above the baseline value, and τ is the time constant of the response or the time for y to increase to 63% of the new steady state. The details of the fitting procedure are described elsewhere (26). Briefly, the Levenberg-Marquardt algorithm was applied to find the minimum sum of squared residuals between the monoexponential function and the experimental data using specialized software (Origin 8.5; OriginLab, Northampton, MA). The phase I-phase II transition was determined by visual inspection of the second-by-second and 5-s averaged data as the point at which there was a sharp decrease from baseline values (20 W cycling) in both RER and end-tidal Po₂. The end of the phase II fitting window was determined by examining the change in τ, 95% confidence interval, χ², and plotted residuals in response to progressive increases in the end of the fitting window. The point immediately preceding a systematic increase in τ, 95% confidence interval, and χ² was considered as the end of phase II. Baseline values for V̇o_2p were fixed as the mean value of the 60-s “window” before the step-transition. The difference between the V̇o_2p at end exercise (V̇o_2 End) and the V̇o_2p at the end of phase II was computed and used to determine the phase III or V̇o₂ slow-component amplitude. Throughout all trials, RER was computed from the ratio of V̇co_2p to V̇o_2p.

The TD for the [HHb] response was determined using second-by-second data and corresponded to the time, after the onset of exercise, at which the [HHb] signal began a systematic increase from its nadir value (by ~1 SD above baseline data). Determination of the TD of [HHb] was made on each individual’s ensemble-averaged response, and the data were modeled using Eq. 1. Baseline [HHb] values were determined by the average of 60 s before the step-transition. The baseline [HHb] was normalized to a zero baseline in each condition.

To observe the changes in [HHb] and unprocessed V̇o_2p with changes in PO within both intermittent conditions, [HHb] and unprocessed V̇o_2p data in each individual were clustered into a series of “recovery” and “work” cycles for analysis. For 25INT, four blocks were compared based on the average variable from each participant over the following time points: 1) 0–3 s (recovery); 2) 4–8 s (work); 3) 9–13 s (work); and 4) 14–28 s (work). Like-blocks were ensemble averaged to yield a single “work-recovery” cycle profile for each individual between 120 and 240 s. For the 10INT condition, three time blocks were computed and corresponded to 1) 0–3 s (recovery); 2) 4–8 s (work); and 3) 9–13 s (work). For [HHb], time-matched profiles identical to both 10INT and 25INT were computed for CONT for comparisons testing.

For each condition, the ratio of [HHb] to V̇o_2p was obtained by normalizing both the [HHb] and V̇o_2p signals as percentage changes (%Δ[HHb] and %ΔV̇o_2p), as previously described (38). Briefly, for both signals, baseline values were considered “0,” and peak values were determined from the final 30 s of exercise ([HHb]_End and V̇o_2 End) were considered as “100%.” The duration required for the matching of %Δ[HHb] and %ΔV̇o_2p within all conditions was then determined.

Statistical analysis.

Data are presented as means ± SD (Tables 1 and 2) and as group means on graphs. A one-way ANOVA with repeated measures was used to compare kinetics responses between conditions. A two-way repeated-measures ANOVA was used to compare physiological responses across time and between the three conditions. A two-way repeated-measures ANOVA was also utilized to compare %Δ[HHb] and %ΔV̇o_2p across time. Where significant main effects were found, a Tukey post hoc analysis was performed for multiple-comparisons testing. All ensemble-averaged data are presented in 5-s averages, unless otherwise stated. All statistical analyses were performed using SigmaPlot version 12.3, (Systat Software, San Jose, CA), and statistical significance was accepted at an α-level of 5%.

Table 1.

Subject characteristics and results from incremental test

Subject No.	Age, yr	Height, cm	Weight, kg	PPO, W	V̇o2peak, ml·kg−1·min−1	LT, l/min	Δ60 PO, W
1	24	178	83.9	317	43.9	1.8	248
2	24	176	71.4	324	50.4	1.7	242
3	22	173	72.3	343	54.6	2.1	262
4	25	183	82.6	367	49.8	2.1	277
5	24	173	69.2	286	45.9	1.3	203
6	31	190	85.0	385	48.5	2.1	293
7	24	185	91.5	305	40.3	1.7	231
8	24	173	76.8	282	41.9	1.2	203
9	24	188	79.2	383	52.1	2.3	300
10	21	183	78.1	329	51.9	2.1	262
Mean	24	180	79	332	47.9	1.8	252
SD	3	6	7	37	4.7	0.4	34

V̇o_2peak, peak oxygen uptake; PPO, power output at V̇o_2peak; LT, lactate threshold; Δ60 PO, power output equivalent to 60% of the difference between LT and PPO.

