Similar fat and carbohydrate oxidation in response to arm cycling exercise in persons with spinal cord injury versus able-bodied

Abstract

Context

Persons with spinal cord injury (SCI) present with low fat oxidation that is associated with poor cardiometabolic health. This study compared changes in fat and carbohydrate (CHO) oxidation during moderate intensity continuous exercise in persons with SCI and able-bodied adults (AB).

Design

Repeated measures, within-subjects study.

Setting

University laboratory in San Diego, CA.

Participants

Nine men and women with SCI (age and time since injury = 32 ± 11 yr and 7 ± 6 yr) and 10 AB adults (age = 25 ± 8 yr).

Interventions

To assess peak oxygen uptake (VO₂peak) and peak power output (PPO), participants performed progressive arm ergometry to volitional exhaustion. Subsequently, they completed 25 min of continuous exercise at 45%PPO.

Outcome Measures

Respiratory exchange ratio (RER), fat and CHO oxidation, and blood lactate concentration (BLa) were assessed.

Results

Data showed a similar RER (P = 0.98) during exercise in SCI (0.97 ± 0.04) versus AB (0.97 ± 0.03) reflecting high CHO use and no differences in BLa (3.5 ± 1.1 and 3.0 ± 0.9 vs. mM, P = 0.56) or fat and CHO oxidation between groups (P > 0.05). However, participants with SCI exercised at a higher relative intensity (P < 0.01, 84 ± 7 vs. 75 ± 7%HRpeak) versus AB.

Conclusion

Data confirm high reliance on CHO during arm ergometry in persons with SCI. To better compare substrate utilization to AB adults, we recommend that exercise be prescribed according to peak heart rate due to differences in cardiorespiratory fitness between groups.

Introduction

Fat and carbohydrate (CHO) are the primary substrates oxidized during moderate intensity continuous exercise (MICE). It is apparent that the ratio of fat versus CHO oxidation depends primarily on exercise intensity,¹ although it is also modified by exercise duration,¹ fed state, and participant fitness level. For example, fat oxidation increases from rest to light exercise until the crossover point is attained at which point CHO oxidation becomes the primary source of ATP supply.² This crossover is highly dependent on exercise mode but can also be influenced by pathology that influences skeletal muscle, endocrine activity, and other functions that determine the physiological response to exercise.

The importance of fat and CHO oxidation was initially identified to optimize athletic performance in endurance athletes,^3,4 but the global rise of pathologies related to fat metabolism warrants the clinical application of exercise as a provocative test of metabolic flexibility. In fact, many studies show that ability to oxidize fat is linked to health status. For example, a lower capacity to oxidize fat is related to onset of diabetes and obesity,^5,6 and in men, there is a positive relationship between insulin sensitivity and maximal fat oxidation,⁷ representing the highest rate of fat utilization attained during exercise. In addition, low fat oxidation during exercise is coincident with a high resting RER has been associated with an unhealthy metabolic phenotype.⁸ Overall, these findings establish the role of fat oxidation in mediating health status and emphasize the importance of assessing the fat oxidation response to exercise in various individuals.

Spinal cord injury (SCI) results in somatic and autonomic changes that accelerate risk of cardiometabolic disease (CMD),⁹ with CMD components risks clustering in this population in a manner causing disorders of metabolism.¹⁰ Concomitantly, the majority of adults with SCI are not physically active¹¹ which places them on the low end of the human cardiorespiratory fitness spectrum.^12,13 Above and beyond a low level of cardiorespiratory fitness, many adults with SCI are obese¹⁴ or experience dyslipidemia,¹⁵ all of which enhance their risk of cardiovascular disease and mortality compared to able bodied (AB) adults.¹⁶ Moreover, fat oxidation during exercise is low in this population. For example, data from Gorgey and Lawrence¹⁷ demonstrated heavy reliance on CHO and attenuated fat oxidation in adults with complete SCI who underwent FES cycling. This diminished capacity for fat oxidation is attributed to their low fitness level, attenuated mobilization of free fatty acid,¹⁸ the blunted neuroendocrine response to exercise,¹⁹ and the small amount of muscle mass activated during upper-body exercise.²⁰ Nevertheless, data from Jacobs et al.²¹ showed that inactive men with SCI exhibit higher fat oxidation during progressive arm ergometry than AB men, which was attributed to the repeated use of the upper body for movement.

