Review Article Volume 7 Issue 5
1Locum Consultant Urologist NHS- UK
2Physical activity and health promotion, Department of Biomedicine and prevention, Faculty of Medicine and Surgery, University of Rome Tor vergata. Rome, Italy
3Clinical Fellow in Urology, Western General Hospital UK
4Consultant Urologist, National Institute of Urology and Nephrology Cairo; Egypt
Correspondence: Abdalla Ali Deb, Locum Consultant Urologist NHS- UK
Received: October 06, 2019 | Published: October 30, 2019
Citation: Deb AA, Emmanuel O, Emara S, et al. Physical activity and prostate cancer: a systematic review. Urol Nephrol Open Access J. 2019;7(5):117-129. DOI: 10.15406/unoaj.2019.07.00258
Numerous studies confirmed that planned exercise therapy is a possible adjunct strategy connected with significant improvements in symptom-related results including exercise tolerance as well as several cancer patients-reported progress such as improvement in quality of life, and physical functioning during conventional adjuvant therapy. The aim of this review was to evaluate the association between physical activity and prostate cancer. Apart from lung cancer, prostate cancer is highly prevalent among men. We searched for original articles, systematic reviews, and meta-analyses that reported on exercise-mediated changes in the prostatic tumour risk and progression from 1980 to 2018. The following electronic databases was used: PubMed, Science Direct, Medline, Sports Discus, Web of Science, Google Scholar and Cochrane database. 85 studies written in English were included in this review. Patient’s cardio-metabolic profile, type of exercise, specific workloads, frequency, duration, intensity and safety precautions are factors to consider when scheduling an exercise program. Regular participation in physical activity is important in the prevention of prostate cancer and it is associated with positive treatment outcomes in patients undergoing Androgen deprivation therapy. Physical Activity may affect prostate cancer progression by reducing insulin resistance, decreasing bioavailable Insulin-like growth factor 1 (IGFI), increasing adiponectin levels and circulating levels of insulin. Interleukin 6 (IL-6) promotes cell proliferation and inhibits apoptosis of prostate cancer cells in vitro. Physical activity is associated with lower circulating IL-6. Based on the information examined in this study, physical activity may be an effective nonpharmacological means in the treatment of prostate cancer.
Keywords: physical activity, exercise, prostate tumor, cancer prevention
For the past 2 decades, improved research and clinical attention has focused on the effectiveness of exercise therapy as an adjunct approach for the treatment of cancer.1 Randomized trials validate that planned exercise therapy is a feasible adjunct tactic connected with significant improvements in symptom-related outcomes including exercise tolerance as well as multiple patient-reported treatment progress such as improvement in quality of life and physical functioning equally during conventional adjuvant therapy.2 In this review, we outline relevant studies related to exercise-mediated changes in the prostatic tumour risk and progression from 1980 to 2018. Prostate cancer is the second most prevalent form of cancer diagnosed among men after lung cancer.3 Androgen deprivation therapy (ADT) is applied in the treatment of patients in the advanced stage of prostate cancer. The side effects of ADT include erectile dysfunction,4 increase fat mass,5 and reduction in muscle strength.6 Combined resistance and aerobic exercise training program was effective in reversing muscle loss in men undergoing ADT due to prostate cancer.7 Pelvic floor/sphincter training is effective in plummeting incontinence in patients with prostate cancer.8,9 The molecular mechanisms behind the positive effects of exercise training programs in addition to ADT has not been well understood, however there was a decrease in inflammation due to low nuclear factor-κB activation in LNCaP cells incubated with post-exercise serum10 and suppressed growth and increased apoptosis of LNCaP cells incubated with post-exercise serum.11 Exercise alters p53, p21 and caspase activities resulting in tumour growth inhibition, tumour apoptosis, tumour suppression and suppressed metastasis.12,13 Physical activity was effective in reducing prostate carcinogenesis in transgenic model.14 The demonstration of possible mechanisms whereby exercise alters the progression of carcinogenesis might strengthen the clinical outcome of cancer treatment.
Exercise could also result to reductions in obesity and oxidative stress and a modulation of immune responses in prostate cancer patients.15 Exercise causes reductions in circulating levels of testosterone and insulin-like growth factors16,17 therefore reducing the development and spread of neoplastic cells. Apart from exercise, testosterone levels are controlled by diet,18 and this may contribute to variances in exercise response among various populations.19 The aim of this review was to evaluate the association between physical activity and prostate cancer. In this review, we outlined relevant studies concerned about exercise-mediated changes in prostatic growth and progression from 1980 to 2018. These mediated changes are linked to the role of consistent physical activity in improving the quality of life, physical fitness and averting the progression of prostate cancer among individuals diagnosed of prostate cancer.