Table 2.

Physiological variables and parameter estimates from CONT, 25INT, and 10INT conditions

	Mean	SD		Mean	SD
Mean PO, W			V̇co2 EndPhase2, l/min
CONT	252	33.6	CONT	3.40	0.44
25INT	225*	29.7	25INT	2.88*	0.36
10INT	198*†	25.9	10INT	2.52*†	0.29
Pre-[Lac−], mM			V̇co2 End, l/min
CONT	1.8	0.4	CONT	4.18	0.43
25INT	2.0	0.4	25INT	3.57*	0.38
10INT	2.0	0.4	10INT	3.06*†	0.29
Post-[Lac−], mM			V̇e EndPhase2, l/min
CONT	14.3	3.1	CONT	73	9
25INT	10.3*	1.9	25INT	82*	9
10INT	7.0*†	1.7	10INT	89*†	14
V̇o2p BSL, l/min			V̇e End, l/min
CONT	0.97	0.09	CONT	139	15
25INT	0.96	0.13	25INT	112*	12
10INT	0.98	0.10	10INT	94*†	17
V̇o2p TD, s			[HHb] BSL, μM
CONT	13	5	CONT	25.8	5.8
25INT	17	4	25INT	26.1	5.7
10INT	15	3	10INT	26.6	5.7
τ V̇o2p, s			[HHb]-TD, s
CONT	28	4	CONT	6	1
25INT	23*	5	25INT	8	1
10INT	24*	4	10INT	9	1
V̇o2 EndPhase2, l/min			τ[HHb], s
CONT	3.01	0.30	CONT	10	5
25INT	2.91	0.35	25INT	9	5
10INT	2.67*†	0.31	10INT	9	4
V̇o2p End, l/min			[HHb]End, μM
CONT	3.69	0.37	CONT	16.1	12.0
25INT	3.29*	0.36	25INT	15.2	11.5
10INT	2.89*†	0.33	10INT	15.0	12.1
V̇o2p SC, l/min			REREnd
CONT	0.69	0.20	CONT	1.13	0.03
25INT	0.38*	0.18	25INT	1.09*	0.02
10INT	0.21*†	0.09	10INT	1.06 *†	0.04

PO, power output; Pre-[Lac⁻], blood lactate concentration before exercise; Post-[Lac⁻], blood lactate concentration 2 min postexercise; V̇o_2p, oxygen uptake; BSL, baseline; TD, time delay; τ, time constant; EndPhase2, end of phase 2; End, end exercise; SC, slow component; V̇co₂, carbon dioxide output; V̇e, ventilation; [HHb], muscle deoxygenation; RER, respiratory exchange ratio.

^*Different from CONT (P < 0.05).

^†Different from 25INT (P < 0.05).

RESULTS

Subject characteristics and results from the ramp-incremental test are presented in Table 1. Mean V̇o_2peak was 3.8 ± 0.4 l/min, which corresponded to a PPO of 332 ± 37 W. The V̇o_2p at LT was 1.8 ± 0.4 l/min. By design, the absolute PO associated with CONT and the work periods for both INT conditions (i.e., Δ60) were identical (group mean = 252 ± 34 W). The mean POs among all conditions were different (P < 0.05; Table 2).

V̇o_2p kinetics.

The V̇o_2p data over the four time blocks of the 30-s cycles of the 25INT (0–3 s, 4–8 s, 9–13 s, and 14–28 s) from 120 s to 240 s, and the three time blocks of 10INT (0–3 s, 4–8 s, and 9–13) over a similar time period, did not indicate any fluctuation (P < 0.05). Figure 1 displays the unprocessed, breath-by-breath data for each condition of a representative subject. Note that any oscillations in V̇o_2p (if present) for 25INT (Fig. 1B) and 10INT (Fig. 1C) are not discernible. The group mean V̇o_2p response profiles for all subjects during the three exercise conditions are displayed in Fig. 2. The τV̇o_2p was shorter in both intermittent conditions compared with CONT (P < 0.05) (Table 2). The V̇o_2p at the end of phase two was lower (P < 0.05) in 10INT compared with CONT and 25INT (Table 2). The amplitude of the V̇o₂ slow component and V̇o_2 End were different across all conditions (P < 0.05; Table 2).