The aim of the present study was to compare substrate metabolism during MICE between active adults with SCI and AB men and women. Previous data in this area stem from studies including athletes with SCI,²² implementing functional electrical stimulation exercise in persons with tetraplegia,¹⁸ and during handgrip exercise in persons with injury above T5.²³ We chose a moderate intensity continuous bout of exercise as it follows recommended guidelines for continuous exercise for adults with SCI.²⁴ In addition, it is apparent that capacity for fat oxidation during submaximal exercise, and not only maximal fat oxidation, is related to health status. Hall et al.²⁵ reported low whole-body fat oxidation in South Asian men that was attendant with elevated fat mass, 2 h insulin concentration, and attenuated insulin sensitivity and concentration of high density lipoprotein. In adults with SCI, few studies have examined fat and CHO oxidation responses in nonathletic adults completing voluntary exercise such as arm ergometry. This line of inquiry is important considering the marked prevalence of obesity in persons with SCI²⁶ and its relationship with cardiometabolic dysfunction in this population.^10,13,27 A prior study showed that chronic arm cycling at a moderate or vigorous intensity increases insulin sensitivity despite no change in body mass or body composition,²⁸ yet potential alterations in fat and CHO oxidation were not examined. Based on their relationship with insulin sensitivity and metabolic health, it seems warranted to further elucidate changes in fuel utilization during exercise in adults with SCI. It was hypothesized that CHO would be the primary substrate oxidized during exercise and that no difference in fat and CHO oxidation would occur between groups due to the anticipated higher VO₂peak seen in AB adults versus persons with SCI.

Materials and methods

Design: During the first session, participants initially completed progressive arm cycling to volitional fatigue to assess VO₂peak and peak power output (PPO). They returned at least 2 d later at the same time of day and performed 25 min of continuous arm cycling at 45%PPO that satisfies current physical activity recommendations for adults with SCI.²⁴ During exercise, heart rate (HR), gas exchange data, and blood lactate concentration were assessed. Both sessions were preceded by 24 h abstention from voluntary physical activity as well as a 3 h fast. Participants were encouraged to arrive to the Laboratory (temperature and relative humidity – 20–22 ^oC and 40–60%) well-rested and hydrated. Results presented in this manuscript for participants with SCI were obtained in a prior study examining the feasibility of high intensity interval exercise in this population during which the bout of MICE was completed²⁹; however, in that publication, no data concerning substrate utilization were analyzed or presented.

Participants: Ten AB participants and nine individuals with SCI participated in the present investigation. Their physical characteristics are presented in Table 1, which shows that age, physical activity, and body mass index were similar (P > 0.05) between groups. Participants with SCI consisted of two men with tetraplegia and six men and one woman with paraplegia. All participants were physically active, with participants with SCI regularly engaging in resistance training, arm ergometry, locomotor training, or wheelchair ambulation; whereas, AB participants participated in resistance training, surfing, aerobic exercise, or played non-competitive sports. However, none regularly engaged in arm ergometry. Inclusion criteria included healthy men and women 18–50 yr old who lacked upper extremity injury that may prohibit intense arm ergometry as well as diagnosis of diabetes, obesity, or heart disease. They initially completed a health-related survey and all provided written informed consent to participate in the study, whose procedures were approved by the University Institutional Review Board.

Table 1.

Participant characteristics and maximal gas exchange data during arm ergometry (mean ± SD).

Parameter	SCI	AB	p value
Age (yr)	32.3 ± 10.6	25.3 ± 8.2	0.12
Gender	8 M/1 W	9 M/1 W	NA
Body mass index (kg/m2)	22.1 ± 1.4	24.6 ± 3.5	0.06
Physical activity (h/wk)	7 ± 3	5 ± 2	0.12
VO2peak (mL/kg/min)	17.4 ± 4.9	26.7 ± 8.1*	0.008
VO2peak (L/min)	1.3 ± 0.5	1.9 ± 0.7*	0.017
VCO2peak (l/min)	1.6 ± 0.6	2.3 ± 0.7*	0.03
RERmax	1.27 ± 0.11	1.24 ± 0.17	0.77
VEpeak (L/min)	52 ± 15	82 ± 28*	0.01
HRmax (b/min)	160 ± 30	169 ± 23	0.47
PPO (W)	95 ± 37	125 ± 33	0.08

SCI = participants with spinal cord injury; AB = participants who are able-bodied; VO₂peak = peak oxygen uptake; VCO₂peak = peak carbon dioxide production; RER = respiratory exchange ratio; V_E = ventilation; HR = heart rate; PPO = peak power output; *= p<0.05 versus participants with SCI.