Search strategy
We searched for studies that reported on exercise-mediated changes in the prostatic tumour risk and progression from 1980 to 2018. The following electronic databases was used: PubMed, Science Direct, Medline, Sports Discus, Web of Science, Google Scholar and Cochrane database. The following search strategy was modified for the various databases and search engines: Prostate cancer, exercise, physical activity, cancer, prostate tumour, cancer prevention, and cancer adjunct therapy. We assessed Full articles and extracted relevant data. We used the MeSH system to extract relevant research studies indexed in PubMed.
Types of studies
Original articles, systematic reviews, and meta-analyses.
Inclusion and exclusion criteria
We selected precise articles that described physical activity and prostate growth, exercise therapy in support of the clinical treatment of prostate cancer and exercise prescription for prostate cancer patients. The selected articles were all written in English. Articles that were not precise, uncertain and with doubtful experimental procedure were excluded. 85 studies were included in this review.
Data extraction and management
We designated all trials retrieved from the databases. We reviewed for relevance based on physical activity and prostate cancer progression, cancer prevention, exercise therapy for prostate cancer patients undergoing ADT and radiotherapy. We retrieved full-text copies of all the articles recognised as hypothetically relevant in this review. Data was reported in a narrative and concise manner. The selection process was elucidated in a Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) flow diagram (Figure 1).
The effectiveness of exercise prescription and dosing for patients diagnosed with prostate cancer
Patient’s cardio-metabolic profile, type of exercise, specific workloads, frequency, duration, intensity and safety precautions are factors to consider when planning an exercise program. Regular involvement in physical activity is vital in the prevention of prostate cancer and it is connected with positive treatment results in patients undergoing ADT.20 Patients diagnosed with prostate cancer should accumulate at least; 150 min per week of moderate-intensity aerobic exercise or 75 min per week of vigorous aerobic exercise, or both, this is in accordance with the reference exercise strategies prescribed by the American College of Sports Medicine (ACSM) for cancer patients.21,22 Cardiovascular diseases are the leading cause of death in men with prostate cancer23 and exercise performed according to the standard prescription improves cardiovascular fitness and averts cardiovascular deaths.24 Galvao et al.25 found a significant increase in muscle strength in prostate cancer patients allocated to the group that took part in chest press, a significant increase in muscle stamina was detected in the group that participated in chest press, there was significant increase in Muscle thickness at the quadriceps position. There was substantial development in general cardiovascular fitness, flexibility, muscle strength, quality of life, and drastic reduction in fatigue among prostate cancer patients undertaking radiotherapy after undergoing an 8-week cardiovascular exercise-training program.26 A randomised controlled trial conducted by Segal et al.27 in which Prostate cancer patients completed resistance exercise training 3 times per week, demonstrated global progresses in quality of life, muscular strength, body fat ratio decrease and lessening in fatigue in the group that partook in resistance exercise and are undertaking radiotherapy, both aerobic and resistance training was found to lessen fatigue. A personalized exercise-training program planned and prescribed according to patients’ cardio-metabolic and functional capacity might be more effective in the treatment of prostate cancer.28 The ideal approach and dosage of exercise for patients diagnosed of prostate cancer has not been established.