Fig. 1.

Unprocessed breath-by-breath V̇o_2p data of a representative participant from a single trial of the CONT (A), 25INT (B), and 10INT (C) are displayed. There were 502 breaths during CONT, 488 breaths during 25INT, and 498 breaths during 10INT. Note that there are no observable oscillations in the V̇o_2p data for 25INT or 10INT. The onset of the heavy-intensity step-transition occurs at 240 s.

Fig. 2.

The group mean V̇o_2p response to CONT (solid circles), 25INT (shaded circles), and 10INT (open circles) are displayed. Overall, the V̇o_2p was highest (P < 0.05) in CONT and reduced further with increased frequency of recovery periods.

Muscle deoxygenation parameters and NIRS-derived [HHb] kinetics.

The group mean [HHb] responses to CONT, 25INT, and 10INT are presented in Fig. 3. A summary of parameter estimates for the on-transient muscle deoxygenation are presented in Table 2. The τ[HHb], [HHb] at the end of phase II, and [HHb] at end exercise ([HHb]_End) were not different among conditions (P > 0.05; Table 2). Oscillations in [HHb] during 25INT were not observed between the 3-s recovery period and the work period corresponding to 4–8 s. However, [HHb] increased above the 3-s recovery period at the work periods corresponding to 9–13 s and 14–28 s (P < 0.05). Within the 10INT, [HHb] was similar between 3-s recovery and 4–8 s of work (P > 0.05), but both were lower than the work period corresponding to 9–13 s (P < 0.05). There were no differences (P > 0.05) in [HHb] across any of the time-matched periods in CONT over the same duration of exercise.

Fig. 3.

The group mean deoxyhemoglobin [HHb] response to CONT (solid circles), 25INT (shaded circles), and 10INT (open circles) are displayed. Mean [HHb] was not different (P > 0.05) among conditions.

Δ[HHb]-to-ΔV̇o₂ ratio.

An overshoot in the [HHb]-to-V̇o₂ signal was evident in all conditions. However, the abolishment of this overshoot occurred more rapidly with the increased frequency of the 3-s recovery periods compared with CONT (CONT: 270 s; 25INT: 150 s; 10INT: 90 s; P < 0.05) (see downward arrows in Fig. 4).

Fig. 4.

The ratio of the change in deoxyhemoglobin to the change in V̇o_2p (Δ[HHb]/ΔV̇o_2p), for CONT (A), 25INT (B), and 10INT (C) is displayed. Time elapsed until abolishment of the overshoot (indicated by downward arrows) was different (P < 0.05) for all conditions.

V̇co_2p, V̇e, and RER.

Mean V̇co_2p and V̇o_2p for all conditions are presented in Fig. 5. The V̇co₂ amplitude and ventilation were different between all conditions at end of phase II V̇o_2p and end-exercise (P < 0.05; Table 2). RER at end exercise was also different among all conditions (P < 0.05; Table 2).

Fig. 5.

The group mean V̇o_2p (open circles) and V̇co_2p (solid circles) CONT (A), 25INT (B), and 10INT (C) are displayed. Respiratory exchange ratio (RER) indicated by V̇co_2p/V̇o_2p was greatest in CONT, reduced in 25INT, and lowest in 10INT (P < 0.05).

Blood lactate concentration.

There were no differences (P > 0.05) in preexercise [Lac⁻] between CONT, 25INT, and 10INT. Postexercise [Lac⁻] differed between all conditions (P < 0.05; Table 2).

DISCUSSION

In this study, we used noninvasive measurements to examine the metabolic and physiological differences associated with continuous high-intensity exercise (CONT) to matched duty cycle PO heavy-intensity (Δ60) intermittent exercise of 25-s work to 3-s recovery (25INT) and 10-s work to 3-s recovery (10INT). These analyses represent the first attempt to measure V̇o_2p kinetics during INT. The main findings were that, with the insertion of the recovery periods, 1) the V̇o_2p response profiles resembled those that would be expected during constant PO step-transitions (oscillations in V̇o_2p were unidentifiable) corresponding to different exercise intensity domains; 2) τV̇o_2p was reduced compared with CONT, whereas τ[HHb] was similar among all conditions; 3) the overall rates of increase in [HHb] relative to V̇o_2p were progressively better matched (i.e., reduced [HHb]-to- V̇o_2p ratio) as recovery frequency increased; and 4) arterialized-capillary blood lactate decreased concomitant with a reduction of V̇co_2p and ventilation. These data suggest that work/rest fluctuations during INT create a metabolic condition that relies less on oxidative phosphorylation during the work period compared with an identical PO performed continuously, and that brief interruptions in PO during step-transitions of identical PO speed V̇o_2p kinetics possibly by improving muscle microvascular O₂ provision.