Assessment of VO₂peak: This session and the subsequent bout of exercise took place on a wall-mounted electronically-braked arm ergometer (Angio, Lode, Groningen, the Netherlands). Before exercise, the participant was seated in a chair placed in front of the ergometer, and the shoulder joint was aligned with the pedals of the ergometer. They were instructed to sit with their back against the chair and minimize movement of the lower extremity. A 5 min warm-up ensued at a work rate equal to 7 W, after which power output was increased in a ramp-like manner by 8–15 W/min in AB and by 3–15 W/min for persons with SCI, with the aim to ensure test duration of approximately 10 min. Cadence was self-selected during the bout, and volitional fatigue occurred when pedal cadence declined below 30 rev/min. Throughout exercise, heart rate (HR, Polar Electro, Woodbury, NY) and pulmonary gas exchange data (Parvomedics True One, Sandy, UT) were continuously obtained. Peak HR and power output were identified as the values coincident with volitional fatigue, and VO₂peak represented the average of the two highest 15 s values occurring in the last 60 s of exercise. Data from our lab show that this exercise protocol elicits ‘true’ peak oxygen uptake in persons with SCI.³⁰

Session of continuous exercise: Upon entering the laboratory, participants were seated for 5 min to enable assessment of blood lactate concentration (BLa). The fingertip was cleaned with a damp towel and then dried. Subsequently, a 23 gauge lancet (Owen Mumford, Marietta, GA) and portable monitor (Lactate Plus, Nova Biomedical, Waltham, MA) were used to assess BLa at rest and 3 min post-exercise. The first drop of blood was wiped away and the second drop was used. The HR monitor was placed on the trunk, and a 5 min warm-up ensued at 10%PPO. Subsequently, the ergometer was placed in manual mode and they cranked for 25 min at a workload equal to 45%PPO. Intensity was prescribed using %PPO as utilized in our prior work,²⁹ as %HRmax can be challenging due to the unique HR response in persons with SCI. Cadence was not standardized during this bout, yet participants were instructed to maintain a value between 40–80 rev/min throughout exercise. Gas exchange data were acquired continuously during this session as well as HR.

Oxygen uptake, VCO₂, and HR from this exercise bout were analyzed from the last minute of the warm-up as well as the last minute of data at 25 (minutes 5–6), 50 (minutes 11.5–12.5), 75 (minutes 17.75–18.75), and 100% (minutes 24–25) of session duration. Fat and CHO oxidation were calculated using the following equations³¹ which are designed for exercise when muscle glycogen contribution is high, as is the case with arm ergometry.²¹ In the event of a respiratory exchange ratio (RER) value equal to or greater than 1.0, fat oxidation was considered zero.

Fat oxidation (g/min) = 1.70(VO₂) – 1.701(VCO₂)

Carbohydrate oxidation (g/min) = 4.21(VCO₂) – 2.96(VO₂)

Respiratory exchange ratio (VCO₂/VO₂) and percent contribution of fat and CHO oxidation were calculated using standard equations (% fat oxidation = 1 – RER/0.3).

Data analysis: Data are reported as mean ± SD and were analyzed using SPSS Version 24.0 (IBM, Armonk, NY). The Shapiro-Wilks test was used to assess normality of all variables. Independent t-test was used to examine differences in physical characteristics and maximal gas exchange data between groups. Two-way ANOVA with repeated measures was used to examine differences between groups (SCI and AB) and across time (3 and 5 levels for BLa and variables related to substrate utilization). If a significant F ratio was obtained, Tukey’s post hoc test was used to locate differences between means. Where appropriate, Cohen’s d was used as an estimate of effect size. Pearson product moment correlation was used to assess associations between variables. Statistical significance was set as P < 0.05.

Results

Maximal gas exchange data: The AB participants exhibited significantly higher (P < 0.01) peak values of VO₂ (d = 1.0), VCO₂ (d = 1.1), and V_E (d = 1.4) than those with SCI (Table 1). The VO₂peak values of our sample are similar to those reported in a prior study²¹ and classify them as having average cardiorespiratory fitness.³² HRpeak did not differ between groups, which suggests that the majority of our adults with SCI maintained normal sympathetic innervation to the SA node to accelerate HR during exercise.