Selected studies on physical activity and prostate cancer
According to the World Health Organization (WHO), physical activity is any physical movement produced by skeletal muscles that involves energy expenditure.29 Based on experimental and clinical studies, physical activity averts the progression of prostate cancer by changing molecular mechanisms resulting to the suppression of tumour growth. In tabulating available epidemiological facts, we categorized them by type of study (cross-sectional, prospective cohort, or case–control) and by findings (an adverse effect, no clear response, a positive trend), and a statistically significant decrease of risk in the more active individuals. There have been many cross-sectional or cohort studies relating occupation to the risk of prostate cancer (Table 1). Leisure-time physical activity have also been linked with the risk of developing prostate cancer based on cohort studies (Table 2). Four retrospective and cohort studies of sport involvement and fitness realization was critically analysed (Table 3)., two of these information found no benefit from sport involvement,70 but Wannamethee et al.64 noted a considered outcome on the reported frequency of sport participation, However, the fourth report observed that a beneficial effect was connected with a high-attained level of aerobic fitness.71
Author |
Sample |
Activity measure |
Outcome |
Comments |
Cohort studies Negative findings |
||||
Hartman et al.30a |
29,133 male smokers, aged 50–69 years followed for an average of 6.1 years; 317 incident cases of PC |
Self-report, sedentary job vs. occupational walkers vs. walkers/lifters vs. heavy laborers |
RR 1.0, 0.6, 0.8, 1.2 (ns) of prostate cancer as stated by Finnish cancer registry |
Attuned for age, urban living, smoking, benign prostate hyperplasia |
Johnsen et al.31a |
127,923 men, aged 20–97 years, followed for 8.5 years; 2458 cases of PC |
Two classifications by interview or questionnaire: sitting, standing, or manual work; inactive, moderately inactive, moderately active, active |
Occupational activity not significantly related to PC (OR manual 0.90 (0.77–1.04), p =0.15 for trend) |
Attuned for leisure activity, height, weight, marital status, education |
Nielsen et al.32a |
22,895 Norwegian men aged 40 to >80 years followed for 9.3 years; 644 cases of PC |
Modest binary classification (high vs. low level of occupational activity) |
No effect of occupational activity ((high RR 1.04 (0.82–1.32); augmented risk in high vs. low education, RR 1.50 (1.11–2.19) |
Age-adjusted relative risks |
Putnam et al.33a |
101 cases of PC were conveyed to State register office,1572 initially cancer-free men aged 40–86 years, followed for 4 years |
Very energetic, ascetically active, or inactive at work, based on work-related codes |
PC unrelated to occupational activity (RR for very active 1.0 (0.6–1.8)) |
Adjusted for age |
Zeegers et al.34a |
58,279 men aged 55–69 years, 1386 cases of PC over 9.3 years of follow-up |
Work-related activities (estimated energy expenditure, sitting time for longest held and for most recent job) |
RRs longest held: >12 vs. <8 kJ/min 0.91 (0.70–1.18) Sitting <2 vs. >6 h/day1.16 (0.91–1.47) |
Attuned for age, alcohol drinking, BMI, energy intake, family history, education |
Positive trend |
||||
Grotta et al.35a |
13,109 Swedish men, initially aged 55 years, surveyed for 13 years; 904 cases of PC |
Low vs medium vs. high level of work-related activity |
HR for high activity 0.81 (0.61–1.07, ns), medium 0.96 (0.77–1.20) |
Attuned for age, education, smoking, BMI, alcohol consumption, diabetes mellitus |
Hrafnkelsdóttir et al.36a |
24-year follow-up of 8221 Icelandic men initially aged 33–79 years; 1052 cases of PC |
Work includes mostly sitting vs standing vs on the move |
HR 1.0, 0.97 (0.80–1.17), 0.91 (0.79–1.06), ns |
Attuned for age, height, BMI, diabetes, family history, education, medical check-ups |
Significant positive findings |
||||
Clarke et al.37a |
5377 men firstly, aged 25–75 years surveyed for 17–21 years; 201 cases of PC |
Very active vs. sedentary |
RR for inactive 1.75 (1.12–2.67), p=0.05 for trend (outcome larger in African Americans) |
Attuned for age, education, ethnicity, family history |
Norman et al.38 |
3 cohorts containing 43,836, 28,702, and 19,670 cases of PC |
Work-related designations (inactive, medium, to very high level of activity) |