Integral to this study was the confidence that the insertion of the 3-s recovery periods within the HVY exercise would facilitate a breath-by-breath V̇o_2p profile that could be subjected to kinetic analyses. Figure 1 displays the raw breath-by-breath V̇o_2p responses of the CONT, 25INT, and 10INT trials of a representative participant. From this figure, it is clear that fluctuations in the V̇o_2p data were not apparent (or that these changes were smaller than the noise amplitude of the V̇o_2p signal (27, 33), and subsequent analyses confirmed that there were no rhythmical oscillations in V̇o_2p with the changes in PO.

Recognizing that the transitions within high-intensity short work/shorter recovery INT may not induce a single “step-change” in ATP demand over the entire exercise protocol, it was hypothesized that insertion of brief recovery periods (3 s) during HVY exercise would contribute to a slowing of phase II V̇o_2p kinetics relative to CONT as the frequency of recovery periods increased. Relative to the CONT condition, we surmised that the forcing stimulus for active muscle V̇o₂ (increased ATP demand) in the intermittent conditions would be periodically “switched off” (or diminished). This would increase phosphate potential (7) and delay the stimulus for oxidative phosphorylation (9). Unexpectedly, V̇o_2p kinetics were speeded with the insertion of the recovery periods. Thus an alternative hypothesis is warranted.

Previous work has suggested that increasing O₂ delivery can speed phase II V̇o_2p kinetics within the HVY domain (11, 19, 35). The NIRS-derived [HHb] signal has been used extensively as a proxy for microvascular muscle O₂ extraction to infer changes in oxidative phosphorylation within the muscle tissue below the NIRS probe (29). When combined with V̇o_2p, the [HHb]-to-V̇o_2p ratio provides insight into the dynamic matching of O₂ provision to O₂ utilization within the active muscle (37). The inclusion and increased frequency of the 3-s recovery periods during high-intensity exercise used herein resulted in a progressively reduced magnitude and duration of the [HHb]-to-V̇o_2p ratio during the on-transient (Fig. 4). Relative to CONT, a reduction in the magnitude of the “overshoot” in [HHb]-to-V̇o_2p signal indicates an improvement in microvascular O₂ delivery throughout the on-transient. It has been suggested that, during the relaxation phase of contraction, there is a marked increase in blood velocity (reflecting blood flow) in comparison to the work phase (53). Thus it is possible that this phenomena would also occur during the 3-s recovery period of the intermittent conditions (44) as intramuscular pressures and impedance to flow would decrease within the working muscle during the recovery periods (1, 17, 34). This increase in microvasculature perfusion could facilitate an improvement in O₂ delivery as recovery frequency increases, and thus any recovery-induced metabolic changes that would be expected to slow the rate of increase of oxidative phosphorylation may have been offset by rectifying limitations associated with O₂ delivery, resulting in faster phase II V̇o_2p kinetics (16, 35). In addition to condition-specific differences in the magnitude of the [HHb]-to-V̇o_2p ratio, the duration for the overshoot to be rectified (i.e., [HHb]-to-V̇o_2p = 1.0) was also reduced with INT and with increased recovery frequency. The inferred increase in microvasculature O₂ provision as recovery frequency increased could account for, in part, the observed reduction in the V̇o_2p slow-component amplitude, which may be reduced under conditions of improved O₂ delivery (18).