Gas exchange data, heart rate, and substrate metabolism during the continuous session: In AB adults compared to those with SCI, continuous arm ergometry elicited a significantly lower relative intensity equal to 75 ± 7 versus 84 ± 7%HRpeak (P = 0.01, d = 1.3) and 60 ± 7 versus 71 ± 9%VO₂peak (P = 0.008, d = 1.6), respectively. Total energy expenditure was 24% higher (P = 0.14) in AB participants versus SCI (129 ± 31 kcal vs. 105 ± 36 kcal) which was due to the higher absolute work rate completed by the former group (56 ± 14 W vs. 43 ± 17 W, P = 0.10).

Table 2 demonstrates heart rate and gas exchange data during MICE in both groups. HR increased from the warm-up (P < 0.001) but there was no group X time interaction (P = 0.85). Absolute oxygen uptake increased from the warm-up (P < 0.001) and there was a group X time interaction (P = 0.015), as VO₂ was higher in AB versus SCI throughout exercise (d = 2.0 - 2.2). Similar results were shown for VCO₂ as it increased from the warm-up (P < 0.001) and was higher (d = 1.9–2.2) in AB participants (P = 0.04 for interaction). RER increased from values recorded during the warm-up (RER = 0.89, P = 0.008) and there was no group X time interaction (P = 0.98). RER obtained at 25% of exercise session was significantly higher than that exhibited at the end of exercise (d = 0.38).

Table 2.

Heart rate and substrate utilization results during moderate intensity continuous exercise (mean ± SD).

Parameter	Warm-up	25%	50%	75%	100%
AB
VO2 (l/min)	0.51 ± 0.10	1.03 ± 0.24*	1.08 ± 0.25*	1.10 ± 0.25*	1.13 ± 0.27*
VCO2 (L/min)	0.45 ± 0.09	1.01 ± 0.24*	1.04 ± 0.24*	1.07 ± 0.26*	1.09 ± 0.26*
RER	0.89 ± 0.15	0.98 ± 0.04	0.96 ± 0.02	0.97 ± 0.03	0.96 ± 0.01
HR (b/min)	87 ± 11	118 ± 19	126 ± 19	129 ± 19	129 ± 19
SCI
VO2 (l/min)	0.48 ± 0.13	0.84 ± 0.25	0.88 ± 0.30	0.89 ± 0.28	0.93 ± 0.29
VCO2 (L/min)	0.43 ± 0.13	0.83 ± 0.26	0.86 ± 0.30	0.86 ± 0.29	0.90 ± 0.30
RER	0.89 ± 0.04	0.98 ± 0.04	0.97 ± 0.03	0.96 ± 0.04	0.96 ± 0.03
HR (b/min)	97 ± 14	128 ± 17	134 ± 17	136 ± 19	139 ± 19

AB = able-bodied participants; VO₂ = oxygen uptake; VCO₂ = carbon dioxide production; RER = respiratory exchange ratio; HR = heart rate; SCI = participants with spinal cord injury; * = p < 0.05 versus SCI at same time point.

Figure 1 shows changes in fat and CHO oxidation in response to MICE in both groups. Compared to the warm-up when fat oxidation ranged from 0.09 - 0.11 g/min, fat oxidation declined with onset of exercise (P < 0.001) and was maintained throughout the bout in both AB and participants with SCI. No group X time interaction was shown (P = 0.88) for the change in fat oxidation. The highest end-exercise rates of fat oxidation (0.07–0.15 g/min) occurred in participants with relatively high VO₂peak whether they were AB (VO₂peak ranging from 27–33 mL/kg/min) or had spinal cord injury (VO₂peak ranging from 15–24 mL/kg/min). Similar results were apparent for CHO oxidation which significantly increased from the warm-up (P < 0.001) and was maintained between 1.0–1.2 g/min in both groups, respectively, with no group X time interaction shown (P = 0.42).

Figure 1.

Changes in a) fat and b) CHO oxidation during 25 min of arm ergometry in able-bodied (AB) adults and those with spinal cord injury (SCI). Data are presented as mean ± SD.

Figure 2 shows the relative contribution of fat and CHO utilization towards energy expenditure during MICE. The contribution of fat peaked during the warm-up (40–45%) after which it declined to approximately 10% in both groups (P = 0.80 for interaction). Percent CHO contribution increased from the warm up (P < 0.001) to 86–90% during exercise and there was no group X time interaction (P = 0.39).

Figure 2.

Changes in a) fat and b) CHO oxidation as a percentage of total energy expenditure during 25 min of arm ergometry in able-bodied (AB) adults and those with spinal cord injury (SCI). Data are presented as mean ± SD.