RR for sedentary vs. high/very high groups 1.11, 1.10, and 1.11 (p=0.0001 for all three groups) |
Attuned for age, year of follow-up, area of residence |
Orsini et al.39a |
45,887 men aged 45–79 years, surveyed for 8 years; 2735 incident cases of PC |
4 categories of occupation (mostly sitting vs. heavy manual) |
RR=0.72 (0.57–0.90); p=0.007 for trend; effects smaller for advanced and fatal cancers |
Attuned for leisure activity, age, smoking, alcohol consumption, education, diet, energy intake, waist/hip ratio, diabetes mellitus |
Parent et al.40a |
449 incident cases of PC; aged 59 years |
High vs. medium vs. low lifetime occupational activity, metabolic equivalents (METs) |
OR intermediate 0.64 (0.41–0.98), high 0.54 (0.31–0.95) |
Data attuned for age, sex, education, ethnicity, smoking, BMI, outdoor activities |
Vidarsdottir et al.41 |
60,194 men initially aged 20–64 years followed for 23 years |
Educational level (basic, medium, high) |
SIR basic =0.92 (0.84–0.99), academic =1.17 (1.05–1.30) |
Greater diagnosis in highly educated group |
Case–control studies Adverse findings Negative findings |
||||
Doolan et al.42 |
1436 cases of PC aged 39–70 years, 1349 coordinated controls |
Finnish occupation background, physical capacity classified by tertiles |
OR highest tertile workload 1.15 (0.95–1.40), ns |
Attuned for age, family history, economic resources |
Hosseini et al.43 |
137 cases of PC, 137 locality controls, men <70 to >80 years |
Walking to work (<10 vs. >10 h/week), intensity of work (sedentary/moderately active vs. highly active) |
OR 0.7 (0.4–1.2) for longer walk (ns), OR=6.7 (1.3–35.1) for highly active work (p=0.02) |
Multivariate adjusted |
Lacey et al.44a |
258 cases of PC, 471 age-matched controls, aged 50–94 years |
Sedentary, moderate, or high work-related energy expenditures at ages 20–29 years, 40–49 years, or 12 years ago |
RR 1.1 (0.7–1.7), 1.3 (0.8–1.9), 0.9 (0.5–1.8) of high vs. sedentary group |
Attuned for age, marital status, education, BMI, energy intake, waist/hip ratio |
Sass-Kortak et al.45 |
760 PC cases aged 50–84 years, 1632 telephone book controls |
Quartiles of lifetime work-related activity |
Active vs. least active workers OR 1.33 (1.02–1.74), p=0.18 for trend) |
Attuned for age, family history, sunlight exposure |
No effect |
||||
Friedenreich et al.46a |
988 cases of PC, histologically confirmed, 1063 population controls |
Energy expenditure <74.2 vs. >161.9 MET h/week |
OR 0.90 (0.60–1.22), ns |
Attuned for age, region, education, BMI, waist/hip ratio, energy intake, alcohol drinking, family and medical history |
Positive trend |
||||
Lagiou et al.47 |
320 histologically confirmed cases pf PC aged <60 to >80 years, 246 hospital controls |
Low, medium, high level of job-related activity |
OR low =1.0, medium =0.95 (0.49–1.84), high =0.69 (0.40–1.22), ns |
Attuned for age and education |
Wiklund et al.48a |
1449 incident cases of PC in men aged 35–79 years, 1118 population controls |
METs h/day of lifetime work-related activity, <11.8, <14.8, <19.8, >19.8 |
OR 1.0, 0.81 (0.65–1.08), 0.87 (0.66–1.15) 0.84 (0.61–1.15), ns |
Attuned for age, region, education, BMI, alcohol consumption, family history, diabetes mellitus, energy intake |
Significant positive findings |
||||
Bairati et al.49 |
64 cases of PC, 5456 cases of benign prostate hyperplasia aged >45 years |
(a) inactive job or light work; (b) 0, 1–49%, >50% of profession spent in inactive or light work |
(a) OR 2.0 (1.1–3.6); 1.0, 1.7 (0.8–3.2), OR 2.8 (1.3–6.0) (p=0.007 for trend) |
Attuned for age, education, total energy intake, smoking, use of vitamin supplements |
Krishnadasan et al.50 |
362 cases of PC, 1805 matched controls; age not specified |
Low vs. moderate vs. high work-related energy outflow |
OR high 0.63 (0.40–1.00), moderate 0.96 (0.7–1.3), p=0.06 for trend) |
Attuned for matching variables, pay, trichloroethylene exposure |
Pierotti et al.51a |
1294 incident cases of PC aged <75 years and 1451 hospital controls |
3-level categorization of work-related activity at ages 12, 15–19, 30–39, and 50–59 years |
OR age 12 years = 0.84 (0.67–1.06), age 15–19 years =0.94 (0.75–1.17), age 30–39 years =0.78 (0.63–0.97), age 50–59 years = 0.75 (0.61–0.93) |
Attuned for age, test centre, education, Sex, BMI, total energy intake, smoking, alcohol consumption, family history |