Based on previous work (7), it is advocated that the requirements for ATP resynthesis during the initial phase of the work periods during short duty cycle INT work are predominated by PCr-derived phosphorylation (7) (as opposed to glycolytic or oxidative phosphorylation) relative to the identical PO performed continuously. It would be expected that [Lac⁻] and/or V̇o_2p would be reduced with increased frequency of recovery periods (20, 21, 30, 36, 56). Recognizing the limitations of using arterialized-capillary lactate as a proxy measure of muscle lactate and pH due to the influence of release and uptake by other tissues (e.g., inactive/active muscle, liver, heart, and brain) in determining blood [Lac⁻] (22), the decreased [Lac⁻] from CONT with increased recovery frequencies may be inferred to reflect a reduced intramuscular [Lac⁻] (25) and lower glycolytic phosphorylation component. The consequence of a reduced reliance on glycolysis during exercise could result in a lower lactate-associated intramuscular acidosis. Using magnetic resonance spectroscopy, we demonstrated that over the last 6 min of INT (10:5 s) the accumulation of intramuscular [H⁺] was 10% lower compared with the CONT (7). Moreover, during the first 120 s of CONT, [H⁺] was 35% greater compared with INT. Although the recovery duration utilized in the present study was shorter than our previous work (from 5 s to 3 s), a greater accumulation of intramuscular [H⁺] in CONT relative to INT conditions is tenable. Given that accumulation of intramuscular H⁺ has been shown to blunt Ca²⁺ sensitivity of the sarcoplasmic reticulum (15) and, through reduced Ca²⁺ release, slows the utilization of oxidatively phosphorylated ATP at the myofilament cross-bridge, and that hypercapnic-induced acidosis elicits a approximately threefold decrease in aerobic capacity (23), this may represent a mechanism by which V̇o_2p kinetics were slower in CONT.

The associated increase of phosphate potential could elicit a downregulation of oxidative phosphorylation and slow V̇o_2p kinetics (44) during the CONT condition compared with both intermittent conditions of the present study. Wilkerson et al. (58) examined the influence of hyperoxia on V̇o_2p kinetics over the continuum from moderate, severe, and supramaximal intensities. Their severe intensity exercise coincided with a V̇o_2p requirement of ~85% of V̇o_2max, which was similar to the 80% V̇o_2max elicited by the present study protocol. These authors observed no effect of hyperoxia on V̇o_2p kinetics at any of the intensities. Unlike the intermittent conditions of the present study, they observed a similar increase in blood [Lac⁻] in both their hyperoxic and normoxic conditions. The previously stated detrimental effects of glycolytic phosphorylation metabolites that would slow V̇o_2p kinetics in the Wilkerson et al. (58) study may have eclipsed any speeding effects of the increased O₂ delivery in their hyperoxic condition. Finally, it is suggested that the previously observed decrease in mean PCr breakdown over repeated 10-s work to 5-s recovery cycles compared with continuous work (7) would also be observed in the intermittent conditions of the present study (35). This decrease in mean PCr breakdown and the associated decrease in creatine kinase activity has been linked to an increase in mitochondrial activity (20, 32) and, as such, could also contribute to the speeded V̇o_2p kinetics of the intermittent conditions in the present protocol.

Further evidence that the differences in [Lac⁻] may reflect a greater acidosis in CONT relative to the INT conditions may be inferred from the RER and ventilation (Table 2). Similar V̇co_2p and V̇o_2p would be expected during steady-state, sublactate threshold exercise, where carbohydrate-derived substrate predominates (10). In contrast, exercise intensities engendering net [Lac⁻] accumulation are associated with [H⁺] accumulation (50). This accumulation increases V̇co_2p relative to V̇o_2p after the transient phase as a result of a shift in the carbonic anhydrase reaction toward CO₂ production (55). This results in an increase in ventilation (47). The average mean RER determined after the completion of phase II to end exercise was greatest in CONT (1.16) and was reduced to 1.09 in 25INT and 1.06 in 10INT. This lowering of V̇co_2p relative to V̇o_2p as recovery period frequency increases (note the overall convergence of V̇co_2p to V̇o_2p in Fig. 5 from CONT to 10INT) intimates a reduction in ventilatory buffering (24) associated with the observed decrease in ventilation in the present study (see Table 2). In combination with the lower overall V̇o_2p in INT relative to CONT, these findings may be interpreted to indicate a reduced contribution of glycolysis and oxidative phosphorylation and greater contribution from PCr-mediated ATP resynthesis to perform the identical PO during the work periods.