Results showed that fat oxidation determined in the last stage of MICE (0.06 ± 0.04 g/min) was significantly associated (r = −0.46, P = 0.04) with overall exercise intensity expressed as %HRpeak (65 ± 9%) as well as fat oxidation during the warm-up (0.11 ± 0.05 g/min; r = 0.51, P = 0.02). There was a trend (r = 0.42, P = 0.07) for a relationship between absolute VO₂peak and fat oxidation; however, all other relationships between fat oxidation and variables including relative VO₂peak, BMI, BLa, and %VO₂peak were not significant (P = 0.19–0.36).

Blood lactate concentration: Results showed that BLa increased from pre- (1.2 ± 0.4 and 1.4 ± 0.6 mM in AB and SCI, respectively) to post exercise (3.0 ± 0.9 and 3.5 ± 1.1 mM, d = 2.7–3.0), yet there was no group X time interaction (P = 0.56).

Discussion

This study compared fat and CHO oxidation in response to a single bout of MICE in physically active individuals with SCI to able-bodied individuals unfamiliar with arm ergometry. In AB adults, low fat oxidation during exercise is related to diminished metabolic health.^8,25 A prior study²¹ showed that sedentary men with paraplegia reveal significant dependence on CHO oxidation during graded arm ergometry, yet higher rates of maximal fat oxidation in comparison to AB. In response to a 25 min bout of MICE, both groups showed heavy reliance on CHO oxidation and similar fat oxidation at workloads equal to 75–84%HRpeak which is a relatively high exercise intensity. However, participants with SCI were exercising at a higher fraction of peak HR and oxygen uptake which suggests some differences in the metabolic response to arm cycling in this population.

In both groups of participants, our results reveal that CHO is the predominant substrate oxidized during continuous, high intensity arm cycling and that the contribution of fat oxidation to energy expenditure is low (approximately 10%). Our results corroborate those obtained during passive and active exercise in persons with SCI³³ and from Jacobs et al.²¹ who reported mean RER equal to 0.97–1.03 during progressive arm ergometry at similar workloads (58 and 68%VO₂peak) to that exhibited by our participants with SCI. In contrast, a prior study in athletes with SCI²² showed maintenance of dramatically higher rates of fat oxidation (0.20 - 0.25 g/min) during progressive exercise at 55, 65, and 75%VO₂peak that would constitute almost 20–30% of total energy expenditure. However, participants in the Knechtle et al.²² study had a VO₂peak that was markedly higher than our entire sample and that used in the study by Jacobs et al.,²¹ which suggests that endurance training of the upper body seems to augment capacity for fat oxidation during arm ergometry in persons with SCI. This is supported by our results showing a positive relationship between VO₂peak and fat oxidation in all participants, which has also been reported in 300 AB adults completing progressive treadmill exercise to exhaustion (r = 0.26).³⁴ Therefore, it seems merited to promote regular physical activity in adults with SCI to enhance cardiorespiratory fitness which is related to capacity for fat oxidation.

A mechanism explaining the relatively low fat oxidation observed is beyond the scope of our investigation, yet several potential explanations exist. First, the intensity of this bout was relatively high despite the low power output used. At similar relative intensities (60–70%VO₂peak) implemented during continuous arm cycling, Kang et al.³⁵ reported RER ranging from 0.94–0.98 in young AB men and women with VO₂peak equal to 29 mL/kg/min. Second, in comparison to the lower body, it is apparent that the upper-body has a greater ratio of type 2 fibers and lower oxidative capacity³⁶ that enhances reliance on CHO utilization through glycolysis for ATP supply.² Third, our data show a significant increase in BLa recorded post-exercise that may inhibit fat oxidation.² Lastly, our participants were at least 3 h post-prandial when they performed continuous exercise which is within a duration where a prior meal could induce an increase in plasma insulin concentration and in turn, attenuate fat oxidation.³⁷ However, previous results³⁸ showed that pre-exercise CHO feeding did not alter fuel use during prolonged arm cycling in persons with SCI in comparison to water, so it is possible that this had little effect upon our results.