Strom et al.52a |
176 cases of PC in Mexican Americans, 176 controls, age ~ 62 years |
None/low vs. moderate/high energy demands of labour |
Reduced risk in active (OR 0.46, 0.28–0.77), p=0.003) |
Attuned for age, education, screening, exposure to agricultural chemicals |
Villeneuve et al.53a |
1623 histologically confirmed cases of PC, 1623 controls, aged 50–74 years |
4-level classification of work (sitting to energetic) |
Significant advantage from strenuous activity in teens or early 20 s, (OR light 0.8 (0.5–1.3), moderate 0.8 (0.5–1.2), strenuous 0.6, 0.4–0.9), ns for 30 s (0.7), 50 s, (0.8) or 2 years before interview (0.9) |
Attuned for age, area of residence, smoking, alcohol consumption, BMI, diet, income, family history |
Table 1 Occupational activity and the risk of developing prostate cancer
HR, hazard ratio; MET, metabolic equivalent, ns not significant; OR, odds ratio; PC, prostate cancer; PMR, proportionate mortality ratio; RR, relative risk or rate ratio; SES, socioeconomic status; SIR, standardized incidence ratio
Author |
Sample |
Activity measure |
Findings |
Comments |
Cohort studies Adverse trend Negative findings |
||||
Crespo et al.54 |
9824 men initially aged 35–79 years followed for death |
Framingham index (quartiles) |
No association between physical activity and prostate deaths |
Adjusted for age, education, urban residence, smoking, BMI |
Giovannucci et al.55 |
47,452 health experts initially aged 40–75 years, followed for 8 years; 1362 cases of PC |
Leisure activity, 1 vs. 46.8 MET h/week |
No significant association to PC except idea of less metastatic activity and lower Gleeson score with vigorous intensity exercise |
Attuned for age, vasectomy, diabetes mellitus, smoking, energy intake, diet |
Grotta et al.35b |
13,109 Swedish men, initially aged 55 years, tracked for 13 years; 904 cases of PC |
Low vs. high leisure activity |
HR 0.93 (0.76–1.14, ns) for incident PC if high physical activity |
Attuned for age, education, smoking, BMI, alcohol drinking, diabetes mellitus |
Johnsen et al.31a |
127,923 men, median initial age 61 years, followed for 8.5 years; 2458 cases of PC |
Quartiles of leisure activity (<25 to >71 MET h/week) |
Leisure activity unrelated to incident PC |
Attuned for work-related activity, height, weight, marital status, education |
Lee et al.56 |
8922 Harvard alumni, mean age 67 years; 439 developed PC during 5 years of follow-up |
Physical activity questionnaire completed twice, weekly energy expenditure quartiles (<4.2 MJ to >12.6 MJ) |
PC disparate to total volume of physical activity or weekly volume of vigorous physical activity |
Accustomed for age, BMI, smoking, alcohol consumption, family history |
Littman et al.57 |
34,757 men initially aged 50–76 years; 583 cases of PC |
MET h/week, walking pace, stair climbing, high-intensity activity, activity at earlier ages |
No association with PC except in sub-group aged >65 years with normal body mass |
Attuned for family history, BMI, income |
Liu et al.58 |
982 cases of PC in 22,071 physicians aged 40–84 years over 11 years of follow-up |
Exercise sufficient to cause a sweat <1/week. vs. >5/weeks |
No relationship of frequent activity to incidence of PC |
Adjusted for smoking, alcohol drinking, height, diabetes mellitus, high cholesterol, hypertension, use of multi-vitamins |
Parent et al.40b |
449 incident cases of PC among 3730 cancer patients |
participation in sports and outdoor activities (never or not often vs. often) |
No significant consequence on risk of PC |
Covariates age, SES, education, ethnicity, smoking, BMI |
Platz et al.59 |
46,786 health professionals, initially aged 40–75 years; 2896 incident cases of PC over 14 years |
Vigorous leisure activity <3, >3 MET h/week |
No relationship to PC |
Attuned for age, family history, BMI, diabetes mellitus, smoking, diet |
Putnam et al.33b |
101 cases of PC in 1572 initially cancer-free men, originally aged 40–64 years, followed for 4 years |
Very active, moderately active, inactive |
Risk of PC unrelated to leisure activity |
Attuned for total energy intake |
Positive trends |
||||
Clarke et al.37b |
5377 men, aged <50 to >70 years, followed for 17–21 years; 201 cases of incident or fatal PC |
Much vs. moderate vs. little or none |
RR much 1.00, moderate 1.10 (0.75–1.61), inactive 1.17 (0.80–1.72), ns |
Attuned for age, education, ethnicity, family history |