As hypothesized, compared with CONT and with increased frequency of recovery periods, the profile of V̇o_2p displayed a smaller phase II and V̇o_2p slow-component amplitude (Table 2). In this way, INT with an identical work phase PO but with different frequency of 3-s (20 W) recovery periods approximated CONT transitions from low baselines to their respective mean PO (~Δ230 W, Δ210 W, and Δ190 W for CONT, 25INT, and 10INT, respectively). While it could be argued that the overall volume of O₂ (VO_2p) consumed relates to the total amount of work performed in the 8-min period, it is apparent from 1) the manner by which V̇o_2p is changing and 2) the observed differences in V̇o_2p kinetics and [Lac⁻] that the relative intensity in relation to exercise intensity domains is dependent on the mean PO. Unfortunately, we did not extend INT protocols to achieve the same total work as CONT. However, had we performed all protocols to the limit of tolerance, we argue that the total tolerable work accomplished in the INT conditions would far exceed that of CONT. For example, Soares-Caldeira et al. (48) demonstrated that critical power associated with INT (using 30-s duty cycles) exceeds that of CONT, indicating that there is an upward shift in the demarcators of each “domain” and the PO ranges that they define. A similar type effect has been observed by manipulating duty cycle (52). It is well established that the metabolic and physiological responses to exercise within the HVY (<critical power) vs. severe (>critical power) intensity domain are drastically different (24, 43) and have implications for muscle fatigue and exercise tolerance (8, 12). Our analyses and the V̇o_2p profiles in Fig. 2 depict responses reflective of exercise performed in different exercise intensity domains (41). This indicates that an identical PO performed intermittently with recovery periods as short as 3 s inserted at different frequencies can cause a shift in the exercise intensity domain paradigm relative to CONT.

Practical applications.

Many sports require short periods of high-intensity exertion followed by brief periods of rest or recovery. Yet the acute physiological responses and metabolic consequences to intermittent type exercise have received far less attention compared with CONT. This study yields an initial assessment of the inherent physiological solutions dictated by the various intermittent models. For example, the present study’s exercise protocol (continuous, 25:3 s, 10:3 s) has particular relevance to elite collegiate level swimmers in the U.S. who may compete or train in pool venues of various lengths. These include 25-yd (NCAA competition), 50-m (Olympic competition), and open-water courses (Olympic competition). The major propulsive arm muscles of elite freestyle swimmers (14) perform work periods of ~10 s and 25 s in 25-yd and 50-m pools, respectively, in one length of the pool. These work periods are preceded by a flip-turn and push off the wall in which these upper limb propulsive muscles are inactive for ~3 s. In contrast, open water races mandate continuous work be performed by these same muscles. Despite the obvious differences between the lower extremity work performed here, and the upper extremity muscle groups associated with swimming, this study assesses the physiological impact of the aforementioned work: recovery durations. Our data suggest that the key consequences of the increased frequency of the recovery periods (for example, as swimming venue size decreases) are a speeding of V̇o_2p kinetics and a reduction in [Lac⁻] and the V̇o_2p slow component. Given the relation of these variables to exercise intensity domains and muscle fatigue, our results indicate that brief recovery periods interspersed in HVY exercise would effectively delay fatigue at a given exercise intensity or allow for a greater intensity to be performed for a given distance.

Conclusions.

To our knowledge, this is the first study to examine V̇o_2p kinetics during intermittent exercise. Here, we established that phase II τ V̇o_2p may be reduced in intermittent compared with continuous exercise, and that insertion of recovery periods as brief as 3 s in heavy-intensity exercise can result in an upward shift in the PO ranges defining the exercise intensity domain paradigm. It is suggested that this speeding of phase II V̇o_2p kinetics may be related to improvements in the matching of local O₂ delivery to O₂ utilization within the active muscle mediated by the brief periods of recovery. Moreover, our evidence shows that inserting brief recovery periods within continuous type exercise, and then increasing their frequency, elicits a lower contribution from oxidative phosphorylation to perform the identical PO.

GRANTS

This study was supported by National Science and Engineering Research Council of Canada Research and Equipment Grant RGPGP-2015-00084.

DISCLOSURES

No conflicts of interest, financial or otherwise, are declared by the authors.

AUTHOR CONTRIBUTIONS

M.C.M. and D.A.K. performed experiments; M.C.M. and G.R.B. analyzed data; M.C.M., D.A.K., and G.R.B. interpreted results of experiments; M.C.M. prepared figures; M.C.M. drafted manuscript; M.C.M., D.A.K., and G.R.B. edited and revised manuscript; M.C.M., D.A.K., and G.R.B. approved final version of manuscript; G.R.B. conceived and designed research.