As stated above, our data showing similar fat and CHO oxidation during arm cycling expand on data from Jacobs et al.²¹ as a direct comparison of studies is inappropriate due to their use of progressive exercise which may elicit distinct metabolic responses versus steady-state continuous exercise. In their study, inactive men with SCI and AB adults unfamiliar with arm ergometry performed successive 3 min stages of progressive exercise at intensities ranging from 20–80%VO₂peak. Their results showed that compared to the AB individuals, men with paraplegia revealed higher maximal fat oxidation and a higher relative intensity at which peak fat oxidation occurred (41 ± 9%VO₂peak). While the current study did not use progressive exercise to compare maximal fat oxidation between groups, in our study continuous exercise was completed at a normalized moderate intensity allowing for isointensive comparison of fat oxidation between SCI and AB. Beyond the methodological differences between Jacobs et al.²¹ and the current study, there are additional potential explanations for the discrepant results across studies. Four of our ten AB participants habitually engage in surfing or martial arts that require repetitive and sustained contraction of the upper body, which may elicit increases in mitochondrial function of the upper extremity, in turn augmenting capacity for fat oxidation. Participants with SCI used in a prior study³⁸ exhibited significantly higher fat oxidation during arm ergometry than AB men, which was likely due to their 25% higher VO₂peak. Second, Jacobs et al.²¹ used different equations to calculate fat and CHO oxidation which may lead to dissimilar estimates of substrate utilization across studies. Third, our participants with SCI were exercising at higher %HR/VO₂peak than AB (see Results) despite being at an equivalent %PPO. This phenomenon also occurred in another study in AB men³⁹ documenting lower RER in cyclists compared to untrained adults at similar absolute yet not relative intensities (59 and 75%VO₂peak), suggesting that specific traits of the exercise bout performed including use of relative or absolute intensity may elicit unique responses between groups differing in cardiorespiratory fitness. In addition, adults with SCI may have a different relationship between HR, VO₂, and exercise intensity due to the loss of lower extremity neural regulation that may elicit an aberrant endocrine or catecholamine response from the adrenal medulla to acute exercise. Fourth, it is possible that the intensity was too high to exhibit any differences between our groups, yet Stisen et al.⁴⁰ identified higher fat oxidation in endurance-trained versus untrained women during cycling at similar intensities to those implemented in the current study. Nevertheless, higher intensity exercise enhances energy expenditure versus workloads commensurate with MFO which better suits individuals completing physical activity for weight control. Lastly, all participants in the Jacobs et al.²¹ study had paraplegia; whereas, our sample included two men with tetraplegia.

Data from AB adults reveal that engaging in exercise training increases capacity for fat oxidation and reduces reliance on CHO oxidation. In overweight men, Rosenkilde et al.⁴¹ showed that 12 wk of different doses of MICE led to significant increases in fat oxidation versus a control group. Similar findings have also been revealed in response to 12 wk of high intensity interval training in inactive women.⁴² Alternative populations showing exercise training-mediated increases in fat oxidation include women with diabetes⁴³ as well as obese boys⁴⁴ which may be related to improved metabolic health. Despite the low fat oxidation revealed in persons with SCI, no study has documented the magnitude of change in this outcome in response to exercise training, so additional study is warranted.

This study has a few limitations. Differences in fat and CHO oxidation were only studied at one intensity, so we cannot describe potential differences at lower or higher intensities of exercise or in response to different exercise modes such as electrical stimulation or circuit training. In addition, despite the use of similar intensities according to %PPO, our participants with SCI completed arm cycling at higher relative intensities versus AB, so different responses may be evident if exercise was prescribed according to an identical %VO₂peak. Our sample of adults with SCI included 2 men with tetraplegia whose peak HR and VO₂peak is much lower than the remainder of the participants, yet their substrate utilization data in response to exercise were similar to those with paraplegia, which led us to include them in data analysis. We required participants to undergo a 3 h fast before exercise, yet precise recording of participants’ physical activity patterns and dietary intake before the trial was not done. Only one woman in each group was recruited, so our data cannot comment on potential sex differences in substrate utilization during arm ergometry, as previously shown in AB adults.⁴⁵ Lastly, our AB participants were completely unfamiliar with arm cycling; whereas, some of our adults with SCI performed it regularly, so further study is merited to denote if differences in substrate oxidation exist between these groups when they are equally trained in arm cycling.

Conclusion

Our results show high reliance on CHO oxidation and low fat oxidation during continuous arm cycling in both adults with SCI and AB. No variable related to substrate utilization differed between groups, which suggests that a lower level of cardiorespiratory fitness characteristic of our participants with SCI does not attenuate capacity for fat oxidation versus AB adults who are unfamiliar with arm ergometry. We recommend that in studies comparing the metabolic response to exercise between persons with and without SCI, scientists prescribe exercise according to %HR/VO₂peak to standardize the intensity that may differ between groups and moreover, when they have similar values for VO₂peak and PPO.

Conflict of interest

No potential conflict of interest was reported by the author(s).