Giovannucci et al.60 |
47,620 health specialists, initially aged 40–75 years, 14 years of follow-up; 2892 incident cases of PC (482 advanced, 280 fatal) |
Vigorous physical activity, 0 vs. >29 MET h/week |
No relationship for all subjects; if >65 years, OR for advanced cancer 0.33 (0.17–0.62) |
Age, BMI, smoking, height, family history, diabetes mellitus, ethnicity, non-vigorous activity, energy intake and diet |
Hrafnkelsdóttir et al.36b |
24 years of follow-up of 822 Icelandic men initially aged 33–79 years; 1052 cases of PC |
Regular physical activity from age of 20 years vs. sedentary |
HR 0.93 (0.83–1.07) for all PC in active individuals, 0.82 (0.63–1.06) for advanced cancers |
Accustomed for age, height, BMI, diabetes, family history, education, medical check-ups |
Nielsen et al.32b |
22,895 Norwegian men, initially aged 40 to >80 years, followed for 9.3 years; 644 cases of PC |
High vs. low leisure activity |
RR 0.80 (0.62–1.03) |
Multivariate adjusted |
Moore et al.61 |
293,902 men initially aged 50–71 years followed for up to 8.2 years; 17,872 cases of PC |
Exercise at starting point and in adolescence (never/rarely to >5 times/week) |
RR of total cases 0.97 (0.91–1.03), p=0.03 for inclination supporting frequent activity during adolescence, but no relationships to exercise habits at baseline |
Accustomed for age, marital status, education, smoking, medical history, BMI, waist circumference, family history, diet and supplements |
Nilsen et al.62 |
29,110 Norwegian men, initially mean age 52 years, followed for 7 years; 957 incident cases of PC |
Activity score based on frequency, intensity and duration of activity (low vs. high) |
Connected to total cancer cases (RR=0.86), but for advanced cancer RR=0.64 (0.43–0.95), p=0.02 for inverse trend |
Attuned for age, marital status, education, BMI, smoking, alcohol consumption |
Patel et al.63 |
72,174 men, initial mean age 64 years; 5503 incident cases of PC over 9 years |
MET h/week (<0.7–35) at age 40 years |
No significant effect (but active have fewer hostile tumours, RR 0.69 (0.52–0.92), p=0.06 for trend |
Accustomed for age, ethnicity, BMI, weight change, energy intake, diet and vitamin use, diabetes mellitus, family and medical history |
Zeegers et al.34b |
58,279 men initially aged 55–69 years; 1386 cases of PC over 9.3 years |
Cycling/walking (min/day), gardening (h/week) |
Gardening unrelated to PC; biking/walking <10 vs. >60 min/d, RR 0.85 (0.69–1.05), ns |
Accustomed for age, alcohol drinking, BMI, energy intake, family history, gardening, sport participation |
Significant positive findings |
||||
Hartman et al.30a |
29,133 male smokers, initially aged 50–69 years, followed for up to 9 years; 317 cases of PC |
Inactive vs, moderate/heavy leisure activity in working men |
RR 0.7 (0.46–0.94) favoring active leisure |
Attuned for age, urban living, smoking, benign hyperplasia |
Orsini et al.39b |
45,887 men, initially aged 45–79 years, followed for 8 years; 2735 incident cases of PC |
Walking or cycling, 5 categories (hardly ever to >60 min/day) |
RR=0.86 (0.76–0.98), p=0.028 for trend; effects greater for advanced (RR=0.74) and fatal (RR=0.72) cancers |
Attuned for work-related activity, age, smoking, alcohol drinking, education, diet, energy intake, waist/hip ratio, diabetes mellitus |
Wannamethee et al.64a |
Potential study of 7588 men aged 40–59 years; 120 incident cases of PC |
6-level classification of leisure activity from none to vigorous |
Advantage from vigorous activity, OR 0.25 (0.06–0.99, p=0.06 for trend |
Attuned for age, smoking, alcohol consumption, BMI, social class |
Case–control studies Adverse findings |
||||
Chen et al.65 |
237 cases of PC, 481 controls aged >50 years |
Mainly a dietary study: 4-level categorization of physical activity |
Adverse effect of high vs. moderate exercise: OR 1.84 (1.01–3.34) |
Multivariate analysis (age, BMI, income, marriage, dietary variables) |
Wiklund et al.48b |
1449 incident cases of PC, 1118 population controls, mean age 67–68 years |
MET h/day lifetime recreational activity, <7.4 to >13.5 |
OR <7.4=1.0, <10.2=1.33 (1.00–1.78), <13.5=1.43 (1.07–1.91), >13.5=1.56 (1.16–2.10), p=0.006 for adverse effect of active leisure |
Attuned for age, region, education, BMI, alcohol consumption, family history, diabetes mellitus, energy intake |
No clear effect |
||||
Lacey et al.44b |
258 cases of PC, 471 age-matched controls, aged 50–94 years |
Tertiles of moderate/vigorous or all physical activity at age 20–29 years, age 40–49 years, and 12 years ago |
No association to PC |
Attuned for age, marital status, education, BMI, energy intake, waist/hip ratio |
Pierotti et al.51a |
1294 incident cases of PC aged <75 years and 1451 hospital controls |
3-level classification of physical activity at ages 12, 15–19, 30–39, and 50–59 years |
No effect on risk of PC at any age |
Accustomed for age, test center, education, SES, BMI, total energy intake, smoking, alcohol drinking, family history |
Sanderson et al.66 |
416 incident cases of PC, 429 Medicare beneficiary controls aged 65–79 years |
Tertiles of strenuous and of moderate physical activity (h/week) |
No relationship to PC in either African American or Caucasian men |
Adjusted for age, geographic region, family history |
Strom et al.52b |
176 cases of PC in Mexican Americans, 176 controls, age ~ 62 years |
Leisure activity (<1/week vs. >1/week) |
No effect on risk of PC |
Attuned for age, education, screening, work-related activity |
Villeneuve et al.53b |
1623 histologically confirmed cases of PC, 1623 controls, age 50–74 years |
5-level classification (<1/month to >5/week) |
No clear relationship to PC |
Accustomed for age, area of residence, smoking, alcohol consumption, BMI, diet, income, family history |
Positive trends |
||||
Friedenreich et al.46b |
988 incident cases of PC, 1063 population controls, mean age 67 years |
<78.5 vs. >25.1 MET h/week |
OR 1.00, 0.80 (0.61–1.04), p=0.06 for trend |
Accustomed for age, region, education, BMI, waist/hip ratio, energy intake, alcohol drinking, family and medical history |
Significant positive findings |
||||
Darlington et al.67 |
752 cases from Ontario cancer registry aged 50–84 years, telephone listing controls |
Strenuous activity mid-teens, early 30 s, early 50 s (yes/no) |
OR for strenuous activity in teens =1.0 (0.8–1.2), early 30 s=0.9 (0.7–1.0), early 50 s=0.8 (0.6–0.9). |
Attuned for age, education, BMI, family history, occupation |
Jian et al.68 |
130 histologically confirmed cases of PC, 274 controls, aged <65 to >75 years |
Reported MET hours of moderate and total activity (<40 vs >120; <44 vs. >135) |
OR moderate activity <40=1.0, <80=0.47 (0.22–1.02), <120=0.46 (0.21–0.99), >120=0.20 (0.07–0.62), p=0.015, Total activity <44=1.0, <90=0.42 (0.18–0.99), <135=0.36 (0.16–0.86), >135=0.39 (0.15–0.99), p=0.50 for trend) |
Accustomed for age, area of residence, education, salary, marital status, number of children, years in labour force, family history, BMI, energy intake |
Yu et al.69 |
1162 cases of PC; 3124 matched hospital controls, age <45 to >75 years |
Leisure activity (active, moderate, or seldom) |
Risk higher in sedentary (OR seldom = .3 (1.0–1.6), moderate = 1.1 (0.9–1.3) active = 1.0 (p=0.03) |
Attuned for age |
Table 2 Leisure-time physical activity and the risk of developing prostate cancer
BMI, body mass index; HR hazard ratio; MET, metabolic equivalent; ns non-significant; NHANES, National Health and Nutrition Examination Survey; OR, odds ratio; PC, prostate cancer; RR, relative risk; SES, socioeconomic status
Author |
Sample |
Activity measure |
Findings |
Comments |
Cohort studies |
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Merrill et al.70 |
PSA levels of 536 partakers in senior citizen games aged >50 years |
Years active >3 times/week |
Total physical activity unrelated to PSA levels |
Attuned for age |
Wannamethee et al.,64b |
Potential study of 7588 men aged 40–59 years; 120 incident cases of PC |
Sporting activity (none, >1/month, >1/week, >2/week) |
RR none =1.00, <1/month =0.98, >1/month to 1/week =0.63, >2/week =0.53, p=0.05 |
Attuned Age, smoking, alcohol, BMI, SES |
Zeegers et al.34c |
58,279 men aged 55–69 years; 1386 cases of PC over 9.3 years |
Sport involvement (never/ever; frequency; duration, year) |
Sport involvement unrelated to PC |
Attuned for age, alcohol consumption, BMI, energy intake, family history, education |
Case-control studies |
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Hållmarker et al.72 |
185,412 partakers in Vasaloppet ski contest and 184,617 non-participants |
1827 vs. 1435 cases PC |
HR 1.22 (1.13–1.30) backing non-participants |
Non-participants matched for age, sex, county of residence |
Galvão73 |
57 prostate cancer patients, aged 70.0±8.4 year |
Randomized to multimodal supervised aerobic, resistance, and flexibility exercises undertaken thrice weekly (exercises (EX); n=28) or usual care (care controls (CON); n=29) for 3 months. |
A significant difference between groups for self-reported physical functioning (3.2 points; 95% confidence interval, 0.4–6.0 points; P=0.028) and lower body muscle strength (6.6 kg; 95% confidence interval, 0.6–12.7; P=0.033) at 3 months favouring EX. |
With bone metastases |
Table 3 Sports involvement, attained aerobic fitness, and risk of prostate cancer
BMI, body mass index; HR, hazard ratio; ns non-significant; PC, prostate cancer; PSA, prostate serum antigen; RR, relative risk; SES, socioeconomic status; EX, exercises
Possible biological mechanisms linking exercise and prostate cancer
EL Richman et al.74 Observed that walking pace was related to a lesser risk of prostate cancer independently of walking period, they stated that men who walked 3 or more hours/week at a brisk pace had a 57% lower risk of prostate cancer. Physical Activity may affect prostate cancer progression by reducing insulin resistance, decreasing bioavailable Insulin-like growth factor 1 (IGFI), increasing adiponectin levels and circulating levels of insulin75 (Figure 2). Interleukin 6 (IL-6) promotes cell proliferation and inhibits apoptosis of prostate cancer cells in vitro;76 however, physical activity is associated with lower circulating IL-6.77 There is an increase in tumor blood flow in animal models, during intense endurance exercise, due to the change in vasculature, thus causing an upsurge in tumor perfusion and oxygenation and in turn decreases the propensity for metastasis.78 Regulation of tumor vasculature might be a likely biological mechanism through which exercise prevents prostate cancer progression. Elevated serum levels of IGF-1, leptin and insulin are related to higher risk of prostate cancer progression.79,80 LNCaP cells cultured with post exercise serum, expresses reduction in cell proliferation and increased apoptosis.81
Exercise lessens the side effects associated with androgen deprivation treatment for Prostate cancer.82 Aerobic exercise exerts cardio-protective effects in animal-subjected to ADT.83 Exercise results to an upsurge in the production of sex hormone–binding globulin (SHBG), dropping testosterone levels.84 Exercise boost antioxidant-enzyme repair mechanisms and drops lipid peroxidation levels, in turn plummeting free radicals and minimizing oxidative stress.85 Regular physical activity combined with lifestyle adjustment and exogenous natural supplements in addition to the pharmacological, surgical and radiotherapeutic treatment of prostate cancer may enable clinicians to attain the anticipated treatment goal.
Based on the information obtained and analysed in this study, a practical exercise and activity goal personalized for prostate cancer patients to increase their chances of survival would be a multidimensional tactic to decrease central adipose tissue deposition and to lessen circulating levels of inflammation, insulin, and unfavourable sex hormones. Further studies aimed to assess the most effective exercise therapy and actual dose, personalised according to patients’ clinical status for averting prostate cancer progression are vital in order to develop a comprehensive prevention and treatment goal for prostate cancer. Physical activity levels, ranging from walking to more intense activities and exercise routines, offers unique benefits. data from Randomized trials continue to accumulate regarding the positive effects of exercise on treatment outcomes for men with prostate cancer and the implementation of exercise during and after treatment for prostate cancer ought to be part of the standard of care and treatment goal. The radiation oncologists are provided with exceptional chance to restate healthy lifestyle methods and modifications owing to the extensive time spent with patients on a weekly basis during treatment. Prostate cancer treatment is one of the lengthiest treatment regimens, and the oncologist is given several opportunities to recommend and aid to implement exercise and lifestyle changes.
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The author declares there is no conflict of interest.
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